A MANUAL 
OF 
DISEASES OE THE NERVOUS SYSTEM “It may be said, without reserve, that this work is the most clear, concise, 
and complete text-book upon diseases of the nervous system in any language. 
And when the large number of such works which have appeared in Germany, 
France, and England within the past ten years is considered, this implies high 
praise.”—The American Journal of the Medical Sciences. 
NOW READY. 
THE SECOND EDITION OF VOL. II OF THIS WORK, 
DEALING WITH DISEASES OF THE BRAIN, CRANIAL NERVES, GENERAL AND 
Functional Diseases. Octavo. 1000 pages. Cloth, $4.50. A MANUAL 
OF 
Diseases of the Nervous System 
BY 
W. R. GOWERS, M.D., F.R.C.P., F.R.S. 
CONSULTING PHYSICIAN TO UNIVERSITY COLLEGE HOSPITAL; PHYSICIAN TO THE NATIONAL 
HOSPITAL FOR THE PARALYZED AND EPILEPTIC 
SECOND EDITION 
REVISED AND ENLARGED 
VOLUME I 
DISEASES OF THE NERVES AND SPINAL CORD 
WITH ONE HUNDRED AND EIGHTY ILLUSTRATIONS, INCLUDING 
THREE HUNDRED AND SEVENTY FIGURES 
PHILADELPHIA 
P. BLAKISTON, SON & CO. 
1012 WALNUT STREET 
1895 Note.—The illustrations of which the source is not stated are original, and 
part of the copyright of the hook. 
PRESS OF WM. F. FELL & CO., 
1220-24 SANSOM STREET, 
PHILADELPHIA. PREFACE TO THE SECOND EDITION. 
The delay that has occurred in the appearance of this volume 
is due to the amount of work that has been expended upon it, 
and the time this has necessarily taken. The whole book has 
been thoroughly revised; many parts have been re-written; 
and additions have been made, the extent of which is shown by 
the fact that the volume is increased in size by about 150 pages. 
These additions, besides those in every chapter and on almost 
every page, include new sections on Multiple Neuritis (extending 
over 50 pages), Beri-beri, Brachial Neuritis, Senile Paraplegia, 
Morvan’s Disease, and the Peroneal Type of Muscular Atrophy, 
as well as extensive additions to the account of the Functions of 
the Spinal Cord and the Symptoms of its Diseases, of Syringo- 
myelia, Tumours, Muscular Dystrophy, Traumatic Lesions, &c. 
An attempt has been made to incorporate the results both of the 
author’s personal experience, and also of the observations and 
investigations of others, during the past five years, especially 
those that are of chief importance and have yielded definite 
facts, either of present significance or future promise. In 
making these alterations and additions, the special aim of the 
work, as stated in the Preface to the first Edition, and especi- 
ally the needs of both the student and the practitioner, have 
constantly been kept in view. 
For most useful and able assistance in the revision of the 
later portion of the book, I have to thank Dr. Risien Russell. 
To Dr. James Taylor I am also indebted for similar help, and 
also for the new and more extensive index, which must facilitate 
the use of the book. 
W. R. GOWERS. 
50, Queen Anne Street, London- 
December, 1891. PREFACE TO THE EIRST EDITION. 
This volume contains the first part of an attempt to give an 
account of diseases of the nervous system, sufficiently concise to 
be within the compass of the time-pressed student or busy prac- 
titioner, and yet adequate in its outline of a subject which has 
become wide and deep beyond any other part of medicine. 
Success in both aims can scarcely be more than approximate. 
Most of the illustrations are printed from blocks prepared from 
original drawings by phototype processes, and I am indebted to 
Messrs. A. and W. Dawson, of the Typographic Etching Com- 
pany (by whom most of the work has been done) for the care they 
have taken in the reproduction. 
The casual reader may perhaps miss subsidiary letters in the 
illustrations of the lesions of the spinal cord. The omission of 
these is intentional. A knowledge of the structural topography 
of the cord is the first requisite in the study of its morbid 
anatomy, and when this knowledge is gained, the figures will be 
understood without difficulty. Familiarity with unlettered illus- 
trations facilitates the comprehension of sections of the spinal 
cord. 
Queen Anne Stbeet, London} 
August, 1886. CONTENTS. 
PAGE 
INTRODUCTION . . . . . . 1 
Classification of Diseases of the Nervous System, 2 
PART I.—GENERAL SYMPTOMATOLOGY . . .4 
Symptoms and their Investigation . . .4 
Motor Symptoms . . . . .4 
Inco-ordination of Movement, 7 
Sensory Symptoms . . . . .8 
Tactile Sensibility, 8 ; Sensibility to Pain, 10 ; Sensibility to 
Temperature, 10 ; Muscular Sensibility, 11 
Reflex Action . . . . .13 
Cutaneous Reflex Action, 14 ; Muscle Reflex Action— 
“ Tendon-reflexes,” 15 ; Paradoxical Muscular Contrac- 
tion, 21 
Changes in Nutrition . . . . .22 
Electrical Irritability . . . . .24 
Muscles: their Action and Paralysis . . .26 
Muscles moving the Upper Limb, 27 ; the Lower Limb, 38 
PART II.—DISEASES OP THE NERVES . . .46 
General Pathology . . . . .46 
Structure of Nerves, 46 ; Physiology of Nerves, 47 ; Lesions of 
Nerves, Secondary Degeneration, 48 
Symptoms of Nerve-injury and Degeneration . 64 
Electrical Changes, 54 ; Sensory Symptoms, 60; Reflex Action, 
61; Vasomotor and Trophic Disturbance, 61 
Injuries of Nerves . . . . .62 
Compression, 62 
Inflammation of Nerves : Neuritis . . .64 
Cai..;es, 64; Pathological Anatomy, 65 ; Symptoms, 67; Dia- 
gnosis, 69 ; Prognosis, 69; Treatment, 70 VIII 
CONTENTS. 
PAGE 
Mobbid Geowths in Neeves : Neueoma . . .72 
Causes, 74; Symptoms, 75; Diagnosis, Prognosis, and Treat- 
ment, 76 
Diseases of Special Neeves . . . .77 
Phrenic Nerve, 77; Nerves of Upper Limb, 79; Combined 
Palsies of the Nerves of the Arm, 89; Diagnosis, 92 ; Treat- 
ment, 92; Nerves of the Lower Limb, 93; Diagnosis, 96; 
Treatment, 97 
Bbachial Neubitis . . . . .97 
Causes, 98 ; Symptoms, 98 ; Diagnosis, 99 ; Prognosis, 100 
Sciatica ...... 101 
Causes, 102; Pathological Anatomy, 103; Symptoms, 103 ; 
Pathology, 105; Diagnosis, 106; Prognosis, 107; Treat- 
ment, 107 
Multiple Neubitis ..... 108 
Varieties, 111; Symptoms, 119 ; Course, 128 ; Cause of Death, 
129; Complications, 129 ; Pathological Anatomy, 130; 
Pathology, 135; Diagnosis, 138; Prognosis, 144; Treat- 
ment, 147 
Endemic Neubitis ..... 150 
Malabial Neubitis ..... 151 
Bebi-beei . . . . .151 
Symptoms, 153 ; Pathological Anatomy, 155 ; Pathology, 155 ; 
Diagnosis, 156 ; Treatment, 157 
Lepbous Neubitis ..... 157 
Symptoms, 158 ; Pathology, 160 ; Diagnosis, 161 ; Prognosis, 
161; Treatment, 161 
PART III.—DISEASES OP THE SPINAL CORD. 
Inteoduction—Anatomy of the Coed . . . 162 
Structure of the Cord ..... 163 
Grey Substance, 165 ; White Substance, 170; Commissure of 
the Cord, 184 
Blood-supply to the Cord .... 187 
Functions of the Spinal Coed .... 189 
Motor Conduction, 190; Representation of Movements in the 
Cord, 191; Sensory Conduction, 194; Reflex Action, 199; 
Adaptation to Posture, 202; Co-ordination of Movement, 
203 ; Influence on Nutrition, 205 ; Visceral Control, 206; 
Mutual Relation of Functions, 209; Table showing approxi- 
mate relation to the spinal nerves of the various motor, 
sensory, and reflex functions of the spinal cord, 210 CONTENTS. 
IX 
PAGE 
Symptoms of Disease of the Cord . . . 211 
Indications of the Seat of the Lesion : Anatomical Diagnosis : 
Motor Symptoms ..... 212 
Loss of Motor Power, 212; Motor Oyer-action—Spasm, 213; 
Muscular Contractions, 214 ; Inco-ordination of Move- 
ment, 215 
Sensory Symptoms ..... 210 
Increased Sensitiveness, 217 ; Pain, 217; Spontaneous Sen- 
sations, 219 
Reflex Action ..... 219 
Loss, Excess, and Reflex Spasm, 219—222 
Vasomotor and Trophic Disturbance . . . 223 
Visceral and other Disturbances . . . 224 
Paralysis of Sphincters, 224; Pyrexia, 225 ; Convulsions, 
226 
Combination of Symptoms .... 226 
Total Transverse Lesion, 226; Unilateral Lesion, 229 
General Pathology and Etiology : Indication of the Nature 
of the Lesion : Pathological Diagnosis . . 231 
SPECIAL DISEASES OF THE CORD . . . 238 
Diseases of the Vertebral Column . , . 238 
Injuries of the Spine ..... 238 
Dislocation, 238 ; Fracture, 239 
Caries of the Spine ..... 243 
Causes, 243 ; Pathological Anatomy, 244; Symptoms, 245 ; 
Complications, 249 ; Course, 249; Diagnosis, 251; Prog- 
nosis and Treatment, 253 
Tumours and Other Diseases of the Spine . . 256 
Growths in the Spinal Column .... 256 
Etiology and Symptoms, 257 ; Diagnosis, 258 ; Prognosis, 
260; Treatment, 260 
Vertebral Exostoses ..... 260 
Syphilitic Disease . . 261 
Erosion by Aneurysm ..... 262 
Hydatid Disease ..... 262 
Diseases of the Articulations .... 263 
Lateral Curvature, 263 ; Vertebral Arthritis, 2C3 
DISEASES OF THE MEMBRANES OF THE CORD . . 265 
Spinal Meningitis : Inflammation of the Membranes . 265 
External Meningitis ..... 266 
Causes and Pathological Anatomy, 266; Symptoms, 268; 
Diagnosis, Prognosis, and Treatment, 268, 269 
Internal Meningitis ..... 269 
Acute Internal Meningitis .... 270 
Causes, 270 ; Pathological Anatomy, 271; Symptoms, 274 ; 
Diagnosis, 276 ; Prognosis, 277 ; Treatment, 277 X 
CONTENTS. 
Spinal Meningitis (continued)— page 
Chronic Internal Meningitis . . . .279 
Causes, 280 ; Pathological Anatomy, 281 ; Symptoms, 284 ; 
Diagnosis, 287 ; Prognosis, 289 ; Treatment, 289 
Hemorrhage into Spinal Membranes: Spinal Meningeal 
Hemorrhage ; Hematorrhachis . . . 290 
Causes, 290; Pathological Anatomy, 291; Symptoms, 292; 
Diagnosis, 294 ; Prognosis, 295 ; Treatment, 295 
DISEASES OF THE CORD . . . .296 
Anemia and Hyperemia ..... 2C8 
Anaemia, 296; Hyperaemia, 298 
Inflammation—Myelitis ..... 299 
Acute Myelitis ..... 300 
Etiology, 300; Pathological Anatomy, 304; Symptoms, 
314 ; Varieties, 321 ; Pathology, 322; Diagnosis, 324; 
Prognosis, 328; Treatment, 329 
Abscess ...... 332 
Embolism ...... 333 
Chronic Myelitis ..... 333 
Etiology, 334 ; Pathological Anatomy, 336 ; Symptoms, 341; 
Diagnosis, 342; Prognosis and Treatment, 344 
Compression ...... 345 
Causes, 345; Pathological Anatomy, 346; Symptoms, 348; 
Diagnosis, 349 ; Prognosis and Treatment, 350 
Anterior Polio-myelitis : Atrophic Spinal Paralysis . 351 
Acute Atrophic Paralysis (Infantile Palsy) . . 351 
Etiology, 352 ; Symptoms, 354 ; Pathology, 364; Diagnosis, 
370 ; Prognosis, 372 ; Treatment, 373 
Subacute and Chronic Atrophic Spinal Para1 jsis . . 378 
Acute Ascending Paralysis .... 380 
Causes and Symptoms, 381; Pathology, 383 ; Diagnosis and 
Prognosis, 385 ; Treatment, 386 
Paralysis from Lessened Atmospheric Pressure—Divers’ 
Paralysis ...... 387 
Pathology, 389 
Hemorrhage into Spinal Cord—Hematomyelia . . 390 
Etiology, 391; Pathological Anatomy, 392 ; Symptoms, 393; 
Diagnosis, 394 ; Prognosis and Treatment, 395 
DEGENERATIONS OF CORD ... 396 
Locomotor Ataxy—Tabes Dorsalis . . . 397 
History, 398; Causes, 398; Symptoms, 401 ; Motor, 402; CONTENTS. 
XI 
Locomotor Ataxy (continued)— page 
Sensory, 403; Reflex, 406; Eye, 407 ; Sphincters, 410; 
Vaso-motor and Trophic, 410; Visceral, 413; Course and 
Termination, 414; Complications, 416; Pathological Ana- 
tomy, 418; Pathology, 425; Diagnosis, 431; Prognosis, 
434 ; Treatment, 435 
Primary Spastic Paraplegia—Primary Lateral Sclerosis . 440 
General Pathology, 440 ; Causes, 442 ; Symptoms, 443 : Patho- 
logical Anatomy, 447 ; Diagnosis, 450 ; Prognosis and Treat- 
ment, 452 
Ataxic Paraplegia ..... 453 
Causes, 453 ; Symptoms, 454; Pathological Anatomy, 456 ; 
Pathology, 458 ; Diagnosis, 459 ; Prognosis and Treatment, 
460 
Pellagra ...... 460 
Causes and Symptoms, 461 
Hereditary Ataxy—Friedreich’s Disease . . . 461 
Symptoms, 463 ; Pathological Anatomy, 465 ; Patholog), 468; 
Diagnosis, 469 ; Prognosis and Treatment, 470 
Simple Senile Paraplegia .... 470 
Chronic Spinal Muscular Atrophy: Progressive Muscular 
Atrophy ...... 471 
Causes, 472; Symptoms, 474: Varieties and Complications, 
482 ; Course, 483 ; Pathological Anatomy, 484 ; Pathology, 
491; Diagnosis, 494; Prognosis, 496; Treatment, 496 
Arthritic Muscular Atrophy .... 498 
Pathology, 500; Diagnosis and Prognosis, 501 ; Treatment, 
502 
Muscular Atrophy from Over-use . . . 502 
Idiopathic Muscular Atrophy : Myopathic Atrophy, Mus- 
cular Dystrophy ..... 503 
Pseudo-liypertrophic Muscular Paralysis : Lipomatous Mus- 
cular Atrophy ..... 505 
Etiology, 506 ; Symptoms, 507 ; Varieties and Complica- 
tions, 514; Pathological Anatomy, 514; Pathology, 
517 ; Diagnosis, 519 ; Prognosis, 520 ; Treatment, 520 
Simple Idiopathic Muscular Atrophy . . . 521 
Causes, 522; Symptoms, 523; Pathological Anatomy and 
Diagnosis, 528 ; Prognosis and Treatment, 529 
Peroneal type of Family Amyotrophy . . . 630 
Muscular Hypertrophy .... 534 
Thomsen’s Disease : Myotonia congenita . . . 536 
Pathology, 538 ; Treatment, 540 ; Congenital Paramyotone, 540; 
Ataxic Paramyotone, 541 XII 
CONTENTS. 
PAGE 
Tumoubs of the Coed ..... 542 
Etiology, 542 : Pathological Anatomy, 543 ; Symptoms, 550 ; 
Diagnosis, 556 ; Prognosis, 560 ; Treatment, 560 
Cavities and Fissubes in the Coed: Syeingo-myelia, Hydeo- 
myelia, Hydeoebhachis inteena . . . 562 
Etiological Pathology, 562 ; Symptoms, 573; Prognosis and 
Treatment, 578 
Analgic panaeitium : Moevan’s Disease . . . 579 
Spina bifida . . . . . .581 
Tbaumatic Lesions of the Cobd .... 586 
Causes, 586; Pathology, 587 ; Symptoms, 588; Diagnosis, 
595 ; Prognosis, 596; Treatment, 596 
Functional and Nutbitional Diseases of the Coed . 598 
Functional Diseases, 598 ; Nutritional Diseases, 601 
IN DEX • *•••»• 605 LIST OE ILLUSTBATIONS. 
Fig. page 
1, 2. The Knee-jerk, mode of obtaining it . . .16 
3. The Foot-clonus, mode of obtaining it . . .17 
4. Tracing of the Foot-clonus . . . . .17 
5. 6. Paralysis and Wasting of the Trapezius . . .28 
7. Paralysis and Wasting of the Deltoid and Trapezius . . 28 
8. Paralysis of the Serratus Magnus . .. . .29 
9. Paralysis of the Deltoid . . . . .30 
10. Motor Points for the Arm, inner side . . . .31 
11. „ „ outer side . . . .32 
12. Paralysis of the Long Radial Extensor of the Wrist . . 33 
13. Contraction of the Palmar Fascia . . . .34 
14. Paralysis of part of the Flexor Digitorum Sublimis . . 34 
15—18. Paralysis of the Interossei . . . 35, 36 
19, 20. Claw-like Hand from Nerve-injury . . .36 
21. The Thumb, normal position of . . .38 
22. Ape-like Position of the Thumb from Paralysis of its Muscles . 38 
23. ,, „ „ in greater 
degree . . . . . .38 
24. Paralysis of tbe Abductor Brevis and Opponens Pollicis . . 38 
25. Motor Points on the Front of the Thigh . . .39 
26. „ of Leg, outer side . . . .41 
27. „ on the Back of Thigh and Leg . . .42 
28. Talipes Calcaneus . . . . . .43 
29. „ Equinus at rest and in Flexion of the Ankle . . 44 
30. „ ,, extreme . . . . .44 
31. Paralysis of the Interossei and Muscles of the Great Toe . . 44 
32. Diagram of Structure of Nerve-fibres . . . .46 
33. Degeneration and Regeneration of Nerve-fibres . . .50 
34. Degeneration of Fibres of Cutaneous Nerves . . .50 
35. Chart of Degenerative Reaction in transient Nerve-injury . . 54 
36. „ „ in permanent degeneration . 56 
37. Tracings of Muscular Contractions in Nerve Degeneration . 57 
38—43. Chai-t of Electrical Reactions in Neuritis . . 58, 59 
44. Neuritis, Microscopical Changes . . . .65 
45. Plexiform Neuroma from the Orbit . . . .73 
46. Neuromata in the Skin of Abdomen . . . .73 
47. „ Multiple, of the Arm . . . .74 XIV 
LIST OF ILLUSTRATIONS. 
Fig. page 
48. Neuromata, Multiple, of the Arm, Nerves dissected out . . 74 
49. Neuroma of the Posterior Tibial Nerve . . .74 
50. „ of Popliteal Nerve . . . .74 
51. Area of Anaesthesia after Division of 8th Cervical and 1st Dorsal 
Roots . . . .81 
52. „ „ from Disease of the Circumflex Nerve . 84 
53. Wrist-drop from Paralysis of Musculo-spiral Nerve . . 86 
54. Carpal Prominence from Paralysis of the Extensors of the Fingers . 86 
55. Palsy of Deltoid, Supra-spinatus, and Infra-spinatus . . 91 
56. 57. Contracture of Hand from a growth in the Cervical Spine . 91 
58. Multiple Alcoholic Neuritis, Palsy of Extremities . . 120 
59, 60. „ „ Microscopical Appearances in the Nerves 132 
61. Leprosy, Areas of Anaesthesia .... 159 
62. • ,, Changes in the Nerves .... 161 
63. The Relation of the Yertebral Spines to their Bodies and to the 
Origin of the Nerve-roots .... 163 
64. Diagram of a Section of the Spinal Cord . . . 164 
65. Diagrams of the Cord at different levels . . . 165 
66. Nerve-cell from the Spinal Cord of Man . . . 166 
67. Nerve-cells sending a Process into the Anterior Root . . 166 
68. Junction of a Divided Nerve-fib re with separate Nerve-cells . 166 
69. The Groups of Nerve-cells in the Anterior Cornu . . 168 
70. The Elements of the White Substance at various levels . . 171 
71. Ascending and Descending Degenerations . . . 173 
72. Descending Degeneration in Hemiplegia . . . 174 
73. Diagram of an Element of the Motor Path . . . 176 
73a. Degeneration of the Antero-lateral Ascending Tract . . 177 
74. „ „ ,, „ and the Postero- 
median Column . . . .. . 177 
75. Degeneration after Injury to the Cauda Equina . . . 177 
76. „ a Lesion in Cervical Region . . .178 
77. „ Injury to the lowest part of the Cord . . 178 
78. Posterior Cornu and Column at the last Dorsal Segment . . 180 
79. Cervical Section; Ascending Degenerations . . . 183 
80. Central Canal in Normal Cords .... 185 
81. The Arteries of the Spinal Cord .... 188 
82. Spinal Cord contused by Gunshot Injury . . . 197 
83. Tracings of the Action of the Sphincter Ani . . . 207 
84. Plan of the Centre for Micturition .... 208 
85. Fracture of the First Lumbar Vertebra . . . 240 
86. Spinal Cord damaged by Fracture .... 241 
87. Fracture of the Fifth Dorsal Vertebra . . . 241 
88. Caries of the Spine ..... 245 
89. External Pachymeningitis in Caries of the Spine . . 267 
90. Purulent Meningitis; Section of Spinal Cord and Membranes . 272 
91. „ „ Infiltration of Arachnoid . . 272 
92. Chronic Alcoholic Meningitis .... 281 
93. Myelitis; Inflammatory Products .... 305 
94. Subacute Myelitis, Lumbar Region .... 306 
95. „ „ more highly magnified . . . 306 
96. Subacute Disseminated Myelitis; Spider Cells . . . 307 LIST OF ILLUSTRATIONS. 
XV 
Fig. page 
97, 98. Acute Transverse Myelitis ; Dilatation of the Central Canal 308, 310 
99. Ascending Myelitis from Fracture of Spine . . 313 
100. „ „ more highly magnified . . . 313 
101. Feet in Myelitis of Lumbar Enlargement . . . 317 
102. Chronic Myelitis ...... 337 
103. Chronic Sclerotic Myelitis ..... 337 
104. „ „ more highly magnified . . 338 
105. Chronic Meningo-mvelitis; Syringo myelia . . . 339 
106. Compression of the Spinal Cord and Pressure-myelitis . . 346 
107. Pressure-myelitis, more highly magnified . . . 347 
108. Atrophic Spinal Paralysis ; Talipes Yalgus and Varus . . 361 
109 „ „ Talipes Calcaneus . . . 361 
110 „ „ Left Arm . . . 362 
111. „ „ afEecting the Hand . . 362 
112. „ „ Microscopic Changes . . 365 
113. „ „ Spinal Cord in Lumbar Region . 366 
114. Double Tabetic Ptosis ..... 408 
115. Perforating Ulcer of the Foot in Tabes . . . 410 
116. Locomotor Ataxy ; Swelling of Elbow . . . 412 
117. „ „ Reti'oflexion of Knee-joints . . 412 
118. Tabetic Foot ...... 412 
119. Locomotor Ataxy; Sections of Spinal Cord . . . 418 
120. „ ., Section of Cervical Region . . 419 
121,122. „ „ complete Sclerosis of Posterior Columns 420, 421 
123. „ „ Chronic Meningitis . . . 423 
124. Osseous Lesions in Tabes ..... 424 
125. Congenital Spastic Paralysis (Cerebral) . . . 446 
126. „ „ „ Cross-legged Progression . 446 
127. Sclerosis of the Pyramidal Tracts .... 447 
128. „ „ in Muscular Atrophy . . 448 
129. Ataxic Paraplegia ; Combined Lateral and Posterior Sclerosis . 457 
130. Hereditary Ataxy; Sections of Spinal Cord . . . 466 
131. „ „ Section of Lumbar Cord . . . 466 
132. „ „ „ Cervical, Dorsal, and Lumbar Regions 467 
133. „ ,. Degeneration of Posterior Nerve-roots . 468 
134. Progressive Muscular Atrophy : Wasting of Back and Arms . 475 
135. „ „ Wasting of the Back Muscles . 475 
136. „ ,, Weakness of the Neck . . 476 
137—140. „ „ Fibres of Wasted Muscles . 485 
141. Normal Anterior Cornu ..... 487 
142. Progressive Muscular Atrophy; Anterior Cornu . . 487 
143. „ ,, Degeneration of the Anterior 
Cornua and Pyramidal Tracts . 488 
144. „ „ Degeneration in Medulla and Cord 489 
145. 146. Pseudo-hypertrophic Paralysis .... 508 
147. „ n Partial Enlargement of Rectus . 508 
148, 149. „ n Absence of Latissimus Dorsi; 
Enlargement of Infraspinatus 509 
150, 151. „ „ Mode of rising . . 510 
152. „ „ Late Stage; Muscular Contraction 
and Wasting . . 512 XVI 
LIST OF ILLUSTRATIONS. 
Fig. page 
153. Pseudo-hypertrophic Paralysis ; Weakness of the Spinal Muscles . 513 
154. „ „ Enlargement of the Yasti . 514 
155. 156. „ „ Muscular Alterations . 515,516 
157. Section of a Myolipoma attached to the Spinal Cord . . 517 
158—160. Idiopathic Muscular Atrophy affecting the Face . . 526 
161. „ „ showing Lordosis . . 527 
162. Advanced Muscular Atrophy, probably of the “ Peroneal Type ” . 531 
163. Myolipoma of the Spinal Cord .... 543 
164. Tumour growing from the Dura Mater . . . 545 
165. Sarcoma between the Arachnoid and Pia Mater . . 545 
166. 167- Tumour growing from the Dura Mater . . 545, 546 
168. „ of the Cauda Equina .... 546 
169. Neuromata of the Cauda Equina .... 546 
170. Central Tumour of Spinal Cord .... 548 
171. Syphiloma in the Spinal Cord .... 549 
172. Central Canal in Normal Cords .... 564 
173. Syringo-myelia from a Child .... 565 
174. „ with extensive Gliomatosis . . . 566 
175. „ with Tumours of the Pons and Cauda Equina . 567 
176. „ associated with Multiple Growths . . 569 
177. „ with Haemorrhage into the Cavity . . 570 
178. „ with irregular Cavities in the Spinal Cord . 573 
179. Spina Bifida; sections of Spinal Cord . . . 583 
COERECTIONS AND NOTE. 
P. 184, line 10, for Fig. 57 read Fig. 64. 
„ 191, „ 26, „ inflammation read information. 
„ 207, „ 1, „ rectum read bladder. 
„ 212, „ 24, „ p. 116 read p. 176. 
„ 400, „ 26, „ puerperal read peripheral. 
The reader is desired to append to the foot-notes on pp. 229 and 316 a refer- 
ence to that on p. 552. DISEASES OF THE NERVOUS SYSTEM. 
INTRODUCTION. 
CLASSIFICATION OF DISEASES OF THE NERVOUS SYSTEM. 
A classification of Diseases of the Nervous System, at once 
scientific, exact, and convenient for systematic description, is not at 
present possible. If we attempt to classify the diseases according te 
either seat or nature, we are met at once by difficulties which prevent 
any complete arrangement. These difficulties arise from the fact that 
many diseases affect more than one part of the nervous system, that 
the precise seat of other maladies is unknown, and that we are still 
ignorant of the nature of a considerable number of diseases. A rough 
division is often made into two broad classes of “ organic ” and 
“ functional ” disease. The first class, that of “ organic diseases,” 
comprehends those in which there is always a visible lesion, manifesting 
sometimes the morbid process which constitutes the disease, sometimes 
only the ultimate degree or result of that process. The second class, 
that of “ functional diseases,” is less definite, comprehending (1) those 
diseases that consist only in a disturbance of function, and are there- 
fore properly so designated; and (2) many diseases which have this in 
common with true functional disease, that they are transient and not 
permanent, and that they are not known to depend on organic changes. 
But there is also a large class of diseases in which no constant lesion 
has been discovered, but which are not transient, and cannot well be 
placed in either of these classes. This simple classification is 
therefore inadequate. It may be well to consider in what respect it 
needs alteration to meet the requirements of our present knowledge. 
The term “ organic disease,” as commonly used, means visible 
disease. But visibility is relative ; it depends on the means of vision. 
The application of the microscope to pathology immediately increased 
the range of organic disease, and a similar increase has resulted, in our 
own day, from the use of staining agents, which render visible many 
changes that could not before be seen. Still it remains true that the 
degree of alteration determines visibility. Molecular changes in 
VOL. I. 
1 2 
INTRODUCTION. 
nutrition, considered as such, must be colossal to be detected. Such 
alterations, not sufficient to be seen, but still considerable, probably 
constitute the morbid process in many diseases that are commonly 
classed as “ functional.” Hence we may distinguish a class of “ nutri- 
tional diseases” as to a large extent distinct from those that consist 
ni a mere derangement of function. While distinguishing these two 
classes, we cannot entirely separate them; nutrition and function are 
mutually dependent, and prolonged functional disturbance must deter- 
mine nutritional change. 
Visible disease varies much in nature and degree. Some forms can 
.-always be seen with the unassisted eye; they change the shape or 
colour or consistence of the part. Other forms can be detected only 
with the aid of the microscope ; while many may be seen with the 
unassisted eye when their degree is considerable, and only by means 
of the microscope in their early stage or when in slight degree. It is 
convenient to term such alterations, the visibility of which is alto- 
gether a matter of degree, “ structural diseases.” Thus we may dis- 
tinguish four pathological classes of disease of the nervous system: 
1. Organic disease (or “ coarse ” organic disease) ; such as tumour, 
haemorrhage, softening. 
2. Structural disease ; such as most forms of sclerosis. 
3. Nutritional disease; such as general paralysis of the insane, 
paralysis agitans. 
4. Functional disease ; such as reflex convulsions, and many forms 
of hysteria. 
In the first class the morbid process always begins outside the nerve- 
elements themselves. In the second class it may begin in them or 
outside them. In the third and fourth classes these elements are 
probably always primarily affected. 
Such a classification helps us to obtain clearer views of the primary 
relations of disease, but is not convenient for systematic description. 
For this a hybrid system is necessary, in which organic and structural 
diseases are classified according to their seat,—in the nerves, spinal 
cord, or brain. With each group may be placed some nutritional or 
funotional maladies of local incidence. The bulk of these diseases are, 
however, best considered separately, after the organic diseases have 
been described, since many of them are of wide distribution or 
uncertain seat. 
Classification has two purposes to serve. It serves to bring out the 
differences in the nature of disease, and thus to define our conceptions 
and make clear our distinctions. But this purpose is less obtrusive 
than the second,—to furnish us, as it were, with shelves on which to 
place our conceptions, and labels with which to ticket them, so that INTRODUCTION. 
3 
we may find them when we need, and study them in a useful order 
with the least loss of time. 
Even if our knowledge were perfect it is not likely that any scientific 
classification, founded on natural distinctions, would serve the prac- 
tical needs of an arrangement for use. Our present knowledge is un- 
questionably so very far from perfect as to be inadequate even for a 
complete natural classification ; while an attempt to construct one of 
this character that shall be also of practical convenience is a mere 
waste of time. For use, we must divide where we ought only to 
distinguish ; and we have to place near together, for convenience’ sake, 
maladies that should be not only far from each other, but sometimes 
far from all others. PART I. 
GENERAL SYMPTOMATOLOGY. 
SYMPTOMS AND THEIR INVESTIGATION. 
The nervous system is almost entirely inaccessible to direct obser- 
vation. The exceptions to this are trifling: the termination of one 
nerve, the optic, can be seen; some of the nerve-trunks in the limbs 
can be felt either in the normal state or when enlarged by disease. 
As a rule, the state of the nervous system can be ascertained only by 
the manner in which its work is done, and morbid states reveal their 
presence by the derangement of function which they cause. 
The functions of the nervous system are often divided into 
mind, motion, and sensation, but they are far more extensive than 
those words denote. The functions of all the organs of the body, all 
states of the blood-vessels and of the circulation within them, and even 
all processes of nutrition, are under the control of the nervous system. 
The disturbance of nerve-function produced by disease is conter- 
minous in extent with the human organism. Our knowledge of 
these svmptoms is constantly increasing in range and in degree. They 
differ, however, very much in relative importance. Some occur more 
frequently than others, and are more direct in significance. Many 
have a special relation to certain parts of the nervous system, while 
others occur in diseases of all parts. It may be well, at the outset,, 
briefly to describe the latter—the general characters of some of their 
most frequent symptoms; while the more special symptoms can be- 
more conveniently considered when we deal with diseases of that part. 
Motoe Symptoms.*—Disturbance of motion is one of the most 
common effects of disease. Movement is produced by muscles, but 
the muscles are excited to contraction by the nervous system. Most 
* Some modification of the words kinesis, aldnesis, Ac., is sometimes used to- 
designate motor symptoms. These words seem to me to add nothing to our know- 
ledge or to its clearness—certainly nothing to compensate for their cumbersome 
character; and the definite addition all such words make to the knowledge that has 
to be acquired is not always sufficiently weighed against their supposed advantage. MOTOR. 
5 
alterations of motility, both defect and excess, are due to nerve de- 
rangement. The conditions are very few in which motor changes 
originate in the muscles themselves. Defect of movement is of 
muscular origin only in some cases of primary alteration in the nutri- 
tion of the muscles. When there is a general impairment of nutrition, 
the muscles participate in this ; they are ill-nourished, and therefore 
feeble. Such a condition is met with in chronic wasting diseases, in 
anaemia, and as an acute affection in all acute febrile diseases. This 
is the chief cause of the muscular weakness that so often succeeds 
fevers ; it may even proceed to the degree of causing visible changes in 
the aspect of some fibres. 
In a few chronic diseases the muscles undergo a primary degenera- 
tion. One is the disease known as “ pseudo-hypertrophic paralysis 
aud allied is an affection in which there is atrophy ot the mus- 
cles. Another is ossification of the muscles. In almost all other 
conditions, loss of power in the muscles is dependent on the state of 
the nervous system, either directly or through defective nutrition of 
the muscles, or both. The nutrition of the muscles depends on the 
motor nerves, although we are still ignorant of the precise nature 
of that dependence. The subject will be referred to again in the special 
account of the changes that result from injuries to the nerves. 
So also with increased and involuntary muscular action—spasm. We 
know even less of what has been termed “ idio-muscular contraction,” 
that is, contraction originating in the muscle itself, than we do of the 
analogous paralysis. Whenever the whole of a muscle contracts, 
the contraction is probably due to the influence of the nervous 
system either directly causing the contraction or indirectly dis- 
posing to it. This is true even when, as in ordinary cramp, a con- 
traction seems to us to be purely local. We can scarcely conceive that 
all the fibres of a muscle can contract simultaneously except under 
central influence. Even muscular “ tone ” is dependent on the connec- 
tion of the muscle with the nerve-centre, since it ceases when the con- 
nection is destroyed. The partial contractions that are termed 
fibrillary ” are perhaps local, since they are so readily produced by 
mechanical stimulation, such as a tap on the muscle. But it is pro- 
bable that fibrillary contractions, although sometimes local, are often 
of central origin. This is also true of the flickering contractions that 
are so common in persons whose nervous system is enfeebled, the 
“ live flesh ” of popular language. They may occur in any muscle, 
from the orbicuhiris palpebrarum (in which they are most common) to 
the gluteus maximus. After a lesion of the nerve-fibres 1o the muscle 
they occur in special degree ; they are often extreme in the calf-muscles 
after sciatic neuritis. 
Defect of movement may present every degree from slight weakness 
to absolute loss. There may be inability even to make the muscle 
contract, or the voluntary contraction may occur, but be too feeble to 
move the parts to which the muscle is attached. The latter difference 6 
SYMPTOMS. 
is to some extent relative, since it varies with the readiness with 
which the part can be moved—i. e. with the resistance to be overcome. 
A contraction that would move a finger may be insufficient to move a 
leg. The difference may vary in the same part according to position. 
A degree of power in the flexors of the hip, that will move the leg 
when the patient is lying on his side, may be insufficient to do so 
when the patient is lying on the back. This difference is even 
more conspicuous in some other muscles; paralysis of the extensors 
of the elbow may be discovered only on an attempt to raise the hat: 
in other positions gravitation really effects that which the muscle 
seems to do. Sometimes the part is moved, but with less force than 
normal. 
The term “paralysis” has long been applied to all degrees of 
defect of power, a distinction being made between complete and in- 
complete paralysis. Partial loss of power is also sometimes termed 
“ paresis.” The advantages of “ paresis ” over the word “ weakness ” 
are chiefly psychical, and depend on the popular horror of “ paralysis,” 
due to its application to absolute as well as to relative loss of power. 
The ideas of progress and incurability seem inseparably attached to the 
term. It is generally wisest to explain its medical use, and the fact 
that it has no significance as to the future. 
Our means of measuring defects of muscular power are very imper- 
fect. The force of some movements can be measured by means of an 
instrument called a “ dynamometer.” Several forms of dynamometer 
have been devised, but that in general use consists of an oval steel 
ring, which can be narroAved either by compression applied to its- 
smaller diameter, or by traction applied to its longer diameter. The 
change in the shape of the dynamometer, and therefore the force 
exerted, is shown by the movement of an index on a scale that has a 
double graduation, a closer for compression, and a wider for traction. 
This form of dynamometer is knoAvn as “ Charriere’s,” from the name 
of its first maker. An older form of dynamometer is that devised by 
Duchenne. It is less convenient fortesting the grasp, although better 
adapted for indicating the force of traction. The use of these instru- 
ments is chiefly confined to the measurement of the grasp. The esti- 
mation of the strength of other movements is difficult, and liable to 
error, but with care a wider use of the instrument is practicable. In 
examining these it is best for the observer to oppose the movement 
and note the resistance that the patient can overcome. The wide 
variations in strength among different persons renders absolute esti- 
mation possible only when the defect is considerable. Slight changes 
are recognised by comparing the power on the two sides. It should 
be remembered that the limbs on the right side are normally stronger 
than those on the left, the relation being about as five to four. Care 
must be taken to secure uniformity of the conditions under which 
the observations are made. 
The two movements that can be most conveniently measured by the 7 
MOTOR 
dynamometer are the flexion of the fingers and of the hip. The former 
is estimated by the grasp; the latter by pressing the raised leg down 
by means of the dynamometer placed over the end of the femur 
above the knee. The person tested being seated on a chair, the knee 
flexed, and the foot raised from the ground, I find that the force 
needed to overcome the contraction of the flexors of the hip is nearly 
the same as that of the grasp of the hand in the same person and on 
the same side. 
Inco-ordination of Movement.—By this term is meant a defect in the 
co-ordination of muscular contractions by which a movement is pro- 
duced. Every movement is due to the contraction of a series of fibres, 
which seldom corresponds to the series massed together in a “muscle.” 
Fibres, not muscles, are represented in the structure of the brain, and 
those that cause a simple movement may be in several muscles. The 
synergic action of these in a definite degree, and at a certain time, is 
essential. So also is the simultaneous contraction of the opponents 
of these acting muscles, which are thus steadied; this antergic* con- 
traction is essential for the exertion of force. Synergic and antergic 
contractions seem to be directly proportioned to the force exerted; 
but the antergic is in inverse degree to the movement. Defect in 
antergy not only does not interfere with movement, but prevents the 
exertion of force by permitting an excess of movement. 
But it is not customary to apply the term “ inco-ordination ” to 
any derangement of movement except that which is irregular in time. 
The variations in the time of the muscular contractions makes the 
form of movement variable and irregular. This irregularity is also 
called “ataxy.” 
A method of estimating its degree consists in making the patient 
suddenly try to touch, with the point of a pencil, a spot on a 
sheet of paper suspended before him, his eyes being closed at the 
moment of the attempt. After a certain number of attempts the 
average distance from the spot of the dots he has made is ascertained, 
and, compared with the result given by a normal individual, affords 
a numerical indication of the degree of inco-ordination. The method 
is effective, although the result is perhaps scarcely worth the trouble.f 
Whenever there is inco-ordination, spontaneous movements occur 
if the patient tries to hold the limb in a certain posture; the varying 
degree of contraction deranges the fixation as well as the movement 
of the limb: deranged fixation means spontaneous movement, co- 
ordination being essential for steadiness of uniform contraction, as 
well as for the steadiness of the varying contractions of movement. 
These involuntary movements constitute a delicate test for the presence 
of ataxy. 
It is necessary to distinguish co-ordination and the direction ol 
* I use this term because we have none to express antagonistic co-operation. This- 
is synchronous with that of the acting muscle, but not synergic, 
f Blix, 4 Neur. Centralb.,’ 1884, p. 83. 8 
SYMPTOMS. 
movement to a definite end. The motor process for the latter depends 
on true sensory guidance, chiefly on the senses of touch and sight. 
It thus depends on peripheral guidance. A sempstress with loss of 
sensation in the fingers cannot sew unless she constantly watches 
them. A compositor, whose sense of touch is dulled upon the tips of 
thumb and index finger, cannot pick up the type, or if he does pick 
it up, drops it again, unless he constantly watches the movement. 
Strictly, this is included in the idea of co-ordination, but its loss is 
not spoken of as inco-ordination. There is also a peripheral guid- 
ance from the muscles, but this is related to co-ordination proper, 
rather than to the direction of movement, and it will be more con- 
veniently considered in connection with the functions of the spinal 
cord. Indeed, the mechanism of co-ordination, and the defect in the 
elements of the process that cause in co-ordination, can only be 
discussed in connection with those functions. 
Sensory Symptoms.—Deranged sensation is another very common 
symptom. It has often to be searched for, as a significant defect may 
be unknown to the patient. Each form of sensation, touch, tempera- 
ture, and pain, must be separately tested, since one may be affected 
and not another. 
Sensibility to Touch.—Tbe structures that subserve tactile sensibility 
are stimulated chiefly by motion—by change in contact. Prolonged 
contact, uniform in its degree and place, is perceived but little, and 
only by close attention. It is the change that excites an impulse. In 
testing tactile sensibility care must be taken that the instrument 
employed does not give an impression of heat or cold, lest the patient 
perceive by the sense of temperature, that which he cannot perceive by 
the sense of touch. The observer’s finger may be used, if it is not cold, 
or the skin may be touched with the featber-end of a quill, a piece 
of string, &c. Tbe eyes of the patient should be closed during the exam- 
ination, and, since he is apt to fancy that he feels a light touch when 
he does not, he should occasionally be asked if he can feel, when no 
contact is made. Loss of sensibility to touch is termed “anaesthesia,” 
but this word is often applied loosely to all forms of impaired sen- 
sibility. 
In examining the tactile sensibility, it is important to ascertain, not 
only whether tbe patient can feel, but whether he is able to recognise 
the place touched,—whether he can correctly “ localise ” the sensation. 
For this he must be asked, not only whether he feels the touch, but 
also to say or point out where he feels it. The part touched should be 
frequently varied. Another test for tactile sensibility depends on the 
fact, ascertained by E. H. Weber, that the distance apart at which 
two points are discriminated is nearly the same in different individuals 
in the same part of the body, although it varies much in different 
parts of the body. The normal distance being known, the increased 
distance at which the points have to he placed for their discrimination 9 
SENSORY. 
is a measure of the degree of defect. The points should not he so 
sharp as to occasion pain. Common compasses may he employed, 
hut the most convenient “sesthesiometer” is one contrived by Sieveking, 
in which the compass points are attached to a graduated bar. The 
greater the degree of tactile sensibility, the nearer together can the 
points be, and still be discriminated. The distance at which they are 
normally distinguished must be known before any inference can be 
drawn. The most important average distances, ascertained by Weber, 
are as follows: the distance is smallest, i. e. the sensitiveness is 
greatest, at the tip of the tongue, where the points are discriminated 
when only 1*5 mm. apart. Then come, in order of sensitiveness, 
the finger-tips, 2 to 8 mm.; the lips, 4 to 5 mm.; the tip of the nose, 
6 mm.; the cheeks and the backs of the fingers, about 12 mm.; the 
forehead, 22 mm.; the neck, 34 mm.; the forearm, lower leg, and 
back of foot, 40 mm.; the chest, 45 mm.; the back, 60 mm.; the 
upper arm and thigh, 75 mm. Slight variations exist in different 
individuals, and a deviation from the normal that is uniform in 
degree throughout the body is probably physiological. In using this 
test it is necessary to touch the skin with the two points at the same 
moment, and with equal pressure. The examination requires time 
•and patience, and the results are considerably modified by the intel- 
ligence of the patient. Moreover, the power of discrimination is 
increased by practice. It is rare to obtain a conclusive result unless 
there is a degree of defect that causes a slight absolute loss, such as 
may be detected with a feather. For these reasons, the practical value 
■of the test is less than was at first anticipated. It is most useful for 
the estimation of changes of sensibility in the same person and the 
same part. 
Another test that has been proposed is to move a pointed object 
along the skin, and note the minimum movement that can be re- 
cognised as such (Leube). This test has not come into general use. 
Curious modifications of tactile sensibility are sometimes observed. 
In one of these, a single touch is felt as if it were two or even three, a 
condition that has been termed “ polysestliesia” (Fischer). In another, 
an im pression on one part is referred to some other part, usually in the 
same limb, rarely in another limb.* In another variety, an impression 
on one part has been referred to the corresponding place on the 
■opposite side of the body ; this has been termed “ allocheiria ” 
(Obersteiner). 
Perception of the degree of pressure on the skin is probably sub- 
* In most persons there are spots in the skin whence a painful sensation seems to 
<!art to a distant place; e.g. a prick on the thigh in a limited area may be felt also 
as a sharp pain near the scapula. This shows how structural connections must exist 
favouring the “ reference ” of sensation to a distance from the nerve stimulated. 
Another instance of the same perverted reference is presented by the frequent 
neuralgic pain in one jaw due to a carious tooth in the other jaw, which seems 
painless. 10 
SYMPTOMS. 
served by the nerves for tactile sensibility. It may be estimated by 
simple pressure applied through any instrument, or by small weights,, 
or by an instrument contrived for measuring the pressure applied to- 
an artery to ascertain the tension of the pulse. In this, a spring 
indicates the degree of pressure applied. The part -tested must be 
supported, so that the muscles are not brought into action. The 
point to be ascertained is the minimum variation that can be recog- 
nised. In health, this is about one twentieth of the total pressure, 
whatever the latter may be (Weber). 
Sensibility to pain is subserved by what are called nerves of “ common 
sensibility.” It may be tested by a prick or a pinch. Tor a prick,, 
too fine a point must not be used, not only because a sharp point may 
penetrate the skin, but because, in the less sensitive parts of the skin, 
where the terminal nerve-plexus is wide, a fine point may here be 
unfelt, although felt readily at a place close by. Nothing answers, 
better than the point of a quill pen. The faradic current may 
be employed to test sensibility to pain, wire terminals being most 
suitable for the purpose. Its advantage is the delicacy with which it 
can be graduated, but it does not furnish any absolute standard, and 
needs more study before it can be usefully employed. 
Sensibility to pain may be changed with or without sensibility to 
touch. Its loss is termed “ analgesia,” but is often included in the 
general term “ anaesthesia.” A painful sensation is often felt more 
acutely than normal; this is called “ hyperaesthesia,” or, more 
correctly, “ hyperalgesia.” Occasionally a touch on the shin gives rise 
to pain, but it is probable that this is due to the stimulation of the 
over-sensitive nerves of common sensibility, and is not an intensifica- 
tion of a tactile sensation. Both tactile and painful impressions may 
produce sensations that are abnormal in character, described as 
“ thrilling,” “ tingling,” &c. This perverted sensation has been termed 
“ parsesthesia,” or “ dyssesthesia,” words that have also been applied 
to purely subjective sensations. 
Sensibility to temperature is usually affected with sensibility to pain, 
but often not in the same degree, and one may be impaired without the 
other. There may be an absolute inability to recognise either heat or 
cold as such, or slight degrees of each may be unperceived while con- 
siderable degrees are recognised correctly. In the latter case there is 
impairment of the power of perceiving differences in temperature, 
analogous to the defect in the perception of differences in pressure. 
There may be observed sensation whereby hot objects feel cold, and 
cold objects hot. The pain that extreme degrees of temperature 
normally produce may be felt with undue readiness, or less readily 
than normal.* When the interval that elapses before a sensation of 
pain is felt is increased, so also is the temperature ; if sensation of pain 
is delayed, that of temperature may be delayed also. It must be 
* See on this point Donath, ‘Arch. f. Psych.,' Bd. xv. SENSORY. 
11 
remembered that, in health, this sensation is slower than that of pain, 
because time is required to raise the temperature of the skin suffi- 
ciently to stimulate its nerves. For coarse examination, hot and cold 
spoons may be employed, or a hinged tongue depressor, one half of 
which is warmed. Both heat and cold must be sufficient in degree to 
be unquestionable, so that hesitation in a patient is certainly subjec- 
tive, and not due to equivocal “ lukewarmness.” For ascertaining the 
power of differential discrimination, test-tubes, containing water at 
different temperatures, are necessary. For practical purposes the 
result thus obtained is hardly commensurate with the time required 
for the examination. 
It is always necessary to test separately the sensibility to heat and 
to cold, as there is strong reason to believe that they are subserved by 
different nerves. If very minute points of the skin are examined, it is 
found that at some points only heat, at others only cold, is perceived. 
The stimulation of points of the skin by electricity shows also that 
at some points the peculiar electrical sensation is produced, at others 
sensation of cold, at others sensation of heat. Further, the points 
identified as “cold points” and “warm points” by the one method 
correspond with the points ascertained by the other method.* The 
conclusion from these observations is confirmed by the fact that in 
disease the sensibility to heat and to cold may be affected in different 
degrees. 
Muscular Sensibility.—The term “muscular sense,” as often used, 
includes more than one form of sensation. There is, first, a true 
muscular sensibility. The muscles are abundantly supplied with 
sensory nerves, which are said to end in the interstitial tissue between 
the muscular fibres (Tschirjew). They seem to be stimulated by pres- 
sure and traumatic processes, like other sensory nerves, and also in a 
special way—by traction on the muscle. Thus a squeeze of the calf 
causes a muscular sensation of an undeniable quality, and strong 
passive flexion of the foot on the leg produces a sensation which is dis- 
tinctly produced in the muscle. They are, moreover, strongly stimu- 
lated when tbe fibres are shortened by extreme contraction, which 
causes the most acute pain that is ever felt in the muscles. It 
must be ascribed to the compression of these nerve-endings, since 
apparently no afferent impressions come from within the fibres. It 
is thus a proof of their susceptibility to pressure-excitation. After 
cramp, the nerves are left in a state of such exalted excitability that 
slight extension of the muscle gives rise to pain, although such 
extension has no sensory effect in the normal state. Thus these two 
mechanical influences are those to which these nerves are chiefly 
sensitive. The muscular pain caused by electrical stimulation, as 
distinct from the pain felt in the skin, may be due to the stimula- 
* Blix, ‘Zeitschr. f. Biologie/ Bd. xx, p. 141; Eulenberg, ‘Zeitschr. f. klin. Med./ 
Bd. ix, Heft ii. The observations have also been corroborated by Goldscheider and 
Herzen. 12 
SYMPTOMS 
tion of these nerves, chiefly direct. But these sensations of pain, 
although due to “muscular sensibility,” are not included in the term 
“ muscular sense.” They are, however, of great importance on 
account of the conclusive evidence they afford of the mode in which 
these nerves can be stim ulated. 
The chief knowledge that is ascribed to the “ muscular sense ” is 
that of the character of movement and posture due to the action of 
the muscles, and also of the character of passive movement (by an 
external force) and of posture when the muscles are at rest. It is 
evident, however, that here we have two very different conditions—in 
one of which there is activity of all the motor elements, while in the 
other these are at rest. Without motor action, there can be only the 
sensory action that never ceases ; in active states this continues, but 
motor action is superadded. Hence, these two elements that are 
comprehended in the term must be separately considered. 
Strange to say, the problem that appears the more complex receives 
most elucidation from certain facts. We have almost direct evidence 
of the source of our knowledge of active posture and movement, while 
we have only indirect evidence of the origin of our knowledge of 
passive movement and rest-posture. 
The evidence shows that the former is due, at least in great 
measure, to the effect on consciousness of the activity of the cells 
causing the movement. The proof of this consists in two facts. (1) 
In palsy of an ocular muscle, objects seen are referred to the position 
(in relation to the body) that they would occupy if the movement 
corresponded to the innervation ; it is the latter, i. e. the activity of 
the nerve-cells, to which the perception of movement corresponds. 
(2) After amputation of a limb, a person who makes an effort to 
move the lost part, seems to feel the part move just as if he did move 
it. These facts show that the motor process is the chief source of 
our knowledge. But, in the case of such a phenomenon, we are 
not justified in assuming that the source of the chief is the source of 
the whole. The perception is not so well defined as to permit us to 
say that it may not in some minor degree be the result of the 
influence about to be described, which may co-operate with the sense 
of active innervation, although we may be unable to discern the 
difference that it makes in the total result. Indeed, if the following 
reasoning is valid, such co-operation must be admitted. 
Our knowledge of rest-posture and passive movement must be 
derived from in-coming impulses. No other source for it is possible. 
The afferent impulses to which the knowledge is due are not those 
from the skin ; the sense of posture may be lost when cutaneous 
sensibility is normal; and conversely, the skin may have lost most of 
its sensitiveness when this knowledge is perfect. These two facts are 
illustrated by unilateral lesions of the spinal cord, as well as by other 
symptoms of disease. The source of these perceptions must there- 
fore be the deeper nerves, those of the muscles and joints, and chiefly SENSORY. 
13 
of the former. When the subject of central co-ordination is dis- 
cussed, evidence will be adduced to show that those afferent impulses 
from the muscles pass to the cerebellum and act through it on the 
motor cells of the cerebral cortex, regulating their state and controlling 
their activity, the continuous slighter activity of “ rest,” and the occa- 
sional greater activity that the will induces. In this influence on the 
cells (or rather in the effect it produces), we have a source for these 
perceptions of passive states. We are thus led to refer our perceptions 
of passive posture to the same cells as give rise to our perceptions of 
active posture. Our knowledge is the result of perception and not of 
sensation proper;—the impulses that cause our perception of passive 
states are not directly/eZf. That these impulses also enter into our per- 
ception of active states, completing them, and rendering them perfect, 
is highly probable. 
Our recognition of resistance to contraction affords one of the 
most delicate tests for “ muscular sensibility.” It is used by testing 
the ability to detect differences of weight, i. e. variations in the 
resistance to contraction. In this examination the patient’s eyes 
should be closed, and the objects used should be of uniform size. 
Leather balls like small cricket balls, containing various weights from 
two drachms to two pounds, are in use at the Queen Square Hospital 
for this purpose. It is desirable to eliminate as far as possible the 
stimulation of the cutaneous nerves. This may be effected in three 
ways: (1) Reducing it to a minimum area, placing the weights in a 
bag suspended by a string to the part to be tested, so that only a 
small area of the skin shall be pressed upon; (2) by increasing it in 
area (Hitzig), so as to lessen the pressure in any given area such as is 
pressed upon in the ordinary way ; (3) by increasing the pressure in 
both area and degree, so that the addition affected by the weight shall 
bear only a small proportion to the total stimulation. This may be 
done by attaching the weight to the lower of two bands, one above the 
other, below the part of the limb to be tested. 
(1) The point to be tested is the power of discriminating weight. 
This is greater than in the case of the nerves of the skin, since a differ- 
ence of one fortieth of the total weight can be recognised under normal 
conditions. (2) The sensitiveness of the muscles to pressure and trac- 
tion. (3) Their sensitiveness to electrical stimulation. It is difficult 
to test accurately the electro-sensibility unless the sensitiveness of the 
'skin is removed, as by the injection of cocain. 
The power of recognising the posture into which the limb is put is 
also regarded as a test for muscular sensibility ; if cutaneous sensi- 
bility is normal the parts handled must be grasped firmly, and pressed 
on both sides, so that the direction of pressure may not suggest the 
posture. Several observations should be made to eliminate the chance 
of accidental error. 
Reflex Action.—Many symptoms of disease of the nervous system 14 
SYMPTOMS. 
are due to derangement of the various reflex actions. These are 
numerous, and we can now only consider their general characters. 
Each action is effected through an afferent sensory nerve, an efferent 
motor nerve, and a system of nerve-cells and fibres connecting the 
two in the spinal cord, the “ reflex centre.” The centre is usually a 
complex and often extensive structure, and in it are paths of different 
“ resistance,” determining the form of reflex action and its extent, accord- 
ing to the source and intensity of the sensory impression. The reflex 
centre is between the roots of the sensoi’y and motor nerves concerned, 
and with them constitutes what may he termed a “ reflex arc.” The 
sensory impulse may not only excite a motor process, it may also pass 
up to the brain, and effect consciousness as a sensation. It is probable 
that these are subserved by the same nerve-fibres, so far as the skin 
nerves are concerned, but by different fibres from the muscles. Further, 
the reflex centre of the spinal cord is to some extent under the control 
•of encephalic centres—a point of very great importance. Two chief 
forms of reflex action must be distinguished. The first is that 
excited chiefly by stimulation of the skin; the second is that which is 
excited by a peculiar mode of stimulation of deeper nerves, probably 
only those of the muscles. The latter is obtained, among other ways, 
by tapping a tendon, and therefore was at first, and still is sometimes, 
called “ tendon-reflex action ”—a most undesirable name. 
Cutaneous Reflex Action.—The reflex movements obtained from the 
skin are excited either by a gentle stimulation, as a touch, than 
by a strong, painful impression. They consist of a single movement 
in most instances, either quick or slow, but often somewhat complex, 
and extensive in proportion to the degree of the stimulation effected, 
and to the character of the sensory stimulation. Often muscles at a 
distance are influenced by a powerful stimulation, either with others 
or alone. A strong impression may cause a reflex action so wide as 
to involve most of the muscles of the body. As a rule a painful 
impression causes a quick flexion movement, as if for escape. Thus 
a prick near the knee causes a reflex flexion of the hip. On the other 
hand, a tactile impression causes a much more complex and irregular 
movement. 
The slighter degrees of excitation cause a contraction in the muscles 
close to the part of the skin that is stimulated, the impulse passing, 
in the spinal cord, only to the related motor centres. This limita- 
tion of the process renders them important in diagnosis, as will be 
shown iu the chapter on the functions of the spinal cord, where they are 
more fully described. The cutaneous reflex actions may be excited at 
almost any part of the skin, but at some parts they are very definite in 
character, and are distinguished by special names. The most important 
are the “ plantar reflex,” from the sole ; the “ gluteal reflex,” a contrac- 
tion in the gluteus when the skin over the muscle is stimulated; the 
cremaster reflex,” a retraction of the testicle on stimulation of the skin 
on the inner part of the thigh ; the “ abdominal reflex,” in the muscles 15 
REFLEX. 
of the abdominal wall when the skin over the side of the abdomen is 
stroked; the upper part of this reflex is a very definite contraction 
<at the epigastrium, and has been termed the “ epigastric reflex.” 
A series of reflex actions may be obtained in the muscles of the back, 
the highest being in the muscles of the scapula. Others may be 
and have been distinguished and named, but this process may easily be 
carried too far. These spinal reflex actions vary in their excitability 
in different individuals, and are always more readily produced in the 
young than in the old. In the region of the cranial nerves the most 
important reflexes are those of the eye—(1) the conjunctival reflex, 
(2) the contraction of the iris on exposure of the eye to light, and its 
dilation on stimulation of the skin of the neck. 
Muscle Reflex Action; “ Tendon-reflexes.”—The second group of 
phenomena which depend on reflex action were first systematically 
studied by Erb and Westphal. All occur in muscles that are in a state 
of slight tension, and are produced by a sudden increase of this tension 
•or by some other sudden mechanical influence, but voluntary contrac- 
tion superadded to passive tension diminishes or prevents them.* 
The first of these is the jerk of the leg which occurs when the 
patellar tendon is tapped. Jt has been called the “ knee-phenomenon ” 
by Westphal, the “patellar tendon-reflex.” by Erb, the “knee-jerk” 
by myself. To obtain the jerk, the knee must be flexed so that the 
•quadriceps femoris is gently extended, and the leg must be free to move. 
If then the patellar tendon is struck, the quadriceps contracts and jerks 
the leg forwards. The most convenient position is with the knee to 
be tested flexed nearly, but not quite, at a right angle. The posture 
■commonly employed is with the leg to be tested across the other, the 
knee of the supporting leg being at a right angle (Fig. 1). But if the 
leg to be tested is stout, its tension in this position may be too great 
to permit of any movement. In such case the observer may place his 
-arm beneath the patient’s thigh, just above the knee, and rest his hand 
on the patient’s other knee (Fig. 2). Children may sit on the edge of 
a chair, adults on the edge of a table. If the legs are vertical, the 
effect of the recoil and of the muscular contraction must be carefully 
distinguished. If the bent fingers of each hand are interlocked, and 
the hands pulled strongly, the knee-jerk occurs more readily (Jen- 
drassik). It is essential that both sets of muscles should be free from 
voluntary contraction. Any contraction of the flexors may be ascer- 
tained by feeling the hamstring tendons, and pressure on these by the 
fingers often helps to secure relaxation. The blow may be given by 
the side of the hand, a percussion hammer (Fig. 2), or a stethoscope 
with an india-rubber edge to the ear-piece. If the jerk is doubtful, 
the skin should be bared. In many cases the movement may be 
obtained by a downward blow upon the patella, by a blow on the 
* This is not in harmony with the results of the experiments of Weir Mitchell; 
but his facts are inadequate to establish his statement. The conditions that influence 
the phenomena, and the effects of these, are very complex. 16 
SYMPTOMS. 
quadriceps tendon above the patella, or by a blow on the substance 
of the muscle—in fact, by any mechanical stimulation that can reach 
the muscle—almost as readily and strongly as by a blow on the 
patellar tendon. "When it is in excess, it may be conveniently 
brought out in a somewhat different way. As the patient lies in 
bed, the finger of one hand is placed across the quadriceps tendon 
just above the patella, and the patella pushed down, so as to make 
Fig. 1.—The Knee-Jerk. 
The dotted line indicates the movement 
which follows the blow on the patellar 
tendon. 
Fig. 2.—The Knee-Jerk. 
Method of obtaining it when it 
is not readily produced in the 
ordinary way. 
tlie quadriceps tense. The finger is then percussed in the direction 
in which the patella is being pushed, so as suddenly to increase 
the tension in the muscle. The blow is instantly followed by a 
contraction, jerking the patella and finger upwards. Yery often this 
single contraction is immediately succeeded by a second, and this by a 
third, and so on—a series of quick clonic contractions, or “ clonus,”- 
recurring as frequently as eight per second. By grasping the patella 
firmly, and suddenly pushing it downwards, so as to make the 
muscle tense, this clonus may also be set up. It may continue a* 
long as tension is kept up, but instantly ceases when the muscle is 
relaxed. 
The next important phenomenon belonging to this group occurs at 
the ankle-joint. If the calf-muscles, which are connected with the 
Achilles tendon, are made tense, and this tendon is tapped, the 
muscles contract, causing a slight extension movement of the foot 
just as the muscles of the thigh contract when the patellar tendon is 
struck. In cases in which these phenomena are excessive,—just as 
sudden tension in the thigh-muscles will cause a contraction, followed REFLEX. 
17 
by others in a continuous series—so, in such cases, if the calf-muscles, 
which extend the ankle-joint, 
are suddenly put on the stretch 
by pressing the hand against 
the sole of the foot (Fig. 3), a 
quick contraction occurs, in- 
stantly ceasing, but if the pres- 
sure is kept up, instantly re- 
newed, and recurring as long 
as the tension is maintained, 
as a clonic series of spasmodic 
contractions—the “ ankle-clo- 
nus” or “foot-clonus” (or 
“ foot-phenomenon ” — West- 
phal). It can often be obtained 
best when the knee is not com- 
pletely extended. The move- 
ment is very uniform under the same conditions, varyingdrom six to 
nine contractions per second. By attaching a writing point to the 
foot, and making it trace a line on a revolving cylinder covered with 
blackened paper, tracings may be obtained (Fig. 4), which are almost 
Fig. 3.—Method of Eliciting the 
Foot-Clonus. 
Fig. 4.—Tracing op the Foot-Clonus in Paraplegia. 
(The tracing reads from right to left.) 
as regular as those of a tuning-fork. The clonus in the extensors 
of the knee has the same time and is evidently of the same nature. 
A clonus quite similar may sometimes be obtained in other muscles— 
peronei, flexor brevis pollicis, flexors of the fingers, &c. 
When a tendon is tapped, and its muscle contracts, the occurrence 
has so much the aspect of a true reflex action that it was assumed by 
most investigators to be such, the stimulus being the excitation of nerves 
in the tendon. This view received apparent confirmation by the dis- 
covery of certain facts : (1) That there are nerves in tendon. (2) That 
these phenomena depend for their occurrence on the integrity of the 
reflex path to, through, and from the spinal cord, and are arrested by 
a lesion in this path. By experiments on animals (in whom similar 
contractions maybe obtained) it has been found that they are prevented 
by division of the nerves to the muscles, by division of either the anterior 
or posterior roots of the spinal nerves, or by destruction of the spinal 
VOL. I. 18 
SYMPTOMS. 
cord.* The knee-jerk cannot be obtained in locomotor ataxy (damage 
to the posterior nerve-roots), or in infantile paralysis (damage to the 
anterior grey matter, part of the reflex centre). (3) That these pheno- 
mena are increased in some cases, together with the reflex action from 
the skin. 
These facts certainly prove that some reflex influence is concerned 
in the production of the phenomena. But (as Westphal has always 
maintained) they do not necessarily prove that the contractions depend 
on a simple reflex action, and it is certain that they do not depend on 
a reflex action from the tendons. Passive tension is necessary for the 
tap on the tendon to be effective. When the phenomena are in excess, 
sudden tension alone will suffice to develope the contraction. Tension 
acts upon the muscle as well as upon the tendon, and frequently the con- 
traction may be distinctly excited by stimuli which act on the muscle 
and have no action on the tendon. For instance, in cases in which these 
phenomena are in excess, if the foot be gently pressed up so as to make 
the calf-muscles tense, and the muscles on the front of the leg be tapped, 
the calf-muscles contract (just as they do Avhen, under the same circum- 
stances, the tendon is tapped), and cause a brief extension movement 
of the foot. I have termed this the “front-tap contraction.” It is a 
very delicate test of increased irritability, and it is also of considei'able 
theoretical interest, since we have in it a contraction developed by a 
stimulus which does not in any way affect the tendon. It can affect 
the gastrocnemius directly, for by placing the hand on the calf, a 
vibration may be felt through the leg. If the tibia, instead of the 
muscle, is tapped, the contraction is much slighter, or does not occur. 
Moreover, a tap on the tendon itself only excites the contraction when 
it increases the tension of the tendon; i. e. when it acts upon the 
muscle also. In the case of the Achilles tendon, this may be easily 
demonstrated with a little care. A gentle tap on the side of the tendon 
will excite the contraction as readily as a tap on the back of the tendon, 
but if the outer edge of the tendon is supported (as by the fingers of an 
assistant), the same tap will no longer be effective, because it no longer 
increases the tension. The strongest proof, however, of the indepen- 
dence of the phenomena on any stimulation of the tendon, is afforded 
by the experiments of Tschirjew, who divided carefully all the nerves 
to the patellar tendon, and still found that the tap upon it made the 
tense muscle contract. 
Thus the evidence seems conclusive that the contractions ai'e not 
excited by stimulation of the nerves of the tendon, but that the 
stimulus originates in the muscle, the tendon being only, so to speak, 
an instrument by which that stimulation is produced. But if the 
muscle is stimulated and then contracts, is not the contraction excited 
locally, as Westphal has, from the first, urged ? A reflex action takes 
a certain time, which is needed for the stimulus to travel to and from 
the cord, and for the reflex process to occur in the centre. According 
See Tscliirjew, * Arcliiv fur Psyciiiatrie,’ Bd. viii. Heft 3. EE FLEX. 
19 
to received physiological data, an interval of at least one fifteenth of 
a second would be needed for the knee-jerk, if it were a reflex process, 
and rather more for the movement at the ankle. I have found that 
when the Achilles tendon, or the front of the leg is tapped, the result- 
ing contraction occurs in about one thirtieth of a second.* The 
interval for the knee-jerk has been found to be about one twenty-fifth 
or one thirtieth of a second.f If the patella is pressed down and 
tapped, in the way I have just described, I have found that the interval 
between the tap and the resulting contraction is often not more than 
one fortieth of a second. The shortness of the interval makes it 
less easy to believe that these contractions are reflex, than that they 
are excited locally. 
At the same time, too much stress must not be laid on time 
measurements. It is certain that some reflex process is concerned 
in the phenomena. If we regard the contractions as local, we have 
still to account for the irritability which permits the local stimulus 
to cause a contraction. This irritability is developed by passive 
tension. If the muscle is relaxed, the fibres may contract if they 
are struck directly, just as do the fibres of a separated frog’s 
muscle, but no contraction can be produced by striking the tendon. 
Hence I have suggested that the tension excites, by a reflex influence, 
a state of irritability to local mechanical stimulation,—such as that 
of a tap on the muscle, on its tendon, or even the vibration from a tap 
on the bone or on adjacent parts. But only that form of mechanical 
stimulation is effective which suddenly increases the previous ten- 
sion. It is only because the tap on the tendon does this so readily, 
that the tendon is the means by which the contractions are most 
easily produced, and through which they have beeu chiefly studied 
and prematurely named. If the tension put on a muscle is gentle and 
gradual, it may only develope the irritability, and an additional local 
stimulation is necessary to produce a visible contraction. J If, however, 
the tension is sudden and forcible, it not only developes the irritability, 
but produces visible contraction in the muscle thus rendered irritable 
—as in setting up the foot-clonus. I have shown that the relaxa- 
tion of the muscle, between the successive contractions, is not com- 
* ‘Med.-Chir. Trans./ 1879, p. 292. The measurement has been since confirmed 
by Waller, ‘Brain/ July, 1880. 
f '039 sec. Burckhardt; '032—‘034 sec. Tschirjew; '04 sec. Brissaud; "03—‘04 
sec. Waller; ’03 sec. Eulenberg. Some measurements which 1 made of the interval 
(‘ Med.-Chir. Trans./ 1879, p. 275) gave a longer interval, probably in consequence 
of the movement of the foot being taken as the indication of the commencing con- 
traction. “ Load” will increase greatly the period of latent stimulation, probably by 
causing the initial contraction to expend itself on the elasticity of the muscle. The 
measurements given above were obtained by recording the commencing contraction 
of the muscle. 
X This explanation was originally given for the “ foot-phenomenon ” alone (‘ Med.- 
Cliir. Trans./ 1879, p. 295). I now think that it is equally applicable to the knee* 
jerk. The evidence of the identity in nature of the two is very forcibly stated by 
Waller (loc. cit.). 20 
SYMPTOMS. 
plete: there is a persistent residual contraction, i. e. a tonic con- 
traction on which the clonic contractions occur. When one clonic 
contraction is over, the tension continuing, a second is instantly 
developed. 
The production of the clonus seems thus to depend on the existence 
of a law limiting the time of muscular contraction. If a fibre can- 
not continue contracted, it relaxes and re-contracts. This is so in 
muscular “tetanus,” although the alternation in different fibres pre- 
vents its manifestation. But in the effect of sudden tension at the 
same instant, both contraction and relaxation occur in all the fibres 
at the same time, because all are stimulated alike and at once. We 
apparently have an example of the “single muscular contraction” 
such as physiologists obtain by an induction shock.* It agrees with 
this in character and time. We have no facts to suggest that such 
contractions could be produced through a reflex mechanism. 
The sensory nerves of muscles have been shown by Tschirjew tn 
commence, not within the muscular fibres, but in the interstitial con- 
nective tissue. The afferent impulse produced by tension is apparently 
due to the tension acting on these nerves: the visible contraction is 
excited by tension or vibration affecting the muscular fibres themselves. 
The latter is ineffective unless the muscles are brought into a state of 
special excitability through the cord. The reality of an afferent impulse 
from the muscle, produced by tension, is demonstrable to anyone who 
will permit his ankle to be suddenly flexed. A distinct pain is felt in 
the muscle (none, be it observed, in the tendon). It is not surprising, 
therefore, that this afferent impulse should, very often, not merely 
develope the reflex excitability or tonic contraction, but also cause a 
more widely-spread reflex action. The attempt to get the foot-clonus,, 
for instance, will cause a flexion of the hip-joint; the attempt to obtain 
the knee-jerk may cause a movement in the opposite leg or a start 
back of the body. But these reflex contractions, if carefully observed, 
may be seen to succeed, at an appreciable interval, the immediate 
contraction. Burckhardt has found that the latent interval for a 
skin reflex is three times as great as for the knee-jerk. This theory 
of reflex irritability and local stimulation affords a full explanation of 
all the relations of these phenomena, and it is the only theory which 
does so. 
It seems, therefore, that the term “ tendon-reflex ” is altogether 
inaccurate. The phenomena are, according to the explanation above 
given, dependent on a “ muscle-reflex ” irritability, which has nothing 
to do with the tendons. If each contraction is reflex, it must be 
generated by an afferent impulse from the muscle-nerves, not from 
the tendon-nerves. This fact seems conclusive and inevitable. Hence 
if we wish to describe them by a general term, it is best to employ one 
which does not involve any special theory of their nature. They have 
been termed “tendon-muscular phenomena,” but the intervention of 
See Foster’s ‘Physiology/ 1888, pt. i, p. 78. REFLEX. 
21 
tendons is not necessary for their production ; the one condition which 
all have in common is that passive tension is essential for their occur- 
rence, and I have suggested* that they be termed myotatic contractions 
(rariKOi, extended). The irritability, on which they depend, is due 
to and demonstrative of a muscle-reflex action which depends on the 
spinal cord. It is highly probable, as Tschirjew suggested, that the 
condition on which the myotatic irritability depends, is identical with 
muscular “ tone.” Since the experiments of Heidenhain, it has beeu 
generally admitted that “ tone ” depends on tension, and is a reflex 
process, f 
A true “ tendon-reflex ” may be excited by pinching the tendon, 
but this is a start of the whole limb, precisely such as results from a 
pinch of the skin. It is an instance of the pain-reflex described above. 
The importance of discarding the tendon-reflex theory (and the name 
that must always involve it to those who have not studied the matter) 
is very great, for it prevents the comprehension of the true nature of 
other phenomena of great importance. 
Paradoxical Muscular Contraction. — This name has been given by 
WestphalJ to a slow tonic contraction occurring in a muscle when its 
attachments are suddenly brought nearer. It is best seen in the 
tibialis anticus ; if the foot is grasped, and passively flexed on the leg, 
the tibialis anticus contracts, sometimes after an appreciable interval; 
its tendon stands out, and the contraction keeps the foot flexed for a 
time which may be some minutes (in one case for twenty-seven) ; the 
relaxation is slow. Repetition lessens the contraction. The contrac- 
tion is not voluntary (although a voluntary contraction may simulate 
it). It may occur on one side only. The contraction produced 
by brief faradism may be similar-ly prolonged in the same case. A 
similar contraction may be observed in the extensors of the toes, 
sometimes in the flexors of the knee, rarely in the arm muscles. Its 
mechanism is uncertain ; whether reflex or not, whether produced 
through the muscle itself, or through the tension on the antagonists, 
(as Erlenmeyer has maintained), we do not know. It seems to be 
an excess of the contraction by which a muscle adapts itself to 
passive shortening of its course. In the cases that have presented 
this phenomenon there has been no muscular rigidity, and no great 
excess (even sometimes a loss) of the myotatic irritability. This 
adaptation to posture seems a phenomena quite separate from that 
which underlies myotatic irritability. It may occur in the early stage 
of tabes, and in some other affections, but its significance is not known. 
A phenomenon somewhat similar occurs in hysteria (Fere) ; it is 
indeed but an isolated and imperfect instance of the condition that 
* ‘ Diagnosis of Diseases of the Spinal Cord,’ 2nd edit., 1881, p. 29. 
f By some interesting researches recently published, Mommsen has reached the 
same conclusion, that muscular tone is dependent on a muscle-reflex action excited 
by teusion acting on the sensory muscle-nerves Virchow’s Archiv,’ Bd. 110, 
p. 22). 
J ‘ Arch. f. Psych.,’ Bd. x, p. 243. 22 
SYMPTOMS. 
when universal and perfect, constitutes the filexibilitas cerea of 
catalepsy. The nature of these contractions will be considered 
further on. 
Changes in Nutrition.—The nutrition of the tissue-elements is 
largely under the influence of the nervous system. Whether this 
influence is exerted through special “trophic” nerves, or through 
the motor, the sensory, and especially through the vasomotor nerves, 
is a question that has been much discussed and is still undecided. 
The balance of evidence is against the existence of special trophic 
nerves. The fact regarding these changes that is surest and most 
important, is that acute disturbance of nutrition is the result of 
irritation of the nerve-trunks and centres, and is in proportion to the 
intensity of that irritation. If a thread is passed through each 
sciatic nerve, and one is also irritated by the application from 
time to time of irritant liquids, trophic changes occur in that limb 
with greater rapidity, and far greater intensity, than in the other 
(Lewaschew). 
The same fact is frequently indicated by the extreme readiness with 
which trophic lesions of the skin and even cellular tissue, occur in 
certain forms of inflammation of the spinal cord especially in those 
that have a strong tendency to spread in the cord, and hence may he 
regarded as possessing more of this peculiar quality that, in our 
ignorance, we term irritative. One theory and one only seems tn 
explain all the facts. It is that the nerve-endings have a structural 
continuity with the tissues,—are related to them in a sort of molecular 
contact similar to that which exists in the tissues themselves—and 
that the nutrition of the molecules of the tissues is determined in its 
character by that of the nerves. The process of irritation descends 
the nerves, it passes from them to the tissues and invades them all. 
Thus we can understand equally the acute changes in the muscles 
which will be described, and also those in the skin and other tissues 
which are under the influence of the sensory fibres. 
Nutritive changes in the shin are easily recognised, but they differ 
much in their character according to their acuteness. When they are 
rapid, and due to very acute irritation of the nerves or the spinal cord, 
such as those just mentioned, the temperature of the limb is raised, 
the vessels readily dilate, and remain dilated for a long time, buli&r 
form, containing a dark-coloured liquid, and slight pressure occasions 
a slough. These changes sometimes occur spontaneously, but are 
more often excited by some cutaneous irritation, and very slight irri- 
tation of the skin will suffice to produce them. Trifling pressure will 
set up a slough, and extensive vesication may result from the applica- 
tion of a hot-water bottle that is not more than pleasantly warm to a 
healthy hand. When the nerve irritation is intense, effusion mav 
occur into the joints. 
In the case of the fifth nerve, acute trophic changes occur in the REFLEX. 
23 
eyeball chiefly when the disease involves the Gasserian ganglion, or 
the nerve in front of it. To produce the same effect, a lesion behind 
the ganglion has to be more irritating than one in front of it, and it is 
probable that a similar relation obtains in the case of the spinal 
nerves and the spinal ganglia. Very intense changes in nutrition are, 
however, common in acute inflammation of the spinal cord. 
The alterations in nutrition in chronic lesions (which have been 
carefully studied by Paget and Weir Mitchell) differ considerably from 
those that result from acute irritation. There is a slow change in the 
nutrition of the skin, which becomes red, thin, and shiny—the “ glossy 
skin” of Paget. The subcutaneous tissue also wastes, so that the 
finger tips become pointed. The growth of the hair and nails is 
retarded, and the latter become brittle. The bones may suffer in their 
nutrition, and may break more easily than in health. If the lesion 
occurs during the period of growth, this is retarded. These changes 
seem to depend on an altered life tendency of tissue elements that 
have been formed without some influence received from the nerves. 
The muscles suffer from lesions of the motor nerves ; the minute 
changes are described at p. 53. At first there may be merely flabbiness, 
, and an appearance of wasting that is not confirmed by measurement, 
but there is soon an actual diminution in the circumference of the limb. 
In extreme cases all the muscular tissue disappears, and the contour of 
the limb is considerably changed. In comparing the size of the limbs 
on the two sides, it should be remembered that the limbs on the right 
side are normally somewhat larger than those on the left side, and that 
the difference varies according to the occupation of the individual, and 
the extent to which this involves an excessive use of the limbs on one 
side. In measuring, great' care is necessary to secure, as nearly as 
possible, the same conditions on each side, both as regards the state of 
the muscles and the place of measurement. It is best, wherever 
possible, to take the maximum measurement in each part, rather than 
to attempt to make the measurement in the same place. In the calf, 
the maximum circumference should always be taken. In the thigh, 
accurate measurement is extremely difficult, because a maximum 
cannot be taken. We may endeavour to measure at the same point 
in the thigh, at the same distance from the condyle, but it is very diffi- 
cult to be exact, and a more accurate comparison can often be made 
by taking the minimum circumference above the knee, in spite of the 
fact that the muscular tissue there is small, and the difference less than 
it is elsewhere. In the forearm the best result is obtained by taking 
the maximum measurement around the muscular prominence below 
the elbow, over the supinator longus. If the upper arm, the circum- 
ference is nearly the same in the middle third, and the middle of the 
humerus may be measured, with little risk of error. In all cases care 
must be taken to draw the tape equally tight at each place. It is 
easier to do this with a flexible steel measure than with an ordinary 
tape measure. Exactness in this respect is best secured by having a 24 
SYMPTOMS. 
spring at one extremity of the tape, with an index that will show the 
tension, which can thus be kept the same at each place.* 
Electrical Ieritability.—The nerves and muscles are excitable 
by electricity, and the excitability is changed by disease, of which the 
change is often an important symptom. It indicates the state of 
nutrition of the nerve-fibres and muscles, and from this we can often 
draw important inferences regarding the condition of the centres. An 
outline of the most important facts regarding electricity in its appli- 
cation to medicine, is given in the Appendix, but it may be well to 
mention here the chief facts of diagnostic importance. 
In the normal state, nerve-fibres are stimulated by either the induced 
or the voltaic current, the stimulation of the motor nerves being shown 
by contraction in the muscles supplied by them, that of the sensory 
nerves by the sensation that is caused. The contraction of the 
muscles is continuous when the faradic current is applied, but if the 
isolated shocks of which the current consists are separately passed, 
each causes a brief, momentary contraction. When the voltaic current 
is applied, contraction occurs, with a current of moderate strength, 
only when the strength of the current is changed, and chiefly when the 
current commences or ceases to pass, i. e. when the circuit is “made” 
or “broken.” The stimulation of the sensory nerves is greatest at 
those times, but occur also, in a much slighter degree, during the 
whole time that the voltaic current is passing. Hence this is probably 
the case also in the motor nerves, although the stimulation is too 
feeble to produce a contraction in health with a strength of current 
that can be borne. In proportion as the nutrition of the nerve-fibres 
is impaired, their excitability is lowered and a stronger current of each 
kind is required to excite them and cause contraction in the muscles 
they supply. When their nutrition is much impaired—i. e. when the 
fibres are “degenerated”—no contraction can be obtained even with 
the strongest currents. 
The changes in the excitability of the muscles are less simple, 
because in them there are two excitable structures—the terminations 
of the nerves, and the muscular fibres themselves. Of these the nerve- 
fibres are the more sensitive to faradism, and the faradic stimula- 
tion of a muscle under normal circumstances is by means of these 
motor nerve-endings. Thus we find that its excitability corresponds in 
degree to that of the motor nerve supplying it. The muscular fibres 
themselves are, even in the normal state, less sensitive to faradism 
than the nerve, apparently because they are incapable of ready response 
to a stimulus so very short in duration as are the shocks of which the 
* As in an instrument contrived l>y Dr. Rus«ell Reynolds (and made by Hawksley) 
in which two rods, to be placed along the middle, one of the thigh, the other of the 
leg, are joined by a hinge that can be tightened at any angle, and on the upper one 
is a tape with the contrivance mentioned in the text. An analogous and most con- 
venient tape measure. REFLEX. 
25 
faradic current consists. (The proof of this consists in the fact that 
under the influence of curara, which removes the excitability of the 
terminations of the motor nerve, the muscle requires a stronger faradic 
current to stimulate it than in the normal state.) But when the nerve 
is degenerated the slowly interrupted voltaic current stimulates the 
muscle as readily as in the normal state ; a contraction occurs when 
the circuit is completed or broken—distinctly slower than that which 
occurs when the nerve-fibres are intact, and due to the stimulation of 
the protoplasm of the muscular fibres themselves. The fact that, 
under normal circumstances, the contraction which is caused by the 
voltaic current is as quick as that produced by the faradic shock, is 
ground for believing that, in health, the voltaic, as well as the faradic 
current, causes the muscle to contract chiefly by exciting the motor 
nerve-endings When the motor nerve is degenerated, and will not 
respond to faradic or voltaic stimulation, the muscle also loses all its 
power of response to the former. Apparently the nerve-degeneration 
is accompanied by changes in the nutrition of the muscular fibre, by 
which any power of response to faradism, which it possessed in 
the normal state, is lost. But the response to the voltaic current 
remains, and becomes quickly more ready than in health, doubtless 
in consequence of nutritive changes which develope what the older 
pathologists called, truly enough, “ irritable weakness.” More- 
over, there may commonly be observed a change in the readiness 
of response to a certain mode of stimulation with voltaism—a “ quali- 
tative ” change, as it is tenned. In health, the first contraction to 
occur, on gradually increasing the strength of the current, is at the 
negative pole when the circuit is closed, and a stronger current is 
required before closure-contraction occurs at the positive pole. But, 
in the morbid state we are discussing, closure-contraction may occur 
at the positive pole as readily as at the negative, or even more readily 
—and contractions, when the circuit is broken, occur far more readily 
than in the normal state. This condition, then—faradic irritability 
lost, voltaic irritability increased and often changed in quality—is 
termed the “ degenerative reaction,” because it occurs when the 
nerve-fibres are degenerated; and if we test them we shall find no 
response to any stimulus, voltaic or faradic. It occurs when the 
nerves are separated partially or completely from their motor nerve- 
cells, and if no such separation exists, it indicates an acute degene- 
rative change in those nerve-cells. 
But the motor nerve-cells and fibres often undergo changes in 
nutrition of a much more chronic character. In this condition the 
irritability of the fibres is lessened gradually and slowly. The irri- 
tability of the inti*amuscular nerve-endings is lessened in the same 
degree as that of the nerve-trunks, and we have a diminution to both 
faradism and voltaism. The nutrition of the muscular fibres i3 
slowly, gradually, impaired; and when the nerve-fibres are much 
affected the muscular fibres are also. There is no stage in which the 26 
ACTION AND PARALYSIS OF MUSCLES. 
nerve-fibre irritability is lost, and the muscle-fibre irritability retained; 
hence there is no condition of lost faradic and increased voltaic 
irritability such as characterises the degenerative reaction just 
described. Irritability is changed to the one form of stimulus just as 
to the other. 
Between these two forms there are intermediate conditions. For 
instance, the nerves may present normal irritability, and the muscle 
the increased voltaic irritability and changed order of contraction met 
with in degeneration. Probably, in these cases, some nerve-fibres are 
degenerated, and lead to the increased irritability of some muscular 
fibres. In both nerve and muscle the character of the reaction is 
determined by the more irritable structures ; hence it is normal in the 
nerve and altered in the muscle. This has been termed by Erb the 
“ middle form ” of degenerative reaction. It would be more accurate 
to call it the “ mixed form.” 
The various changes in irritability have been thought to indicate the 
existence, and various affection, of separate centres for the nutrition 
of the nerves and muscles, apart from, though acting through, the 
motor nerve-cells. Remembering that the nerves and muscles contain 
fibres which suffer in different degrees, the phenomena at present 
ascertained may all be explained on the simpler principle stated, without 
the assumption of these special centres, of the existence of which there 
is, indeed, no evidence. 
Frequently the lowered irritability of degeneration in the nerves is 
preceded by a slight increase of irritability, very transient when the 
degeneration is acute, of longer duration when the degeneration is of 
the slower variety just noticed. In some morbid states, again, in which 
the change of nutrition in the cells and fibres is extremely slight, an 
increase may alone be discovered. I have found such an increase, for 
instance, in diseases regarded as functional, as paralysis agitans and 
chorea, and it is an interesting proof of the molecular changes which 
underlie, or result from, “ functional ” maladies. 
TEE MUSCLES: TEEIR ACTION AND PARALYSIS. 
Disease of the motor nervous system is largely manifested by loss 
of muscular action. Individual muscles, as well as groups of muscles, 
are often separately affected. Hence it is desirable to consider the 
symptoms of the paralysis of the more important muscles, before we 
enter on the study of special diseases. 
The symptoms of the palsy of any muscle is a loss of its normal 
action, and a knowledge of this action is essential for the comprehend 
sion of those symptoms. The two must therefore be considered 
together. They are positive and negative aspects of the same facts. MUSCLES OF UPPER LIMB. 
27 
It may be well, at the same time, to mention the nerve by which each 
muscle is supplied. 
The action of muscles is threefold. (1) By their tonic contraction 
they maintain the parts in a certain posture, independently of volun- 
tary effort. By actual contraction they (2) produce certain movements, 
and also (3) oppose the action of other muscles by a feebler contrac- 
tion, and thus steady the movement that results. 
The complex way in which muscles act together, and modify each 
other’s effect, renders the subject a very large one. Here, only an 
outline can be given of the more salient facts concerning the most 
important muscles. The reader who desires to pursue the subject 
further can do so in the 4 Physiologie des Mouvements,’ of Duchenne, 
to whose researches our present knowledge is largely due. 
The Diaphragm (phrenic nerves from the fourth and fifth cervical) although 
a double muscle with two nerves, habitually acts as a whole, the two halves 
contracting simultaneously and diminishing each lateral curve of the arch. The 
central tendon descends but little. The abdominal viscera are depressed, and 
the parietes protruded. If the hand is placed beneath the ribs, the descent of 
the viscera beneath the diaphragm can be felt. When the diaphragm contracts 
alone, as when the intercostals are paralysed, or the phrenic nerve is faradised, 
the ribs to which the muscle is attached are slightly raised during its action, and 
this elevation causes a slight expansion of the thorax. In ordinary breathing 
this expansion is lost in the action of the intercostals. In paralysis the inspi- 
ratory protrusion of the upper part of the abdomen is lost; it even recedes 
during inspiration instead of advancing, and a descent of the viscera can no 
longer be felt by the hand. There often results a remarkable alternation in the 
respiratory movements of the thorax and abdomen, the retraction of the one 
corresponding to the protrusion of the other. 
Sterno-Mastoid (spinal accessory nerve), passing from the sternum and 
adjacent part of the clavicle to the mastoid process, inclines the head towards, 
and rotates the face from, the side on which the muscle contracts. B >th 
muscles together support the head in the vertical position, and, if it ia 
bent back, they bring it forwards into, but not beyond, this position. 
Paralysis of one muscle has no influence on the position of the head, and but 
little on its movements. Other muscles supplement the loss. This is no such 
thing as a “ paralytic torticollis.” In palsy of both muscles, the head can be 
balanced in the vertical position, but if it falls back, it can be brought forward 
only with great difficulty. Each sterno-mastoid is associated in action with the 
muscles of the other side ; it is a “ contra-lateral muscle.” Eor instance, in 
using the right arm, the head is turned to the right by the left sterno-mastoid. 
This association is sometimes reproduced in disease. 
Muscles moving the Upper Limbs. 
Muscles moving the Scapula and Shoulder-Joint.—The Trapezius 
(special accessory, lower cervical and upper dorsal nerves) consists of three parts. 
The first, from the occipital bone to the outer end of the clavicle, is rarely used 
except in breathing (respiratory portion, Duchenne). The second part is that 
which passes from the lig. nuchae, lowest cervical, and upper three dorsal spines, 
downwards and outwards to the acromion and outer part of the spine of the 28 
ACTION AND PARALYSIS OF MUSCLES. 
scapula. The lowest part passes from the dorsal spines below the third, outwards 
and partly upwards, to the inner half and base of the spine of the scapula. The 
Fig. 5.—Paralysis and wasting of tra- 
pezius ; alteration in contour of 
shoulder at rest. 
Fig. 6.—Ditto, when the arms are 
raised (the right one being aided 
by another person). 
second part is the chief elevator of the scapula and shoulder. With the third 
part it brings the scapula towards the spine, and puts the shoulder back. Both 
parts tend to rotate the scapula—acromion up, lower angle 
out. By this rotation the arm is carried above the 
horizontal level, to which the deltoid raises it. Para- 
lysis of the highest part has little influence on the move- 
ment of the scapula, but causes a change in the content 
of the neck (Fig. 5) especially conspicuous on deep in- 
spiration. The change in the shape of the neck is verv 
great, when the arms are raised, if the whole trapezius is 
wasted (Fig. 6). In palsy of the middle part, the eleva- 
tion of the shoulder is imperfect; in that of the third 
part, the scapula is farther from the spine than normal. 
In palsy of all parts, the scapula becomes rotated (acro- 
mion down, inferior angle in) by the weight of the arm 
and the contraction of the opponents (Fig. 7). The 
rotation may mask the displacement outwards, due to 
the paralysis of the lowest part. If the clavicular part 
remains, there may be no rotation, but the scapula is 
lower than normal. 
The Rhomboids (fifth cervical nerve, by a branch 
that passes through the scalenus) first rotate the scapula 
on the outer angle, moving the lower angle inwards, 
and then move the whole scapula upwards and inwards. 
In strong elevation, they aid the trapezius, which pre- 
vents the rotation of the scapula. The rotatory action 
aids forcible depression of the raised arm. The muscles 
also fix the scapula for the action of the teres major. 
Their tone helps to keep the scapula against the thorax (opposing the pectoralis) 
and in its vertical position (opposing the serratus), and hence, in paralysis, the 
FlO. 7 —Paralysis and 
wasting of deltoid 
and trap'zius; ro- 
tation of scapula, 
from weight of arm, 
in consequence of the 
paralysis of the tra- 
pezius ; progressive 
muscular atrophy. MUSCLES OF UPPER LIMB. 
29 
edge of the scapula, at rest, stands out a little, leaving a furrow, and the scapula 
is slightly rotated (lower angle out). Movement is hut little interfered with by 
the paralysis of the rhomboids, the most important effect being that the move- 
ment backwards of the raised arm by the teres and deltoid is feeble for want 
of the fixation of the scapula. 
The Levator anguli scapulae (third cervical nerve) first rotates the scapula 
on the outer angle and then raises it. The muscle is usually paralysed with the- 
trapezius, and then the scapula falls, but the special effect of its palsy is lost in 
that of the trapezius. If the levator is preserved, and the trapezius paralysed, 
there is great rotation of the scapula, which is, as it were, suspended by its inner 
angle (Fig. 7). 
Serratus magnus (posterior thoracic nerve, from the fifth and sixth cervical) 
carries the scapula outwards, forwards, and slightly upwards, when the arm is 
put forwards. It tends to rotate the scapula on the inner angle (acromion up),, 
the lower fibres most powerfully, but this rotation is prevented by the rhom- 
boids and levator anguli. It does not raise the shoulder when the arm is 
hanging. It helps to fix the scapula when the posterior fibres of the deltoid 
move the raised arm back. If the scapula is fixed by the rhomboids, the serratus 
can act on the ribs, and aid forced 
inspiration. It has most inspiratory 
effect when the arms are elevated. 
In paralysis there may be little 
change in the position of the scapula 
at rest, but often there is slight rota- 
tion (lower angle in) from the un- 
opposed tone of the rhomboids. When 
the arm is moved forwards by the 
anterior part of the deltoid, the 
scapula, no longer held against the 
thorax and moved forwards by the 
serratus, is rotated on its vertical axis 
by the action of the anterior part of 
the deltoid on the humerus, and of 
the middle part on the scapula. Thus 
the posterior edge recedes from the 
thorax, leaving a groove into which 
the hand can sometimes he placed 
(Fig. 8). The scapula is, at the same 
time, rotated ; lower angle inwards 
and upwards. Elevation of the arm 
above the level of the shoulder is much weakened, but can be imperfectly 
effected by the middle part of the trapezius. Loss of the serratus weakens 
other movements, but does not abolish any. Inspiratory expansion of the thorax, 
when the arms are raised, is distinctly less on the paralysed side (Poore). 
The Deltoid (circumflex nerve, from the four lowest cervical) abducts the 
humeruj, the anterior and posterior fibres also moving the arm forwards and 
backwards respectively. The arm is raised least by the posterior, and most by 
the anterior fibres, hut even the latter only elevate it to a right angle with the 
trunk. Hence, if raised by the anterior fibres, and then moved back by the 
posterior, it is at the same time depressed. Elevation above a right angle is by 
rotation of the scapula (trapezius and serratus). These muscles also fix the 
*capula for the deltoid, preventing the rotation (acromion down, lower angle 
Fig. 8.—Paralysis of the serratus magnus;. 
eversion and rotation of scapula when 
the arm is put forwards. 30 
ACTION AND PARALYSIS OF MUSCLES. 
in) that the deltoid, acting alone, would cause. In paralysis, abduction of the 
arm, direct, forwards, and backwards is almost lost. All the abduction that 
remains is a trifling movement by 
the supraspinatus. An attempt to 
abduct results in rotation of the sca- 
pula and elevation of the shoulder 
(Fig. 9) from an excessive innervation 
of the associated trapezius and ser- 
ratus, which, as we have seen, fix the 
scapula when the deltoid acts. Para- 
lysis of single parts of the deltoid 
causes loss of the corresponding move- 
ments of the arm, but if the middle 
part only is paralysed, there is still a 
limited power of direct abduction by 
the conjoined contraction of the ante- 
rior and posterior parts, aided by the 
supraspinatus. 
The Supraspinatus (suprascapular 
nerve) abducts the arm, moves it for- 
wards, and rotates it in. It thus aids 
the deltoid. Isolated paralysis of the 
supraspinatus has little influence on 
movement or position, hut if the deltoid is also paralysed, the head of the humerus 
falls away from the acromion far more than when the deltoid is paralysed alone. 
The Infraspinatus (suprascapular nerve) rotates the humerus outwards, and 
in paralysis this movement is lost. A difficulty in writing is produced, the 
movement along the line being by this rotation of the humerus. 
The Teres minor (circumflex nerve) has a similar action to the infraspinatus, 
and its palsy has a similar effect. 
The Subscapularis (short subscapular nerve, from the fifth and sixth cervical) 
rotates the humerus in, and its paralysis lessens this movement. 
The Latissimus dorsi (long subscapular nerve, from the brachial plexus—last 
four cervical nerves) lowers the raised arm, and puts it back ; the upper part 
adducts the scapula, the lower depresses the shoulder by acting on the humerus, 
which it tends to drag out of the socket. It inclines the trunk a little, and 
both muscles together extend the trunk. In paralysis, forcible backward de- 
pression of the raised arm is lost, and the shoulder cannot be put back without 
being also raised (by the trapezius). 
The Pectoralis major (anterior thoracic nerves from the brachial plexus) con- 
sists of two muscles, the action of the clavicular and sternal parts being different, 
The clavicular (which arises also from the highest part of the sternum), if the 
arm is hanging, brings the shoulder forwards and upwards, as if shivering; 
if the arm is raised, it is bi’ought forwards and lowered to the horizontal posi- 
tion. The muscle is thus concerned, Duchenne says, in the “ cut ” of the swords- 
man and the benediction of the priest. The sternal portion lowers the raised 
arm from every position, and if the arm is hanging, it draws the shoulder 
down. Paralysis of the upper part has little effect on the movement of the 
arm, because the anterior fibres of the deltoid have the same action. It is easily 
recognised by making the patient put his arms in front of him and press the 
palms together. In paralysis of the lower part, even with the lattissimus, the 
raised arm can still be lowered accurately, by the weight of the arm and relaxa- 
Fr&. 9.—Paralysis of right deltoid; ele- 
vation of shoulder by trapezius on an 
attempt to raise the arm, which is 
slightly abducted by the supraspinatus. MUSCLES OF UPPER LIMB. 
31 
tion of the elevators, but it cannot be lowered against even a slight resistance. 
Thus a blacksmith with this defect could wield a heavy hammer, but could not 
blow the bellows by pulling downwards a cord (Duchenne). 
The Teres major (short subscapular nerve) approximates the humerus and 
the outer edge of the scapula, by bringing the former to the side of the trunk, and 
rotating the latter. The simultaneous contraction of the levator anguli and 
rhomboids, fixing the inner angle, causes this rotation to raise the prominence of 
the shoulder Hence, in a forcible elevation of the shoulder, the arm is pressed 
Pelfoid 
(ant. half) 
Triceps (long head) 
Mus.-cut. ». 
Triceps (inner head) 
Biceps 
Ulnar n. 
~ Brach. ant. 
Median n. 
— Supinator long. 
Flex, carpi ulnar.' 
- Pronator teres 
Flex. dig. profund. 
— Flexor carpi radialis 
Flex. dig. sub. (II & III) 
- Flex, digitor sublim. 
- Flex. long, pollicis 
Flex, d git. sub. (I & IV) 
- Median n. 
Ulnar n. 
_ Abductor pollicis 
Palm. brev. 
- Opponens policis 
Abd. minim, digit. 
Flex. min. dig. 
Oppon. min. dig. 
- Flex. brev. pollicis 
Adductor pollicis 
Lumbricales - 
Fig. 10.—Motor points for the arm, inner side (from Erb). The points at which the 
muscles and nerves can most effectively be stimulated. 32 
ACTION AND PARALYSIS OF MUSCLES. 
against the side, the lower fibres of the latissiraus and pectoralis major aiding 
the adduction. The teres cannot alone put the arm behind the trunk. In 
paralysis, the elevation of the shoulder, with the arm against the side, is lost. 
Muscles moving the Foeeaem.—Triceps (musculo-spiral nerve).—The long 
head has an action similar to the teres, hut feebler. It contracts when the arm 
is forcibly lowered, and prevents the displacement downwards of the head of 
the humerus by the actual depressors, the latissimus and pectoralis. All parts 
extend the elbow, the long head with less force than the others, but its action on 
the shoulder-joint, just mentioned, is important, because forcible depression of the 
raised arm is often associated with extension of the elbow. In paralysis of the 
triceps, the elbow can only be extended by the weight of the forearm, and ex- 
tension against gravitation is impossible. Thus a man with paralysis of the 
triceps cannot raise his hat in the customary manner. Flexion of the elbow 
is uncertain, on account of the loss of the antagonistic steadying force. 
FlQ. 11.—Motor points for the arm, outer side (Erb). MUSCLES OF UPPER LIMB. 
33 
The Brachialis anticus (musculo-cutaneous and mnsculo-spiral nerves) flexes 
the elbow simply. Its rai-e isolated palsy has little effect, since it is supple- 
mented by the biceps and supinator longus. 
The Biceps (musculo-cutaneous nerve) supinatesthe forearm if it is pronated, 
and then flexes the elbow. In paralysis the flexion can still be effected, hut the 
traction on the humerus causes pain at the shoulder, from the loss of the support 
of the long head of the biceps. 
The Supinator longus (musculo-spiral nerve) places the forearm midway 
between pronation and supination, and then flexes the elbow. If it is paralysed, 
there is a tendency for supination to accompany flexion (biceps); and if the 
brachialis anticus is also paralysed, the elbow can only be flexed when the fore- 
arm is supinated. 
If the three direct flexors of the elbow are paralysed, feeble flexion is still 
possible by the extensors of the wrist, which cross the elbow-joint, but only 
after the forearm has been pronated and the wrist over-extended. 
The Supinator brevis (musculo-spiral nerve by posterior interosseal branch) 
is the only simple supinator. If it is paralysed, supination can still be effected 
by the biceps, and also by the supinator longus as far as midway between 
pronation and supination. 
Pronators.—The p. teres and p. quadratus (median nerve) both pronate 
strongly, and their palsy causes loss of this movement, hut pronation to the 
mid-position is still possible by the supinator longus. 
Muscles moving the Hand.—Flexors of Wrist.—The F. carpi ulnaris 
(ulnar nerve) and F. carpi radialis (median) flex the wrist. The ulnar flexor 
tends to turn the supinated hand still more out, but neither moves the wrist- 
joint laterally. Flexion indeed hinders the lateral movements of the wrist, in 
consequence of the shape of the articular surfaces. The f. c. ulnaris flexes the 
fifth metacarpal bone on the carpus, as well as the wrist-joint. In paralysis, 
flexion of the wrist can only be effected by the flexors of the fingers when these 
are extended. Extension of the wrist is unsteady from the loss of the antergie 
contraction of the flexors (see p. 7). 
Extensors of Wrist.—Extensor carpi radiales brevis et longus ; E. c. ulnaris 
(musculo-spiral nerve and its radial branch). The short 
radial is a direct extensor; the long radial and the 
ulnar move the hand laterally as well. In paralysis of 
all three extensors the wrist can only he extended by 
the extensors of the fingers when the phalanges are 
flexed. In loss of the short radial, direct extension is 
still possible by the long radial and ulnar, and lateral 
extension by one of these alone. If either is para- 
lysed, together with the short radial, direct extension 
is lost, and only lateral extension, in the direction of 
the remaining muscle, is possible. Paralysis of either 
lateral extensor, long radial or ulnar, leads to perma- 
nent deviation of the wrist in the direction of the 
remaining muscle (Fig. 12). The loss of the long 
radial is more serious than that of the ulnar, because 
the radial lateral movement is of more importance, being 
needed for the convenient motion of the hand to the 
mouth. Paralysis of the extensors impairs flexion of 
the fingers, from the great shortening of the course of 
the tendons, by the flexion of the wrist that occurs. The ulnar extensor acts 
Fig. 12. — Paralysis of 
the long radial ex- 
tensor of the wrist in a 
young child ; habitual 
deviation of the hand 
towards the ulnar side, 
(After Duchenne.) 
YOL. I. 34 
ACTION AND PAPALYSTS OF MUSCLES. 
also synergically with the extensor of the metacarpal hone of the thumb, as may 
he noted if the finger is placed on the tendon beneath the styloid process of 
the ulna. Hence, in paralysis of this extensor, the hand deviates laterally when 
the thumb is strongly extended. 
Extensors of the Fingers.—Extensor communis digitorum; E. indicis; 
E. minimi digiti (musculo-spiral nerve). The common extensor moves the 
fingers and then the wrist. When the muscle is faradised, the extension begins 
at the distal phalanges, and these become flexed again, when the hand is 
extended beyond the plane of the forearm, by the tonic force of the flexors, 
the course of their tendons being elongated by the extension of the wrist. 
Moreover, the muscle has little action on the last two phalanges, since they 
cannot be extended by the long extensor, if the interossei, their proper exten- 
sors, are paralysed. During extension by the communis the fingers are sepa- 
rated from the second. The extensors of the first and last fingers have a 
similar extensor action, but, in addition, they adduct their respective fingers 
towards the middle finger. In paralysis, the extension of the fingers is im- 
Fig. 13. 
Fia. 14. 
Fig. 13.—Posture of the hand in contraction of the palmar fascia, resembling 
that in paralysis of the long extensors of the finger. 
Fig. 14.— Paralysis of the fibres of the flexor sublimis which act on the two 
middle fingers: twelve years’ duration. The second phalanges of these fingers 
are bent backwards and subluxated from the contracture of the unopposed 
interossei, while the last phalanges are kept in position by the unaffected 
flexor profundus. (After Duchenne.) 
possible ; but if the proximal phalanges are passively extended, the middle 
and distal joints can be extended by the interossei. For the lateral move- 
ments of the digits, extension of the proximal phalanges is essential, and hence 
these movements are lost, hut they can he performed if the proximal phalanges 
are passively extended. The posture of the fingers due to contraction of the 
palmar fascia resembles that in palsy of the long extensor (see Fig. 13), but an 
examination of the palm shows the cause of the flexion. 
Flexors of Fingers.—F. sublimis (median nerve); F profundus (median and 
ulnar nerves). These muscles flex chiefly the second and third phalanges, the 
first phalanx being flexed by the interossei. The superficial muscle flexes the 
second phalanx on the first, the deep flexes both. The action on the first phalanx 
is confined to extreme flexion of the fingers, and is the less, the more the wrist 
is flexed. But if the flexion of the middle and distal phalanges is prevented 
the first is strongly flexed. In extreme shortening of the course of the tendons MUSCLES OF UPPER LIMB. 
35 
by flexion of the wrist, the action on the fingers is very feehle, evidence of 
a normal antergic action of the extensors of the wrist. When the extensor of 
the fingers is in strong action, extending the proximal phalanges, the action of 
the flexors on the second and third joints is very strong (tearing position). In 
paralysis of these muscles the power of flexing the last two joints is lost, but the 
interossei still flex the metacarpo-phalangeal joints. Paralysis of the deep flexor 
alone causes merely loss of the power of flexing the distal joint, but this impairs 
many movements, such as playing on the piano. In paralysis of these muscles, 
the unopposed tone of their opponents, the interossei, which extend these joints, 
leads in time to over-extension, and, with repeated passive pressure in using the 
fingers, may even produce a subluxation backwards. In palsy of the sublimis 
this effect is chiefly seen at the middle joint (Pig. 14), in that of the profundus 
at the distal joint. 
Interossei and Lumbricales (ulnar nerve, except the outer two lumbricales, 
which are supplied by the median).—The Interossei abduct and adduct the 
fingers, but only when these are extended at the metacarpo-phalangeal joints, 
and some effort is required for adduction, since the tendency of the long 
extensor is to separate the fingers, and this influence has to be overcome. They 
also extend the second and third phalanges on the first, and flex the first on the 
metacarpal bones. The lumbricales aid the flexor-extensor action of the inter- 
ossei, but do not move the fingers laterally. The opposite action of the fore- 
arm muscles and of the interosseal extensors and flexors is very important. 
Their synergic action steadies movements, and in many actions they contract 
alternately. Thus in making a down-stroke with a pen or pencil the long 
flexors bend the last two joints; while in making an upstroke these are ex- 
tended, and the metacarpo-phalangeal joint is flexed, by the interossei. In para- 
lysis of these muscles the lateral movements are lost, but a slight abduction 
and adduction of the index can still be effected by its long extensors. Only the 
first phalanx can be extended, and flexion is almost confined to the last two 
phalanges. The first three lumbricales, being supplied by the median nerve, 
often escape when the other muscles are paralysed by an injury to the ulnar 
nerve, and they aid the others when these are merely weak ; hence the index 
and middle fingers seem to recover before the others (Pig. 15). The position of 
Fig. 15. 
Fig. 15.—Recent incomplete paralysis of the interossei from a punctured 
wound of the ulnar nerve at the wrist: attempt to extend fingers. The loss 
of extension of the last two phalanges is chiefly marked in the third and fourth 
fingers, from the influence of the lumbricales (supplied by the median) on the 
others. (After Duchenne.) 
Fig. 16.—Paralysis of the interossei (ulnar nerve) slight in degree: attitude 
of fingers at rest. 
the hand at rest becomes altered. Normally there is slight flexion at all joints 
by the tone of the muscles, interossei and long flexors. In paralysis the first 36 
ACTION AND PARALYSIS OF MUSCLES. 
phalanx is in a line with the metacarpal bones, while the other phalanges are 
flexed, the middle more than the distal (Fig. 16). In action this flexion is 
always increased, the metacarpo-phalangeal joints become over-extended, and 
the other joints strongly flexed (Fig. 17). Gradually the hand assumes this 
Fia. 17. 
Fia. 18. 
Fia. 19. 
Fig. 20. 
Fig. 17.—Attempt to unbutton waistcoat by the band shown in the last 
figure; extreme flexi >n of the last two phalanges, and extension of the first, on 
the attempt to use the fingers. (From nature.) 
Fig. 18.—Old-standing palsy of interossei and thenar muscles, showing the 
over-extension of the first and flexion of the last two phalanges. 
Fig. 19.—Paralysis of all the intrinsic muscles of the hand and of the long 
flexor of the thumb, in consequence of an injury to the brachial plexus in dis- 
location of the sh ulder. The fingers present the claw-like attitude; the thumb 
is in extension. (After Duehenne.) 
Fig. 20.—Paralysis of the ulnar nerve from a wound at the wrist (indicated 
in the figure). Extreme claw-like hand from the unopposed contracti on of the 
common extensor and long flexors of the fingers and thumb. (After Duehenne.) 
posture even at rest (Fig. 18), and ultimately the posture becomes warped into 
a deformity by the over-extension of the first phalanges, and extreme flexion 
of the others, due to the contracture of the long extensor and of the flexors 
the tendons of these muscles stand out conspicuously on the back and in the 
palm, and a claw-like attitude is developed, the “ main en griffe ” (Figs. 19 and 
20). Changes in the articulations may ultimately limit even passive movement. 
Muscles of the Thumb.—Extensor secundi internodii pollicis (musculo- 
spiral nerve) extends both phalanges, and moves the whole thumb backwards 
and from the fingers, so as to bring it behind the plane of the metacarpus. It 
may ultimately extend the wrist-joint, but it never supinates. It is not used in 
extending the thumb when this is opposed to the first finger. In para- 
lysis, the metacarpal bone of the thumb is slightly flexed on the carpus, and is 
inclined forwards. The second phalanx is flexed on the first, and can only be- 
extended (by the abductor and outer part of the short flexor) when the meta- 
carpal bone is adducted and the first phalanx is flexed. The constant flexion of 
the second phalanx interferes with the movement of the index finger, unless the MUSCLES OF UPPER LIMB. 
37 
patient remembers to move the thumb out of the way by the extensor of the 
metacarpal bone. Writing is not interfered with because the muscle is not con- 
cerned in extension with opposition. 
The Extensor primi internodii pollicis (musculo-spiral nerve) is the true 
abductor of the thumb. It moves the metacarpal bone outwards, and extends 
the first phalanx. It would move the whole hand in the same direction as the 
thumb, were not this tendency counteracted by the antergic contraction of the 
extensor carpi ulnaris (q. v.). It does not pronate or supinate. In paralysis 
abduction of the metacarpal bone is less than normal. There is an undue flexion 
of the first phalanx, and the metacarpal bone is flexed on the carpus, so that the 
thumb is drawn towards the palm. The loss of this muscle is, however, compen- 
sated to a considerable extent by other muscles. 
The Extensor ossis metarcarpipollicis (musculo-spiral nerve) is really the long 
abductor of the thumb. It moves the metacarpal bone outwards and forwards, 
flexing it on the carpus, and then flexes the wrist with slight pronation. It thus 
moves the thumb as much forwards as outwards. In paralysis the metacarpal 
bone is, at rest, less inclined forwards than normal, and somewhat abducted, but 
the first phalanx is in its normal position. Movement of the thumb is but little 
interfered with. 
In combined palsy of the extensors of the first phalanx and of the metacarpal 
bone the thumb becomes adducted, and is parallel to the radius. The first 
phalanx is slightly flexed by the thenar muscles. 
The Thenar muscles constitute two groups: (1) The short abductor and 
outer portion of the short flexor (median nerve) move the metacarpal bone for- 
wards and inwards (flexing the first phalanx), incline it outwards, and rotate it 
inwards, so as to place its palmar aspect opposite the fingers. The second 
phalanx is ultimately extended. If the metacarpal bone is previously abducted 
the movement is greater, and amounts to circumduction. (2) The adductor 
and inner part of short flexor (ulnar nerve) go to the inner side of the first 
phalanx. The metacarpal bone is moved towards that of the second finger: if 
previously flexed, it is extended ; if previously opposed to the index, it is moved 
a little outwards. The phalanges follow the movements of the metacarpal bone, 
but the first is slightly flexed and the second is extended, as the fingers are 
by the interossei. 
The Opponens pollicis (median nerve) flexes the metacarpal bone on the 
carpus, and abducts it, but this movement is insufficient to oppose the thumb 
to the index ; the conjoint action of the abductor is necessary (see above). 
The Flexor longus pollicis (median nerve) flexes the second phalanx forcibly 
and the first feebly. It has no action on the metacarpal bone. It is used in 
writing (making a stroke towards the body) and in picking up a small object, 
&c. In paralysis this flexion is lost, and with it these actions ; if an object is 
held between the tips of the thumb and forefinger, the last phalanx of the 
thumb is bent back. Other movements of the thumb are not interfered with. 
If all the thenar muscles are paralysed the metacarpal bone is in the plane of 
the index, and drawn towards it by the extensor of the second phalanx, which 
moves the metacarpal bone inwards and backwards. The whole thumb corre- 
sponds with the metacarpal bone in position, the phalanges being normal. In 
paralysis of the short abductor and flexor the second phalanx cannot be extended 
unless the metacarpal bone is abducted. These shoi't muscles normally prevent 
the abduction that the extensor of the second phalanx tends to produce. The 
latter, moreover, prevents undue adduction when the special abductors are para- 
lysed, but brings the metacarpal bone into the plane of the index. Thus the 38 
ACTION AND PAEALYSIS OF MUSCLES. 
posture of the hand at rest resembles that of the hand of an ape (Figs. 21 and 22). 
If the abductor and opponens are paralysed, the tips of the thumb and fingers can 
Fig. 21. 
Fig. 22. 
Fig. 23. 
Fig. 21.—Normal position of the thumb (for comparison with the succeeding 
figures). 
Fig. 22.—Position of the hand in long-standing paralysis and wasting of the 
tlenar muscles. Under the influence of the long extensor the metacarpal bone 
of the thumb has been brought into the same position as the other metacarpal 
bones, being rotated slightly, so that the back of the thumb is in the plane of 
the back of the hand, like the hand of the ape. (Alter Duclienne.) 
Fig. 23, from another case, shows the same condition, hut still greater dis- 
placement of the metacarpal bone has taken place, from the greater contraction 
of the extensor. (After Duchenne.) 
only be brought together by flexing the last 
phalanges of the digits (Fig. 24). Then the 
thumb can be brought into contact with the 
finger by means of the short flexor, which 
inclines the metacarpal bone sufficiently to 
effect this, although not enough for the tip 
of the first finger to touch the thumb when its 
phalanges are extended. 
If the short flexor is paralysed, the thumb 
can still be opposed to the first two fingers by 
the abductor, hut it cannot he opposed to the 
last two fingers, on account of the deficient 
lateral inclination of the thumb, which should 
be produced by this muscle. Writing is easy 
by means of the short abductor, whereas, if 
this is lost, although the thumb can be opposed 
to each of the fingers, writing is much inter- 
fered with. 
If all the thenar muscles are paralysed, a 
certain amount of opposition of the thumb and 
fingers is still possible, by means of the flexion 
of the last phalanges of the thumb and fingers. 
If all are paralysed except the adductor, objects 
can still he held between the thumb and side of 
the palm. 
Fig. 24.—Paralysis of the ab- 
ductor brevis and opponens 
polbcis. From the want of 
these muscles the thumb can 
only be brought in contact 
with the tip of the index by 
strong flexion of the last two 
phalanges of the fingers, other- 
wise the tip of the thumb 
only reaches the middle of 
the second phalanx. (After 
Duchenne.l 
Muscles moving the Hip-Joint.—The Gluteus maximus (small sciatic 
nerve chiefly) extends the hip-joint, and freely rotates the thigh outwards. It 
is the most powerful extensor of the hip, and it is chiefly used when a forcible 
Muscles of the Lower Limb MUSCLES OF LOWER LIMB. 
39 
extension is required, and the joint has been previously flexed. It is employed, 
not in standing, or in walking on level ground, but in going upstairs, or uphill, 
and in rising from a seat. When it is paralysed these movements are 
difficult. 
The Gluteus medius (gluteal nerve) is the chief abductor. All parts of the 
muscle have this action, but, in addition, the anterior third moves the thigh 
forwards and rotates it inwards, while the posterior third moves it backwards 
and rotates outwards. The successive action of the several parts causes circum- 
duction. The Gluteus minimus (gluteal nerve) has probably the same action. 
In paralysis, abduction and circumduction are lost; in standing on the other foot 
the pelvis is inclined from the affected side, and hence, in walking, there is an 
oscillation of the trunk, which becomes very considerable if the muscles of both 
Crural n 
J- Tensor vaginm femoris. 
Obturator n 
Pectineu 
Sartorius. 
Adductor map 
Adductor long 
Quadriceps. 
Rectus femoris. 
Crureu 
j- Vastus extern. 
Vastus intern. 
Fig. 25.—Motor points on the front of the thigh (Erb) 
sides are affected. Moreover, the unopposed tone of the outward rotators pro- 
duces a permanent rotation of the leg, so that the toes are directed outwards, 
and, from the altered position of the foot, the propulsion of the body in walking 
is deficient. 
The Pyriformis, Gemelli, Obturator internus, and Quadratus femoris (special 
nerves from the sacral plexus) all rotate the thigh outwards, and the first- 
named muscle, in addition, carries the thigh obliquely backwards and outwards, 
in the same way as the posterior fibres of the gluteus medius. In paralysis of 
these muscles external rotation is impossible, and the unopposed tone of the 
internal rotators (anterior fibres of the gluteus medius and minimus) causes the 
leg and foot to be habitually turned inwards. 40 
ACTION AND PARALYSIS OF MUSCLES. 
The Psoas (lumbar nerve) and Iliacus (anterior crural nerve) flex the hip- 
joint, and, in doing so, cause also a slight rotation outwards. In paralysis, 
flexion is lost, and the use of the leg in walking becomes impossible. 
The Tensor vaginae femoris has a slight power of flexing the hip, and at 
the same time rotates the thigh in. It normally counteracts the tendency of 
theilio-psoas to rotate outwards. If it is paralysed, there is a tendency for the 
foot to turn out when it is being brought forward in the act of walking. 
Adductors of the Thigh.—The Pectineus (obturator nerve) causes an oblique 
movement forwards and inwards, i. e. a combined flexion and adduction, as in 
crossing the legs. It also rotates outwards. The Adductor longus, and pro- 
bably the Adductor brevis (obturator nerve), have the same action, but the 
flexion is less than by the pectineus. The Adductor niagnus (obturator and 
great sciatic) causes a similar adduction, but while its upper fibres rotate out- 
wards its lower fibres rotate in, and ai-e employed in keeping the foot straight 
during adduction in riding. This is very difficult if these fibres are paralysed. 
The foot then turns out when the hip is flexed, either in the recumbent posture 
or in walking, from the preponderance of rotation out by the other adductors. 
When all the adductors are paralysed, not only is adduction lost, but in flexion 
of the hip the foot is moved forwards and outwards, instead of directly for- 
wards, showing that there is normally a synergic action of the abductors and 
adductors with the flexors in this movement. 
Muscles moving the Knee.—Extensors: Rectus, Vasti, and Crureus, 
together called the E. quadriceps (ant. crural nerve).—The vasti act solely on 
the knee-joint; the rectus also aids in flexing the hip, but chiefly when the 
knee is bent. In consequence of its passage over the hip-joint, moreover, the 
force with which it extends the knee is increased by the simultaneous extension 
of the hip. This effect is useful in the propulsion forwards of the body in 
walking. The crureus is unimportant. 
In paralysis of the extensors of the knee, standing is still possible if the knee 
is extended, since the arrangement of the articulation renders a contraction of 
the extensors unnecessary. But secondary shortening of the flexors is apt to 
occur, and then standing becomes impossible because the knee cannot be perfectly 
extended. In the same way, walking is possible if the leg is not moved forward 
beyond the vertical position ; if it is, the knee becomes flexed by the weight of 
the leg and foot, and the patient falls when he attempts to rest upon it. 
liisingfrom the kneeling posture in the ordinary way is impossible. In partia 
paralysis of the muscles, as in pseudo-hypertrophic paralysis (q. v.), the exten- 
sion of the knee, in rising, is facilitated by placing the hand upon it, and so 
bringing the centre of gravity of the body near the fulcrum of the lever formed 
by the femur. If the vastus internus aud rectus are paralysed, the vastus 
cxternus may dislocate the patella by the obliquity of its traction. The vastus 
internus never does so in the opposite condition, because its action is less oblique. 
Flexors of the Knee.—The Sartorius (ant. crural nerve) flexes the hip- and 
knee-joints, and has a feeble power of rotating the thigh outwards and the knee 
inwards. It is a muscle of small importance. 
The Gracilis (obturator nerve) adducts the thigh more powerfully than it 
flexes the knee. It rotates the leg inwards. 
The Semitendinosus, Biceps, and Semimembranosus (great sciatic nerve) 
are not only flexors of the knee but extensors of the hip-joint, and are the 
muscles that extend the hip during ordinary walking, the gluteus maximus 
(q. v.) being called into action only during special efforts. The leg is rotated 
inwards by the semitendinosus, outwards by the biceps. 41 
MUSCLES OF LOWER LIMB. 
In paralysis of the flexors, the resulting loss of the power of flexion interferes 
with walking, since the knee-joint cannot be bent, in the forward movement of 
the leg, until the thigh is flexed sufficiently to permit the weight of the foot to 
flex the knee. To prevent the toes striking the ground the foot is unduly flexed 
on the leg. The loss of the support that the flexor tendons give to the knee- 
joint leads to an undue strain on the ligaments, which become stretched, and 
slight retroflexion of the joint may occur. 
In paralysis of the muscles that extend the hip, there is a tendency to fall 
forwards in walking. To counteract this the trunk is carried backwards, and a 
fatiguing strain on the flexors of the hip results. 
In paralysis of the biceps, the leg, during flexion, is rotated inwards ; when the 
biceps remains and the other muscles are paralysed, there is an undue rotation out- 
"Ext. poplit. n. 
Tibialis anticiis 
Extensor digit, 
Gastrocrem. (outer head) 
Peroneus lougus. 
| Soleus. 
Peroneus brevis, 
Extensor long, 
Flexor long, pollicis. 
Extensor brev. digit. 
Dorsal interossei 
Abductor minim, digit. 
Fig. 26.—Motor points of leg, outer side (Erb). 
wards. The effect of these abnormal movements on the ligaments of the joint is 
such that, after a time, the amount of rotation becomes greater than is possible in 
health. 
The Popliteus (internal popliteal nerve) has but a feeble power of flexing the 
knee. Its chief action is to rotate the leg inwards when the knee-joint has been 
flexed. 
Muscles moving the Foot.—Extensors of Foot on Leg*—The Gastrocnemius 
* These muscles are sometimes termed “ plantar flexors,” because they are homo- 
logons with the flexors of the wrist. The term is a bad one, since it involves a use 42 
ACTION AND PARALYSIS OF MUSCLES. 
and Soleus (internal popliteal nerve, from the sciatic) have the same action. 
They extend the hinder part of the foot and draw down the outer side of the 
forepart of the foot, but very little the inner side. Hence the foot is rotated, 
j-Gluteus maximus, 
Sciatic n 
Adductor magnns. 
■ Semitendinosus. 
’■Semimembranosus. 
Biceps (long head) 
Ext. poplit, 
poplit. ». 
Gastrocnem. (ext. headl- 
'Ga'trocnem. (int. head), 
Soleus< 
Soleus. 
Flexor long. poll. 
Flexor digit, comm. 
Tibial n. 
Fig. 27.—Motor points, back of thigh and leg (Erb) 
so that the dorsum looks outwards, while the whole foot is turned inwards on 
the axis of the leg. The peculiar inversion and adduction that thus accompanies 
of the word “flexor” in absolute contradiction to its proper signification. We 
ought not to frame a descriptive term such as this on an analogy which involves a 
contradiction to the description. Flexion is bending, a movement from a straight 
line; and extension is less bending, a movement towards a straight (stretched, 
extended) line. To call a movement toward a straight line “flexion,” because in the 
arm the similar movement produces this effect, is a process that is not description, 
but the statement of an analogy—the worst possible kind of nomenclature. Names 
should be descriptive or they should be arbitrary. Neither theory, nor analogy, 
nor homology should have any part in them. What we call homology is merely a 
species of analogy; it rests on inference and reasoning, not on simple absolute 
aspect. Nothing that rests on reasoning is inherently stable and free from change. MUSCLES OF LOWER LIMB. 
43 
extension is due to the form of the articular surfaces. The gastrocnemius has 
very little power of flexing the knee, but the extension of the knee increases the 
effect of the muscle on the ankle-joint, especially in walking, just as we have 
seen that the extension of the hip.augments the force with which the contracting 
rectus extends the knee. For direct extension of the ankle, the peroneus concurs 
and opposes the inversion. The only difference between the gastrocnemius and 
soleus is that the latter, having no attachment to the femur, can extend the 
ankle when the knee is flexed as well as when it is extended. In paralysis of 
these muscles, extension of the ankle (by the peroneus longus and flexor longus 
digitorum) is extremely feeble, and the foot can scarcely he canned beyond a 
right angle. Walking is greatly interfered with ; standing on tiptoe is im- 
possible. The unopposed peroneus longus causes eversion of the foot, lowers the 
head of the first metatarsal bone, and deepens the plantar arch. In time the 
ankle-joint becomes over-flexed, the heel considerably lowered, and the plantar 
muscles and fascia become shortened. The resulting deformity is termed talipes 
calcaneus (Fig. 28). 
Fig. 28.—Talipes calcaneusfrom atrophic paralysis of the calf muscles, with 
flexion of the middle and distal phalanges of the toes, from paralysis of 
the interossei. 
The Peroneus longus (musculo-cutaneous nerve, from external popliteal of 
sciatic) everts the foot, lowering the inner border, narrowing the foot, and in- 
creasing the plantar arch. It also turns the whole foot out on the axis of the leg. 
It has a very feeble power of extending the ankle. It keeps down the inner part 
of the foot during extension by the calf muscles, as in walking. In paralysis 
of this muscle the inner part of the front foot is not supported during extension, 
and yields to slight force. The foot becomes adducted and rotated, so that the 
sole is direct 'd inwards, in consequence of the unopposed action of the sural 
muscles. The inability to press the inner part of the ball of the foot firmly 
against the ground leads to over-action of the flexors of the great toe. The 
plantar arch is lessened ; there is “ flat foot.” 
Flexors of the Foot.—The Tibialis anticus (anterior tibial branch of ext. 
popliteal nerve) produces simultaneously three movements : it elevates the inner 
part of the front foot (opposing the peroneus longus) ; it flexes the ankle-joint, 
and adducts the foot. The Extensor longus digitorum (ant. tibial nerve), besides 
extending the toes, flexes and abducts the foot. The abduction is in consequence 
of the outward position of its tendons beneath the annular ligament. These 
two muscles together produce direct flexion of the foot, or flexion with adduction 
or abduction, as the force of one or the other preponderates. Paralysis of either 
weakens flexion, and the corresponding lateral movement is lost, flexion being 
accompanied by the deviation effected by the muscle that remains. The defect 
in flexion is greatest in paralysis of the tibialis, and the loss of the instinctive 44 
ACTION AND PARALYSIS OF MUSCLES. 
flexion, when the leg is brought forward in walking, causes the foot to catch 
against the ground. Paralysis of the flexors is followed by secondary contrac- 
ture of the extensors, and talipes equinus results (Fig. 29), which is the greater 
the longer the palsy has lasted (Fig. 30). Its occurrence is facilitated, in many 
Fig. 29.—Talipes equinus, due to atrophy of the tibialis anticus and 
secondary contracture of the calf muscles. In A the foot is shown at 
rest; there is slight equino-varus. In B it is shown during flexion, 
and the varus is changed to valgus by the action of the peroneus 
longu8. Note the increased extension of the toes in B from the com- 
pensatory over-action of the long extensors of the toes. (After 
Duehenne.) 
cases of palsy, by lessened growth of the hones of the leg, so that the ball of the 
foot only touches the ground when the foot is extended. There is usually slight 
Fig. 30. 
Fig. 31, 
Fig. 30.—Extreme talipes equinus from o'd-standing palsy of the tibialis 
antirus (infantile paralysis) and extreme contraction of the calf muscles. No 
flexor movement was possible. 
Fig. 31.—Paralysis of the interossei and the adductor and short flexor of the 
great toe. The first phalanges are over-extended and the second are flexed, 
while the hollow of the sole is increased. (After Duehenne.) 
rotation inwards of the foot at rest, even when the tibialis is paralysed (see Fig. 
29, a), because such rotation is produced by the sural extensors (p. 42); but in MUSCLES OP LOWER LIMB. 
45 
this case the slight valgus at rest is changed to varus on an attempt to flex the 
ankle (Fig. 29, b). 
The Peroneus brevis (musculo-cutaneous [peroneal] branch of ext. popliteal 
nerve) abducts the foot and rotates it, raising the outer edge. 
The Tibialis posticus (posterior tibial nerve from int. pop.) adducts the foot 
and curves it, rendering the outer border and instep more convex. Its power of 
adduction is greater than that of the tibialis anticus, and it does not rotate the 
foot in the same manner. 
These two muscles alone have the power of adducting and abducting without 
flexing or extending; and in their paralysis these simple movements are lost. 
If one only is paralysed, a deformity develops corresponding to the action of 
the other muscle,—talipes valgus in paralysis of the tibialis posticus ; t. varus 
in that of the peroneus brevis. 
The muscles moving the toes present, in their mode of action, a close corre- 
spondence to those of the fingers. 
The Extensor longus digitorum and the Extensor longus pollicis (anterior 
tibial nerve) extend chiefly the first phalanges, while the Flexor longus digitorum 
and Flexor brevis (posterior tibial nerve) flex the lust two phalanges. The 
Lumbricales and the Interossei (post, tibial nerve by ext. and int. plantar), 
together with the Abductor and Flexor brevis minimi digiti, opoose both the 
other extensor and flexor muscles, flexing the first phalanx and extending the 
others. This action is of great importance in walking, since they give the last 
propulsion to the body as the ball of the foot leaves the ground. The Abductor, 
Adductor, and Flexor brevis pollicis (plantar nerves from post, tibial) have a 
similar action on the great toe, but with adduction or abduction respectively. 
The interossei also produce a lateral movement of the toes, but this action is of 
little practical importance. In paralysis of the common extensor of the toes, 
and of the proper extensor of the great toe, the tonic force of the interossei and 
analogous muscles produces persistent flexion of the first phalanges and exten- 
sion of the others. If the conditions are reversed, and the latter muscles are 
paralysed, the first phalanges are over-extended, sometimes even subluxated, 
and the two other joints are flexed, so that a claw-like form of foot is the 
result (Figs. 31 and 28). The final propulsion in walking, above described, is 
much interfered with, and the attempt is painful because the ends of the toes 
are turned towards the ground. 
Other examples of the effects of paralysis of the muscles of the arm 
and leg are given in the illustrations to the chapter on Infantile 
Paralysis (Acute Polio-mj elitis). PART II. 
DISEASES OF THE NERVES. 
GENERAL PATHOLOGY. 
Structure.—The individual fibres consist of a central “axis- 
cylinder,” which is the chief functional element, surrounded by the 
“ medullary sheath,” or “ white substance of 
Schwann,” composed of myelin (M, Fig. 32), a 
liquid fatty material supported by a fine network 
of horny substance, “ neurokeratin.” The myelin 
is absent in the “ non-medullated ” fibres of the 
sympathetic. A delicate membrane surrounds the 
white substance, the “primitive sheath,” or “ neuri- 
lemma,” or “sheath of Schwann ” (S). Nuclei (n) 
lie at intervals within the sheath, between it and 
the myelin. The white substance is interrupted at 
regular distances by what are termed “ nodes,”—some- 
times, from their discoverer, “nodes of Ranvier” 
(N). The end of each portion, or “internode,” is en- 
closed by the sheath, through which the axis-cylinder 
passes. Between the incurved extremities of the 
sheath is a little clear cementing substance, shown 
by the fine dotting in the figure. There is one 
nucleus (n) to each internode, about its middle; 
hence they are sometimes called “internodal nuclei.” 
Around the nucleus is a little protoplasm, and it 
is probable that a very thin layer of protoplasm 
everywhere lies between the sheath and the myelin. 
Each internode may be conceived as a cell, a fat- 
cell according to Ranvier, consisting of membrane, 
nucleus, protoplasm, and fatty matter, the cells being 
arranged end to end, and the axis-cy.inder pass- 
ing through them, as a string passes through a 
series of tubular beads. The internodes are shorter 
towards the termination of a nerve. It is important 
not to confound the nodes with other, imperfect 
divisions, sometimes termed the “ incisions of 
Schmidt” (IS, Fig. 32,1). These are oblique, incomplete divisions 
of the white substance. Many exist in each node. They are believed 
Fig. 32.—Diagram 
of the structure 
of nerve-fibres. I 
and II, medul- 
lated, III, non- 
medullated fibre; 
S, sheath ; M, 
myelin, or white 
substance of 
Schwann; Ac,axis- 
cylinder; n, nu- 
cleus; N, node; 
IS, incision of 
Schmidt. (From 
a preparation of 
the nerve-fibre of 
a frog,stained with 
osmic acid.) PHYSIOLOGY OF NERVES. 
47 
by some histologists to be of artificial origin, but their uniform 
character seems conclusive evidence that they depend on structural 
conditions. 
The myelin, Banvier suggests, must protect the axis-cylinder, since 
its almost liquid consistence will diffuse pressure on the nerve. It 
may also have an insulating action, which, while not essential for 
conduction, may render conduction more perfect, and possibly more 
rapid. The nodal segmentation keeps the almost liquid myelin uni- 
formly distributed along the fibre, and permits nutrient material to 
reach the axis-cylinder. 
The “grey fibres,” “ non-medullated fibres,” consist of an axis- 
cylinder, sheath, and nuclei (Fig. 32, III), but contain no myelin. They 
constitute the sympathetic nerves, but some (probably sympathetic 
fibres) are found in all the spinal nerves. They are absent from the 
nerves of special sense, except the olfactory, which contains no other 
fibres. 
The nerve-fibres are united into “ fasciculi ” by delicate nucleated 
connective tissue, and these fasciculi are similarly connected into lai-ger 
bundles, while the whole nerve is surrounded by a dense connective- 
tissue sheath. From this a very delicate “ sheath of Henle ” extends 
on to the single nerve-fibres at the final distribution of the nerve. All 
these tracts of connective tissue are continuous. In them the blood- 
vessels run and nerve-fibres are distributed. These “ nervi nervorum ” 
are derived from the nerve they supply.* Each nerve (“including 
its sheath”) is thus part of the area of distribution of its own fibres. 
Physiology op Nerves.—The first greatfact to be kept in view is that 
the axis-cylinder of each nerve-fibre is the prolonged process of a nerve- 
cell, which passes gradually into the axis-cylinder, without any abrupt 
or visible change in structure. This unity explains the secondary 
degeneration described in the next section; the axis shares the life of 
the cell, and cannot maintain a separate existence. Further, the fibre 
shares all modifications in the nutrition of the cell, manifesting it 
perhaps in a different way, but never preserving a perfectly normal 
state if the nutrition of the cell is changed. 
In the function of nerve-fibres we can see another aspect of the 
same fact. We speak of cells producing and of fibres conducting 
what is termed nerve-energv. But fibres also can produce nerve- 
energy. The stimulation of a fibre is sufficient proof of this. More- 
over, if we pass up to the nerve-cell we are met by the necessity of 
recognising the fact that this function of the fibre is not peculiar to it. 
The process of the cell must conduct, and the cell must itself conduct. 
Each motor cell of the cord is part of the path through which the 
nerve-energy from the brain passes. That which passes through 
must be conducted, however it may be changed in amount. Even if 
it is renewed, we cannot so distinguish this function of the cell from 
that of the fibre as to say that there is not conduction. Nor can we stop 
* Horsley, Koy. Med. and Chir. Soc., January 22, 1885. 48 
PHYSIOLOGY OF NERVES. 
here. A fibre can generate nerve-energy, and a cell can conduct: does 
the whole function of the two differ except in degree ? If they are 
of the same nature, and can perform the same function, we seem unable 
to avoid the conclusion that the nature of the function must be the 
same, and that the difference we recognise must be in degree. 
The great contrast between them is not in function ; it is in vitality. 
Function differs only in degree, just as their structure differs in 
degree. But the cell possesses an independent vitality, and with this 
it possesses also that mysterious body—a nucleus. Fibres have nuclei 
in abundance outside the axis-cylinder; they have no nucleus within 
their functional element. We seem to have in this feature a vital 
difference, pregnant alike with meaning and effect. 
Further, so far as is yet known, the cells within the central nervous 
system, from which fibres spring, are those from which they conduct. 
Hence the direction of conduction is the same as that of degeneration. 
But this relation does not exist everywhere; it is so in the motor 
nerves, but the sensory peripheral nerves degenerate downwards and 
conduct upwards. Here, however, the conditions are manifestly excep- 
tional. Their vitality depends on the cells of ganglia on the posterior 
roots. These are vital as far as we can see alone ; they are not related 
to function. The function is towards, not from them. The impulses 
come from the structures in which the nerves end—structures that 
seem to be developments of the axis-cylinder, far lower in nature 
than nerve-cells, but possessing the same power of generating an 
impulse when some form of energy acts on them from without. 
These upbearing nerves end peripherally in most cases by dividing 
into many branches. Thus each fibre is brought into much more 
extensive relation with the external forces than would otherwise be 
possible, and may end in an amount of receptive material not incom- 
parable to that of a nerve-cell itself. 
The endings of the motor nerves are those to which impulses proceed, 
and hence have no relation to the considerations just mentioned. 
These structures in some way transfer the nerve-energy to the 
muscular protoplasm, at least it disappears in making the muscle 
contract; and the only fact with which we are immediately concerned 
is that this must involve continuous molecular contact. In such 
continuity we probably have the means through which the nutrition 
of the muscular fibres is influenced by that of their nerves. 
Lesions of Nerves.—Secondary Degeneration.—As we have seen, a 
nerve-fibre undergoes the structural changes known as “degeneration” 
whenever it is separated from the cell from which it springs. We 
have also seen that, as a rule, the degeneration is in the direction 
of conduction, i. e. the cell from which the nerve-fibre conducts is 
that which governs its nutrition, with the exception of the sensory 
fibres in the peripheral nerves. The degeneration is commou'y 
termed “ secondary ” because it is dependent on a “ primary ” lesion of LESIONS OF NERVES. 
49 
another kind—as division of the nerve. Degeneration also follows 
many slighter lesions of a nerve-compression, over-extension, and the 
like; but it is not certain that this is always the same as that which 
follows a total lesion. The secondary degeneration is often called 
*• Wallenan,” from the name of the pathologist who first studied it. 
It is of great importance, practical and theoretical. The medullary 
sheath breaks up into segments, and these into smaller and smaller 
fragments, and the minute globules and granules are ultimately 
removed from the nerve-sheath. This is then empty, the axis-cylinder 
having also perished during the process. The nature of this process of 
destruction has been studied by Erb and others, but has been chiefly 
elucidated by the researches of Ranvier, and must be considered in 
some detail. Ranvier has shown that it is not a mere process of death 
or decay, but au active process, a destruction of the nerve as such by 
the protoplasm and nuclei of the internodal cells that constitute it. 
The nature of the process has been chiefly studied in animals. The 
most important facts are illustrated in Eig. 33, in which the examples 
have been selected from Ranvier’s figures and reduced to one tint. 
In the rabbit the first changes are to be perceived at the end of 
twenty-four hours. The nuclei are increased in size (A n, B n); 
the amount of protoplasm about them is greater than normal, and 
is granular; there is in places a local increase in the amount of 
protoplasm within the sheath, compressing the myelin (A x, B xr 
C x). The nuclei then become detached from the sheath; the proto- 
plasm everywhere increases, and encroaches on the myelin, until here 
and there it meets across the tube, c mpletely separating the myelin 
(A, lower part; B, upper part), and with the myelin the axis-cylinder 
(D). This process then goes on with increased rapidity; the myelin 
is broken up into smaller and smaller fragments (C, E, E) which are 
globular in the watery protoplasm, just as oil forms globules in water. 
The nuclei meanwhile continue to enlarge, and then divide, first the 
nucleolus and then the whole nucleus (F). The two nuclei may 
again divide, until (as in G) there are four or more nuclei in each 
internode, instead of one only as in health. The small globules of 
fatty myelin seem to become changed in chemical composition, since 
they are stained less deeply by osmic acid. Ranvier suggests that 
their fatty matter may undergo a process of saponification. Ultimately 
they seem to pass through the sheath, are taken up by connective- 
tissue cells and lymphatic cells in the vicinity (as in J), and are 
gradually, for the most part, removed. By the time the myelin is in 
small globules the nuclei cease to multiply. On the removal of the 
products of degeneration the sheath shrinks, and looks empty in 
places, but here and there it is enlarged by the nuclei, protoplasm, 
and a few remaining myelin globules (H). Hence in transverse 
section many small sheaths are seen with a few of larger size where 
they have been cut across at these swellings. 
In the rabbit the first changes are visible at the end of twenty-four 
YOL. I. 50 
LESIONS OF NERVES. 
hours; tlie first complete interruption of the myelin and axis-cylinder 
occurs about the end of the second day ; the process of destruction is 
Fig. 33. 
Tig. 34. 
Fig. 33.—A-J, Degeneration of nerve-fibres (osmic acid and carmine 
staining). A, from sciatic of rabbit four days after section; B, C, same, 
fifty hours after section; D, a fibre stained with carmine only, to show 
the axis-cylinder ; F, G, fibres from pigeon three days after section ; H, two 
fibres from pneumogastric of rabbit six days after section ; J, a lvmphatic 
cell from interfibrillar connective tissue, containing globules of myelin 
that it has taken up. In all the figures n, n, nuclei; x,x, constrictious of 
the myelin produced by the growth of the protoplasm; ac, axis-cylinder. 
K, L, Regeneration of nerve-fibres. K, from pneumogastric of rabbit 
seventy-two days after section ; L, from sciatic of rabbit ninety days after 
section; e, rounded end of white substance of Central end of nerve; it, 
sheath ; na, new axis-cylinder. In L are two globules of myelin remaining 
from the degeneration of the old fibre. 
Fig. 34.—Degenerating fibres from cutaneous nerves of man. (After 
Pitres and Vaillard.) A, from near a bedsore in a case of fracture of the 
skull; B, C, D, from the fifth nerve in a case of neuralgia and ulceration of 
the lip; n, n, nuclei. In A the protoplasm and nuclei are increased, and 
the myelin is breaking up, the processes having proceeded furthest in the 
neighbourhood of the nucleus in the middle of the fibre; in B the segmenta- 
tion has gone on to the formation of globules, which in C are, for the most 
part, small, and many have been removed, so that the fibre is narrow; 
while in I) all tbe products of degeneration have been removed from con- 
siderable tracts of the sheath. 
considerably advanced at tbe end of tbe fourth day, and is finished, 
ajid the multiplication of the nuclei ceases, towards the end of the GENERAL PATHOLOGY. 
51 
second week. In peripheral nerves the changes seem to progress 
from the lesion to the periphery, but within the central nervous 
system they are said to begin at the same time in all parts of the 
fibre. It is uncertain to what extent the difference is real or 
apparent, being simultaneous in the whole extent of the separated 
portion of the nerve. They progress more rapidly at its peripheral 
extremity than elsewhere. At the end of the second day, in the rabbit, 
stimulation of the nerve by electricity no longer causes muscular 
contraction. Thus the disappearance of the electrical excitability 
coincides in time with the first complete segmentation of the myelin 
and axis-cylinder. This interruption explains what is termed the 
“loss of excitability.” It must be remembered that the loss of 
continuity is not the only cause of loss of excitability. (See p. 52.) 
If the ends of a divided nerve are brought quickly into perfect appo- 
sition secondary degeneration does not occur in animals, and probably 
not in man.* Simple division appears to be a less serious injury 
than the extensive displacement of myelin in a contusion. 
Thus the process is the result of an active growth of the nuclei and 
protoplasm of the nerve, i. e. of the cellular elements of which the 
uerve is composed. Why does this occur? The determining cause 
is the interruption of the axis-cylinder—its separation from the cell 
of which it is a process. It follows equally destruction of the nerve- 
cell. Eanvier points out that the destructive growth of the proto- 
plasm, which follows loss of function in the axis-cylinder, suggests 
that normally its function restrains the vital energy of the cell- 
elements. But it is possible that changes in the nutrition of the axis- 
cylinder precede the segmentation. 
A process of destructive cell-activity suggests the idea of inflam- 
mation. The degeneration maybe regarded as a process of parenchy- 
matous inflammation. Several observers have described other indica- 
tions of inflammation outside the fibres, especially increase of nuclei, 
and accumulation of leucocytes in the interstitial connective tissue, 
and even in the nerve-sheath, and also dilatation of the blood-vessels. 
Such changes are intense at the primary lesion. Their degree in the 
nerve below the lesion is very variable, and seems to be proportioned 
to that in the primary process. This is another mode of stating the 
important fact that the irritative character of the secondary process is 
determined by the irritative nature of the primary disease. 
The process of secondary degeneration occurs more slowly in the 
rabbit than in a bird, and seems to be still slower in man, in whom 
it is probable that complete segmentation does not occur until between 
the fourth and eighth days. It is certain that an identical process 
occurs in man. Changes in peripheral nerves near bedsores and in 
the fifth nerve, found by Pitres and Vaillard, are shown in Pig. 34, a 
comparison of which with Pig. 33 will show the identity of the process. 
It is highly probable that after complete division of a nerve in man the 
See Bowlby, * Injuries and Diseases of Nerves/ p. 32. 52 
LESIONS OF NERVES. 
changes are the same as in animals. But the most common lesion in 
man is neuritis, and in this the process of degeneration is probably 
greatly modified by the severity of the primary lesion ; in some cases 
it occurs rapidly, in others very slowly. In the latter cases, which 
are chiefly those of focal neuritis, the process cannot be the same as 
that which follows division of a nerve. The change in irritability, 
which will be more fully described in the account of the symptoms, 
is a slow depression, sometimes moderate in degree. The depression 
may be preceded by an increase in irritability. In such cases there 
can be no complete segmentation of the nerve-fibres. There must be 
a gradual alteration in the molecular nutrition of the axis-cylinder,, 
changing its excitability. Even in severe cases there is not usually a 
sudden loss of irritability; the current necessary for stimulation has 
to be made stronger, until at last in seven or eight days the strongest 
endurable current fails to cause muscular contraction. But we 
cannot infer, from this alone, that there is an actual interruption of 
the axis-cylinder. A stronger current might still excite the nerve, 
because, as we shall presently see, when a nerve is being regenerated, 
an axis-cylinder may conduct, and still not be excitable by currents of 
ordinary strength. 
All severe changes in the nutrition of the fibres involve the intra- 
muscular nerve-endings in the same degree. The evidence of this is 
that the faradic irritability of the muscles (which depends on the 
nerves within them) presents changes quite similar to that of the 
nerve-trunk. But this is not always true in slight changes of nutrition 
of the nerve. We shall presently see that the slight alterations of 
irritability in the nerve and muscle do not always correspond. The 
nerves terminate in structures of special nature, and these may well 
have some slight degree of nutritional independence. 
Regeneration may occur in the nerve after the degeneration is over. 
It is a slow process, occupying the second, third, and fourth month 
after division. According to Ranvier, it occurs always by the growth 
of new axis-cylinders from the central end of the nerve (see Eig. 33, 
K and L), which ultimately become covered with myelin. One or more- 
new fibres may spring from each central fibre, and these may subdivide. 
All are enclosed in a sheath which is continuous with that of the 
central end (Eig. 83, E, s.). We must assume that only some of 
these axis-cylinders persist and achieve functional permanence. Some- 
times these fibres twist about, and even turn back and grow upwards, 
probably in the direction of least resistance. In animals, new fibres 
may grow through a considerable extent of cicatricial tissue between 
the divided ends of a nerve, but in man it is doubtful whether regene- 
ration of a divided nerve occurs unless the extremities are brought in 
contact, or at least close pi-oximity. Some investigators believe that 
there is a formation of fibres in the peripheral extremity independ- 
ently of the growth of new fibres from the central end.* In cases 
U.ff. by Neumann, Mayer, &c. A full abstract of their observations is given GENERAL PATHOLOGY. 
53 
of slight injury, regeneration occurs more readily; in these it is 
probable, as we have just seen, that degeneration has been incom- 
plete. The regenerated nerve-fibres regain some conducting power 
while they are still much narrower than normal, and before they can 
be excited by electricity. 
Muscles.—The degeneration of the motor nerves is attended by 
changes in the nutrition of the muscles. These commence in or after 
the second week. The muscular fibres become narrower, and may be 
reduced, ultimately, to one-third of their former width. An increase in 
width has been said to precede the narrowing for a few days.* The 
transverse striation becomes less distinct, and the striae seem to be nearer 
together than in health. The fibres may become cloudy or granular, 
but do not present actual fatty degeneration except in some very acute 
cases. If no regeneration of the nerve takes place, the transverse 
situation gradually disappears, and may be replaced by a longitudinal 
striation, or the fibres may undergo certain chemical changes, and pre- 
sent a peculiar glassy appearance, which has been called “ vitreous 
degeneration.” During the progress of the changes in the fibres, the 
nuclei of the sarcolemma and of the interstitial tissue are increased in 
number, and cellular elements, either newly formed, or migrated from 
the vessels, develop into fibres, so that ultimately the muscular fibres 
are separated by considerable tracts of connective tissue, and a state of 
cirrhosis results. If regeneration of the nerve occurs, the muscular 
changes are arrested, and the normal condition of the fibres is slowly 
restored. The amount of connective tissue in the muscle is often 
permanently increased, but the fibres are narrowed out of proportion 
to the increase in the connective tissue, and this undergoes contrac- 
tion so that the muscle is for a long time smaller than normal, and its 
natural bulk may never be regained. If no regeneration of the nerve 
•occurs, the muscular fibres gradually disappear; fibrous tissue takes 
their place, and, slowly contracting, permanent shortening may result. 
Similar shortening sometimes occurs when there is partial recovery of 
the nerve and muscle. In most lesions of nerves, other than actual 
division, some fibres recover, even though others are permanently 
by Bowlby (loc. cit.), and also by Allen Starr in the Middleton Goldsmith Lectures 
for 1887 (‘ New York Med. Record/ February, 1887). By some the new axis- 
cylinders are said to be formed by elongation of the fragments of the old axis; 
by others from the nuclei of the sheath of Schwann, and appearances have been 
seen by Bowlby (loc. cit.) in man which seemed to him to bear this interpreta- 
tion. But Rauvier’s careful investigations have been fully confirmed by the 
minute researches of Vanlair (‘Arch, de Biologie/ 1885), and it is difficult to 
understand that perfect axis-cylinders should be formed and remain unexcitable, 
as the peripheral segment certainly does. Structures may he formed resembling 
axis-cylinders that are not really capable of the proper function. The weight of 
Ranvier’s undisproved and confirmed observations is very great. It is possible 
that the process, in the peripheral part of a nerve, is influenced by the connec- 
tion with other nerves and the recurrent influence of anastomosing fibres. 
* Steinert, * Verli. Phys. Ges. Wurzburg/ 1888, No. 10. 54 
LESIONS OF NERVES. 
destroyed. The muscular degeneration is the result of that of the 
motor nerves, as described at p. 22. 
Symptoms of Nerve-injury and Degeneration.—The symptoms 
that attend the lesions of motor nerves and the consequent degene- 
ration are of great importance. The lesion of the nerve causes 
paralysis of the muscles supplied by it, due to, and in propor- 
tion to, the interference with the conducting power of the nerve. 
The muscles at once become flabby from loss of tone, and to this 
atony actual wasting is added in the course of a few weeks. The 
wasting is due to the reduction in size of the muscular fibres. If the 
sensory nerve-fibres are not interrupted, the muscles become tender to 
the touch, and pain is caused by their strong contraction, due probably 
Fig. 35.—Type of degenerative reaction in a case of nerve-injury of mode- 
rate severity. (After Krb.) Muscle irritability lowered Irom middle of 
first week ; farad ic, extinct in middle of third, reappearing in ninth ; 
voltaic, increased from middle of second week until tenth, then de- 
pressed until fourteenth. Nerve irritability (changed alike to both cur- 
rents) is lowered from middle of first week, lost at end of second, 
reappearing at seventh. Power lost until end of fifth week. 
In this and the following figures the normal degree of irritability (ascer- 
tained from the healthy side) is represented by the finely dotted 
horizontal line (n.l.); faradic irritability, F, by a line of larger dots ; 
voltaic irritability, V, by a broken line; M, muscle; N, nerve; P, 
power of voluntary contraction, its degree shown by the vertical lines; 
the asterisk marks the occurrence of the lesion. The vertical divisi ns 
represent time intervals. (Many of these iudicatiug letters are given only 
in subsequent figures.) 
to the effect ot' interstitial inflammation on the sensory nerves, which 
end in the connective tissue. 
The most important symptoms are those that are afforded by elec- 
trical examination of the muscles and nerves, since they enable the 
degenerative changes to be ascertained and followed during life. The 
alterations in the electrical reaction, consequent on this degeneration, 
have been already briefly mentioned (p. 24), but must now be described 
in greater detail. The rapid degeneration of a nerve, which follows a 
severe lesion, is attended by a loss of irritability on electrical stimu- 
lation, the loss being the same to faradism and voltaism. After such 
lesions as are common in man, neuritis for instance, there is no sudden 
loss, such as occurs after injury of a nerve in an animal, when the 
nerve becomes segmented, but there is a more or less rapid diminution SYMPTOMS. 
55 
of excitability, and this goes on until no stimulation can be produced, 
even by a strong current. The progressive changes in irritability may 
be conveniently represented on a chart. Fig. 35 shows the typical 
course of the changes of irritability in a case of moderate severity. In 
the muscle (M) a fall of irritability (due to the degeneration in the 
nerve-endings) occurs simultaneously with that in the nerve trunk (N), 
and the faradic excitability becomes extinct at the same time in both 
nerve and muscle. The fall in voltaic irritability is quickly arrested 
by the change in the muscular fibres, through which they soon become 
more excitable than normal to the voltaic current. This change usually 
occurs during the second week, and the irritability continues to increase 
during the third and fourth weeks. At its maximum it may amount 
to three, four, or five cells of the battery i e. contraction can be 
obtained in the paralysed muscles with a current weaker, by so many 
cells, than is necessary to cause contraction in a corresponding un- 
affected part. The further course of the changes in irritability depends 
on the severity of the lesion and the intensity of the degeneration. In 
a case of moderate degree, such as is shown on the chart, nerve irrita- 
bility reappears about the end of the second month, usually after some 
voluntary power is regained. It is at first low, so that a strong current 
is required. It gradually increases, but for a long time continues a 
little below the normal degree. This return of nerve irritability is 
accompanied by a corresponding return of faradic irritability in the 
muscles (i.e. in the intra-muscular nerves). The increase of voltaic 
irritability often persists long after recovery of power, but it lessens 
as faradic irritability returns, and, as shown in the chart, it may 
fall below the normal before it ultimately regains its original degree. 
Slight changes in irritability can be ascertained only by a comparison 
with the corresponding part on the other side in the same individual. 
Moreover, when we speak of excitability being “ lost,” we mean that 
we can obtain no stimulation by any strength of current that can be 
borne. This strength varies in different persons and in different parts. 
The more sensitive the part, the earlier irritability seems to be lost, 
and the later it seems to return; and the greater the resistance of the 
skin, the stronger must be the strength of current.* In many cases, 
if we could use very strong currents, the irritability would be found 
to be merely much lowered, although it seems to be extinct when we 
can only test it with currents of moderate strength. 
If the lesion is very severe, so that there is no recovery, and no 
regeneration of the nerve, the loss of nerve irritability, and of the 
faradic muscular irritability, is permanent. The increase in voltaic 
irritability persists for months, and then gradually falls as the 
muscular fibres waste, and becomes lower and lower (see Fig. 36) 
* Hence the importance of ascertaining what current is actually passing by the 
use of a galvanometer, which may be thus used when the comparison with the other 
side is made by a number of cells, to spare the patient the longer and more paiuful 
process which the more exact comparison by absolute current strength involves. 56 
LESIONS OF NERVES. 
FiO. 36.—Type of reaction in a case of complete and permanent damage to 
a nerve. (After Erb.) Early course as in the last d agram ; no return of 
power, nerve irritability, < r faradic irritability in the muscle. The early 
increase in voltaic irritability gradually lessens, and at the end of ten 
months falls below the normal, but is not extinct until nearly two years. 
until ultimately no reaction can be obtained, the fibres having perished. 
It does not become extinct until at least a year has elapsed, and some- 
times (as in the chart) only towards the end of the second year. 
Often, when no contraction can be produced on the first attempt, after 
two or three applications, distinct contractions are obtained. 
The changes we have hitherto considered are in the degree of irrita- 
bility, “ quantitative ” changes. But the quantitative increase in the 
muscular irritability is often accompanied by a change in the order of 
response, according to the pole that is applied and the strength of 
current—a “ qualitative ” or “ polar ” change. We have already con- 
sidered its general characters (p. 24), and have seen that it consists 
in an undue readiness of response at the positive pole (Anode) com- 
pared with that at the negative pole (Kathode) (Fig. 37, B and C), 
the muscle being normally the more sensitive to the latter (Fig. 37, A). 
Writing Cl. for the closui-e of the circuit, O. for its opening, and C. 
for contraction, the normal reaction is— 
1. K.C1.C.; 2. 3' K0C* 
In disease— 
L 2. An.O.C.; 3. K.O C.: or even 
1. An.Cl.C.; 2. K.C1.C.; 3. K.O.C.; 4. An.O.C. 
This qualitative change is not always present, at any rate in recog- 
nisable degree. Even when there is a marked quantitative change, the 
kathodal closure contraction may still occur first. When the change 
is present, it is only in the muscles, and it must depend on the 
muscular fibres themselves. In the motor nerve the kathodal response 
is always the first, although a qualitative change has been detected in 
degenerated sensory nerves. 
The muscular contractions which occur thus with undue readiness 
differ from normal contractions, excited through the nerves, in their 
distinctly deliberate character. Instead of the quick, lightning-like 
contraction, the movement is distinctly longer in reaching its maximum 
and longer in its duration. This difference is very well shown in the 
accompanying tracings of contraction (Fig. 37). Sometimes a slight SYMPTOMS 
57 
FlO. 37.—Tracings of the muscular contractions in nerve-degeneration. (After 
Erb.) Ka, Kathodal closure contraction; An, Anodal closure contraction. 
A, tracing in health; Ka much stronger than An; contractions sudden. B, 
tracing in nerve-degeneration with moderate current. An much greater than 
Ka, the latter scarcely visible. Contraction slower, shown by the more 
sloping upstroke. C, the same, with a stronger current. Ka greater, but 
still less than An; the slow character of the contraction and its long duration 
well marked. 
abnormal tetanic contraction during the passage of the current also 
occurs. During the period of increased voltaic irritability the 
mechanical excitability of the fibres is often increased. If they are 
directly percussed, they respond with a distinct slow contraction (Erb). 
Such are the changes in irritability which occur in cases of nerve- 
lesion and degeneration of moderate and considerable degrees of 
severity. Certain variations are occasionally met with, and these 
occur especially in cases of neuritis of slight degree. In severe cases 
the fall in nerve irritability, which usually commences in the middle 
of the first week, may not take place until the end of this week, 
although it may then progress so rapidly that no stimulation can be 
obtained at the end of the second week. An example of this is shown in 
Eig. 38.* The same chart, and some of those that follow it, illustrate 
another very common variation from the type above described. There 
may be no fall in the voltaic excitability of the muscles before the 
commencement of the degenerative increase. Indeed, this initial 
fall is as often absent as present.f The change in the nutrition of 
* This and the following charts are from cases of neuritis of the facial nerve, 
f The fall seems to suggest that the voltaic irritability of the muscular fibres is 
normally below that of the nerve-endings, and this is intrinsically probable. The 
presence or absence of the fall may depend on the rapidity with which the nerve- 
endings degenerate. Some facts, moreover, that have come under my notice, 
suggest that the motor nerve-endings possess some nutritional difference from the 
fibres, in consequence of which the relative condition of the two, especially as 
regards excitability, varies in different cases, especially in the early stage. 58 
LESIONS OF NEHVES. 
the muscle may then coincide with, instead of succeeding, the degene- 
ration of the nerve-endings (Figs. 38, 40). Sometimes, if the degene- 
ration is rapid, there is an interval of a few days before the secondary 
changes in the muscle have reached the degree necessary to produce 
increased irritability. In a slight degree of degeneration, the 
increase in the voltaic irritability of the muscles may be postponed 
for a week or more after the nerve irritability begins to fall, and until 
Fig. 38.—Severe neuritis, paralysis comp’ete for months; recovery imper- 
fect. Irritability of nerve normal during first week; fell rapidly during the 
second; lost at its close. Simultaneous increase in voltaic irritability. The 
divisions on the left side represent cells of the voltaic battery, and half- 
centimetres of the secondary coil of Stohrer’s induction apparatus, in this and 
the following charts. 
Fig. 39.—Slight neuritis; slight return of power on seventh day, slowly in- 
creasing ; normal in fifth week. Muscle: faradic irritability lessening from 
fourth day, lost on fifteenth, reappearing on twentieth. Voltaic irritability 
normal till twelfth day, then augmented. Nerve-trunk : lowered from fourth 
day without initial increase, reappearing on twenty-third day; changed alike 
to faradism and voltaism. 
the rise occurs the voltaic irritability of the muscles may remain 
normal, even when their faradic irritability falls with that of the 
nerve-trunk. An instance of this is shown in Fig. 39. 
When the nerve-lesion is very 
slight in degree, the fall in nerve 
irritability may be preceded by 
a rise, which may be far greater 
in degree than the subsequent 
fall. The fall may indeed be not 
only slight, it may be altogether 
absent, so that the rise consti- 
tutes the only symptom. Thia 
initial increase in irritability is 
of considerable interest as the 
manifestation of the slightest 
degree of alteration in the nutri- 
tion of nerve-fibres.* It may 
last for a few days or for twa 
weeks (Fig. 40), and I have 
once known it to continue for five weeks (Fig. 41). Although the 
* A similar change is met with in some central diseases, as chorea and paralysia 
agitans. 
Fig.40.—Slight neuritis; power not entirely 
lost, and In coming normal during the third 
week. Slight deg. react, in muscle deve- 
loped during second week, and continued 
till seventh. Nerve irritability increased 
during second week, passing during the 
third into transient depression, the vol- 
taic irritability falling more than the fara- 
dic. 59 
SYMPTOMS. 
Fig. 41.—Slight neuritis; quick recovery of power durng third and fourth 
weeks. Degen. react, in muscles present at the end of the second week, 
slowly lessening, but present in slight degree until the fourth month. 
Considerable increase in irritability in the nerve-trunk at the end of the 
second week, greatest to the faradic shock (crosses) and lasting until the 
fifth week. 
change in irritability of the nerve is usually the same to both cur- 
rents, a partial exception to this rule is presented by the increase 
in irritability we are now considering The change is not always 
quite equal to faradism and to voltaism, and it is frequently much 
more marked to the isolated faradic shocks than it is to either the 
voltaic current or the rapid succession of shocks that constitutes the 
faradic current. This is shown very strikingly in Fig. 41, and in less 
degree in Fig. 43. In the former the irritability to the two currents 
was the same ; in the latter that to voltaism was distinctly the greater. 
I have once met with a slight but distinct and prolonged diminution 
in faradic irritability when no change could be found to voltaism (see 
Fig. 42). Bernhardt has observed lessened irritability to faradism 
Fig. 42. 
Fig. 43. 
Fig. 42.— Slight neuritis; power regained during the second week. 
Deg. react, in muscle di-tinct on eighth day, lessening during second 
and third weeks. Nerve: lowered faradic, normal voltaic irritability. 
Fig. 43.—Very slight neuritis. No change in muscular in it ability ; irri- 
tability of nerve-trunk increased from fourth to eighth day, most to faradic 
shock crosses), least to faradic current. 
with distinct increase to voltaism in an ulnar nerve the seat of 
traumatic paralysis. In one singular case of double facial palsy, with 
weakness of the limbs, and changes in their muscular irritability, 
the voltaic excitability of the facial nerves was Dot lessened, although 
faradic irritability was lost to such a current as could be borne. The 
case was probably one of non alcoholic peripheral neuritis.* 
* The observations were made with great care and with full knowledge of a 60 
LESIONS OF NERVES. 
Moreover, the law that the faradic irritability is changed in the 
same degree in the muscles (nerve-endings), and in the nerve-trunk, 
is also not always true of slight cases. The muscle-nerves may 
present no change when the excitability of the nerve-trunk is consi- 
derably increased (Fig. 48). The probable significance of this differ- 
ence has been already mentioned (pp. 52 and 57, note). 
The electrical excitability of a nerve and its power of conduc- 
tion are usually lost together. But when a nerve is recovering 
from a local lesion, and regeneration is in progress below the lesion, 
some power of conducting the voluntary stimulus may return in 
the peripheral portion before it becomes excitable by any form of 
electricity. This seems to show that the nerve-fibres can con- 
duct, that is, pass on the nerve-foi'ce they receive as such, before 
they can produce nerve-energy in response to the influence of a 
4t stimulating ” force acting on them. Another rare anomalous con- 
dition has been noted by Bernhardt and Griinberg, in recent cases of 
nerve-injury. When the lesion arrests all conduction of the voluntary 
stimulus a strong faradic stimulation of the nerve above the lesion 
may still cause slight contraction in the paralysed muscles. It is 
probable that this difference is simply one of strength of stimulus, and 
that the nerve impulse generated by the electricity is stronger than 
that descending from the brain. 
Recovery of the nerve is attended by gradual restoration of power 
over the muscles, the nutrition of which slowly improves; but if the 
wasting has been considerable, a long time elapses before they regaiu 
their normal size. Indeed, as already stated, they may be always 
somewhat smaller than the corresponding muscles on the unaffected 
side. Curious secondary spasmodic symptoms are common after palsy 
of the facial nerve (q. v.)—spontaneous muscular contractions, and 
associated over-action of the affected muscles. This associated over- 
action is very rarely met with after palsy of the nerves of the limbs, 
but coarse, fibrillary, muscular contractions, and a tendency to cramp, 
are not uncommon, and may persist for years. (See also Neuritis.) 
Sensory symptoms also result from lesions of the nerves that contain 
sensory fibres. The interruption of the fibres arrests conduction, and 
causes loss of sensation in the part supplied by the nerve, just as it 
causes motor palsy. But a slight lesion of a mixed nerve may cause 
persistent muscular paralysis, and sensation be unaffected, or im- 
paired only in slight degree, and for a short time. This result is 
so frequent that we cannot ascribe it to a difference in the relative 
damage to the motor and sensory fibres. It must be due either to (he 
fact that the sensory fibres recover more readily, or that a slight degree 
of conduction may suffice for the stimulation of the sensory centres in 
the brain, and not for that of the muscular fibres. There is also a 
third hypothesis, and that is a difference in the sensory and motor 
frequent source of fallacy—the diffusion of the voltaic current to the muscles them- 
selves. Cyon has observed a similar change after injury to a nerve in an animal. SYMPTOMS. 
61 
impulses in physiological character.* In another class of cases, 
however, we must seek a different explanation of the persistence 
of sensibility in the area supplied by the nerve. There may be no loss 
even when a nerve is completely divided. This is observed chiefly near 
the extremity of a limb. It can only be explained by what is termed 
“recurrent sensibility.” Anastomoses exist between the terminal fibres 
of different nerve-trunks, and it would seem that, in some individuals, 
the connection of sensory fibres suffices for conduction. Thus, of 
two persons in whom the ulnar nerve at the wrist has been divided, one 
may have total anesthesia in the fingers supplied by the nerve, and in 
the other there may be little or no loss. 
The peripheral segments of the sensory fibres degenerate, like the 
motor nerves. We cannot test them, and ascertain the degeneration 
in the same way, in severe lesions, because their stimulation cannot be 
perceived. Nevertheless an altered polar reaction has been observed 
in slight cases, analogous to that which occurs in the muscles. A 
sensation is produced with the positive pole by a weaker current than 
is required with the negative pole. In some cases of nerve-injury 
and neuritis a delay in conduction of pain may be observed. 
Increased sensitiveness in the area of distribution of the nerve, 
with or without spontaneous pain, is very common in cases of partial 
lesions of nerves. It must be referred to the morbid changes in their 
fibres, alterations in the nutrition of the axis-cylinder or nerve-endings, 
probably analogous to the slight changes in the motor nerves which 
increase their excitability. Pain and tenderness of the nerve-trunk 
are also frequent in the same cases, due no doubt to the increased 
sensitiveness of the “nervi nervorum” distributed in the sheath. The 
sheath of each nerve is part of the distribution of its own fibres, and 
those that end in the sheath seem to be very readily deranged. We 
shall see the importance of this consideration in relation to neuritis 
and neuralgia. The pains, both local and distant, are sometimes 
very severe and persistent. 
Reflex Action.—All lesions of nerves abolish reflex action in the area 
of the distribution of the nerve affected. Myotatic irritability is also 
lost, from damage to either the motor or sensory fibres concerned, and 
this loss may persist long after the other symptoms. 
Viso-motor and trophic disturbance occurs frequently in consequence 
of lesions of nerves. The vaso-motor nerves run in the mixed nerve- 
trunks, and suffer with the other fibres. The general character of the 
disturbance has already been described (p. 22). When the lesion is 
acute and irritative, vascular dilatation and an increase of temperature 
occur at first, and are followed by passive hypersemia and lowered tem- 
perature. There may be oedema, and an increased secretion of sweat. 
The changes in the skin, acute and chronic, are those that have 
been already described. “ Glossy skin,” red, smooth and thin, is 
* The experiments of Leuderitz (‘Zeitschr. f. klin. Med.,’ Bd. iii) merely confirm 
the fact, and do not really explain it, as he and others have assumed. 62 
COMPRESSION. 
especially common, and is frequently accompanied by atrophy of tha 
subcutaneous tissue, and perhaps of the bone, so that the finger-tips 
become narrow, and present an aspect that is very characteristic. 
Burning pain, with tenderness, often accompanies the change, and may 
continue for long. Occasionally, instead of becoming thin, the epi- 
dermis increases in thickness, the nails often become thick and rough, 
and present transverse or longitudinal furrows.* In parts where there 
is much subcutaneous tissue this may also become thickened and 
have a peculiar doughy feel, resembling that met with in myxcedema. 
The growth of the hair may be lessened or increased. Sloughing of 
the skin is far less common than in central diseases, but vesication 
occurs with extreme readiness, and sometimes vesicles or bullse appear 
to form spontaneously. Ulcers result which erode and destroy the 
tissues, especially of the finger-ends. Mustard plasters also blister 
the skin more readily than in health. It is important to remember 
these facts, because the affection is one in which hot applications are 
often recommended. A gentleman dislocated his shoulder, and either 
by the displaced bone, or in the reduction, the brachial plexus was 
seriously injured. The muscles of the hand wasted, and the skin 
became glossy. He was advised by a surgeon to bathe the hand daily 
in hot water. One day his wife bathed it in water which to her was 
pleasantly warm, and which caused him no discomfort, but the result 
was that the hand was covered with blisters, and ulcers were left 
which did not heal for months. 
The joints often suffer in their nutrition. Acute inflammation, such 
as occurs sometimes in spinal affections, is rare, but chronic changes in 
the joints are frequent, with much tenderness ; alterations in the 
articular surfaces, and fibrous adhesions result, which limit move- 
ment. When the muscular wasting is slight, the condition may 
resemble a primary joint affection, and this mistake in diagnosis is 
sometimes actually made. 
INJURIES OF NERVES: COMPRESSION. 
Traumatic lesions of nerves are in the province of surgerv. Thev 
belong to the physician only in so far as their effects are produced 
by the agency of a neuritis, the mechanical origin of which mav 
escape notice. Neuritis is described in the next section. A word is 
needed, however, on the subject of simple, slow compression of nerves, 
not because the symptoms are grave, but because they often give rise 
to very grave mental concern on the part of the patient, and to occa- 
sional doubts in the mind of his medical attendant. Sudden compres- 
* Several excellent illustrations of these changes are given by Bowlby, loo. cit., 
where also a full account of traumatic lesions is given. NEURITIS. 
63 
sion bruises the nerve-fibres, and only concerns ns as a cause of 
neuritis. Slow pressure on an)' nerve, however slight, if maintained 
for a time, causes a familiar tingling in the region of distribution of 
its fibres, often with a sense of warmth, with disordered sensations and 
even a loss of sensibility in the skin. Often this is accompanied by an 
inability properly to put in action the muscles that are supplied by the 
nerve. All the symptoms pass away in a few minutes, a sense of cold 
and an inability to direct movements being often the last effects. If 
they do not pass away, the persistent effects are ascribed to a neu- 
ritis such as is produced by any other cause. 
But neuritis is not the primary lesion, and the initial symptoms 
are not produced by the agency of inflammation. Hence, when 
they persist, it is doubtful whether we should ascribe them to the 
inflammation unless thej occur after an interval. The mechanism 
by which the tingling and early anaesthesia are produced, probably 
causes also the lasting symptoms. The compression no doubt 
causes anaemia, but the known sensitiveness of nerves to mechanical 
stimulation makes it probable that the effects are chiefly produced 
by the mechanical influence of the pressure on the elements of the 
nerve-fibres, and that a compression for a few hours has such an 
effect in separating the molecular elements of the white substance, 
as to set up a secondary degeneration of the same character as that 
which results from division of a nerve. The neuritis is thus no 
more the cause of symptoms in compression than in division. In 
each there is a displacement of molecules interrupting conduction. 
This is also the conclusion of Weir Mitchell, who found that a 
pressure of eighteen to twenty inches of mercury for twenty seconds 
abolished the power of conduction, though only for a few minutes, in 
spite of conspicuous change in the white substance. The latter is 
still greater, and the effects more enduring, in a contusion. 
The cause of the tingling in the region of distribution of the sciatic 
nerve is recognised when it is due to pressure by sitting. But it 
is otherwise when the pressure is on the nerves of the arm and is 
produced during sleep. The tingling may be felt in the region of 
the ulnar nerve, in consequence of flexion of the elbow, or in the 
whole hand from the pressure on the nerves of the brachial plexus 
on the side on which the patient is lying. Waking up with the 
tingling, and sometimes with cramp or powerlessness in the hand, he is 
naturally alarmed. The diagnosis, however, is rendered easy by the 
unilateral character of the symptoms, and by the fact that they are 
always felt on the side that is bearing the weight of the body. The 
symptoms are produced much more readily when the general health 
is bad; they last longer and more often end in neuritis. The pres- 
sure of crutches on the brachial plexus may have the same effects. 64 
NEURITIS. 
INFLAMMATION OF NERVES: NEURITIS. 
Neuritis, or inflammation of nerves, presents various characters, 
which have led to the distinction of numerous forms. The inflam- 
mation of single nerves usually begins in the outer sheath of the nerve, 
and this has been distinguished as “perineuritis ” It may involve 
also or chiefly the connective tissue between the bundles of nerve-fibres 
(“interstitial neuritis”), or the nerve-fibres themselves (“parenchy- 
matous or degenerative neuritis ”). Some forms of neuritis have a 
tendency to ascend the nerve, and this variety has been termed 
“ ascending neuritis ” or “ neuritis migrans.” One nerve-trunk may 
be primarily affected, or many nerves may suffer at the same time. 
The latter condition, “primary multiple neuritis,” is of great import- 
ance, and will be described in a separate section. 
Most forms of neuritis may be either acute or chronic. Acute 
neuritis usually subsides into a chronic stage, and its symptoms may 
thus persist for a long time. Other varieties that have been distin- 
guished depend upon the cause to which the inflammation is secondary. 
Thus we have eaucerous, syphilitic, gouty, diabetic, and other forms. 
Causes.—Injury causes more or less inflammation which occurs 
readily, and follows very slight damage. Neuritis may thus be set 
up by all sorts of wounds, by contusions, by compression from with- 
out or by adjacent stuctures, and by over-extension of the nerves. 
Those nerves that pass by joints are liable to injury from disloca- 
tions, either by the displacement of the bones, or during reduction. 
In fractures the nerves may be injured directly, or may be compressed 
by the callus that is formed. Nerves are sometimes damaged by a 
violent contraction of the muscles through which they pass. It is 
probable also that muscular effort excites neuritis in other situations, 
especially in persons who are predisposed. Moreover, a strain on the 
fibrous tissues of joints, fasciae, &c., may set up inflammation in 
them, which may spread to the nerves. 
Neuritis may arise by extension from adjacent inflammation. The 
nerves near suppurating joints may be involved, and even, it is said, 
those that pass by a joint the seat of simple inflammation. The 
latter is certainly rare. The intercostal nerves have been affected by 
extension from an inflamed pleura. The cranial nerves and the spinal 
nerve-roots are involved by extension from the membranes. 
Exposure to cold is another cause of neuritis. It is then often 
called “ rheumatic.” The nerve, or rather its sheath, may be primarily 
affected, or the first effect may be inflammation of the fasciae, from 
which the inflammation spreads to the nerve-sheath. Persons who 
are liable to muscular rheumatism, and those who are gouty, suffer 
thus with especial frequency. But exposure to cold also acts in PATHOLOGICAL ANATOMY. 
65 
another way, causing a blood-state which acts on many nerves at 
the same time. Many general diseases have a similar power of 
causing either an isolated or a multiple neuritis. It is through this 
agency that diphtheritic paralysis is produced, and the same effect 
may he due to the presence of other toxic material in the blood, 
metallic poisons, alcohol, &c., an account of which will be found in 
the section on “ multiple neuritis.” When an isolated neuritis occurs 
during an acute disease it is probably produced through the agency 
of compression, unnoticed during the prostration. Neuritis has also 
been found in the vicinity of bedsores (Pitres), and though pro- 
bably due to pressure may be part of the mechanism by which 
they are caused. Some chronic general diseases cause only isolated 
neuritis,—either simple, as that which is due to gout (when the 
general disease must be regarded chiefly as a predisponent) ; or 
special, as syphilitic, cancerous, or leucocythsemic neuritis, in which 
there is an infiltration of the nerve with the special tissue-element 
characteristic of the general disease. 
The characters of the simple isolated form constitute the chief 
subject of this section. 
Pathological Anatomy.—The changes differ according as the 
inflammation affects primarily the adventitial connective tissue, 
“adventitial neuritis,” or the fibres themselves in the “ paren 
chvmatous ” form. Isolated neuritis is generally adventitial, and 
will be first described. In acute inflammation the affected part 
of the nerve is red and swollen. The redness depends on distended 
vessels, which may be visible on the surface. The swelling is due to 
oedema, or to a sero-fibrinous 
exudation, sometimes jelly-like 
in aspect. The microscope shows 
leucocyte-like corpuscles sur- 
rounding the vessels, infiltrating 
the sheath (Pig. 44) and ac- 
cumulating between it and the 
nerve. There may be even small 
extravasations of blood. These 
changes may be limited to the 
sheath in what is called “ peri- 
neuritis,” or may extend into 
the substance of the nerve in 
“interstitial neuritis.” In the 
latter case the lymphoid cor- 
puscles infiltrate the septa, and 
may even be seen in the sub- 
stance of the fasciculi, between 
the nerve-fibres. These changes may be continuous along a con- 
siderable tract of the nerve (diffuse neuritis), but more frequently 
they are chiefly marked at certain places, which are separated by, por- 
Fig. 44.—'Neuritis : degeneration of nerve- 
fibres, the myelin broken up into masses, 
globules, and granules. Accumulation of 
leucocytes in nerve-sheath. From a case- 
of multiple neuritis. (After Leyden.) 
vol. I. 66 
NEURITIS. 
tions of the nerve which are so little affected as to appear to the naked 
eye to be normal (“ focal ” or “ disseminated neuritis ”). The foci of 
inflammation are chiefly situated at places where the nerve turns round 
a bone, or emerges from canals or fasciae, or divides. 
The extent to which the nerve-fibres suffer varies much. They 
usually present little change when the inflammation is limited to 
the sheath, unless the nerve lies in a bony canal, or in rigid fibrous 
tissue, within which the sheath cannot expand; its swelling then exerts 
pressure on the fibres. When the inflammation is interstitial the 
fibres suffer more readily, although not invariably. On the other 
hand, they are sometimes found much altered, when the connective- 
tissue elements are but little affected. In this case the inflammation 
is “parenchymatous” and begins in the nerve-fibres, the interstitial 
tissue being secondarily involved or unaffected. The changes in the 
fibres are almost the same as in degeneration (Figs. 33 and 34). 
It was pointed out how closely the two processes of inflammation 
and degeneration are connected, and how difficult it is to separate, 
or even to distinguish them, in many cases. The myelin of the white 
substance first breaks up into segments, more or less elongated, often 
with smaller globules of myelin between or beside them. The masses 
are cloudy or finely granular in aspect. The axis-cylinders are 
interrupted where the myelin is divided. The nuclei of the sheath are 
increased in number, and the protoplasm around them is increased in 
quantity. Next the myelin is divided into smaller globules and 
granules, and the axis-cylinder is no longer recognisable. The myelin 
then disappears in parts of the tubes, while it remains at other parts, 
but is still more finely divided. Lastly, the sheaths become empty 
and very narrow, containing only nuclei at intervals, with here and 
there a little finely granular material, or sometimes some brownish 
pigment granules. The process may thus go on to complete destruc- 
tion of the fibres. These commonly suffer unequally ; fibres that 
have a normal appearance are scattered among those that are much 
altered. 
In chronic interstitial neuritis the axis-cylinders often suffer less than 
the white substance. The latter becomes atrophied, so that the fibres 
are smaller than normal. If the interstitial inflammation is very intense 
the fibres may break up as above described. As the inflammation sub- 
sides, the new cellular elements that have made their appearance assume 
the aspect of fusiform cells, and fibrous tissue is developed, either from 
these cells, which become less numerous, or from the intercellular exu- 
dation. This fibrous tissue surrounds and encloses the fasciculi, a 
condition that has been termed “ sclerosis of the nerve.” A firm 
fusiform swelling may remain at the affected spot, and this may be 
adherent to adjacent structures. Sometimes fat is ultimately formed in 
the new connective tissue, a condition that has been rather unnecessarily 
termed “ lipomatous neuritis ” (Leyden) ; the fatty deposit does not 
seem to be related to any special form of neuritis. SYMPTOMS. 
67 
In syphilitic neuritis, which affects chiefly the cranial nerves, thei’e 
is a cellular growth in the sheath and interstitial tissue similar to that 
which constitutes other syphilitic new formations, with a variable 
amount of alteration of simpler inflammatory character. The growth 
in the sheath may amount to a distinct syphilitic tumour, with or 
without interstitial changes. In cancer, nerves adjacent to the new 
growth may present simple interstitial neuritis, or may he infiltrated, 
by a growth of cancer-elements spreading to the nerve by direct 
extension. Inleucocythsetnia there is a dense infiltration of the nerve 
with leucocytes. 
The destructive changes in the nerve-fibres extend down the nerve 
to the periphery in a process of secondary degeneration, more or less 
inflammatory in nature, as already described in secondary degeneration. 
Usually the central portion of the nerve remains free, the alterations 
ceasing a short distance above the seat of the primary inflammation. 
In rare cases an ascending neuritis (n. migrans) passes up the nerve, 
and may spread, at a plexus, to other nerve-bundles and other nerve- 
trunks. The formation of fibrous tissue in the inflamed part, and 
the cicatricial contraction of this tissue, often prolong the irritation 
of the nerve-fibres, and the symptoms due to this and a state of 
“ chronic neuritis ” is said to be left. 
Symptoms —The symptoms of neuritis vary extremely according to 
its intensity, its extent, and the nerve that is affected. In two places, 
the brachial plexus and the sciatic nerve, the symptoms are suffi- 
ciently special to make their separate description desirable, although 
the general account applies to them also. 
The onset of the acute form is sometimes attended by some con- 
stitutional disturbance, especially when many nerves are affected. 
The chief symptoms are local. The most prominent is pain, felt in 
the inflamed part of the nerve, and also often in the part to which it 
is distributed (see p. 61). Sometimes the pain involves the whole 
limb, and in severe cases it may be most intense, burning, boring, 
rarely darting, in character; usually worse at night; increased by 
movement, by postures that involve tension or pressure on the nerve, 
and by whatever causes passive congestion of the limb, such as the 
act of coughing. Sometimes it seems to radiate into distant parts, 
and not rarely pain is also felt in the corresponding region of the 
opposite limb. The sensitiveness of the whole of the affected region 
is increased, and even the bone may be tender, so that at first attention 
may not be directed to the nerve, but when this is pressed great pain 
is always produced. In slighter cases the pain is usually limited to 
the nerve and its distribution. It may, indeed, be absent when the 
nerve or branch is chiefly motor, a fact difficult to explain unless the 
sheaths of such nerves contain fewer sensory fibres than usual. If 
the nerve is accessible to direct examination it may be felt to be 
distinctly swollen at the affected part. Occasionally the skin over it 
has been observed to be red, and rarely there has been slight oedema. 68 
NEUR1TJS. 
Spontaneous sensations may be felt in the region supplied by the 
nerve, tingling, &e., and the skin may be hypersesthetic. After a time, 
as the nerve-fibres suffer, sensation may be perverted, or even lessened ; 
complete anaesthesia is usually confined to small areas. The muscles 
supplied by the nerve become weak in various degree, tender, and 
present fibrillar twitcbings; they are seldom powerless, but pain may 
prevent their contraction. They present the altered electrical reac- 
tions characteristic of nerve-lesions. Increased perspiration has been 
observed in the part of the skin supplied by the inflamed nerve, very 
rarely it is arrested, and sometimes, although rarely, eruptions occur. 
Herpes is not common from ordinary acute neuritis. .The epidermis 
may become thickened into a state like ichthyosis, or atrophy as 
“ glossy skin.” Effusion into joints has been observed in very rare 
cases. The constitutional disturbance which may attend the onset 
subsides in the course of a few days, but the pain and other sym- 
ptoms usually persist in undiminished severity for several weeks. 
They ultimately slowly subside into a chronic stage, and may continue 
as a secondary neuralgia due to a habit of over-action set up in the 
centre. 
In the chronic form constitutional disturbance is absent, and pain 
is the prominent symptom from the first. The affection of motion, 
sensibility, and the trophic changes are similar to those met with in 
the acute form. In both forms the muscles may waste, and present the 
reaction of degeneration when they are tested with electricity (p. 45). 
In slight cases the initial increase of excitability in the nerve is often 
well marked. Trophic changes in the skin are very common; so is 
alteration in the nutrition of the joints, and adhesions form, limiting 
the movement, and fixing the parts in the position corresponding to 
the muscular inaction. 
When neuritis ascends a nerve, the symptoms gradually extend in 
area; and if it reaches the plexus from which the nerve proceeds, they 
may extend to most or all the nerves of the limb. This “ascending 
neuritis ” is not rare in man, may even reach the spinal canal, 
and there produce various disturbances. The inflammation may 
spread in the tissue outside the dura mater, or may extend to 
the cord, and cause subacute or chronic myelitis with or without 
meningitis. The paralysis that occurs secondarily to some visceral 
diseases, as those of the bladder, and commonly regarded as reflex 
paralysis, are probably produced through the agency of an ascending 
neuritis. Lastly, the inflammation may extend to the nerves of the 
other side, usually to those that correspond to the primary seat of the 
disease. Such extension may be through the spinal cord or the 
membranes, but in some cases symptoms occur in the nerve of the 
opposite side, without any indication of an affection of the centres. 
Experiments on animals have demonstrated that such implication of 
the opposite nerve may occur when the centres are unaffected. It has 
been called “sympathetic neuritis.” We have seen that reflected DIAGNOSIS PEOGNOSIS. 
69 
pains are occasionally felt in the corresponding nerve on the opposite 
side, and it is probable that, as in neuralgia, vaso-motor disturbance 
in the nerve-sheath may accompany such pains, and, in a predisposed 
person, may cause actual neuritis. 
The Duration and Course of neuritis vary much. A slight acute 
neuritis may run its course in a few weeks and then subside. Much 
more commonly the affection persists in a chronic stage for many 
weeks, or even months, and slowly passes off. The rheumatic and 
gouty forms are as a rule much more tedious than those that result 
from injury, although traumatic neuritis is sometimes very insidious 
and may last a long time ; it may ascend the nerve from its starting- 
place and become localised in certain situations, where it may develop 
afresh, and give rise to symptoms that may seem to be independent 
of their cause. In the predisposed, it may set up troublesome local 
functional disturbance, hysterical contracture, and the like. 
Diagnosis.—The diagnosis of neuritis depends, first on the locali- 
sation of the symptoms to the distribution of a certain nerve-trunk, and 
secondly on the pain and tenderness in the nerve. The diffuse pains 
that attend the onset may be readily mistaken for the pains of acute 
rheumatism, or for those due to an inflammation of the bone, but in the 
course of a day or two the localisation of the symptoms declares their 
nature. The chronic form is easily and often mistaken for neuralgia, 
and the diagnosis is the more difficult because many so-called neu- 
ralgias are really due to neuritis. The distinction can only be fully 
fliscussed when we have considered the symptoms of neuralgia, but it 
rests chiefly on the fact that in neuralgia the pain intermits more 
completely than in neuritis, there is not the same initial tenderness in 
the nerve-truuks, and the tender spots have a more uniform localisation. 
Lessened sensibility or change in the muscles, showing organic damage 
to the nerve-fibres, are conclusive evidence of neuritis. The pains in 
some central diseases, chiefly those of the spinal cord, may be thought 
to be due to neuritis, but there is not the local tenderness of the 
nerve-trunk, and the pain is not limited to the distribution of a single 
nerve. As we shall see presently, the diagnosis of multiple neuritis 
from affections of the cord is far more difficult. 
Prognosis.—The gravest form of simple neuritis is that in which the 
nerve is affected secondarily to a local suppurative inflammation. The 
prognosis is best, as a rule, in traumatic neuritis, but the rule is one 
to which the exceptions are occasionally very considerable in degree. 
A neuropathic disposition makes the prognosis worse. In all cases 
the intensity of the symptoms, and the evidence of descending degene- 
ration, furnish a more trustworthy guide to prognosis than does the 
mere form of the affection. The effects of complete degeneration 
always endure for some months. Regeneration does not occur until 
the original cause has ceased to act, and then occupies many weeks in 
its progress to the restoration of functional competence. In all forms 
pain is apt to linger on, and the longer the older the patient is. 70 
NEURITIS. 
Treatment.—The first consideration in the treatment of neuritis is 
the removal of its cause, if this can be discovered. A wound or injury 
or local inflammation adjacent to the nerve must be dealt with by 
appropriate measures. Any constitutional cause, such as gout, must 
be treated. For the inflammation of the nerve, it is of the first 
importance to secure to the part as perfect rest as possible. Move- 
ment causes mechanical irritation of the nerve, and involves functional 
stimulation of its fibres, both of which are injurious. The nerves of 
a limb run between muscles, and the contraction of these muscles 
causes pressure on the inflamed nerve, and irritates it, as the pain thus 
produced sufficiently shows. Pain is indeed a useful indication of the 
harmful influence of movement, since the stimulation of the nerves of 
the sheath, in which the pain is produced, doubtless has also a reflex 
effect, increasing the vaso-motor element in the inflammation. Hence 
it is most important that all movement that causes pain should be 
avoided. The posture of the limb should be such as to involve the 
least pain and the least danger of secondary contracture. The general 
treatment of an acute neuritis nust be that suitable for any acute local 
inflammation, whatever its seat,—an uustimulating diet, an aperient, 
and diuretics. In gouty cases a brisk purgative may, with advantage, 
be given. G-eneral diaphoresis is useful in cases that are due to cold, 
and in others local sweating is often of distinct service. The limb 
may be steamed, or exposed to hot air. This should be followed bv 
hot fomentations applied along the course of the affected nerve, and 
these by linseed-meal poultices. Leeches may also be employed at the 
onset of severe cases. When the inflammation results from injury, 
cold may be applied along the course of the nerve instead of heat;, 
both probably modify the vascular disturbance of inflammation in a 
similar manner. Counter-irritation maybe used at the onset of slight 
cases, but when the inflammation is severe, this agent is more effective 
during the subsidence of the inflammation than during its active 
stage. Blisters, repeated mustard plasters, or stimulating liniments 
may be used, but care must be taken not to blister skin that is 
anaesthetic, or troublesome ulceration may be caused. The same 
caution is necessary in regard to hot applications, as is shown by the 
case mentioned on p. 62. 
Spontaneous pain requires sedatives, of which the hypodermic injec- 
tion of morphia is by far the most potent. It should be used only 
for spontaneous pain, and not to enable the patient to use the limb in 
a way that would produce pain if morphia were not given. Mechanical 
irritation may be equally injurious, although the pain which it would 
cause is obviated by the sedative. Moreover it should only be used 
as a last resort, when the agent to be mentioned next is inadequate. 
Morphia has little influence on the morbid process; it lessens the 
effect of the disease on the brain only by acting on the brain. 
In cocaine we have an agent capable to a large extent of replacing 
morphia, and of a greater therapeutic capacity. Although it has less. 71 
TREATMENT. 
power of relieving pain, it is capable of doing much more than that. 
It arrests the local transmission of the impulses that cause pain, and 
so, at a limited region, it does lessen pain and often remove it for a 
time, and the local character of its action enables it to exert a simul- 
taneous influence on the morbid process. It prevents the irritative 
influence on the inflamed structures of the impressions that are felt as 
pain, which we have just considered ; and the entire arrest of the influ- 
ence, even though the region is small, seems to produce a much greater 
effect on the process than might be anticipated. It is instructive to note 
the opposite influence, revealed by the occasional redness of the skin 
and subcutaneous oedema, along the course of the inflamed nerve. The 
injection should be made at one of the seats of pain. In the rheumatic 
form salicylate of soda has been given, but is of doubtful value. 
Iodide of potassium sometimes seems to be useful, but no agent has 
so distinct an influence on the process of inflammation in the nerve 
as small doses of mercury. A grain of blue pill may be given once or 
twice a day ; and if morphia has to be injected at the same time, the 
mercury is useful also in correcting the constipating influence of the 
morphia. 
In the chronic stage or form, counter-irritation, by blisters or 
cautery, is of great value. So also is electricity, which has little 
influence during the acute stage. The voltaic current should be 
used. The positive electrode may be placed over the inflamed part of 
the nerve, or over the seat of pain, and kept there for ten minutes at 
a time, the strength of current being slight, such as the patient 
can just perceive. In very chronic cases a stronger current, sufficient 
to cause actual pain, is of service, applied in a similar manner, but 
for a shorter time. It has probably chiefly a counter-irritant influence, 
and faradism may be used in the same wav. All painful impressions 
on the skin lessen, for a time, the nerve-pain. 
The muscles supplied by the inflamed nerve may be left alone, 
unless their wasting is marked, or the degenerative reaction shows 
serious damage to the motor fibres. In cases of moderate severity 
ihey will recover when the nerve recovers. All that is desirable is 
that they should be gently rubbed once or twice a day. If the wasting 
is considerable, however, or there is degenerative reaction, they should 
be stimulated, to gentle contraction by a weak, slowly interrupted 
voltaic current. They should on no account be faradised during the 
active stage of the affection, even if they act to faradism. The acute 
pain that the faradie stimulus causes, and the increased tenderness 
that lasts for hours afterwards, are evidence of its injui-ious effect. 
In all cases attention to the general health is of great importance. 
Tonics are needed during the chronic stage. Change of air will some- 
times remove, in a few weeks, symptoms that have previously been 
stationary for months. 
The modifications of treatment that are rendered necessary bv 
the position of the neuritis will be considered when we come to speak 72 
NEUROMA. 
of the affections of the several nerves. The pathological varieties of 
neuritis only need special treatment in so far as they depend upon 
special causes, and this point, as already mentioned, must always be 
one of the first considerations. 
MORBID GROWTHS IN NERVES : NEUROMA. 
The term “ neuroma ” has been applied indiscriminately to all 
morbid growths situated on the peripheral nerves. The discovery, by 
Virchow, that many of these consist of a growth of nerve-fibres, while 
others consist of heterologous tissue such as constitutes morbid 
growths elsewhere, has led to the distinction of the former as “ true 
neuromata” and the latter as “false neuromata,” or “pseudo-neuro- 
mata,” and even to the limitation of the term “neuroma” to a growth 
of nerve-tissue, whether in the central or peripheral nervous system, 
the heterologous growths being called by the names they bear in 
other situations, as “ fibroma,” “ sarcoma,” &c. The latter system of 
nomenclature, although certainly more consistent, has not become 
current in this country. 
The true neuromata may consist of medullated or of non-medullated 
nerve-fibres, termed “myelinic” and “amyelinic ” forms by Virchow. 
The latter were for a long time regarded as fibrous. The occurrence 
of ganglion-cells has been proved in only one or two instances. There 
is connective tissue between the nerve-fibres, which varies in amount 
and in character, and hence the firmness of these tumours also varies. 
This interstitial tissue may be so abundant as to constitute an inter- 
mediate form between the true and false varieties. This is probably 
the condition in most cases of multiple neuroma. The “ false neuro- 
mata” may be of various nature, but fibrous growths, “fibromata,” 
are far more common than any other kind. Myxoma occasionally 
occurs, the new mucoid tissue growing from the nerve-sheath. Grlioma 
is very rare on the peripheral nerves, although occasionally found on 
the auditory nerve. Various forms of sarcoma have been met with. 
Carciuoma also occurs, very rarely as an isolated growth, but not 
uncommonly as a more or less diffused or nodular infiltration of the 
nerve, arising by extension from a contiguous growth. Syphilitic 
growths are common on the cranial nerves within the skull, but are 
rare elsewhere. In lepra anaesthetica the nerves are infiltrated with 
fibrous tissue, enlarging them to many times their normal size. The 
enlargement is rarely nodular, and is rather a chronic cirrhotic inflam- 
mation than a growth. (See “ Leprous Neuritis.”) 
A curious variety of neuroma, consisting of interlacing cords, more NEUROMA. 
73 
or less nodular and tortuous, is termed plexiform neuroma. About 
i wenty cases have been recorded. The disease commonly begins in 
foetal life, and is most common on some branch of the fifth nerve in 
the orbit or the upper eyelid, but has been met with over the temporal 
bone, in the lumbar, cervical, brachial, and solar plexuses, on the penis 
and the mamma. It may be quite superficial or deeply seated. The 
cords, from 1 mm. 
to several centime- 
tres in diameter, con- 
sist of a clear outei 
7one of concentric 
fibrillar connective 
tissue, of innerlooser 
nucleated tissue,and, 
in the middle, a 
bundle of nerve- 
fibres, some normal, 
others dt generating. 
The cords are con- 
nected together by 
loose tissue, sometimes myxomatous, separated from the proper tissue 
of the cords by an epitheliated space. The growth of this form is 
extremely slow, but it may exert compression on adjacent structures.* 
A remarkable case of extensive myxomatous disease of the nerves of 
the forearm, congenital in origin, presenting analogies to plexiform 
neuroma, is recorded by Mr. De Morgan.f 
The subcutaneous extremities of sensory nerves are sometimes 
enlarged into minute tumours which, 
when painful, have been termed “ tu- 
bercula dolorosa.” Neuromata in the 
skin may co-exist with similar tumours 
on the nerve-trunks. Those shown in 
Fig. 46 are from the same case as the 
tumours represented in Figs. 47—49. 
The size attained by growths on 
nerves varies from that of a child’s 
head to a nodule only just visible. 
They rarely exceed the dimensions 
of the closed fist. The variation 
in size of multiple neuromata is illustrated in Figs. 47—49, after 
Smith. J The large tumour (Fig. 47) was the size of a lemon, but in 
the same case a growth from the sciatic plexus almost filled the pelvis. 
They may occur on any nerve in the body, cranial or spinal, and are 
Fig. 45.—Plexiform neuroma from the orbit. (After Mar- 
chand.) The connective tissue surrounding the cords 
has been removed except at a, and irregular, cylindrical, 
nodular cords are seen anastomosing. A nerve passes 
into the tumour and suddenly becomes enlarged. 
Fig. 46.—Cutaneous neuromata from 
skin of abdomen. (After Smith.) 
* Marchand, * Virchow’s Arcbiv/ Bd. lxxvi, p. 36. 
f * Path. Trans./ vol. xxvi, p. 2. 
J R. W. Smith, ‘Treatise on Neuroma/ 1849. Many instructive cases have been 
collected by Bowlby (‘ Diseases and Injuries of Nerves ’). 74 
NEUKOMA. 
Fig, 47. 
Fig. 48. 
Fig. 49. 
Fig. 50. 
Fig. 47.—Fight elbow of a man, set. 30, with multiple neuromata; those on the 
nerves of the arm are visible beneath the skin as moniliform series of swellings 
along the course of the nerves. (After Smith.) 
Fig. 48.—Part of the brachial plexus and nerves of the arm. 
Fig. 49.—Neuroma of the posterior tibial nerve, same case. The tumour was the 
size of a lemon, and could be felt in the popliteal space. The flattened bundles of 
fibres of the nerve were separated and passed over the surface of the tumour. The 
portion of nerve to the right is a piece of the external popliteal. The tumours caused 
no interference with function. The patient died of enteric fever. One large tumour 
filled the pelvis. 
Fig. 50.—Small neuroma of popliteal nerve laid open. It is seen to lie within the 
sheath. It caused no symptoms during life. (After Smith.) 
sometimes numerous on the pneumogastrics, spinal roots, and sympa- 
thetic plexuses. When neuromata are multiple they are often extremely 
numerous, and almost every nerve in the body may be transformed into 
a chain of growths. In the case figured more than 200 were counted 
in the right arm alone, and the total number of growths in the body 
cannot have been less than 1000, while in another 3020 were counted.* 
The tumours are almost always within the sheath of the nerve (Fig. 
45). Sometimes they are on one side, and the nerve may pass by 
unchanged. More often the substance of the nerve is involved, and 
the fibres may be separated and spread out on the surface (Fig. 44). 
Even then they may not be damaged. They suffer far more in hetero- 
logous growths than in true neuromata. 
Causes.—The causes of neuroma are generally obscure. Multiple 
neuromata are sometimes hereditary, and are probably due, in most 
cases, to a congenital tendency of tissue growth. Plexiform and 
multiple neuromata have been met with in the same family. Thev 
are said to be sometimes the result of general neurotic predisposition, 
and evidence of this is found in the occasional occurrence of ueuro- 
mata in the subjects of cretinism or idiocy, of which some remarkable 
examples have been recorded. Multiple neuromata are said to be 
almost confined to men. The isolated form is not uncommon in women. 
‘ Med. Times and Gaz.,’ 1883, i, p. 152. SYMPTOMS. 
75 
They id ay occur at any age. Yirchowbelieves that they are unusually 
common in the phthisical and scrofulous. 
Of traceable immediate causes the most frequent is traumatic 
injury. Pressure, punctured wounds, or division of the nerves may 
give rise to them, apparently by a perversion in the process by which 
cicatrisation takes place. A well-known instance is the formation of 
the so-called “ amputation neuromata,” or “ bulbous nerves,” round 
or oval growths, the size of a bean or larger, which form on the 
divided extremities of the nerves in the stump left after an amputation. 
The occurrence of new growths containing nerve-fibres may seem to 
be very remarkable. We must remember, however, how frequently 
they are connected with traumatic causes, i. e. take origin in cicatricial 
processes. In such processes the nerve-fibres present a remarkable 
power of growth. Banvier has shown that from the end of each old 
fibre several new fibres grow, only one of which probably ultimately 
persists. Under apparently mechanical influences some of these fibres 
may twist about, aud even turn and grow upwards. It is thus not 
difficult to understand that a true neuroma may result from injury to 
a nerve; it is said, indeed, that the ends of the nerves in amputation 
stumps are generally enlarged into minute bulbs, which contain more 
fibres than do the nerves on which they are situated.* 
Symptoms.—These may be entirely absent, especially in the case of 
multiple (true) neuromata, which are sometimes discovered post 
mortem, when their existence has not been suspected. Often, however, 
they cause marked symptoms. The most frequent is pain seated in 
the tumour (which may be extremely tender) or referred to the dis- 
tribution of the nerve, often acute, burning, or darting, and frequently 
intermittent. It may be increased by pressure on the tumour. In 
the case of the terminal neuromata local pain may be the only sensory 
symptom ; but when the nerve-fibres suffer, parsesthesise, numbness, 
or formication may be complained of, and ultimately sensation may 
be lessened or lost. Paralysis of the muscles supplied by the nerve 
is occasionally met with, the region paralysed corresponding to the dis- 
tribution of the nerve on which the tumour is situated, except in the case 
of neuromata in the cauda equina, from which paraplegia may result, 
with flexor spasm. A neuroma of the pneumogastric may cause grave 
cardiac disturbance, sometimes increased by pressure on the tumour. 
More common motor symptoms are reflex spasms in adjacent or even 
distant muscles. For instance, in a case of “ bulbous nerves ” in tbe 
stump after amputation at the shoulder-joint, the muscles on that 
side of the neck were in constant clonic spasm. Occasionally epilepti- 
form convulsions are produced, and have been known to cease when a 
painful neuroma had been excised. The occurrence of these symptoms 
has little relation to the size of the tumour. 
When the neuromata are in accessible situations they may be felt. 
Sometimes they give rise to visible tumours, and in multiple neuroma 
* Bowlby, loc. cit., p. 20. 76 
NEUROMA. 
the course of the superficial nerves may be marked out by lines of 
head-like swellings, as in Fig. 47. The cutaneous neuromata also 
cause visible swellings. The whole abdomen was covered with such 
nodules in the case recorded by Smith (Fig. 46). They are sometimes 
not sensitive, sometimes exquisitely tender and most painful, especially 
when closely united with the skin. Pressure on the nerve above the 
tumour commonly lessens the pain. 
Plexiform neuroma rarely causes other symptoms than the signs 
manifesting its local presence. The functions of the nerve-fibres 
involved are not usually interfered with. Once or twice anaesthesia 
of the skin has been observed. 
Course.—The growth of neuromata varies greatly in rapidity. 
When symptoms occur they most commonly last for a long time, 
increasing in severity, and from the long-continued pain the patient 
may ultimately be worn out. In other cases the symptoms show 
little tendency to increase, and in rare instances they may lessen in 
severity and even disappear. 
Diagnosis.—The recognition of the existence of a neuroma depends 
on its superficial position, or on the production of symptoms of damage 
to the nerve. The latter, when existing alone, are equivocal, since they 
may be due to pressure on the nerve from an adjacent growth, or even 
to neuritis. The disease maybe suspected if symptoms—pain, numb- 
ness, weakness—occur, limited to the distribution of a nerve-trunk, 
and no cause of external pressure can be discovered, and the long 
course of the symptoms makes it unlikely that they are due to 
neuritis. The diagnosis can, however, only be certainly made when 
the tumour can be felt. Secondary subcutaneous sarcomata may very 
closely resemble neuromata. 
The diagnosis of the kind of neuroma, whether “ true ” or “ false,” 
i. e. composed of nerve-fibres or other tissue, is very difficult. Multiple 
neuromata are usually true, and of very slow growth ; false neuromata 
are rarely multiple unless they are of infecting nature and rapid iu 
development. The existence of idiocy, or other neuropathic indication, 
is in favour of the neural nature of the tumours. The lateral position 
of the growth on the nerve is in favour of its “ false ” character. 
The diagnosis of plexiform neuroma is only possible when the tortuous 
nodular cords can be felt. 
Prognosis.—This depends on the existence of symptoms. If these 
are absent, unless the tumour is of rapid growth, there is good reason 
to hope that they will not occur. In multiple (true) neuromata the 
nerve is less likely to suffer than in isolated growths. If symptoms 
are present the prognosis is less favorable, and depends on the ten- 
dency which they exhibit to increase. 
Treatment.—Medicines are useless except in the syphilitic forms of 
nerve-tumour, not here considered. Extirpation is the only remedy. 
If the tumour is lateral, and can be shelled out, the removal entails 
little risk. If, however, the growth infiltrates the substance of the NERVES OP THE ARM. 
77 
nerve, the affected part must be excised, and the ends brought 
together. The risk of permanent loss of function in the nerve is great, 
and in deciding on such an operation, the urgency of the symptoms, and 
the importance of the function of the nerve, must be taken into consi- 
deration. After the extirpation of such tumours, the tendency of cica- 
tricial processes in nerves to go on to the formation of similar growths 
(seen in “ bulbous nerves ”) renders the chance of relapse considerable. 
The operation reproduces conditions favorable for the activity of what- 
ever predisposing influence aided in the original development of the. 
disease. When neuromata are multiple, surgical treatment is out of 
the question, except for isolated tumours that cause distress. 
In the case of terminal neuromata—whether the cutaneous “ tuber- 
cula dolorosa ” or the amputation neuromata—excision is practicable, 
and it is unattended with the risks attending interference with a nerve 
in its continuity. In amputation flaps the chance of a relapse is 
considerable. 
In plexiform neuroma excision is undesirable, and no other treat- 
ment is of any use. 
Pain, and the reflex spasm, that are so distressing in amputation 
neuromata, need relief when attempts to cure have failed. By nerve- 
stretching we may perhaps give relief without the effects that follow 
excision, and in cocaine we have a means of arresting for a time the 
ingoing impulses that play an important part in generating the sym- 
ptoms. The rest thus given to the centre is absolute, and its degree 
and frequent repetition may compensate for its brevity. 
DISEASES OF SPECIAL NERVES. 
The diseases of the cranial nerves may he most conveniently 
considered in connection with the diseases of the brain. Here, 
therefore, only the affections of the spinal nerves will be described, 
in so far as they present special features. The effect of paralysis 
of the individual muscles has been already described in detail, and 
need not be here repeated, except in general terms, or in so far as the 
association of palsies resulting from a nerve-lesion presents a parti- 
cular character. 
Phrenic Nerve.— Impaired function of the phrenic nerve is 
commonly the result of disease of the spinal cord, or of the roots of 
the nerve from disease of the membranes or the bones. The deep 
position of the nerve-trunk protects it from injury, but it is occasionally 
damaged in wounds of the neck, and in its course through the thorax 
it may be compressed by tumours, aneurisms, &c. Paralysis sometimes 
follows exposure to cold, and is ascribed to neuritis. This has been 78 
SPINAL NERVES. 
met with in multiple neuritis. In disease of the spinal cord and 
membranes both nerves are usually paralysed; causes acting on 
the nerve-trunk usually affect one only. The effect and symptom of 
paralysis is inaction of the diaphragm (see p. 22). If one nerve only 
is affected, the diaphragm does not descend on that side, but the 
movement of the other side lessens the resulting defect of movement, 
and it can then be detected only by close observation. The loss of the 
action of the diaphragm has little effect on the respiratory functions 
while the patient is at rest, but dyspnoea is said to be readily pro- 
duced by exertion ; the breathing then becomes quick and the voice 
feeble. At the same time this is probably chiefly because too much 
and too constant work is thrown on the upper thoracic muscle of 
extraordinary breathing. Any lung disease, such as an attack of 
bronchitis, is rendered far more serious by the diminished breathing 
power. When the diaphragm is paralysed, the movement of the 
thorax is often increased, and the expansion of the lower part may 
draw forwards the adjacent abdominal wall. This must not be mis- 
taken for the effect of the descent of the diaphragm. Paralysis has 
to be distinguished from (1) abnormal nervous breathing. The dia- 
phragm is used little in extraordinary breathing, which is chiefly by 
the upper part of the thorax, of the “superior costal type,” as it is 
called. Hysterical and nervous patients will often breathe, for a 
time, only in this manner, even when at perfect rest, especially when 
they are under observation. Such breathing is no doubt facilitated 
in women by the fact that the diaphragm is habitually used by them 
less than by men. Repeated examination may be necessary to deter- 
mine whether there is any real paralysis of the diaphragm in these 
cases. A single diaphragmatic inspiration settles the point. The 
patient’s attention should be distracted, and she should not be aware 
of the object of the examination. (2) Inflammation of the diaphragm 
may arrest its movement, and so also may diaphragmatic pleurisy or 
peritonitis—each distinguished by the fact that it is usually secondarv 
to adjacent inflammation, and any movement, if effected, causes 
characteristic pain. (3) A primary and isolated degeneration of the 
muscular fibres of the diaphragm has been described by Callender and 
others as common after death, but it has not yet been proved to cause 
such inaction, during life, as might be confounded with paralysis. 
Paralysis may be due to disease of the nerve or of the spinal cord. 
In the latter case other muscles always suffer; in the former the 
diaphragm usually suffers alone unless it is part of multiple neuritis. 
In disease of the nerve-roots there are other indications of the position 
of the disease. The affection is often overlooked because not searched 
for, especially in disease of the spinal cord. The observer forgets that 
its associations are not with the lower dorsal muscles, and he omits 
to look for it in cases in which the cervical cord is suffering and other 
respiratory muscles act well. 
If there is reason to suspect neuritis, counter-irritation should be NERVES OF THE ARM. 
79 
applied over the lower aud inner part of the anterior triangle of the 
neck. The only other special point in treatment is the application of 
electricity. The nerve may be stimulated by pressing the rheophore 
deeply outside the lower part of the clavicular portion of the sterno- 
mastoid. The other pole may be placed at the epigastrium or over the 
corresponding half of the diaphragm. But the influence of electricity 
on paralysis of the diaphragm is not sufficient to make its use desir- 
able. In the cases in which such treatment could do good the affec- 
tion is transient and comparatively unimportant. In central disease 
electricity has very little influence. 
Nerves of the Upper Limb. 
The nerves of tlie arm and shoulder are derived from the five lower 
cervical and the first dorsal nerves. These interlace in the brachial 
plexus in such a complex manner that most of the nerves of the arm 
are derived from many spinal roots. 
The nerve-roots form, by their union, three trunks, which we may indicate by 
Roman numerals. They are formed thus :—I, by the branch from the fourth, and 
the roots of the fifth and sixth cervical; II, by the seventh; and III, by the eighth 
cervical and the first dorsal. Each trunk divides into two parts, and the union of 
these divisions forms the three cords of the brachial plexus from which the nerves 
of the arm proceed. But before the primary trunks divide, certain nerves arise, 
the origin of which is thus less doubtful. The fifth and sixth cervical roots give 
origin directly to the posterior thoracic nerve for the serratus, and from the cord 
formed by their union springs the supra-scapular nerve. The three cords of the 
plexus have the following relations:—The posterior is derived from all three 
primary trunks, and gives rise to the subscapular nerve, the circumflex, and the 
musculo-spiral (or radial, as the whole nerve is sometimes termed). The upper 
or outer cord is derived from the two upper primary trunks, i. e. from the fourth, 
fifth, sixth, and seventh cervical roots, and from it proceed one anterior thoracic 
and the musculo-cutaneous nerves, together with the outer head of the median. 
The inner or lower cord is derived only from the lowest primary trunk, i. e. 
from the last cervical and first dorsal, and gives rise to the ulnar, the inner 
head of the median, the internal cutaneous, the intercosto-humeral, and to the 
second anterior thoracic nerves. It may be convenient to put these coarse 
anatomical relations in the form of a table. 
Primary Trunks. 
Nerves. 
I. 
4, 5, and 6 C. 
II. 
6 and 7 C. 
III. 
(8 CU 
vi D.J 
Nerves. 
Upper 
cord 
'External ant. thoracic. 
[ Musculo-cutaneous. 
Subscapular . 
Circumflex 
Musculo-spiral 
Post. 
cord 
Outer head of 
median. 
Lower 
cord 
dinner head of 
Ulnar. 
Internal cutaneous. 
Intercosto-humeral. 
'-Internal ant. thoracic. 80 
SPINAL NERVES. 
These anatomical facts, however, give us little help in tracing the relation of 
the nerves to the spinal roots. The investigations of Ferrier and Yeo,*, who 
ascertained the movements produced hyfaradising the several spinal roots in the- 
monkey, show us the way in which the movements, muscles, and nerves are 
represented in the spinal roots. Their results are therefore of great interest, 
although we are not justified in transferring the facts to man except in so far 
as they receive confirmation from human anatomy and pathology.f Subject to 
this reservation, the chief results are important, and may be thus stated.^ 
The roots to which the several nerves are thus traced are as follows : Sub- 
scapular, 6 and 7 C.; cii'cumflex, 4 and 5 C.; musculo-spiral, 4, 5, 6, 7, 8 C.; 
musculo-cutaneous, 4, 5 C. ; median, 5, 6, 7, 8 C.; ulnar, 8 C., 1 D. 
Still more important are their observations on the relation of various move- 
ments of the arm to the nerve-roots, and these are as follows : 
Cervical 4.—Elevation and retraction of the arm, flexion and supination of 
the forearm ; by the rhomboids, supra- and infra-spinatus, biceps, brachial is, 
and supinators. 
Cervical 5.—Similar to the last, hut without retraction of the arm, and with 
extension of the wrist and first phalanges ; by the deltoid, serratus, flexors of 
elbow, extensors of wrist, and long extensors of fingers. 
Cervical 6.—Adduction and retraction of the upper arm, extension and pro- 
nation of the forearm, flexion of the wrist; by contraction of the pectoralis, 
latissimus dorsi, triceps, flexors of wrist, pronators. 
Cervical 7.—Adduction and rotation inwards at the shoulder-joint, flexion of 
the wrist, and of the fingers at the second phalanx ; by the teres major,, 
latissimus dorsi, subscapularis, triceps, and long flexors of the fingers. 
Cervical 8.—Flexion of fingers and thumb so as to close the fist; flexion of 
wrist towards the ulnar side, pronation of forearm, extension of elbow ; by the 
intrinsic muscles of the hand, the long flexors of the fingers and thumb, the 
flexoi-s of the wrist, and the triceps. 
Dorsal 1.—Adduction of the thumb, flexion of the fingers at the metacarpo- 
phalangeal joints ; by the interossei, &c. 
Thus most movements are related to many spinal roots. The most important 
relations are these : that of the deltoid, rhomboids, supra- and infra-spinatus, 
flexors of the elbow, and supinators, to the fourth and fifth cervical; that of the 
adductors of the arm and extensors of the elbow to the sixth and seventh nerves ;. 
pronation to the sixth and eighth ; extension of the wrist to the fifth ; flexion 
to the eighth ; extension of the first phalanx to the fifth ; flexion of the fingers 
to the seventh and eighth, and the action of the intrinsic muscles of the hand 
to the first dorsal. These facts will probably, in the future, find important 
practical applications. 
Regarding the relation of the sensory branches to the nerve-roots, we have 
* * Proc. Rov. Soc.,’ March 21, 1881. Careful dissections by Herringham (c*'. 
March 25th, 1887) give somewhat different results, but this method of investigation 
is open to more uncertainties than that of stimulation. Herringham’s conclusions 
should, however, be noted by future investigators. 
f In the case of the leg there are some important discrepancies between the 
results in the ape and the conditions that obtain in man. These will be noticed in 
their proper place. 
X Ferrier has since stated that the relations he gave (followed in the text) were all 
one nerve too high (‘ Proc. Roy. Soc.,’ 1883, vol. xxxv, p. 229), but this would make 
the innervation of the intrinsic muscles of the hand from the second dorsal nerve,, 
which is certainly not the case in man. NERVES OF THE ARM. 
81 
besides the facts of anatomy, only the evidence furnished by rare cases of 
injury or disease in which the lesion and its effects are well-defined.* Few 
facts of this character are, however, so conclusive as that illustrated in Fig 51, in 
which the area shaded by slanting lines was rendered anaesthetic by the division 
of the posterior roots of the last cervical and first dorsal nerves. The general 
indications are that the distribution of the sensory fibres of the nerve roots is 
along the axis of the limb and not across it. The last two pairs of nerves 
supply the ulnar side of the limb and the finger tips, the fifth pair the radial 
side and the middle roots of the brachial plexus, the middle zone of each side of 
the limb and the thumb.f 
Fig. 51.—Area of impaired sensation after division of the posterior 
branches of the 8th C. and 1 I). nerves, by Professor Horsley for inveterate 
paroxysmal neuralgia in that region. 
Paralysis of the nerves of the upper limb may be due to disease of 
the nerve-roots, of the plexus, or of the trunks that arise from these. 
It is convenient to consider, first, the diseases of the nerve-trunks, and 
afterwards those of the nerve-roots and of the plexus. Prom the 
roots themselves only one important nerve-trunk is derived: the pos- 
terior thoracic nerve. The others spring from the plexus. 
The morbid influences that affect the nerves of the arm are very 
varied. The brachial plexus passes close to the shoulder-joint, and 
hence dislocation often damages the nerves, sometimes one only, some- 
times several, and occasionally all the trunks. In fractures of the 
bones, the nerves adjacent may be torn, or may be compressed by 
the ends of the bone, or by the callus that is formed, or by bandages 
that are applied. The course of certain nerves is, in some parts of 
the arm, especially apt to be the seat of wounds of various kinds. 
They may be compressed by cicatricial fibrous tissue when the 
wound is merely near the nerves, while the position of some exposes 
them to pressure against the unyielding bone. Even slight pressure 
on these nerves is effective when prolonged, as it often is during 
sleep, when warning sensations are unperceived. The sleep induced 
by alcohol is especially apt to be attended by this accident. Hence 
there is a group of “ Sleep-palsies ” of the arm, chiefly of the musculo- 
spiral and median nerves, rarely of the plexus itself. 
* Instructive f;icts of this character will be found in papers by Thorburn, 
Brain,’ January, 18S7, and October, 1887. 
f This is due to the mode of growth of the arm-bud in the embryo; as 
shown by Boss in a most instructive paper, ‘Brain,’ January 7th, 1888. See 
also chapter on the Functions of the Spinal Cord. 
YOL. I. 82 
SPINAL NERVES. 
Primary neuritis may involve any nerve, or the brachial plexus, or 
the nerve-roots; certain nerves also suffer in multiple neuritis. 
Secondary neuritis, set up by injury or by adjacent inflammation, 
may extend upwards, and, reaching the plexus, spread to other nerves. 
Neuromata are rare. Various morbid processes in the neck may involve 
the nerve-roots. Neuritis of the plexus, and the multiple form, are 
separately described. 
Posterior Nerve—Nerve to the Serratus.—In consequence 
of its position and long course, the nerve to the serratus often suffers. 
After being formed in the substance of the scalenus medius muscle, 
by the union of branches of the fifth and sixth cervical nerves, it passes 
behind the brachial plexus and along the side of the chest to the 
lower border of its muscle. It is in the neck that the nerve is most 
often injured. It may be damaged there by direct pressure—as in 
carrying on the shoulder a heavy sharp-cornered object—or by severe 
muscular efforts, such as carrying a weight that does not press into 
the neck, wielding a heavy hammer, or long-contined exertion with 
the raised arm, as, for instance, in whitewashing a ceiling. In such 
cases a traumatic neuritis is set up by the violent compression of the 
nerve consequent on the forcible or prolonged contraction of the mus- 
cle through which it passes. When the onset of the palsy occurs 
immediately on the exertion, a paralysing injury to the uerve must 
have occurred, which will be followed by secondary neuritis. Falls 
and blows on the neck and shoulder are occasional causes; there is 
usually much bruising of the adjacent parts. Punctured and gun- 
shot wounds occasionally involve the nerve. The least frequent 
cause is exposure to cold, such as a draught on the neck, or 
sleeping on damp earth. I have once known it to follow par- 
turition, developing four days afterwards, doubtless from neuritis 
excited either by the muscular exertion, or by exposure of the neck to 
cold during the labour. The serratus suffers also in central disease, 
chiefly in progressive muscular atrophy and infantile paralysis ; but 
in these it is always associated with palsy of other muscles. Isolated 
paralysis of their nerves is nine times as frequent in men as in women 
It occurs chiefly in muscular workers, and during the active period of 
life, twenty-five to forty. The immediate causes sufficiently explain 
this relation to age and sex, and they also account for another fact—■ 
that it is far more frequent on the right side than on the left. It is 
sometimes bilateral, but the two nerves are never damaged at the same 
time. One man was affected on the right side after carrying heavy 
beams on the shoulder; he then carried them on the left shoulder, 
and the left serratus became paralysed. 
Severe neuralgic pains in the neck and about the shoulder commonly 
precede and accompany the onset of the affection when due to neuritis. 
The symptoms of the paralysis of the serratus have been already de- 
scribed (p. 29). It is readily recognised by the recession of the posterior 
edge of the scapula from the thorax when the arm is put forwards NEUVES or THE A KM. 
88 
{Fig. 8, p. 29). In severe cases the muscle is found to have lost fara- 
dic irritability, although it may still contract to the voltaic current. 
The course of a severe case is always tedious. Months may pass 
before improvement is manifested, and the paralysis is sometimes per- 
manent. In treatment it is desirable to maintain the nutrition of the 
muscle, as far as possible, by electrical stimulation, and its superficial 
situation renders this easy. If counter-irritation is desirable, it should 
be applied over the position of the scalenus, since the .lesion of the 
nerve is commonly at this place. The use of the arm should be 
limited. When practicable, the elbow should be carried in a sling of 
such a length as slightly to raise the shoulder. All movements that 
may involve contraction of the scalenus, i. e. all movements needing 
elevation of the shoulder, must be prohibited. 
The Suprascapular nerve arises from the trunk formed by the 
union of the sixth, fifth, and a branch of the fourth cervical nerves, 
but its fibres come from the fifth and partly from the fourth. It is 
occasionally damaged alone, or with the circumflex, in dislocation 
of the humerus, and by falls on the shoulder, and by carrying 
heavy weights. In some cases the injury may be to the upper part 
ot' the plexus (see p. 91), which may recover except this nerve. The 
result of its disease is palsy of the supra- and infra-spinatus (p. 30). 
The latter is the more important, and causes a defect of the rotation 
outwards of the humerus, interfering with many movements, and, 
among others, with the movement of the pen along the line in writing. 
Undue work is thrown on the posterior part of the deltoid and the 
teres minor; the deltoid may become hypertrophied, and its poste- 
rior edge is conspicuous against the wasted infra-spinatus. The 
scapula is rotated, so that the lower angle is moved upwards and 
inwards. The paralysis of the supra-spinatus is unimportant, except 
that the humerus is less firmly fixed and the deltoid more readily 
fatigued. It can, in very slight degree, supplement the deltoid, and 
if paralysed with the deltoid, the head of the humerus falls more than 
it does when the deltoid is paralysed alone. Some anaesthesia over 
the scapula often results from disease of this nerve. 
The Circumflex nerve, although arising from the posterior cord of 
the plexus, seems to derive its fibres from the same source as the 
supra-scapular, the fourth and filth cervical nerves. It supplies the 
deltoid and teres minor, and the skin over the deltoid. The course 
of the nerve renders it very liable to injury from dislocations and falls 
on the shoulder, and from the pressure of a crutch. Simple neuritis 
and so-called “ rheumatic palsy ” are rare, but the nerve has been 
affected in some acute diseases, possibly from pressure, and in rheumatic 
fever, perhaps by inflammation extending from the joint. It suffers, 
with other nerves, from disease of the upper part of the brachial 
plexus. 
The chief symptom is paralysis of the deltoid (p. 29), which abolishes 
almost all power of raising the arm, a very trifling degree of abduc- 84 
SPINAL NERVES. 
tion by the supra-supinatus alone remaining. The slight nerve-supply 
that the fore-part of the deltoid receives from one of the anterior 
thoracic nerves is insufficient to mitigate the effect of the paralysis of 
the circumflex, although it may maintain slight power of voluntary 
contraction in the anterior fibres, and this sometimes gives rise to an 
erroneous impression that the paralysis of the circumflex nerve is in- 
complete. The effect of the conjoined palsy of 
the teres minor is unimportant. The wasting 
of the deltoid causes a change in the shape of 
the shoulder (Figs. 7 and 9). Sensation may 
be lost in the skin over the lower part of the 
muscle, and the loss sometimes extends on to- 
the shoulder (Fig. 53). In some cases there is 
no auaesthesia, even when the muscle is wholly 
paralysed; we have seen that this is often the 
case in nerve-lesions (p. 60). Adhesions are 
apt to form in the shoulder-joint, in part pro- 
bably the result of trophic changes, since the 
circumflex supplies the articulation as well as 
the chief muscle that moves it. 
The diagnosis of the paralysis of the cir- 
cumflex nerve is easy. The only condition 
readily mistaken for it is anchylosis of the 
shoulder-joint in a stout individual, in whom 
the state of nutrition of the muscle is not readily 
perceived. The risk of error is increased by the 
fact that arthritis and paralysis may result from the same cause—a fall 
on the shoulder. Passive movement at once solves the problem. The 
scapula moves with the arm in anchylosis, and not in palsy. The 
importance of examining the joint is very great in all cases of inter- 
ference with movement of the shoulder. A patient had an epileptic 
fit which was supposed to have left brachial monoplegia, merely because 
he fell on the shoulder, and the movement of the arm was lessened first 
by pain, and then by arthritic adhesions. 
Tne Musculo-cutaneous nerve supplies the chief flexors of the elbow 
and the skin over the radial side of the forearm. It is scarcely ever 
paralysed alone, but often suffers, with other nerves, in disease of the 
brachial plexus. The symptoms correspond to its function; there is 
paralysis of the biceps and bracliialis (see pp. 32, 33), the effect of 
which is especially conspicuous when the arm is supinated and the 
supinator longus cannot flex the elbow. There may also be anaesthesia 
of the radial side of the forearm, front and back. 
The Musculo-spiral nerve is more frequently paralysed alone than 
any other nerve of the arm. Arising from the posterior cord of 
the brachial plexus, it seems to derive its motor fibres from all the 
nerve-roots that enter the plexus except the first dorsal. It supplies 
the triceps, all the muscles on the back of the forearm, the extensors 
Fig. 52.—Disease of the 
circumflex nerve from 
pressure-neuritis during 
acute illness ; wasting of 
deltoid. Tlie dotted line 
indicates the area of cu- 
taneous anaesthesia. NERVES OP THE ARM. 
85 
of the wrist and fingers, both the supinators, also the skin on the 
radial side of the back of the hand, the back of the thumb, index 
finger, and half the middle finger. It is thus the extensor nerve of 
the arm, and has a more complete relation to a single function than 
is common among the nerves of the limbs ; a fact that has given rise 
to diagnostic error, since a palsy limited to a single function suggests 
a central cause. The frequency with which this nerve suffers is due 
to its course. As it leaves the brachial plexus to wind round the bone, 
its position exposes it to injury in dislocation or from the pressure of 
a crutch; the most common form of “crutch palsy” is paralysis of 
this nerve. Lying as it does close to the humerus, it is readily torn 
in fracture, or compressed by callus, and it suffers gravely from even 
temporary pressure against the hard bone. Such pressure is often 
exerted during sleep. The nerve may be paralysed by the pressure to 
which it is exposed when the body, with the arm beneath it, rests on 
the ground or on a hard bed. Thus, a man slept all night on a bench, 
lying on his right side with his arm beneath him, and woke in the 
morning with this nerve paralysed. Curiously, a precisely similar event 
had occurred to him three years before. In other cases the pressure 
on the nerve is that of a hard and sharp object over which the arm is 
placed during sleep, as the edge of a chair or the side of a couch. 
The Continental custom of tying together, behind the body, the arms 
of a prisoner, often causes paralysis of this nerve, sometimes on both 
sides. In Russia it is not uncommon in infants, from the popular 
practice of binding the arms to the body and then laying the child to 
sleep on its side. I have three times seen paralysis from a violent 
contraction of the triceps, once during the act of pulling on a tight 
pair of boots, once from throwing a stone with energy, and once from 
grasping a lamp-post to avoid a fall during a severe attack of giddi- 
ness In each the nerve was at once completely paralysed ; and in the 
second, in which the palsy was severe, a bruised appearance was ob- 
served over the lower part of the triceps. Neuritis due to cold is often 
assumed to be a cause, and is possibly sometimes effective, but the 
exposure has usually been during alcoholic sleep, and it is probable that 
the paralysis is due to compression rather than to cold. The same 
influence may also have been operative in cases in which the nerve has 
been paralysed during an acute disease. Although in a case of para- 
lysis during typhus, described by Bernhardt, neuritis was found after 
death, this was at the spot at which pressure is usually effective, and 
the inflammation was probably thus excited. Pressure always sets 
up neuritis, and the diagnosis of a primary neuritis is never justified 
if the spot affected is one liable to compression. 
The symptoms of disease of the musculo-spiral nerve are paralysis 
of the extensors of the elbow and of the wrist, the long extensors of the 
fingers and thumb, and the supinators (see pp. 33, 34). All these are 
paralysed by a complete lesion of the nerve near the brachial plexus. 
When the lesion is near the middle of the humerus, as it is in most 86 
SPINAL NKRVFS. 
cases of compression, the triceps generally escapes, but not always 
The supinatus longus is usually paralysed, but escapes if the lesion 
is below the origin of its branch, and may also escape if the injury to 
the nerve is incomplete. In sleep palsy it usually suffers, but I have 
seen it unaffected, in a case in which the ext. carpi radialis was also 
but little affected, and Bernhardt has noted the escape of the supinator 
in an otherwise complete paralysis from dislocation of the humerus. 
The extensor palsy causes characteristic wrist-drop, and loss of the 
power of extending the first phalanges of the fingers and the thumb 
(see p. 34). There is sometimes a gradation of palsy from the first 
finger, in which it is least, to the fourth, in which it is greatest (Fig. 
54). The same gradation is seen in lead palsy, &c. It is not easy to 
explain. The action of the flexors is feeble, from the loss of antergic 
support; in most cases of complete palsy I have found the power of 
flexion reduced from this cause to one third of the normal. The loss 
of the power of supination is a grave inconvenience. If an object is 
grasped firmly the arm becomes pronated. The patient tries to com- 
pensate for the loss by putting the elbow against the side and rotating 
Fig. 53.—Paralysis of the musculo-spiral nerve; maximum extension of 
wrist and fingers. The extension of the fingers progressively diminishes 
from the first to the fourth. (From a photograph.) 
the humerus. The pronators may ultimately become shortened. The 
over-flexion of the carpus, and its deficient support by the extensor 
tendons, leads to a pro- 
minence of synovial sacs, 
and perhaps of the bones, 
at the back of the carpus 
(Fig. 55). In severe cases 
the muscles waste, and the 
maximum circumference of 
the limb below the elbow 
may be a quarter or half an 
inch less than on the other 
side. The electrical reac- 
tions depend on the seve- 
rity of the lesion of the nerve; commonly there is well-marked degene- 
FiG. b4.—Prominence at back of band from para- 
lysis of the extensors. The patient was suffering 
from wrist-drop due to silver-poisoning (see vol. 
ii, “ Argyria.”) NtiltVES OF THE ARM. 
87 
rative reaction. The affection of sensibility in the area supplied by 
the nerve is very variable. The skin of the upper arm rarely loses 
feeling; in the hand sensation may be normal, although the muscular 
paralysis is complete. There may be subjective “ tingling ” in the part 
although there is no loss of sensibility. 
The diagnosis is easy in most cases. The affection is distinguished 
from lead palsy by its common limitation to one arm, by the affec- 
tion of the supinator, and often by the sudden onset; that from lead 
is gradual. These characters, and the commonly obtrusive cause, 
always suffice for the diagnosis. It must be remembered, however, 
that this nerve is one most frequently affected in many other forms ot' 
multiple neuritis (q. v.). The prognosis in disease of the musculo- 
spiral nerve depends on the severity of the lesion, as indicated by the 
electrical reaction. When there is evidence of nerve-degeneration the 
paralysis usually lasts for some months. Recovery ultimately occurs 
in almost all cases. The treatment is that for neuritis, already 
described, but attention should be paid to the posture of the limb, so 
as to avoid tension on the affected part of the nerve. For this reason, 
and also because strong contraction of the triceps may further injure 
the nerve, extension of the elbow should be avoided in cases of lesion 
of the nerve as it winds round the humerus. 
The Median nerve supplies the pronators, the radial flexor of the 
wrist, the flexors of the fingers (except the ulnar half of the deep 
flexor), the muscles that abduct and flex the thumb, and the two 
radial lumbricales. Its motor fibres seem to have an extensive origin 
from all the cervical roots that enter the brachial plexus. It subserves 
sensation on the radial side of the palm, on the front of the thumb, 
of the first two fingers, and of half the third finger, and also, at least 
in many persons, on the back of the last phalanx of the index and 
middle finger; sometimes also on the adjacent part of the back of the 
ring finger and the back of the last phalanx of the thumb. Isolated 
palsy of this nerve is not frequent, and generally results from wounds 
of the forearm, or fractures of the forearm bones rarely from injuries 
in the upper arm. The nerve is occasionally the seat of neuritis, 
which may be induced by compression, especially in those who, in 
their work, have to hold an object between the hand and upper arm. 
I have known it to be paralysed at the wrist a few hours after a severe 
sprain of this joint. Webber has recorded a case in which it seemed 
to be injured by a violent contraction of the pronator teres. When 
there is complete damage to the nerve, pronation is impossible beyond 
the mid-position, to which the supinator longus can bring the forearm, 
and an attempt is made to supplement this by rotating the humerus 
inwards, and separating the elbow from the side. The wrist can only 
be flexed with a strong inclination towards the ulnar side. The 
thumb is in persistent extension and adduction (like the thumb of the 
ape, Figs. 22 and 23, p. 38), and cannot be opposed to the tips of the 
fingers. The power of flexing the second phalanges on the first is lost, 88 
SPINAL NERVES. 
and also that of flexing the distal phalanx of the first and second 
fingers, but this phalanx can still be flexed in the third and fourth 
fingers, by the ulnar half of the flexor profundus (see p. 29). Inter- 
osseal flexion of the first phalanx is still possible, and the unopposed 
extensor action of the interossei on the middle and distal phalanges 
tends to cause a subluxation of the articulations concerned. The 
wasting of the thenar muscles is usually conspicuous. The resulting 
condition is very characteristic, but if the damage is at the wrist 
flexion of the wrist and distal phalanges remains. The sensory loss is 
variable; it may be absolute or absent. If there is anaesthesia it is 
greater on the palmar surface, and will often be found also on the 
dorsal aspect of the extremities of the first two fingers. 
The TJlnar nerve comes, through the inner cord of the plexus, from 
the last cervical and first dorsal roots, and its origin from the lowest 
part of the cervical enlargement gives it an important relation, since it 
is the first of all the brachial nerves to be affected by disease that 
ascends from the dorsal to the cervical region of the spinal cord. The 
nerve supplies the ulnar flexor of the wrist, the ulnar half of the deep 
flexor of the fingers, the muscles of the little finger, the interossei, 
some of the lumbricales, the adductor and inner head of the short flexor 
of the thumb. Its sensory area is the ulnar side of the hand, back 
and front, generally more extensive on the back (two fingers and a 
half) than on the front (one finger and a half). The course of the 
nerve, superficial behind the elbow and at the wrist, renders it liable 
to separate injury. It is often implicated in wounds of the forearm, 
and about the elbow-joint, by dislocations of the shoulder and elbow, 
enlargement of the elbow bones, and by fractures of the bones of the 
forearm. It is occasionally the seat of neuritis, and, like the musculo- 
spiral nerve, it is sometimes paralysed by pressure. At the elbow, the 
projecting bones preserve the nerve from direct pressure; although 
Duchenne describes paralysis in men who, while at work, rest the bent 
elbow on a hard substance, this mechanism is certainly rare. It is much 
more common for the nerve to suffer in long-continued flexion of the 
elbow, without external pressure; and from this cause the nerve is 
sometimes paralysed during sleep. I have three times seen a sleep 
palsy of the ulnar nerve. The tension may set up neuritis, and is 
especially effective if the resistance of the tissues to morbid influences 
is lessened by general ill health. Many persons must have noticed 
that if, when out of health, they sleep with the elbow bent, they wake 
with tingling, and even loss of feeling, in the region supplied by the 
ulnar nerve, although this may not happen when they are in good 
health. If the ill-health is profound, as in an acute illness, local 
neuritis of considerable intensity may be set up. Thus a lady, a few 
days after childbirth, who was prostrated by a long, exhausting 
labour, noticed tingling in the side of the hand, and, whenever she 
bent her elbow, a sensation “ as if she had knocked her funny-bone.” 
Paralysis of the muscles supplied by the ulnar nerve followed in a few NERVES OF THE ARM. 
89 
hours, and in a fortnight there was distinct wasting. When I saw 
her, six months later, the ulnar nerve behind the elbow was distinctly 
thickened. She had had a similar, but more transient attack after a 
previous confinement. A similar palsy has occurred during the course 
of typhoid fever, and both nerves have been known to suffer (Bern- 
hardt). In such conditions, not only is the tissue-health lowered, but 
warning sensations are often unperceived. 
The importance of the interosseal flexion of the fingers for many 
actions, such as writing, renders palsy of the ulnar nerve peculiarly dis- 
abling. Several illustrations of the symptoms have already been given 
(p. 36). In flexion of the wrist, the hand deviates towards the radial 
side, and persistent distortion may take place. Adduction of the 
thumb is lost, and so are most movements of the little finger. The 
fingers cannot be flexed at the first or extended at the other joints, 
but the loss is slighter in the first two fingers than in the others, because 
their lumbricales ai'e supplied by the median nerve, In time the 
opponents of the interossei, by their contracture, lead to over-exten- 
sion of the first phalanges and flexion of the others; the “claw-like 
hand” is produced (see p. 36), but this is less complete than in cases 
of progressive muscular atrophy, on account of the escape of the first 
two lumbricales. When the palsy is imperfect it may be possible to 
■extend the second and third phalanges, if the first can be over-extended, 
and an advantage thus given to the interossei by the lengthening of 
the course of their tendons, just as in partial paralysis of the long 
extensors they may be able to extend the digits if the wrist is flexed, 
but not if it is extended. In lasting damage the hypothenar eminence 
may disappear, the palm is hollow, the thenar muscles that remain 
stand out, and the opponens may cause a slight forward rotation of 
the thumb. 
The loss of sensation, as in the case of the other nerves, varies much, 
both according to, and irrespective of, the degree of lesion of the nerve. 
Subjective sensations are common, with and without anaesthesia, and 
those who have had neuritis are sometimes unable to bend the elbow 
for a few minutes without a sensation of tingling in the area supplied. 
The diagnosis of disease of the ulnar nerve is easy. A difficulty is 
occasionally caused by the circumstance already mentioned, that dis- 
ease at the lowest part of the cervical enlargement may cause sym- 
ptoms limited to the region of this nerve, but a knowledge of the fact 
is usually sufficient to prevent an error. 
Combined Palsies of the Nerves of the Arm.—Paralysis in the 
region of two or more of the nerves of the arm is very common, and 
results from many causes. It may be due to disease of the spinal 
cord or the nerve-roots within the spinal canal, but with these we are 
not now concerned. The most frequent causes outside the spinal 
canal are the following:—(1) Morbid processes in the neck, affecting 
the nerve-roots outside the spine or the upper part of the brachial 
plexus, especially growths and exostoses. (2) Diseases of the plexus CO 
SPINAL NERVES. 
itself, neuritis or injury, dislocations of the shoulder, the stretching 
by a sudden wrench of the arm,* or actual rupture of the nerves 
entering the plexus by great local violence. (3) Fractures of the 
bones. (4) Ascending neuritis, “neuritis migrans,” which, com- 
mencing in a single nerve, may ascend to the plexus, and there 
spread. 
We may consider first the cause last named. An injury of a single 
nerve is sometimes followed by an extension of the motor and sensory 
symptoms to the regions supplied by other nerves. This can only be 
explained by an ascending neuritis reaching the junction of the nerves 
at the brachial plexus, and there spreading, often in what seems a 
random manner. Thus a lady cut her wrist so as to leave a scar an 
inch long, over the position, and in the direction, of the median nerve. 
The injury caused paralysis and wasting of all the muscles in the 
hand supplied by this nerve. This palsy was followed by a gradual 
loss of power, with diminished faradaic irritability, in the long 
extensor of the fingers, the ulnar flexor of the wrist, and also by 
defect of sensation in the skin supplied by the ulnar nerve. Hence 
the neuritis must have ascended to the plexus, and there have spread 
along each root of the median nerve. Again, a woman cut her right 
hand with a broken stone bottle, along the hypothenar eminence. 
Three weeks afterwards the muscles of the hand supplied bv the 
ulnar nerve gradually became paralysed, with wasting and loss of ii-ri- 
tability, and in the area of the skin supplied by the nerve there was 
first tingling and then diminished sensibility. Burning pain spread 
up the front of the forearm, and inner side of the upper arm, to the 
axilla ; all the forearm muscles lost power, the flexor carpi ulnaris, 
and the flexor sublimis digitorum in greatest degree; the tingling and 
lessened sensibility spread to the fingers supplied by the median 
nerve, and the abductor pollicis wasted. In this case also there must 
have been an ascending neuritis of the ulnar, spreading to the median 
at the brachial plexus. 
The brachial plexus is occasionally the seat of a primary neuritis. 
This is described in a separate section (p. 97), as it is a defined and 
important disease. Another cause of damage to the plexus is dislocation 
of the shoulder, especially sub-coracoid dislocation, in which the dis- 
placed head of the humerus necessai’ily compresses the nerves. The 
extent of injury varies greatly; only one nerve may suffer, or not one 
may escape. Every muscle of the arm may be paralysed, from the 
deltoid downwards. In most cases the injury is severe in degree; 
there is rapid wasting of the muscles, with the reaction of degenera- 
tion, and there is a great tendency to the occurrence of trophic changes 
in the skin. It was in a case of this character that the forearm and 
hand were covered with blisters from the application of water that 
seemed merely warm to a healthy hand (p. 62). 
Fracture of the humerus may damage both the musculo-spiral and 
* Bowlby, loc. cit., p. 225. 91 
NERVES OF THE ARM. 
ulnar nerves, rarely the median. Fracture of the bones of the forearm 
often injures both the median and ulnar nerves. 
Injuries to the neck sometimes cause a partial paralysis of the arm 
of peculiar distribution, the special characters and significance ot' 
which were first made known by Erb.# A similar paralysis may 
come on apart from injury. The muscles affected are the deltoid, 
often the supra-spinatus and infra-spinatus, the biceps and brachialis 
anticus, and the supinators. Erb found that there is one spot between 
the scaleni, corresponding to the sixth cervical nerve, at which electrical 
stimulation puts all these muscles in action. Hoedemaker, who has 
described two cases of this palsy, finds the motor point in a line drawn 
from the sterno-clavicular articulation to the seventh cervical spine, 
1*5 centimetres from the edge of the trapezius. The palsy is appa- 
rently dependent on disease of the roots of the fifth and sixth cervical 
nerves, and the fifth, it will be remembered, receives a twig from 
the fourth.f Besides injuries, this group of palsies may result from 
Fig. 55. 
Fig. 56. 
Fig. 57. 
FiG. 55.—Combined palsy of deltoid, supra-spinatus, and infra-spinatus, from a fall 
on the shoulder. 
Figs. 56,57 —Left hand of a patient suffering from a growth beside the lower cervical 
spine compress:ng the nerve-roots. There was anaesthesia of all parts supplied 
by the brachial and cervical plexus. The arm was adducted, the elbow flexed, the 
hand in the posture shown, flexion of first, extension of second, strong flexion 
of last phalanges, the first phalanx of the thumb over-extended, the second fluxed. 
Rigidity extreme, and an attempt to overcome it caused great pain. There 
was also some contracture of the loot (equino-valgus). 
* Heidelberg Society, 1874, ‘ Ziemssen’s Handbuch/ 1874, Bd. xii, pt. 2, p. 504; 
see also Bernhardt, * Zeitsch. f. Id. Med./ 1882, Bd. iv, p. 415. A previous descrip- 
tion by Duchenne had escaped notice. 
f Erb referred the palsy to disease of the sixth nerve. The experiments of 
Ferrier and Yeo point to the fifth and fourth roots as those innervating these 
muscles but his subsequent correction indicates the fifth and sixth (see p. 80). 92 
SPINAL NERVES. 
non-traumatic processes, probably from neuritis, and also from 
groAvths in this situation. Ducbenne and Seligmiiller bave also 
described paralysis of similar distribution produced in infants during 
birth, either by pressure from the position of the arm, or by traction 
on the neck with the finger or hook. Most obstetrical cases slowly 
recover. Those due to injury in adult life are often severe; the 
symptoms continue for a long time, and may be permanent. 
Morbid processes connected with the bones of the cervical spine 
sometimes produce combined symptoms of irritation and palsy of 
the nerves of the arm, pain, hypersesthesia, anaesthesia, paralysis 
of mnscles, and extreme muscular contractures, often very irregular in 
distribution (such as are shown in Figs 56,57). I have several times 
known sensory symptoms in the arm to be due to a chronic syphilitic 
oellulitis beside the vertebrae, causing deep-seated induration and 
severe compression of the nerves ; in each case it was completely 
removed by anti-syphilitic treatment. Growths at the part may also 
■compress the subclavian artery and the weaker pulse may aid the 
diagnosis.* 
Diagnosis.—The diagnosis of diseases of the nerves of the arm has 
been for the most part sufficiently considered in connection with the 
special nerves. It consists chiefly in an application of the facts there 
stated. One or two more general considerations deserve, however, 
a brief mention. Some diseases of the spinal cord are first manifested 
in the arm, by muscular palsy, wasting, or by anaesthesia. The risk 
of error is prevented, in most cases, by the abseuce of any corre- 
spondence between these symptoms and the functions of special 
nerves, by the absence of any indication of morbid processes in the 
neighbourhood of the nerves, and by the presence of other signs of 
disease of the spinal cord. It has been mentioned that disease in the 
lowest part of the cervical enlargement may be manifested only in the 
region of the ulnar nerve, the lowest in origin of all the brachial 
nerves. Such disease is, however, usually bilateral, and secondary to 
disease in the dorsal region of the cord, the indications of which have 
preceded the symptoms in the arm. A knowledge of these facts, and 
a careful consideration of the distribution and course of the symptoms, 
will rarely leave the observer in doubt. 
Treatment.—There is little in the treatment of the diseases of the 
nerves of the arm that requires special mention. The chief measure 
is the treatment of the cause of the paralysis. Any present source of 
pressure must be removed as far as possible. The ends of a divided 
nerve must be sutured. It is remarkable how quickly this has some- 
times been followed by the restoration of conducting power. The 
posture of the arm must, in all cases, be such as to avoid tension on 
an injured or inflamed nerve. The treatment of neuritis is described 
in the next section. Electrical stimulation of the muscles is of great 
Bowlby, loc. cit. 93 
NERVES OF THE LEG- 
importance in all cases of severe damage to the nerves. Even in 
old and stationary cases it sometimes starts some improvement. 
Nerves of the Lower Limb. 
Disease of these nerves is far less common in the lower than in the 
upper limb, with one important exception,—the primary disease of the 
sciatic nerve that goes by the name of “ sciatica.” This affection is 
reserved for separate description in the next section. 
The nerves of the leg are derived from the lumbar and sacral 
plexuses. The lumbar plexus, consisting of the first three and a half 
lumbar roots, supplies the skin of the lower part of the abdomen, of 
the front and sides of the thigh, of the inner side of the lower leg and 
foot. It supplies also many muscles—the cremaster, and those that 
flex and adduct the hip-joint, and those that extend the knee. Its 
branches for the leg are the obturator and anterior crural nerves. 
Tne sacral plexus consists of the fifth lumbar root and half the fourth 
(lumbo-sacral cord) and the first four sacral nerves, of which, however,, 
only the upper three have to do with the leg. This plexus innervates 
the extensors and rotators of the hip, the flexors of the knee, and all 
the muscles that move the foot, together with the skin of the gluteal 
region, the back of the thigh, the outer side and back of the lower leg,, 
and most of the foot. Its chief nerves are branches to the outward 
rotators of the hip, the gluteal nerve, and the small and great sciatic. 
The results obtained by Ferrier and Yeo (see p. 80) on stimulating the roots 
of the lumbar and sacral plexuses in the monkey, may be thus summarised : 
Lumbar I and II. Lower abdominal muscles (not cremaster). 
III. Psoas and iliacus, sartorius, extensors of knee ; (flexion of hip and 
extension of leg). 
IY. Glutei, adductors, extensor cruris, pei’oneus longus ; (extension of 
hip and knee, elevation of outer side of foot). 
V. Glutei, hamstrings, and all the muscles in front and back of 
lower leg; (rotation of thigh outwards, flexion and rotation inwards 
of leg; extension of foot with elevation of outer edge ; flexion of 
distal phalanges of toes). 
Sacral I. Hamstrings, calf muscles, long flexor of toes, intrinsic muscles of 
foot; (slight outward rotation of thigh, flexion of knee, extension 
of foot, adduction of great toe, flexion of first phalanges of all toes 
and of both phalanges of great toe). 
II. Intrinsic muscles of foot; (“ interosseal ” flexion of toes, similar to 
the last). 
These results cannot be simply applied to man. For instance, it is certain 
that in man, one flexor of the hip, the psoas, and the cremaster, are largely 
innervated from the second lumbar, but no indication of the action of either of 
these could be observed on stimulating this root in the monkey. 
The distribution of the sensory fibres of the nerve-roots is considered in the 
chapter on the Spinal Cord. 
The Lumbar plexus itself is sometimes damaged by growths in the 
abdomen (especially by those that spring from the lumbar glands) and 
by psoas abscess, while the nerve-roots may suffer in disease of the 94 
SPINAL NEIlVES. 
bones of the vertebrae and in meningitis. The plexus may also be in« 
vaded by inflammation ascending the lumbo-saeral cord from the sacral 
plexus, and it is occasionally the seat of spontaneous neuritis. The 
obturator nerve is rarely affected alone; it has been sometimes damaged 
in the course of parturition. The anterior crural nerve has suffered 
from the same cause, and is sometimes injured by wounds of the 
groin or thigh, or by dislocation of the hip-joint. Symptoms may be 
limited to it in disease of the nerve-roots. 
Of the interference with movement that may result, the paralysis of 
the flexors of the hip depends on the position of the disease. This 
paralysis is total only when the lumbar plexus is damaged. Disease of 
the anterior crural nerve, within the abdomen, does not affect the psoas, 
but may paralyse the iliacus, and so weaken, without abolishing, the 
power of flexion. The chief symptom of disease of this nerve is the 
loss of power in the extensors of the knee, and the wasting of these 
muscles, together with loss of the knee-jerk which results from the 
interruption of the reflex arc. The effect of these palsies on movement 
is very serious (see pp. 40, 41). Anaesthesia involves the w7hole of the 
thigh (except a strip along the middle of the back), the inner side of the 
leg and foot, and the adjacent sides of the first and second toes. In many 
cases the paralysis is incomplete, and the symptoms present corre- 
sponding variation. Irritation of the nerve may cause severe pain in 
the region supplied by it. This is sometimes an early symptom of a 
growth near the spine. The pain in neuritis of the plexus may extend 
along the course of the ilio-hypogastric, ilio-inguinal, and genito- 
crural nerves, to the lower part of the abdomen and groin. 
Paralysis of the obturator nerve causes a loss of the power of adduc- 
tion of the thigh, so that the patient cannot put one leg across the 
other. Rotation of the thigh outwards is interfered with, but in 
slighter degree than adduction. The effect of these palsies (described 
on pp. 39, 40) is far less serious than is the disability which results 
from disease of the anterior crural. 
The superior gluteal nerve occupies an intermediate position between 
the two plexuses, arising as it does, from the lumbo-sacral cord, which 
descends from the fourth and fifth lumbar roots. Its disease, which 
is very rare in isolated form causes paralysis of the gluteus medius 
and minimus, with a loss of abduction and circumduction of the thigh 
(see p. 39). 
The Sacral plexus is sometimes damaged by growths in the pelvis, 
by pelvic inflammation of various kinds, and by compression during 
parturition. It is also often the seat of neuritis, which, however, less 
frequently begins in the plexus, than ascends to it from the sciatic 
nerve. Apart from spontaneous neuritis, which will be separately- 
described, the sciatic nerve outside the pelvis is occasionally injured by 
wounds, rarely by dislocations of the hip, often by disease of the bone, 
and by adjacent morbid growths. It is also a relatively frequent 
seat of neuroma. Of the terminal branches, the external popliteal, by NERVES OF THE LEG. 
95 
its superficial course, and proximity to the hard bone, suffers from 
traumatic lesions of various kinds; it is also prone to spontaneous 
neuritis. This nerve is homologous with the musculo-spiral nerve of 
the arm, and presents an analogous liability to disease. The posterior 
tibial nerve is more secure in its deeper course, but may be damaged 
by fracture of the bones. 
The symptoms of palsy of the sciatic nerve vary much in their 
character, according to the position of the disease. The small sciatic 
is implicated only when the mischief involves the pelvic plexus, and it 
scarcely ever suffers alone. The effect is palsy of the gluteus maximus, 
which interferes with rising from a seat more than with walking 
(see p. 39). There is also anaesthesia of the skin in the middle third 
of the back of the thigh, and in the upper half of the calf. A lesion 
of the sciatic nerve, near the sciatic notch, paralyses the flexors of the 
leg (which are also extensors of the hip ; see p. 42), and all the muscles 
below the knees. Often the lesion is below the upper third of the 
thigh, and then the flexors of the leg escape. Even when all the 
muscles below the knee are paralysed, walking is still possible, the 
foot being raised by over-flexion of the hip. The anaesthesia that 
results from a lesion of the nerve below the origin of the small sciatic, 
involves the outer half of the leg, the greater part of the dorsum of 
the foot, and all the sole, but the leg may escape, perhaps through 
union with other nerves. 
The symptoms of disease of the branches are as follows:— 
That of the external popliteal or peroneal nerve causes paralysis of 
the tibialis anticus, long extensor of the toes, peronei, and extensor 
brevis digitorum. The effect of this is a loss of all power of flexing 
the ankle and of extending the first phalanx of the toes (see p. 44). 
The foot cannot be raised from the ground in walking, and talipes 
equinus ultimately results (Eig. 30, p. 44), which may be attended 
with persistent flexion of the first phalanges of the toes from contrac- 
ture of the unopposed interrossei. There is also anaesthesia on the 
outer half of the front of the leg, and on the dorsum of the foot. 
Disease of the internal popliteal nerve paralyses the popliteus, calf 
muscles, tibialis posticus, and long flexors of the toes, as well as the 
muscles of the sole. In addition to the disability which characterises 
paralysis of the plantar muscle, there is loss of the inward rotation of 
the flexed leg, if the disease is so high as to involve the branch to the 
popliteus, and there is also loss of the power of extending the ankle- 
joint. Talipes calcaneus results (Fig. 28, p. 43). The sensory loss 
is on the outer lower part of the back of the leg, and on the sole, but 
varies much. 
The plantar nerves rarely suffer alone. A lesion of the internal nerve 
causes ansesthesia on the inner part of the sole, and plantar surface of 
the three inner toes and half the fourth, together with paralysis of the 
short flexor of the toes, the plantar muscles of the great toe (except 
the adductor), and of the two inner lumbricales. 96 
SPINAL NERVES. 
Disease of the external nerve produces anaesthesia of the skin on the 
outer half of the sole, the little toe aud half the fourth, paralysis of 
the flexor accessorius, the muscles of the little toe, all the interossei, 
the two outer lumbricales, and the adductor of the great toe. The 
effect of this palsy (see p. 45) is serious, since the toes cannot take 
their proper share in propelling the body forward in walking, and they 
gradually become flexed at the last two joints and extended at 
the others, from the contracture of the opponents of the inter- 
ossei,—aposition of the toes that causes serious inconvenience in 
walking. 
Diagnosis.—The diagnosis of diseases of the nerves of the leg is 
determined by the same general principles as those that have been 
mentioned as applicable to the nerves in general, and to the nerves 
of the arm in particular. The limitation of the symptoms to the 
functional areas of individual nerve-trunks, the evidence afforded by 
nutrition, irritability, and reflex action that the muscles are separated 
from the spinal cord, the implication of the sensory functions, and 
often the tenderness of the affected nerves, indicate, in most cases, 
the seat of the disease. To these signs, are often added other indica- 
tions of a local cause, corresponding, in its position, with the nerve 
to which the symptoms point. 
The relation of nerve-trunks to nerve-roots, although by no means 
simple, is certainly less complex in the case of the nerves of the leg 
than in those of the arm. This is especially the case in the lumbar 
plexus, and it leads to an occasional difficulty in diagnosis. Pressure 
on the spinal cord, for instance, at the level of the origin of the fourth 
lumbar roots, may cause symptoms identical with those of a partial 
lesion of the anterior crural nerve. For instance, I have known para- 
lysis of the extensors of the knee, loss of the knee-jerk, with anaesthesia 
in the f rout of the thigh, to be the result of a gumma at the side of the 
cord at this level. But other evidence of a spinal lesion is rarely absent 
under such circumstances, and, in this patient a foot-clonus, due to the 
pressure on the pyramidal fibres, left no doubt as to the situation of the 
disease. Another difficulty arises from the long course of the nerve-root s 
in the cauda equina, disease of which may simulate that of the nerves of 
the leg. But the symptoms are commonly bilateral in consequence of 
tlie proximity of the nerve-roots of the two sides. In all cases in which 
symptoms are bilateral (unless there is evidence of a disease known 
to cause symmetrical lesions, such as multiple neuritis), the suggestion 
is that the disease is situated where the motor or sensory paths of 
each side are so near that they can be affected by a single lesion, i. e. 
that the disease is within the spinal canal. But here, as in other 
cases, we cannot reverse our diagnostic rules. Disease of the spinal 
cord does not always cause bilateral symptoms. A limited lesion of 
one anterior cornu may be so placed as to paralyse the muscles supplied 
by a single nerve, and a doubt may be felt as to the central or peri- 
pheral origin of such palsy. The muscles supplied by the anterior 97 
BRACHIAL NEURITIS. 
crural nerve, and the muscles in the front of the lower leg supplied 
by the external popliteal, are those of which the central palsy most 
often leads to doubt. The mode of onset, the presence or absence 
of sensory symptoms, the rarity of acute spinal palsy except in child- 
hood, and of nerve-lesions except in adult life, the wider initial pre- 
valence of the palsy in acute, and its later extension in chronic, 
cornual disease,—these suffice as a rule to remove any doubt. 
It is important to remember that the pressure of a growth may 
cause either a chronic or an acute affection of the nerves. The chronic 
symptoms result from compression ; the acute from a neuritis set up 
by the pressure and irritation. 
Treatment.—The treatment of disease of the nerves of the leg 
does not differ from that of disease of the nerves of the arm. More- 
care, perhaps, is needed to avoid increasing present mischief, or 
inviting a relapse, by exposure to cold or by fatiguing exertion. More- 
care is also needed to obviate the tendency to secondary contractures in 
the case of palsies of long duration, aud in those attended by pain, in 
which the patient seeks ease in postures to which the muscles only too 
readily adapt themselves. The contraction of the hamstrings, from con- 
stant flexion of the knees, occurs very readily and is most troublesome ;. 
that of the calf muscles, which occurs when the flexors of the ankle are 
paralysed, also constitutes a serious obstacle to walking after recovery. 
A little timely care, by attention to posture, will often save a vast 
amount of later trouble. That of the calf muscles, however, which 
is due to the extension produced by the weight of the foot, as the 
patient lies, cannot always be entirely prevented, but may be lessened 
by a board or large sand-bag against which the feet can rest. 
BRACHIAL NEURITIS. 
Besides the forms of inflammation of the nerves of the arm alreadv 
described, a primary inflammation of the brachial plexus occurs in a form 
as well defined as sciatica, and equally meriting a separate description. 
This, however, need only include its special features; those that are 
common to other forms of neuritis have been already described. It 
is so closely analogous to sciatica that it may be called “ sciatica of the 
arm.” It is essentially a perineuritis,—a primary inflammation of 
the sheaths of the branches that enter and form the brachial plexus. 
Cases occur, however, in which the symptoms correspond in general 
character to the rest, but in which their distribution suggests that the- 
nerve-roots rather than the plexus are the seat of the inflammation,, 
and pain about the spine supports the opinion. This form may be 
called Radicular Neuritis. Although its existence has not been 
VOL. I. 08 
BRACHIAL NEURITIS. 
established bv pathological evidence, the symptoms mentioned admit 
of no other explanation. A knowledge of their significance is of great 
practical importance on account of the closeness with which they may 
simulate those of organic disease of the bones of the spine, or a growth 
in the spinal membranes. 
Causes.—The influence of gout in causing local neuritis is very 
conspicuous in the brachial form, with the special characteristic that 
this occurs chiefly late in life, very often from the inherited disease, and 
with greater frequency in females than any other form of neuritis; 
their liability is at least equal to, if not greater than, that of men. 
Five-sixths of the cases occur after fifty, and it may be met with up 
to extreme old age. In men there have usually been the ordinary mani- 
festations of gout, but in women the tendency is often only indicated 
by the family history, and by previous muscular rheumatism, especially 
lumbago and sciatica,—which have seldom been absent in either sex. 
In one case the onset of the bi’achial neuritis occurred immediately 
after an attack of sciatica. 
Symptoms.—Pain, the great symptom of the inflammation of all 
mixed and sensory nerves, is greater in this than in most forms of 
neuritis. It is usually the first symptom, and lasts long after the in- 
flammation is over ; its severity, coupled with the age of most sufferers, 
renders the malady one of a peculiarly trying character. The first 
pain is often referred to a distance from the seat of the inflamma- 
tion, perhaps because this begins at the plexus, where, at divisions, 
it is facilitated by motion, and the conducting fibres are readily 
reached and early irritated. Frequent seats for the first pain are 
the region of the scapula (sometimes beneath the bone) and the 
wrist or back of the forearm, with or without the hand. In other 
cases, however, the first pain is at the plexus itself, above the clavicle 
or in the axilla, and these are the places in which it is commonly 
most intense throughout the attack. As the pain increases it extends 
along the course of the nerves of the arm, which the patient will often 
accurately indicate with his finger when tracing the lines of pain. 
The pain is sometimes sudden in onset and severe from the beginning; 
more often it is at first occasional, or felt on certain movements, bxit, 
as it increases, it becomes more continuous, with variations that soon 
rise to paroxysmal degree. Ultimately there is always more or less 
dull wearying pain in the whole arm, but especially in the region of 
the plexus, varied by attacks of great severity. In these the pain 
is acute and lancinating, or stabbing, or burning ; it usually takes the 
course of the nerves, diffusing itself from them, and often passing 
to the side of the chest, and to the neck,—seldom to the head. The 
pain often varies in character according to intensity ; at the height of 
the paroxysm it may be sharp and stabbing, or such darting pains may 
be superadded to a more diffused burning pain, which lasts longer 
than the acute pain, and may be folloxved, as the paroxysm subsides, 
by general tingling of the skin of the whole limb. The paroxysms are DIAGNOSIS. 
99 
induced by movement or occur spontaneously. In slighter cases the 
pain is paroxysmal only, and then the relation to movement is a very 
conspicuous feature. Although it is seldom confined to movement, this 
never fails to induce severe pain, and the patient avoids the slightest 
use of the limb. Elevation of the arm especially causes distress. 
With the pain there is usually undue sensitiveness of the skin, 
which may be much increased during and after the paroxysms. Loss 
of sensation is rare, and is met with only in cases that are not only 
severe but prolonged. The two may concur, as “ anaesthesia dolorosa.” 
The muscles usually present the flabbiness and slight wasting 
common in neuritis, but the damage to the motor fibres is seldom 
sufficient to cause considerable atrophy. Sometimes, however, there 
is enough damage to cause wasting of some group of muscles, with the 
reaction of degeneration. This is most frequent in the radicular form, 
in which the damage is to the upper part of the plexus and nerve- 
roots. There may then be anaesthesia of the skin over the affected 
muscles. It is difficult to ascertain the existence or the amount of 
motor weakness; effort induces pain so readily that the patient can 
seldom be induced to make an attempt to exert force. Power is often 
said to be almost lost, when it is probably greater than is believed. 
Besides the muscles, the subcutaneous tissue of the limb may also 
waste, and the skin may become thin and shining, and present the 
aspect already described. Subcutaneous oedema is also common. 
Arthritic changes in the joints of the fingers are almost constant in 
the cases that occur in later life; the adhesions may be permanent. 
Diagnosis.—Few maladies, as a fact of experience, give rise to greater 
diagnostic difficulty. This is due to several causes: the affection is 
rare; its symptoms are sometimes equivocal; the subjects are usually 
in the degenerative period of life, when many obscure diseases attended 
with pain in the arm occur to the mind of the physician ; and lastly, 
the distinction between neuralgia and neuritis is often difficult, although 
less so than is supposed. The last is indeed the most frequent 
source of error. The most severe and characteristic cases of brachial 
neuritis are frequently mistaken for pure neuralgia, on account of the 
paroxysmal character of the more severe pain, and because the cha- 
racters of neuritis are unfamiliar. The points to determine the 
diagnosis are those described in the sections on neuritis and neuralgia; 
-—the degree of persistent tenderness of the nerves and the influence 
of movement, together with the history of the attack, the locality of the 
pains, and especially any evidence of damage to the fibres. A history 
of neuralgia in the person or the family is of slight weight only ; the 
tendencies to true neuralgia and to neuritis are often combined, and 
each is a frequent result of gout. A far greater difficulty is presented 
by the cases in which the inflammation remains slight and is confined 
to the plexus, affecting branches where the conducting fibres can be 
so irritated as to cause distant pain, which then becomes the leading 
symptom. This is often paroxysmal, and, when on the left side, may 100 
BRACHIAL NEURITIS. 
radiate to the chest and be associated with disturbed action of the 
heart. Angina pectoris is often thought of in such cases ; and here 
again the degenerative age may increase the difficulty by leading to- 
the presence of some coincident disease of the heart, or by making true 
angina not unlikely. The distinction afforded by the nerve-tenderness 
is then of great importance, because the disproportionate amount of 
tenderness (compared with the amount of pain) is more emphatic in 
slight than in severe cases. Persistent tenderness with only parox- 
ysmal pain should always suggest neuritis. When the position of the 
pain is carefully examined, its relation to the plexus and branches is 
often clear. It is important to remember that all nerve-pains in the 
brachial region on the left side have a tendency to resemble anginal 
pain in distribution, and to be associated with cardiac distress. 
Probably there is some peculiar tendency for pains in this part to 
disturb the action of the heart; a common physiological relation may 
underlie both the nerve-pains of cardiac angina and the cardiac sym- 
ptoms of nerve-pains. Hence this secondary disturbance does not 
neutralise the significance of the special signs of neuritis. In some 
cases of the slighter class, the pains suggest the idea of an aneurism 
in many cases of brachial neuritis this diagnosis has been made, and 
the patient has had to endure months of mental distress, for which 
no real cause was in existence. Such a suspicion, in the absence of 
special signs, such as pressure-symptoms, should only be entertained 
if the paius are persistently and increasingly severe, and unaccom- 
panied by any considerable amount of tenderness. In all these cases,, 
moreover, the presence of the gouty diathesis may be allowed weight 
in the diagnosis. 
The muscular wasting, slight in degree, added to the arthritic 
changes, gives rise to a condition which maybe mistaken for a primary 
joint affection with secondary “ arthritic atrophy ” of the muscles. It 
is only in the chronic stage that this error is possible. A careful 
attention to the history of the case will show its real nature, but with- 
out this attention the mistake is easy, and it is often made. 
Prognosis.—Except in its most trifling degree, brachial neuritis is 
a tedious malady ; the duration of every severe case is to be measured 
by months, and often more than a year elapses before the patient is free 
from pain. Post-neuritic pain is always more prolonged in the old than 
in the young, and the age of the subjects, together with the amount of 
damage to the nerves, causes suffering to last longer than in almost any 
other form. To these causes also must be added the degree of sen- 
sitiveness of the affected nerves, exceeded only by that of the fifth 
nerve, and also the mobility of the parts in which the plexus lies ; this 
involves a continued cause of irritation, brought into play as soon as the 
diminution in the severer pain permits the patient to employ the long 
useless arm. Relapses, moreover, are not uncommon. Recurrence 
may take place after moderate attacks, but seldom occurs after those 
of extreme severity. SCIATICA. 
101 
Recovery from the consequences of the inflammation is not always 
complete. The limb often remains smaller and feebler, with a liability 
to tingling and to cramp, and also to neuralgic pains under the influence 
of changes in the weather, &c. But the most serious consequences 
are the alterations in the joints. These are very frequent: the fixa- 
tion occasioned by the pain permits, and the tendency to perverted 
nutrition produces, adhesion between the articular surfaces, in con- 
sequence of which the movement becomes permanently restrained. 
It is probable, moreover, that the constitutional state which underlies 
the primary malady often increases the degree of these joint-alterations. 
The shoulder, wrist, and fingers are the joints that are most frequently 
thus rendered stiff. The interference with the movement of the fingers 
is especially troublesome; the joints become painful in consequence of 
the unavoidable strain on the tissues when an attempt at use is made. 
Treatment.—The treatment that has been described, as needed in 
neuritis generally, is suitable also for this form, and its details need 
not here be repeated. Abstinence from movement is of great import- 
ance ; the occurrence of stiffness of the joints in consequence of the 
immobility of the limb must be risked. It is doubtful, indeed, whether 
the tendency to this is much increased thereby, for the effect of pain, in 
preventing sufficient movement to maintain the normal state of the 
joints, is not materially increased by rest otherwise enforced; while 
the difference between a little movement and none, during the acute 
stage of the affection, is enough to make a considerable difference in 
the effect on the inflammation of the nerves. The influence of cocaine, 
injected under the skin, is very beneficial, but it is needed frequently 
in severe cases, and two injections (each TV—gr.) may be given 
■daily during the height of the disease. It is important that the nerves 
should not be irritated by massage in the state of active inflammation ; 
indeed, no therapeutic measure which occasions pain can do as much 
good as harm. After the tenderness has subsided, gentle rubbing, 
such as is agreeable, may be employed with advantage. Electricity is 
only needed for muscles that present the reaction of degeneration, or 
to aid in removing after-pains. 
SCIATICA. 
As the word sciatica is commonly used, it is a general designation 
for all affections of which the chief symptom is pain in the region of 
the sciatic nerve. It is thus often applied to the pain which results 
from pressure on the nerve in the pelvis, as by a tumour. In a stricter 
use of the word, however, it is applied to painful affections of the nerve 
not due to any cause outside it. The two varieties may be distinguished 102 
SCIATICA. 
as secondary and. primary sciatica. Primary sciatica is commonly 
regarded as a neuralgia. This view is in the main erroneous; the 
vast majority of cases of sciatica are really cases of neuritis of the 
sciatic nerve. The reasons for this opinion are given in the section on 
the pathology of the disease. 
Causes.—Sciatica is far more frequent in males than in females; 
the proportion has been very variously estimated. It is difficult to 
obtain statistics on the malady that are free from sources of fallacy, 
since comparatively few cases enter general hospitals. The incidence 
of severe sciatica seems to be fairly presented by the 137 cases that 
were treated in the Devonshire Hospital, Buxton, during the year 1883, 
and there is no reason to suppose that slight cases differ, in this 
respect, from those that are severe. The percentage of males is 82 ; 
of females, 18; giving a ratio of 4 to 1, which is probably very near 
the truth—a remarkable contrast to the analogous affection of the- 
arm. The disease is unknown in childhood, and rare in the second 
decade of life. It is most frequent between forty and fifty, next 
between fifty and sixty, and next between thirty and forty. The per- 
centage distribution of the 137 cases at Buxton is as follows:—Ten 
to twenty, 3 per cent.; twenty to thirty, 9 per cent.; thirty to forty, 
19 per cent.; forty to fifty, 29 per cent.; fifty to sixty, 2S per cent.; 
sixty to seventy, 13 per cent.; over seventy, 1 per cent. The influence 
of age is nearly the same in each sex. 
Two constitutional conditions are potent factors in the production of 
sciatica—gout, and that form of rheumatism which affects chiefly the 
fibrous tissues of the muscles. These two constitutional states cannot 
be entirely separated, but many of the sufferers are of opposite types: 
some are stout, plethoric, distinctly gouty; others pale, weakly, and 
rheumatic. Many of the latter owe their rheumatism to inherited 
gout; rheumatic fever is certainly one of the effects of this family 
tendency. Sciatica is most common among those who are gouty 
but do not suffer from articular gout, and such individuals often have 
many attacks. Gouty inheritance is generally to be traced in those 
who suffer early from the disease. Syphilis has been supposed in 
some cases to be the cause of a sciatic neuritis, but the cases are so rare 
as to make strong and clear evidence desirable. 
An exciting cause is to be traced in many of the cases. Exposure 
to cold is the most common. It is usually local exposure, as by wet 
boots, standing in water, &c.; sometimes, however, a general chill 
of the body determines an attack. The exposure to cold may be 
even more direct, as by sitting on wet grass. I believe that draughty 
water-closet seats are answerable for some cases. The neuritis often 
arises by the extension of an adjacent rheumatic affection of the 
fibrous tissue, especially of that form of lumbago which involves 
the fibrous attachments of the muscles at the back of the sacrum. 
This passes down, extending along the fasciae, to the nerve-sheath in 
the neighbourhood of the sciatic notch. (The fact is of much interest,. SYMPTOMS. 
103 
because it shows that this form of rheumatism must be regarded as 
inflammatory since it ran spread as inflammation.) A few days 
after the pain reaches the nerve-sheath there may be all the signs 
of intense inflammation. Mechanical causes also sometimes excite 
the disease, and still more often co-operate with other influences. 
The pressure of the edge of the chair, in those who sit much, is the 
most frequent mechanical cause. Muscular over-exertion has been 
thought occasionally to excite the disease. If the nerve is already 
tender, a strong contraction of the muscles at the back of the thigh, 
especially when the knee is flexed, and the muscles can freely shorten 
and widen, may produce acute pain in the nerve, evidently by its 
compression. It is conoeivable, therefore, that this cause may be 
effective in a predisposed person. Various morbid processes within the 
pelvis may cause symptoms of sciatica, usually by acting on the sacral 
plexus. Thus rectal and other tumours, pelvic inflammation, and 
injury during labour are occasional causes. A loaded rectum has been 
thought to be capable of producing sciatica. Mechanical congestion of 
the plexus of veins which lies over the sacral plexus of nerves is usually 
regarded as an occasional cause, but this is somewhat hypothetical, 
and its efficiency can scarcely be demonstrated. Lastly, the sciatic nerve 
may be secondarily involved in mischief that is outside the pelvis. The 
most frequent cause of this is disease of the bone, and especially disease 
of the hip-joint. In all these forms of secondary sciatica the symptoms 
are due partly to pressure on the nerve, partly to inflammation 
excited in it by the pressure, or extending to it from the adjacent 
disease. 
Pathological Anatomy.—Sciatica being a disease that does not 
itself cause death, observations of the morbid changes are few. In 
most cases that have been examined, distinct evidence of neuritis has 
been found, chiefly involving the nerve-sheath, but extending in some 
cases to the interstitial tissue. The changes are those that have been 
already described in the account of neuritis (p. 54). In recent cases 
there is swelling and redness of the sheath, sometimes there are small 
haemorrhages, and, in severe cases, similar but slighter alterations in 
the instertitial tissue, with secondary damage to the nerve-fibres. The 
signs of inflammation are most intense at the sciatic notch, and opposite 
the middle of the thigh. They may be limited to one or both of these 
picices, or they may be greatest there, and extend, in slighter degree, 
over a considerable tract of the nerve. 
Symptoms.—The chief symptom of sciatica is pain along the course 
of the nerve-trunk, often also along that of its branches, and sometimes 
in the area of its distribution. The affection may begin suddenly, 
especially in cases of rheumatic origin,— as suddenly as lumbago— 
generally about the hip or sacrum. Some sudden movement seems 
to excite it, but there has usually been slighter rheumatic pain in 
the neighbourhood for a day or two. More frequently the onset 
is gradual; slight pain is felt along the back of the thigh, on move- 104 
SCIATICA. 
ments and in postures that make the nerve tense, or cause pressure 
upon it. As the disease increases, the pain is more readily pro- 
duced, and becomes greater in degree, until at last the patient is 
free from induced pain only when at rest and the leg is in a 
certain position. Any movement that makes the nerve tense causes 
extreme suffering, a nd to avoid this the knee, in walking, is kept slightly 
flexed, and the leg held stiffly so as to avoid painful changes in the 
tension of the nerve. As the pain on movement increases, spontaneous 
pain is added, at first chiefly felt in the nerve-trunk;, but soon spreading 
to its branches and distribution. It is usually most intense in certain 
spots—(1) above the hip-joint, near the posterior iliac spine, (2) at the 
sciatic notch, (3) about the middle of the tbigh, (4) behind the knee, 
(5) below the head of the fibula, (6) behind the external malleolus, 
(7) on the back of the foot. The pain may radiate over the whole 
distribution of the nerve, but it is often so distinctly limited to the 
course of the trunk and branches, that the patient points these out 
with exactness when he indicates the course of the pain. It may 
be dull or acute, is often burning in character, and worse at night. 
It may seem to dart downwards, starting from the highest point. 
As the pain on movement increases, the nerve-trunk becomes ex- 
tremely tender to pressui’e, especially along the back of the thigh. 
Even before the tenderness becomes considerable it may often be 
elicited in the following manner. Let the patient sit on a chair with 
the knee at a little more than a right angle. If the finger is then 
pressed into the popliteal space, so as to make the nerve a little more 
tense, a pain is felt in the course of the nerve at the back of the thigh 
or above the sciatic notch. It is due to the sensitiveness of the nerve 
to tension, and is a very useful test. It is of much diagnostic value, 
especially when the part inflamed is high up within the pelvis, and 
there is no tenderness to pressure at the back of the thigh. 
Abnormal sensations other than pain are often felt in the area of 
■distribution of the nerve,—tingling, formication, and the like; and in 
severe cases there may be irregular spots of anaesthesia on the back of 
the thigh, on the leg, or the foot. The affection of sensibility at the 
back of the thigh indicates that the disease extends up the nerve, above 
the sciatic notch, to the origin of the small sciatic, or that this is 
involved in a simultaneous neuritis. In severe cases the muscles 
supplied by the nerve become flabby, tender to the touch, and sometimes 
distinctly weak and wasted. This is chiefly noticeable in the calf 
muscles. There may be slight alteration in the electrical irritability, 
but this amounts to a distinct degenerative reaction only in very severe 
cases. Slight fever and corresponding constitutional symptoms may 
attend an onset that is acute, or an inflammation that is intense. 
Chronic cases, however, are usually not attended by elevation of 
temperature. 
The duration and severity of the affection are extremely variable. It 
may be trifling in degree, causing pain on movement only, and this PATHOLOGY. 
105 
may pass away in the course of a few weeks. On the other hand, the 
spontaneous pain may be so continuous and intense that sleep can be 
obtained only by the help of narcotics, and the disease may last for 
many months, and even for a year. In most cases that last more 
than a year there is really a relapse of the affection. Improvement is 
shown by the subsidence of spontaneous pain, followed by the slow 
diminution of the pain on movement, and of the tenderness of the 
nerve. The muscular wasting, which occurs in severe cases, may lust 
long after the active stage of the disease in the nerve ; and fibrillary 
•contractions in the muscles that have been affected may continue for 
years, and are sometimes accompanied by a tendency to painful 
eramp. For a long time after the attack is over, pain is felt in the 
nerve in certain postures. Occasionally a secondary neuralgia is set 
up, extending outside the sciatic area. The disease is prone to relapse, 
•and still more prone to recur after recovery. A second attack may 
occur in the same or in the other leg, but both legs are scarcely ever 
affected at the same time. I have only once known a true primary 
sciatic neuritis to be bilateral. 
The cases of secondary sciatica depending on disease outside the 
nerve, compressing or irritating it, differ, in some respects, from the 
primary form. Pain is felt less in the nerve-trunk than in its distri- 
bution. The difference is not absolute ; it is one of degree. There is 
rarely, however, the tenderness of the nerve that is so common in 
primary sciatica. The course of the secondary cases is also different, 
and depends on the course of the original disease. 
Complications of sciatica are rare, but one or two deserve mention. 
Cutaneous eruptions, usually herpetic in character, have been occa- 
sionally met with. These may heal slowly, but, in themselves, they 
are unimportant. Sometimes the epidermis exfoliates; oedema of 
the limb occurs iu rare cases. A graver complication, but happily a 
rare one, is a tendency of the mischief to ascend the nerve. Thus sym- 
ptoms may spread from the region of the sciatic to that of the lumbar 
plexus ; the pain may spread to the front of the thigh, and the exten- 
sors of the knee may become flabby and weak. This is probably due to 
the passage of an ascending neuritis up the lumbo-sacral cord. In 
extremely rare cases the morbid process has apparently reached the 
spinal cord, and indications of cord disease have thus succeeded those 
of a primary and apparently simple sciatica. 
Pathology.—The nature of the disease has been already indicated. 
The evidence that the disease is a neuritis, and not a neuralgia, is 
chiefly threefold. The conditions under which the disease occurs 
are very different from those that attend unquestionable neuralgia in 
other situations. This has been remarked with surprise, even by those 
who regard it as a neuralgia, but who have failed to see the signifi- 
cance of the difference. Secondly, the neui-itic nature of the affection 
is clearly indicated by the facts of pathological anatomy, scanty though 
these are. Thirdly, the symptoms in severe cases are proof of the 106 
SCIATICA. 
existence of neuritis, the wasting of the muscles and the anaesthesia 
indicate structural damage to the nerve-fibres, and preclude any other 
explanation. There is every gradation between these severe forms 
and those which are slight, and the symptoms in the latter are 
identical with those of the earlier stage of the severe cases. 
The symptoms find their explanation in the character of the morbid 
process, and the facts of neuritis in general, already described, apply 
to this disease in every point. It is primarily a perineuritis; the 
pain in the nerve and its tenderness are due to irritation of the sheath- 
nerves. The pain referred to the distal portions of the nerve is due to 
the irritation of the proper fibres by the interstitial inflammation, while 
their greater damage explains the anaesthesia and muscular wasting. 
Diagnosis.—The diagnosis of sciatica rests on the position of the 
pain—on the relation of this to the trunk of the nerve, and to its area 
of distribution. But the recognition of this relation does not alone 
suffice for the diagnosis. We have to consider the distinction from 
other pains in the sciatic area, to discriminate, if we can, sciatic 
neuritis from sciatic neuralgia, and to decide whether the affection 
of the nerve is primary, or is secondary to mischief outside it. It 
should be needless to say that pain felt only on the outer side of the 
thigh is not sciatica, although the name is sometimes applied to such 
cases, apparently because, some name being needed, that of the 
nearest affection is chosen. 
Branches of the sciatic nerve and sacral plexus ramify over the hip- 
bone, and pain in sciatica may be felt near the hip-joint; hence disease 
of this joint and sciatica may be confounded. The pain in simple 
disease of the hip-joint does not extend down the back of the thigh 
in the course of the sciatic, and there is no tenderness of the nerve. 
The danger of this error is not great if a careful examination is made, 
and has been much exaggerated by writers unfamiliar with the charac- 
teristic symptoms of true sciatica. 
The distinction between a sciatic neuritis and a sciatic neuralgia is 
sometimes difficult, although less frequently than might be inferred 
from current accounts of these diseases, in which the history of the 
neuralgia has been written from the symptoms of the neuritis. If we 
recognise that all cases of sciatica with persistent tenderness of the 
nerve are really neuritic, cases of sciatic neuralgia become extremely 
rare. The two diseases occur usually under different conditions : the 
subjects of neuralgia have often suffered from neuralgia elsewhere, 
and are generally weakly and anaemic. The pain is from the first 
spontaneous; posture has little influence upon it; movement is not 
itself painful, although it may excite paroxysms of pain. The pain is 
referred to the branches and distribution of the nerve rather than to 
its trunk, or it darts up or down the trunk ; and tenderness of the 
nerve, if it exists, is altogether subordinate to the spontaneous pain. 
Secondary sciatica is usually produced by disease of bone about the 
hip-joint, or of the joint itself, or by disease in the pelvis. In the TREATMENT. 
107 
former case a careful examination (never to be omitted in any case 
of sciatica) at once reveals the mischief. When the disease is within 
the pelvis, the tenderness of the trunk of the nerve is slight in pro- 
portion to the pain, and this circumstance should always lead to a 
careful search for any indication of pelvic mischief. In any case of 
doubt a rectal examination should be made. 
Sciatic pain occurs in some diseases of the bones of the spine, in 
lesions of the cauda equina, and occasionally in disease of the spinal 
cord itself. In these cases we have little or no tenderness of the 
nerve ; the pain is chiefly peripheral, and very often bilateral. Double 
true sciatica is so rare that bilateral pain should always suggest disease 
of the nerve-roots. The pains of locomotor ataxy are often felt in 
the sciatic area, and occasionally follow the course of the sciatic nerve 
but their wider range, their fugitive character, and their association 
with other symptoms of tabes, should prevent an error. 
Prognosis.—The prognosis of sciatica, not dependent on disease 
outside the nerve, is always good as regards ultimate recovery. As a 
general rule, the probable duration of the disease is proportioned to 
the severity of the symptoms. The practicability of adequate rest is 
an important element in the prognosis. Irritating exertion may 
lengthen the duration of the disease by many months, and indeed 
relapse may follow each partial recovery until one or even two years 
may pass before the sufferer at last becomes free from pain. When 
the nerve is so sensitive that the patient cannot stand, the affection 
will continue for some months. 
Treatment.—The principles of the treatment of sciatica are those 
of neuritis already described, and only the points of special importance 
need be here repeated. In all cases rest to the limb is essential, and 
its urgency is proportioned to the acuteness and severity of the sym- 
ptoms. Many slight cases are converted into severe ones by unwise 
exertion. All postures and all movements which increase pain should 
be avoided. The same principle applies to mechanical compression of 
the nerve by hard seats, and by strong contractions of the flexors of the 
knee. In more positive treatment the possible causes of the disease 
must be remembered. In gouty cases saline purgatives are often of 
signal service, and are distinctly useful in preventing attacks in those 
who are liable. In the acute stage of a severe attack, hot linseed-meal 
poultices should be applied along the course of the nerve. Counter irri- 
tation is of great value, and cannot be employed too early. A com- 
mencing attack may often be cut short in a few days by rest, and a 
series of mustard plasters or small blisters applied over the seats of 
pain, as this changes under their influence, chasing it, as it were, from 
one spot to another, until it disappears. Internally, whenever there is 
reason to believe that active inflammation exists, mercury should be 
given—a grain of blue pill twice daily ; nothing else seems distinctly to 
influence the process. Salicylate of potash or lithia and nitrous ether 
should also be given at the onset—soda salts being avoided. Sponta- 108 
MULTIPLE NEURITIS. 
neous pain can only be relieved by sedatives. Morphia is the surest, but 
it should only be used for the relief of severe spontaneous pain. In no 
malady has cocaine proved of more signal service. It should be injected 
pretty deeply at the seat of pain, but never into the nerve. One twelfth 
of a grain may be first used, increased rapidly to a third or half a grain. 
It relieves pain, although not in the same degree as morphia, but it has 
a powerful action in promoting the subsidence of the inflammation, 
as described in the account of neuritis. Morphia, although equally 
effective elsewhere, may also be injected with advantage over the 
inflamed part of the nerve, so as to combine the counter-irritation of 
eutaneous acupuncture with some local as well as general sedative 
influence. Simple acupuncture along the course of the nerve has 
been recommended; it gives temporary relief to the sciatic pain, as 
does any superficial pain, but the cases are very few in which it has a 
permanent effect. Sedative or counter-irritant liniments and oint- 
ments may also be applied along the course of the nerve ; the most 
useful are belladonna liniment mixed with an equal part of chloroform 
liniment, and aconite ointment, rubbed in until distinct tingling is 
produced. Electricity is chiefly useful in the later stages; its method 
of use has been described in the account of the treatment of neuritis. 
In very obstinate cases, nerve-stretching has done good; sometimes, 
perhaps, by releasing the nerve from compressing adhesions, but pro- 
bably more often by effecting an energetic counter-irritation, and 
enforcing a beneficial rest. 
To prevent recurrence the causes should be carefully avoided, and 
any gouty state lessened by an appropriate regimen. Slight threaten- 
ing pain should be met by more rest, counter-irritation by sinapisms, 
and the careful avoidance of sudden movements especially. If there 
is the sacro-lumbago that often precedes sciatica, the pain produced by 
rising from a seat may often be lessened by a few moments’ rubbing. 
MTJLTIPLE NEUEITIS. 
The term “ multiple neuritis,” or “ polyneuritis,” is applied to the 
condition in which many nerves are inflamed simultaneously or in 
rapid succession. This multiplicity is its most obtrusive feature. 
In most forms, moreover, the nerves affected are the same on the two 
sides; the neuritis is not only multiple, it is symmetrical; and when, 
as is sometimes the case, only a few nerves ai’e involved, even one 
only on each side, the symmetry becomes a more salient feature than 
the multiplicity. Another important characteristic is its peripheral 
distribution; usually most intense at the extremities of the nerves, it 
lessens progressively towards the centre, commonly ceasing long before 
the nerve-roots are reached. Hence it has also been termed “ peri- PATHOLOGY. 
109 
pheral neuritis,” a name that is accurate but somewhat confusing, 
inasmuch as the term has been applied to affections of nerve-trunks 
generally, in distinction from central diseases causing similar sym- 
ptoms. 
The discovery that certain combinations of symptoms, formerly 
thought to depend on disease of the spinal cord, are really due to 
disease of the peripheral nerves, is one of the most important steps 
in the recent advance of pathology. It has profoundly modified 
many of our conceptions, not only of the processes of disease, but of 
the range and action of certain morbid influences, and has shown that 
much of our supposed knowledge of the central affections of corre- 
sponding aspect was erroneous, and the history of these maladies has 
to be reinvestigated. 
The occurrence of multiple neuritis was first demonstrated by 
Dumenil, of Rouen (1864), although the leprous form had been pre- 
viously described by Virchow. Graves, indeed, long ago suspected 
that many cases of paralysis were due to disease of the nerves, but he 
based his opinion on the normal aspect of the spinal cord ; and in 
most of the cases he describes it is probable that modern methods of 
examination would have revealed disease. Naturally, also, symptoms 
so peculiar had attracted the notice of clinical observers, and were 
described from time to time; first, perhaps (1822), by Dr. J. Jackson, 
of Boston, U.S.A., and, much later, but fully, by Duchenne (1858).* 
Dumenil’s observations attracted little notice, and it was not until 
fresh facts were brought forward by Joffroy (1879), Leyden (1880), 
and Grainger Stewart (1881), that attention was generally directed 
to the subject. During the last ten years a very large number of 
observations have been published, and the general history of the 
disease is now established on an adequate basis. 
The peculiarities of distribution of multiple neuritis harmonise with 
what is known of its pathology. In isolated neuritis the primary 
affection is of the nerve-sheath and connective tissue—the neuritis 
is “ adventitialin the symmetrical multiple forms the nerve- 
fibres themselves are almost always the seat of the primary process; 
the connective tissue and sheath suffer secondarily and in proportion 
to the acuteness of the process in the nerve-elements—the neuritis is 
“ parenchymatous.” 
The forms of multiple neuritis which are thus characterised by 
their symmetry and parenchymatous nature are due entirely to a 
morbid blood-state having a direct influence on the nerve-tissue. 
Their cause is the presence in the blood of some virus, often an organic 
* The first ascription of a form of paralysis to this lesion was by Dr. Todd, in the 
case of lead palsy. “I believe that the muscles and nerves are early affected, and 
that at a later period the nerve-centres become implicated. The nervous system is 
thus first affected at its periphery, in the nerves, and, the poisoning influence con- 
tinuing, the contamination gradually advances towards the centre” (‘Clin. Lect.,* 
1854, p. 9). 110 
MULTIPLE NEURITIS. 
or inorganic chemical compound, to which the nerve-fibres are sus- 
ceptible, just as they are susceptible to curara, or the motor-cells to 
strychnia, or the nerves for accommodation to atropia. It is an 
instance of what has been termed “ selective action,” the mani- 
festation equally of a peculiarity in the acting virus and in the 
structures acted on. The peripheral distribution of the affection is 
probably due to the fact that the vital and nutritional energy of the 
nerve-fibres lessens with the distance from the cells of which they are 
part, and from which their vitality is derived. The relation to a. 
blood-state as the cause explains also the symmetry of the affection, 
since the like structures on each side possess the same characteristics, 
and, being equally exposed to the morbid influence, there is no reason 
why the nerve-elements on one side should suffer alone, or even in less 
degree, than those on the other side. 
Isolated neuritis may be caused in part by a constitutional or blood 
state, but is not due to this alone ; some exciting cause is in operation, 
acting locally and determining the position of the affection. Hence 
it is rare for such neuritis to be multiple, and when more than one 
nerve is affected the distribution is irregular and not symmetrical. 
Gouty neuritis affords an illustration of this. Moreover, in these 
forms the connective tissue, and especially the sheath of the nerve, is 
the part primarily affected, and the nerve-fibres are damaged only in a 
secondary manner. Between the two chief forms of neuritis, the isolated 
or irregular adventitial and the parenchymatous symmetrical forms, 
there is thus an essential difference. 
Between the two classes, however, certain forms seem to occupy 
an intermediate position. These are the forms of multiple neuritis 
in which sometimes the one and sometimes the other element in the 
nerve seems to suffer most, or in which both are involved. We must, 
however, distinguish from these the cases in which mere acuteness of 
the process causes both elements to be involved; in which, for in- 
stance, a very acute parenchymatous neuritis causes some degree of 
adventitial inflammation, or acute adventitial inflammation involves 
the nerve-fibres. These cases conform in distribution to the type to 
which they belong; the primary parenchymatous neuritis, and it 
alone, being strictly symmetrical. But there are other cases in which 
the causes are combined. Alcoholism, for instance, the most common 
toxic cause, may be due to a mode of life that has also produced gout, 
and then isolated gouty perineuritis may accompany general poly- 
neuritis of parenchymatous nature and symmetrical distribution. 
Exposure to cold, again, may cause a “ rheumatic ” perineuritis, 
either of a single nerve, or of a few nerves irregularly distributed ; 
and it may also produce a blood-state allied to that of acute rheu- 
matism, and thus a symmetrical parenchymatous polyneuritis. An 
important cause of neuritis is toxaemia due to the development of 
specific organisms in the blood, sometimes those that cause a definite 
disease, as diphtheria or smallpox. Such organisms seem occasionally ETIOLOGY. 
Ill 
to fix themselves in the connective tissue of the nerves, causing an 
irregular adventitial neuritis, and also to leave behind a product, 
perhaps a chemical substance, comparable to alcohol, capable of causing 
a parenchymatous neuritis. The two forms may then be conjoined in 
a puzzling manner. It is probably thus that the forms of diffuse or 
total neuritis are produced, occasionally met with in diphtheritic 
paralysis. 
From these considerations it follows that symmetrical multiplicity 
means a blood-state acting alone; irregular multiplicity generally 
means a constitutional state combined with local determining causes. 
When very few nerves are affected irregularly, the general influence 
sinks to the level of a predisposition, and this is not always to be 
recognised when a single nerve is affected. 
The classes into which multiple neuritis may be divided can now be 
better understood. They depend chiefly on the several causes to 
which the affection is due. The acuteness or slowness of its onset 
has also been made a ground of distinction. As we have seen, the 
less acute the process the more perfect is the limitation to the one 
element, the sheath or the nerve-fibres. In the most chronic form the 
process in the nerve-elements resembles a degeneration, and has been 
termed “degenerative neuritis.” Underlying this distinction, however, 
was the idea that only the chronic forms commence in the nerve-fibres 
themselves, and that in the more acute forms the connective tissue is 
also primarily involved. It is certain, however, that this is not the 
case, although the secondary affection of the connective tissue is 
intense in proportion to the acuteness of the disease. From most 
causes we meet with cases both acute and chronic. 
The forms of multiple neuritis, classified according to what is 
known of their causes, may be provisionally thus tabulated. No 
arrangement can be free from anomalies until we know more of the 
causes and of the mechanism by which the varieties are produced. 
Provisionally, however, that we may survey their relationship, the 
forms may be divided into five groups. 
I. Toxic : due to the presence in the blood of a known poison, which maybe— 
(а) Metallic: lead, arsenic, silver, &c. 
(б) Non-metallic, as alcohol—the most frequent cause. With this may 
perhaps be placed the neuritis that occurs in diabetes, which 
probably depends on the presence in the blood of some substance 
allied to sugar, and formed only during the altered metabolism 
of this disease. 
II. Toxemic : due to some virus in the blood, the precise nature of which is 
unknown, but which is probably in mcst cases either an organism or a 
chemical product of the growth of organisms. These cases may be divided 
into two classes. 
(a) Primary, in which the neuritis is part of the first effects of the 
virus, as distinguished from the cases in which this first pro- 
duces some other disease. The primaiy forms again may be 112 
MULTIPLE NEURITIS. 
subdivided, according as the virus is derived from without, or 
(apparently) generated within the body. 
(1) Extraneous, the virus being derived from without, as are 
the organisms that cause directly the neuritis of leprosy ; 
and probably also some forms of neuritis the origin of 
which has not yet been based. 
(2) Intrinsic, in which the virus is produced within the body, 
as probably in many cases of septicaemic neuritis after 
wounds, &c. It is possible, however, that these cases 
may ultimately be found to have an extraneous origin. 
(&) Secondary, in which the toxaemic agent first causes some definite 
disease, which is followed by polyneuritis as a sequel, an interval 
of some weeks or even months elapsing between the two effects* 
The neuritis is then sometimes said to be caused by the disease. 
Probably, as already explained, the neuritis is generally due to 
some chemical product of the growth of the organisms in the 
body. Examples of this are the polyneuritis that follows diph- 
theria, smallpox, variola, typhoid, tubercle, and perhaps syphilis. 
In some of these, as ali-eady explained (p. 110), two mechanisms 
may be at work—one direct, the other indirect. 
III. Endemic : the neuritis that is due to local organisms which have this for 
theii primary or secondary effect. The chief forms are malarial neuritis 
and the disease called beri-beri. Strictly, however, these belong to II, a, 1, 
primary toxaemic neuritis due to a cause acquired from without; but their 
peculiar local characteristics make it convenient to sepai-ate them. 
IV. Rheumatic : the multiple neuritis that follows exposure to cold, and is 
probably due to a morbid blood-state like that which gives rise to rheu- 
matic fever, pneumonia, polio-myelitis, and the like. It is possible that 
these belong strictly to II, a, 2, the primary neuritis due to a blood-state 
of intrinsic origin, but they constitute a well-marked group. 
V. Cachectic and senile forms, in which degeneration of the nerves seems part 
of general mal-nutrition, and begins at the periphery where their vitality 
is lowest. Some of these cases may be really neuropathic, and due to the 
same causes as produce degeneration in the spinal cord; while among the 
senile forms must be reckoned not only those due simply to age-failure of 
nutrition, but the rare instances in which arterial degeneration and 
lessened blood-supply produce local necrotic changes in the nerve. 
It is not necessary to consider here the particulars regarding the 
causation of all these forms. The neuritis due to the Metallic Poisons 
is described in Vol. II in connexion with their other effects on the 
nervous system; there also Diphtheritic Neuritis is considered in the 
account of this paralysis (which is not wholly peripheral), and most 
of the secondary toxaemic forms find their place in the account of the 
Paralyses after Acute Diseases. Malarial neuritis, Beri-beri, and 
Leprous neuritis are considered separately at the end of this section. 
The forms that need special consideration in this place are certain 
varieties of “ primary ” polyneuritis, toxic or toxaemic, the “ secondary 
toxaemic forms of intrinsic origin, the rheumatic, diabetic, and the ETIOLOGY. 
113 
cachectic forms—in most of which the symptoms of polyneuritis 
develop as an apparently independent disease, and not as the sequel 
to some other affection. Of the other forms, however, some notice 
must be taken where they come into important contrast or comparison 
with those now specially considered. 
By far the most common cause of multiple neuritis is alcoholism, and 
this variety must therefore furnish us with the most important facts 
regarding the clinical history of the disorder. But it may be well first 
to consider briefly the causation of some of the less frequent varieties. 
Syphilitic neuritis is mainly an affection of single nerves, and, as 
such, has been already considered. These probably suffer in conse- 
quence of the direct action of the organisms on the adventitial tissues,, 
and coincide in time with other “secondary” syphilitic lesions. It 
has been conjectured that true acute multiple neuritis may be directly 
syphilitic, but the evidence of this is insufficient. We may, however, 
see a true pareuchymatous syphilitic polyneuritis in the tabetic form, 
in which the sensory fibres are affected at the periphery; tabes is 
generally a post-syphilitic disorder, and parenchymatous degenerative 
neuritis is a common, and sometimes the only lesion in this affection. 
This “ peripheral neuro-tabes,” as it is termed, may not unreasonably 
be regarded as an effect of some product of the specific organisms, 
comparable to the less chronic forms of neuritis that succeed less 
chronic specific diseases, such as diphtheria or smallpox. The subject 
is considered in the section on Locomotor Ataxy, but it is important 
to mention it here, because this disease presents an example of central 
and peripheral lesions due to the same cause, and because an affec- 
tion of the sensory nerves almost identical in distribution and nature, 
and giving rise to similar effects, is sometimes the consequence of 
alcohol, and occasionally also of other agents, as arsenic. 
Tubercular polyneuritis is a form regarding which we have still 
much to learn. It has occasionally developed in the course of phthisis, 
and has been found to be of the purely parenchymatous or degenera- 
tive variety. Severe cases, with characteristic motor and sensory 
symptoms, in which other causes, such as alcohol, can be excluded, are 
rare, but their occurrence is well established,* and they seem to justify 
the conclusion that the tubercle bacillus is capable of producing a 
poison having a specific action on the nerves—a mechanism also indi- 
cated by the fact that the bacilli themselves cannot be found in the 
affected structures. It is said that similar slighter neuritis is frequently 
to be found after death in cases of phthisis, and probably produces sym- 
ptoms that are overlooked in the general prostration of the later stages 
of the disease. Some severe cases recorded as tubercular are, however, 
not free from the suspicion that alcohol was in part or wholly the 
cause of the neuritis. There is, moreover, another relation between 
multiple neuritis and phthisis; the latter often develops in the course 
of alcoholic neuritis, and is a frequent cause of death. It is not im- 
VOL. I. 
* See Oppenlieim, ‘ Zeitschr. f. klin. Med.,’ 1886, p. 230. 114 
MULTIPLE NEURITIS. 
probable that a neuritis of the pulmonary branches of the vagus leads 
to the low pneumonic form of phthisis that is generally found in such 
cases, and this may even render the tubercular organisms more effec- 
tive if they find entrance into the lungs. Although gout is so power- 
ful a cause of isolated neuritis, there is no evidence that it causes the 
multiple form, although it may perhaps modify the symptoms of this 
by adding to it an isolated perineuritis. 
The Acute Diseases that may be followed by neuritis are especially 
diphtheria, variola, measles, typhus and typhoid fevers. The interval 
that usually elapses between the acute disease and the neuritis supports 
the opinion that the latter is due to a chemical poison produced by the 
specific organisms; and so also does the perfect symmetry of the 
symptoms, since the toxic agent must be such as can have an equal 
action on all similar structures. Moreover, the occurrence of the 
neuritis is not related to the severity of the primary disease, and thus 
seems to be due rather to some peculiarity in the special organisms, 
such as so often determines peculiar features in an epidemic. In one 
case, which developed six weeks after varioloid, with pains in the limbs, 
atrophy of the arms and legs, &c., the purely nem’itic nature of the 
morbid process was ascertained six months later, when the patient 
died from pneumonia. In diphtheria, as already pointed out, we seem 
to trace a double mechanism,—an early direct action of the organisms 
on the adventitial tissue in some cases, and a later parenchymatous 
neuritis due to some product of their growth, more abundant and 
effective in some cases than in others. Malarial neuritis seems to 
occupy a position intermediate between the secondary and primary 
forms, since it sometimes follows malarial fever, and sometimes develops 
without previous fever in those who have been exposed to the influence 
of malaria. It is described separately as one of the endemic forms. 
Of the Primary Toxsemic varieties a typical example is presented by 
another endemic form, beri-beri, which is the sole result of an organised 
virus, or of a product of the organisms. This also is considered in a 
separate section, but its history deserves careful study on account of the 
light it throws on the pathology and causation of other forms of poly- 
neuritis, in which the processes are less simple and therefore less clear. 
An instructive contrast to beri-beri, which is a purely parenchyma- 
tous form, is presented by leprous neuritis, also described sepa- 
rately. Here we find a purely adventitial form, due to the direct 
presence of the organisms in the connective tissue. The contrast 
presented by these two forms is almost complete. 
Septicsemic polyneuritis follows some wound or injury or local in- 
flammation capable of giving rise to blood-poisoning. In some cases 
it has been unaccompanied by the usual symptoms of septic blood- 
states, but has followed its cause at an interval that suggests, taken 
with other analogous facts, that it is due to some virus produced 
probably by the presence of septic organisms of a special character. 
For instance, a man, thirteen days after a stab-wound beneath the ETIOLOGY. 
115 
■clavicle, which healed well, had an attack of parotitis with facial palsy. 
Ou the fortieth day there developed paralysis of tongue, vocal cords, 
and limbs, and on the sixth day after the onset of these symptoms he 
died from respiratory palsy. Extensive peripheral neuritis was the 
■only nerve lesion.* 
In a less severe case recorded by Barrsf the symptoms commenced 
three weeks after a neglected wound of the hand, which produced in- 
flammation of the lymphatics, extending up the arm to the axilla. 
The symptoms of neuritis began in the injured limb, and invaded 
successively the other extremities, causing characteristic weakness in 
the lower legs, with loss of the knee-jerk. He slowly recovered. It 
is possible that some cases of this class result from unsuspected foci 
of inflammation within the body, in which pus becomes pent up and 
causes the blood-state. 
In such cases as those due to a possible internal source of blood- 
poisoning, multiple neuritis develops as a disease apparently primary 
without obvious cause if the source of the septicaemia has been undis- 
covered. Other primary cases occur, however, in which there is no 
cause for septicaemia, and the only explanation we can give of these is 
that they are probably due to a virus received from without, the 
precise nature of which is unknown. I have met with some cases in 
which the symptoms of multiple neuritis, perfectly characteristic, 
came on without any discoverable cause, and ran a course in most 
cases mild, and ending in recovery; in one or two others severe, and 
ending in death. Some cases of what is popularly termed “ blood- 
poisoning ” are probably of this nature. If certain drain poisous, 
probably organismal, are capable of giving rise to a disease, diphtheria, 
of which multiple neuritis is often part, there is no improbability in 
some forms of virus of similar character and analogous source, having 
such neuritis for their chief effect. In this connection it is instructive 
to note that an epidemic is on record in which paralysis preceded the 
throat affection (see ‘ Diphtheritic Paralysis,’ vol. ii). As an 
instance of this primary form may be mentioned the case of a medical 
practitioner who was attacked with obstinate vomiting and diarrhoea 
succeeded by constipation, for which no cause could be discovered, 
quickly followed by “ numbness ” in the hands and feet, and a diffi- 
culty in using them. When I saw him, a fortnight later, there was 
loss of tactile sensibility, limited to the palms and soles, weakness of 
the legs, and no knee-jerk. The weakness rapidly increased and ex- 
tended, and at the end of five weeks from the onset he died. Such 
a case presents all the features of the toxic form. J 
* Roth, ‘Corr.-Bl. f. Schw. Aerzte,’ 1883, No. 13. 
f ‘Amer. Journ. Med. Science,’ Feb., 1889. 
X It should be mentioned that other circumstances excited a suspicion of inten- 
tional chronic poisoning. This fact does not lessen the suggestiveness of the case. 
Multiple neuritis must henceforth constitute an element in many questions of medical 
jurisprudence. Its discovery might give greater weight to indications of some forms 
of poisoning. 116 
MULTIPLE NEURITIS. 
The Rheumatic form embraces all the cases of polyneuritis that are 
due to exposure to cold. In the typical cases of this class the general 
distribution of the affection and other features indicate that a blood- 
state must be the immediate mechanism by which it is produced. 
We know that rheumatic fever, due to a similar exposure to cold, must 
depend on such a morbid blood-state, produced in some way by the 
disturbing influence of the chill on the chemical or other processes 
within the body. We know also that the rheumatic poison thus 
generated must, vary much in its precise nature by the great variations 
in the acute rheumatic lesions that it causes (see ‘ Chorea,’ vol. ii). The 
same exposure, in another person, may give rise to pneumonia. Hence 
it is not surprising that the effect of the exposure should, in some 
persons, be such as to cause a blood-state capable of producing 
multiple neuritis, symmetrical and parenchymatous, especially when 
we know that this may actually be accompanied by acute pneumonia,, 
and by other evidence of profound toxic state of the blood. In a case 
recorded by Putnam, fatal in seven days from paralysis of the respi- 
ratory muscles, and distinctly due to cold, there was swelling of the 
spleen such as is met with in typhoid and other acute toxsemic states. 
But exposure to cold has also the power of causing an isolated neuritis 
(e. g. of the facial or the sciatic nerve), a neuritis adventitial in nature, 
essentially a perineuritis. Nor is it surprising that such an adven- 
titial neuritis should occasionally involve more than one nerve—should, 
in fact, be a polyneuritis. The evidence that such polyneuritis may 
be produced by cold is given in the chapter on Acute Atrophic Para- 
lysis (Polio myelitis), with which it may coincide, as a result of the 
same exposure. The connective tissue of nerves is of the same nature 
as that on which the rheumatic poison exerts its special influence, and 
the modes of onset of sciatica have shown us that the rheumatic pro- 
cess may pass from the fasciae to the nerve-sheaths. A consideration 
of these and other facts makes it probable that cold may cause (1) an 
isolated adventitial neuritis; (2) a multiple neuritis of the same 
character, irregular in distribution, probably by the agency of a blood- 
poison related to that which causes muscular rheumatism and the 
affection of the fibrous tissues of the joints in rheumatic fever; (3) 
a symmetrical parenchymatous polyneuritis due probably to a special 
blood-state of greater specificity than that which produces the adven- 
titial form, and perhaps allied to that which gives rise to pneumonia 
and to cerebro-spinal meningitis. Pneumonia, at least, may be com- 
bined with multiple neuritis as a result of the same exposure. 
The diabetic form presents many varieties, and our knowledge of it 
is still imperfect. It is supposed that inflammation of single nerves 
frequently underlies the obstinate forms of neuralgia met with in this 
affection; but besides this a symmetrical multiple neuritis, parenchy- 
matous in nature, is occasionally met with, and is said to present all 
the varieties that are produced by alcohol, and of various degrees of 
severity. It is not, however, related to the amount of sugar in the ETIOLOGY. 
117 
urine—in many of the sufferers this has been small (in one, indeed, as 
low as one half per cent.) ; nor is it readily influenced by a dietetic 
reduction of the amount of sugar in the blood. Hence it is supposed 
to be due to some toxic product that is formed in the perverted meta- 
bolism of the diabetic, comparable to acetone, although certainly not 
acetone itself. The fact that the reduction of the amount of sugar 
formed has little influence on the condition suggests that the poison is 
not a product of the decomposition of sugar, but rather a material 
formed in the place of sugar by some modification of the chemical 
processes that lead to the increased production of the latter. This 
form is of special interest on account of the close chemical rela- 
tion between sugar and the most potent cause of multiple neuritis, 
alcohol. 
Alcoholic polyneuritis is the form most frequently met with, at any 
rate so far as well-marked cases are concerned ; this form preponderates 
in most countries over all others put together, but at present many of 
the slighter sensory forms escape recognition, and the preponderance 
will probably be much less when all cases are recognised. It results 
chiefly from the stronger forms of alcoholic drinks, and especially 
from spirit-drinking. It is more common among those who take 
small quantities frequently than among those who indulge in an 
occasional “bout” of intemperance, probably because the total 
quantity consumed is greater by the former. It is far more frequent 
among women than among men—probably three times as frequent. 
How far this is due to a special predisposition on the part of women, 
or to the conditions under which it is taken, is yet doubtful. On the 
one hand continuous drinking is more common among women than 
is occasional intoxication; and women who take alcohol to excess 
generally do so in the form of spirits, while men often take it in the 
form of beer. At the same time the opposite proclivity is seen in the 
case of delirium tremens, and it would seem as if there were a differ- 
ence in the nervous system of the two sexes, whereby a susceptibility 
of the nerves of women replaces that of the brain in men. 
The amount of alcohol habitually taken, and the duration of the 
habit before the onset of the affection, vary much. It has been thought 
that a neuropathic disposition renders a less quantity and briefer 
period adequate. Other causes often co-operate with alcohol in 
exciting the disease, especially exposure to cold, and, in the lower 
classes, insufficient nourishment. Exposure is especially effective in 
those in whom slight symptoms exist but attract little attention, and 
the condition of the nervous system is, as it were, prepared for a 
severe outbreak. 
Cachectic and Senile Forms.—Regarding these little remains to be 
added to what has been stated atp. 112. The evidence rests chiefly on 
the post-mortem discovery of the changes in the nerves, but it is 
probable that more careful attention to the point will show that sym- 
ptoms are not unfrequent which now receive little attention, or are 118 
MULTIPLE NEURITIS. 
regarded as functional only. More attention is also needed by tlie 
cases in which a neuropathic tendency or some depressing emotion 
seems to be the cause of this disease, as they may be of the corre- 
sponding degeneration of the pyramidal fibres within the cord in 
“lateral sclerosis,” a degeneration which also begins at the extremity 
of the fibres and extends upwards. 
Atheromatous Neuritis, already mentioned as a variety of the 
senile form, merits separate recognition on account of its peculiar 
mechanism. In these cases the nerves of the limbs have been exten- 
sively damaged through atheroma (or “arteritis obliterans”) of their 
arteries. Necrotic inflammatory processes take place in the parts of 
the nerves supplied by the affected vessels, and there result symptoms 
that resemble those of the toxic form in character, although differing 
in the greater irregularity of distribution. The symmetry that consti- 
tutes so striking a feature of the common cases is absent, but arterial 
degeneration may be symmetrical, and an incomplete rough symmetry 
may thus result. It is conjectured that such disease of the nerves will 
be found to be frequent in the cases in which senile disease of the 
arteries gives rise to gangrene, and that it is partly through the 
, agency of the neuritis that the gangrene is produced; but this view 
overlooks the potent influence of the arterial obstruction itself. 
General Etiology.—Multiple neuritis is a disease of adult life. 
The only form met Avith in children is that which sometimes accom- 
panies polio-myelitis, and may perhaps now and then be met with 
apart from the spinal malady, as an infantile variety of multiple 
adventitial neuritis, irregular in distribution. The other common 
forms occur chiefly between twenty and fifty; the alcoholic between 
thirty and forty twice as frequently as in either the previous or later 
decade, but it may be met with up to sixty years of age; while the rare 
senile (purely degenerative) variety, and the still more rare arteritie 
form are met with at still later ages. Females constitute a majority 
of the cases, the degree of which cannot yet be estimated; it is due 
solely to their liability to alcoholic neuritis, in which they amount to 
at least 70 per cent. The rheumatic and toxsemic forms, on the other 
hand, occur more frequently in males, probably from their greater 
exposure to the causes of the disease. 
More than one cause may co-operate in producing the affection, and 
then we may distinguish the one as “ predisposing,” the other as- 
“exciting,” although, as a rule, either would be adequate alone Avere 
its degree more intense. The double causation can most often be 
traced when cold or some depressing influence co-operates with alcohol, 
or Avhen the influence of the latter is conjoined with that of tubercle, 
as either the primary or secondary cause. Even more frequently the 
symptoms folloAV some cause of constitutional depression, inadequate 
alone. In one case this was an attack of acute gastric catarrh with 
vomiting, the result of the alcoholism which was the real cause of the- 
neuritis. In other cases a depressing emotion has seemed to be the SYMPTOMS. 
119 
excitant, and, as we have seen, this appears to be sometimes alone 
sufficient. In one alcoholic case the injurious effect of painful emo- 
tion (due to the death of a son) was at once to arrest improvement, 
and to excite a progressive increase in the symptoms, which continued 
until death a few months later. Anaemia probably acts chiefly as a 
predisponent, lowering the nutrition and resisting power of all the 
tissues, and rendering a slighter cause effective. Thus, in the case of 
an anaemic girl recorded by Barrs, the symptoms followed immediately 
on bathing the feet in cold water, when heated. 
Symptoms.—The symptoms produced by multiple neuritis differ 
widely, as has been already intimated, according to the character of 
the affection of the nerves. They are of three classes—motor weak- 
ness, sensory disturbance, and inco-ordination. The motor weakness 
depends on an affection of the motor nerve-fibres, and usually 
involves first and chiefly the flexors of the ankle and extensors of the 
toes, and the extensors of the wrist and fingers in the forearm, 
muscles that are homologous and supplied by corresponding nerves, 
the anterior tibial or peroneal nerve in the leg, the radial branch of 
the museulo-spiral in the arm. The result is the characteristic 
“ wrist-drop ” and “ foot-drop,” shown in Fig. 58. Other muscles 
suffer in severe cases. The sensory symptoms consist of subjective 
sensations of tingling, &e. ; pains of various character, seat, and 
degree, often referred to the nerves or deep parts; tenderness 
of the skin, nerve-trunks, and muscles, and loss of cutaneous sensi- 
bility. The inco-ordination resembles that present in the slighter 
degrees of locomotor ataxy, and is often associated with loss of the 
muscular sense. These symptoms will be considered in detail. Ac- 
cording to the predominance of one or another of the three sets, 
corresponding varieties are distinguished,— (1) a motor form, in 
which there is loss of power with or without the other symptoms; 
(2) a sensory form, in which there is no marked muscular weakness 
or inco-ordination, but in which sensory disturbance—irritation or 
loss—is the chief symptom ; (3) an ataxic form, in which, without 
marked loss of power, with or without sensory symptoms, inco- 
ordination is the dominant symptom. 
As mentioned in the introductory section, the varieties of poly- 
neuritis that are due to special metallic poisons and to certain acute 
specific diseases are described separately, in the second volume of this 
work, among the general diseases of the nervous system. The 
common alcoholic form is alone suitable to convey a knowledge of the 
general features of the affection, but the account of its symptoms 
must be completed by some mention of those of the less common 
forms, which do not need separate description elsewhere. 
It should be clearly understood at the outset that no set of sym- 
ptoms is exclusively related to a single cause. The various forms 
which depend on the incidence of the disease on the motor or the 120 
MULTIPLE NEURITIS. 
sensory nerves in preponderant degree, are met with in consequence 
of each of the common causes, although, as we shall see, some causes 
give rise more frequently to one form than to another. 
The onset and course of multiple neuritis vary much in different 
cases, both of the same class and of the several classes. Premonitory 
Fig. 58.—Multiple alcoholic neuritis ; palsy of extensors of wrist and flexors 
of ankle. (From a photograph by Mr. Hyde Marriott, B.Sc.J 
symptoms occur in some cases. They have been observed chiefly in 
the alcoholic form, hut occur in others also. When due to cold or 
other causes of constitutional disturbance, the special symptoms of 
the general state may immediately precede the onset. Thus, after 
exposure to cold, general rheumatic symptoms, with fever, bron- 
chitis, and other signs of catarrh, may immediately be followed by 
the symptoms of neuritis. The symptoms that have been regarded as 
premonitory are especially “ numbness ” and tingling of the fingers 
and toes, or of the palms and soles, or the lower parts of the limbs, 
vaso-motor disturbance in the extremities (as pallor of the fingers), 
and painful cramp in the calves or elsewhere, together with dull 
rheumatoid pains. These constitute the first symptoms of the disease, 
but when they exist alone for months before the onset, they may 
be regarded as “ premonitory.” All these symptoms are probably 
due to the influence of alcohol on the nerves, disturbing the function 
of the structures whose nutrition undergoes subsequently a correspond- 
ing impairment. 
The onset itself may be acute or subclironic, and is sometimes so slow 
as to deserve the name of chronic, especially in the slighter sensory 
form. An acute onset is on the whole rare in alcoholic cases unless 
the malady is “excited” by some cooperant influence. Thus, in one 
alcoholic, a prostrating attack of vomiting, lasting for ten days, was 
followed by an onset of the symptoms of neuritis so acute that at the 
end of a week the patient was unable to stand, and there was general 
impairment of sensibility. It is met with chiefly in cases due to 
cold or toxsemic states; in these it may be attended by severe con- 
stitutional disturbance, rigors, and considerable pyrexia. In other SYMPTOMS. 
121 
forms the elevation of temperature is usually slight or moderate, but 
sometimes amounts to 8° or 4°, and may last from one to three or 
four weeks. The first definite symptom (if it has not existed before) is 
often the tingling, or “ pins and needles ” in the extremities, already 
mentioned, with vague “ rheumatic” pains, which become more acute. 
Motor symptoms are usually soon added, palsy or inco-ordination, 
or both. They are seldom absent in acute cases. The pronounced 
symptoms of the disease may resemble in character those produced 
by the inflammation of single nerves, differing only in distribution, 
and involving all the functions of the affected nerves; this is often 
the case when the malady is acute in onset. But when chronic, 
as already stated, the fibres may be affected according to their 
specific function, and to this the symptoms are then limited, so that 
they resemble those that are ascribed to a disturbance of special 
elements of the spinal cord, rather than the affection of isolated nerves. 
The motor form involves either the upper or lower limbs or both, 
but always the corresponding limbs on both sides, and their distal 
extremities, the hands or the feet, first and chiefly.* Whichever limbs, 
arms or legs, present the first symptoms, suffer in greater degree 
throughout, and it may be alone. The feet suffer more frequently 
than the hands; motor symptoms may exist in the legs, and only 
sensory symptoms in the hands, and this when the weakness in the 
legs is extreme. In whatever part the affection occurs various sen- 
sory disturbances, and especially pains, commonly precede the weak- 
ness, and increase with it. They are accompanied by tenderness 
generally along the nerve-trunks, but almost invariably in the mus- 
cles, and sometimes of the skin. These pains may occur in the 
limbs that do not become paralysed if the action of the cause 
can be arrested. Although loss of power is the obtrusive feature, 
some loss of co-ordination generally accompanies it, and is often 
the means by which the attention of the patient is first directed 
to the commencing disability. He finds a difficulty in balance when 
standing, or in performing the finer movements with his fingers; and his 
attention being thus drawn to the part, he finds, on further investiga- 
tion, that there is some actual defect in the power of extending the 
wrist and fingers, or in raising the toes or foot from the ground during 
the forward movement of the foot in walking. Tremor is often con- 
spicuous in alcoholic cases long before the loss of power. When- 
ever there is weakness in the leg the knee-jerk can no longer be 
obtained, probably because the afferent muscle-nerves suffer more 
widely than the motor nerves. The constancy of this loss is very 
great, and it is not related to any one class of symptoms, but occurs 
equally in the paralytic and ataxic forms of neuritis. At the same 
time it is not absolute; the knee-jerk seems to persist in very rare 
cases of slight degree, as mentioned on p. 126. 
* The very various symptoms of the disease are well illustrated by an instructive 
series of cases published by Ur. Buzzard, ‘Paralysis from Peripheral Neuritis/ 1886. 122 
MULTIPLE NEURITIS. 
When the first symptoms are in the legs the first motor loss is 
the inability to raise the toes from the ground in walking, owing to 
imperfect flexion of the ankle-joint and extension of the toes. But 
this symptom may be to a large extent obscured by the interference 
with movement occasioned by the tenderness of the muscles and the 
liypersesthesia of the skin, which commonly coexist and prevent the 
exertion of the amount of power that is possessed. There is a 
tendency for the nerves of the sole and the palm of the hand to be 
especially involved in the byperaesthesia—in obedience to a law of 
pathological susceptibility which is to be traced not unfrequently in 
polyneuritis, especially in the tabetic, diphtheritic, and toxsemic 
forms. 
These effects of the sensory irritation may render it difficult to deter- 
mine the common course of the motor weakness, the order in which the 
muscles suffer, and the relative degree of their impairment at different 
periods. The conspicuous fact is that the muscles first to suffer are 
those supplied from the external popliteal nerve (anterior tibial group), 
and these are followed by other muscles below the knee, except 
in the very rare instances in which palsy does not spread beyond the 
muscles first affected. The muscles above the knee suffer later and less, 
and more frequently escape considerable impairment. The flexors of the 
knee, although supplied by the sciatic nerve, do not suffer more than the 
extensors, or more frequently, so far as the tenderness permits us tojudge. 
Least frequently and in least degree the muscles suffer that move the 
hip-joint; it is only in the most severe cases that these are appreciably 
affected. Very rarely is the innervation of the bladder or rectum 
involved in the disturbance of polyneuritis. Interference with these 
functions may generally be regarded as evidence that the morbid 
changes are not limited to the nerves, but involve the spinal cord 
itself. 
In the arms, the first and chief defect in power is in the extensors 
of the wrist and fingers. Both arms are affected together or in quick 
succession—one never suffers alone in considerable degree. Thus 
the palsy resembles at first, and sometimes throughout, that which is 
familiar as the effect of lead poisoning. The resemblance may extend 
to the escape of the extensor of the metacarpal bone of the thumb, 
and of the supinator longus. Lead palsy, indeed, is an example of 
peripheral neuritis of the “ toxic form,” and differs from the general 
form in the limitation of even severe palsy. It seems that the radial 
nerve (of the museulo-spiral) is that which, in the upper limbs, is 
the most prone to suffer—a fact which is at present unexplained. It 
probably depends not on any peculiarity of position, but on some 
deeper functional relation and position among the nerves of the body, 
6ince it obtains when the affection is of the peripheral extremities of 
the fibres and does not involve all the fibres of the nerve. The radial 
nerve is homologous with that in the leg of which the fibres are the 
first to suffer—the peroneal,—regarding which the same facts are true. SYMPTOMS. 
123 
It is only in the cases due to metallic poisons that the palsy becomes 
considerable without spreading to other muscles. Generally the flexors 
of the wrist and fingers become weak, and so do the interossei, while 
the last to suffer are the thenar and hypothenar muscles. It is rare 
for the palsy of any muscles except the extensors to be complete. In 
more severe degree the muscles above the elbow suffer, last and least 
those of the shoulder. The muscles below the elbow may be almost 
powerless when those above it are scarcely affected. 
In severe cases the trunk muscles are involved—the diaphragm, 
and the muscles of the thorax and abdomen. Less rarely, but also 
only in severe forms, increased frequency of the pulse and palsy of 
the vocal cords indicate that the fibres of the vagus are suffering. 
Yery seldom the facial muscles, or those of the tongue, are in- 
volved. Affection of the motor ocular nerves, of the pupils, and 
nystagmus, have been met with only in the most severe cases, aud 
chiefly in those due to toxaemia. The nerves of the pharynx and 
alimentary viscera seem always to escape. It is more doubtful 
whether this is true of the branches of the lung. 
Thus the stress of the affection falls on the muscles of the extremities, 
and those that are affected first also suffer alone in slight cases, and 
most in those that are severe. As they become weak, and sometimes 
even earlier, they become tender, and this muscular tenderness usually 
increases to an extreme degree, and becomes even more obtrusive, in 
many cases, than the tenderness of the nerves. The limb cannot 
be grasped, even gently, without cries of pain being elicited, and 
every change of posture gives rise to distress. This is an important 
sign, and is no doubt due to the fact that all the nerves of the muscle 
suffer, the afferent as well as the motor twigs. Yery rarely it is 
absent. It increases the pain of an electrical examination, and, after 
a strong current has been applied, the muscles may ache for hours— 
a fact that should inculcate scrupulous consideration in all such 
procedures. 
The affected muscles quickly become flabby and waste, and their 
prominences disappear. The muscular atrophy becomes extreme in 
some instances, but the aspect of the limbs differs from that in pro- 
gressive muscular atrophy on account of the partial distribution of the 
affection, and because it is only in a few muscles, such as the extensors 
of the fingers and the interossei, that the wasting is as great as in 
that affection. Changes in the electrical excitability of the muscles 
concur with these symptoms; they present the reaction charac- 
teristic of nerve lesions, described at p. 54. The faradic irritability is 
lost, and that to voltaism is increased in amount, and often but not 
always altered in quality, in the usual manner. In slight cases, 
however, increase in voltaic irritability may be trifling, and may be the 
chief change. In the nerves the irritability to both currents lessens 
and is ultimately lost. If a case is examined in the very early stage* 
the increased irritability mentioned at p. 58 may be found, and after-- 124 
MULTIPLE NEURITIS. 
wards replaced by diminution and loss. In the most severe cases the 
muscles most affected may quickly lose all irritability, on account of 
the intensity of the secondary changes in the muscular tissue, which 
destroy instead of merely changing their special structure and 
characteristic functions. Occasionally the wasting is concealed by 
(edema, but now and then (as I have seen) the size of the muscles 
may be little reduced even when they are totally paralysed, with 
extinction of faradic and great reduction of voltaic irritability. But 
the wasting is only deferred, and extreme atrophy ultimately occurs. 
In such cases there is probably a rapid fatty degeneration of the 
muscles, and the fat accumulates between the fibres so as to main- 
tain, for a time, the bulk of the muscle. An extremely rare alteration 
is the preservation of some voltaic irritability in the nerves as well 
as in the muscles, faradic irritability being lost in both. 
As in other cases of unequal palsy, the less affected muscles of the 
limbs are apt to undergo contracture and shortening, especially when 
the palsy causes the part to assume habitually a certain position 
under the influence of gravitation, or a certain posture is adopted 
by the patient in order to lessen pain. These contractures occur 
chiefly in the lower limbs. The foot-drop shown in Fig. 58 is especially 
frequent, from the palsy of the flexors permitting the foot to fall as 
the patient lies in bed, under the influence of gravitation and of the 
unopposed extensors. The effect of posture is seen in the contraction 
-of the flexors of the knee, which may be fixed at a right angle, and to 
a less degree of those of the hip, on account of habitual flexion of 
these joints to escape the pain occasioned when the parts are nut on 
the stretch in the extension of the limb. 
The affection of the sensory nerves of the skin is sometimes absent, 
more often it is conjoined with that of the motor nerves, and some- 
times only with that of the sensory muscle-nerves. It very seldom 
exists alone. Its first manifestation is the tingling and other sub- 
jective sensations already mentioned, to which is soon added the 
byperaesthesia which is often so troublesome throughout the disease. 
Sensory disturbance is usually more extensive than the motor palsy, 
but is greatest at the most affected parts, the extremities of the limbs. 
Except in slight cases, the damage to the sensory fibres becomes suffi- 
cient to lessen the sensibility of the skin to touch. A faint touch 
may be unfelt while over-sensitiveness to pain continues, and is even 
so intense that a strong touch may cause distress. Barely, as I have 
twice seen, sensibility to pain is lost, that to touch being preserved. 
The temperature sense is usually normal. These sensory changes are 
first developed on the extremities, sometimes on the palms and soles; 
they may even be still more local, and only considerable on the tips 
of the fingers, or the hvperaesthesia may be chiefly under the nails. 
Spontaneous pains accompany the hvperaesthesia, dull, or acute, or 
“burning” in character, referred to the deeper parts of the limb, or 
the nerve-trunks, or the joints, and increased or excited by any SYMPTO MS. 
125 
attempt at movement. The pain referred to the joints may he really 
in them, especially in the gouty, or it may be in the nerves that pass 
by the joints and are disturbed mechanically by tlieir movement. 
The sensory change increases in area as the disease develops, and 
usually extends first up the outer side of the leg and the radial side 
of the forearm. Although sensibility to pain is seldom lost, the 
conduction of pain is delayed in some cases. 
In the ataxic form, inco-ordination is the chief symptom, and it 
may accompany the onset of muscular weakness in the motor form. 
It is usually accompanied by muscular tenderness, and exists with or 
without the affection of cutaneous sensibility just described. It pro- 
bably depends on changes in the afferent muscle-nerves, the impres- 
sions from which are chiefly concerned in the process of co-ordination 
(see Spinal Cord, Functions). The implication of these nerves is 
shown by the muscular tenderness that is so marked a feature. The 
inco-ordination in these cases resembles closely that which exists in 
tabes, and the knee-jerk is lost as in that disease, while the frequent 
occurrence of pains in the limbs increases the resemblance. Hence 
the form in which this symptom is predominant has been called jpseudo- 
tabes, often with the prefix alcoholic, from the fact that this is its most 
frequent cause. It has, however, also been met with from arsenical 
poisoning. The ataxy may involve the arms or the legs, but is most 
frequent in the latter. It never reaches the degree met with in advanced 
tabes, probably because very extensive and intense damage to the 
muscle-nerves only occurs when the toxic cause is intense; its effect 
then is not limited to a single set of nerves, but, involving the motor 
also, produces a loss of power, before which the inco-ordination 
ceases to be prominent, if it does not of necessity disappear. The 
general law that limitation needs chronicity of course and moderation 
of degree holds good in these cases on the sensory as well as on the 
motor side. When the inco-ordination is the prominent symptom the 
disturbance of sensory nerves is slight, and if there is extreme 
hypersesthesia and much loss of sensation there is usually also motor 
palsy; and thus this ataxic form is not commonly accompanied by the 
intense sensory disturbance of the complete and characteristic cases. 
Sensory loss, chiefly to touch, is, however, occasionally met with in 
chronic cases of the ataxic type. The resemblance to tabes is then 
still greater. The distinction is considered in the section on “ Dia- 
gnosis.” 
Tenderness of the nerve-trunks in the region of whose supply the 
symptoms are greatest is a very common symptom, although not 
always readily recognised, because they are only more tender than the 
adjacent structures, and the degree of difference may seem not great 
when all the parts are extremely sensitive. It is less frequently a 
marked symptom than the tenderness of the muscles, and must 
depend (since the pain is felt at the spot) on the involvement of the 
nerves of the sheath. It is only in very rare cases, chiefly of irre- 126 
MULTIPLE NEURITIS. 
gular adventitial neuritis, that any swelling of accessible nerves can 
be distinguished. 
Reflex action from the skin varies much in its condition. In cases 
with hyperaesthesia it is often increased, even when there is considerable 
motor palsy ; the muscles that escape cause the movement, and the 
impression that reaches the reflex centre is doubtless increased in 
degree just as is that part of it which reaches the brain and is felt 
as increased sensation. But in severe cases, with extensive loss of 
power and sensation, the skin-reflex may be lost. The loss may be 
observed to coincide with an increase in the other symptoms, and 
generally to be related to loss of sensibility to touch with extensive 
motor palsy; it may, however, be lost when sensation is perfect. Occa- 
sionally it is lost out of proportion to the other symptoms, motor 
or sensory. The muscle-reflex action (myotatic irritability), as we 
have already seen, is almost invariably lost. Although the knee-jerk 
has been observed to persist in rare cases (Dejerine), its persistence 
is quite exceptional, and probably depends on the escape of at least 
some of the fibres on which the action depends. Possibly, however, 
the knee-jerk is sometimes excessive in the early stages of the disease 
in consequence of an irritable state of the nerves on which it depends, 
similar to that which gives rise to the hvpersesthesia. I have more 
than once found it increased in cases of slight sensory neuritis (e. g. 
with symmetrical tingling and slight anaesthesia on the soles), and in 
one such case it disappeared as the disease progressed. On the other- 
hand, it is often lost when there is scarcely any appreciable weakness 
of the extensors, although usually some tenderness of these muscles 
suggests an affection of the afferent path. 
Trophic changes occur in prolonged cases—in the nails, skin, and 
hairs, and are similar to those of ordinary neuritis; glossy skin, 
arthritic adhesions, and thickening being the most common. Bedsores 
are not common—a fact well established, but not altogether easy to 
explain. The vaso-motor nerves may present disturbance of function, 
and some oedema of the limbs is common, especially in cases that are 
due to alcohol: the blood-state or impaired function of the kidneys 
probably aids in its production. It occurs about the ankles, back of 
the foot, and very frequently about the wrist and back of the hand. 
In one very severe and fatal alcoholic case the legs and back were 
the seat of a peculiar brawny oedema, pitting very slowly, and 
attended with lividity of the skin in the depending parts, which 
became brighter in colour on pressure. In this case endocarditis 
developed during the course of the malady. In one recorded case 
oedema was present only over the nerve-trunks in the neighbourhood 
of joints—a place in which the movement of the limbs especially 
disturbs the sheath-nerves of the trunks, to which the vaso-motor 
nerves of the part are probably related. Indeed, it is common for 
oedema to be present about the joints when it is not elsewhere, and 
this may be the explanation. Pain in the joints and even some SYMPTOMS. 
127 
effusion into them have been observed, especially in association with 
an acute onset, but it is perhaps more often gouty* than rheumatic 
in alcoholic cases, and its significance as to the “ rheumatic ” nature 
of the neuritis must be looked on with some suspicion. It may 
be occasionally a result of the disease of the nerves, since chronic 
changes in the joints often take place just as they do, in the inflam- 
mation of single nerves. It is especially common in the finger-joints 
and in the wrist, but it occurs also in the shoulder and knee, less 
frequently in the elbow and other joints of the legs. There is pain 
on movement and thickening about the joint, with ultimate limitation 
of movement. It is a troublesome effect of the disease, because it 
interferes with movement when power returns. There is much more 
tendency to it in some cases than in others, and it may be so extensive 
as permanently to cripple the sufferer, f The adhesions commonly 
re-form after they have been forcibly broken down. 
The symptoms are wide-spread in proportion to the acuteness and 
intensity of the malady, but differ in these respects also accord- 
ing to its cause. The effect of metallic poisons is usually limited and 
confined to the arms, as in lead palsy. In alcoholism all the limbs 
are often affected, but the arms escape more often than the legs. 
From malaria the legs usually suffer alone ; such cases are considered 
at p. 151. In cases with complex causation a general parenchymatous 
neuritis may be accompanied by a preponderant adventitial inflam- 
mation of some one nerve, as the facial or sciatic. The cases with 
most widely distributed symptoms are those that result from obscure 
toxsemic states, from cold, and from alcoholism. It is in these, and 
especially in the first, that the nerves of the heart, larynx, and of the 
muscles of respiration most frequently suffer. When the laryngeal 
nerves suffer it is usual for both adduction and abduction of the 
vocal cords to be weakened, seldom one movement only. The optic 
nerves have been affected only in rare cases with considerable blood- 
change. In the case mentioned on p. 126 (in which there was brawny 
oedema and endocarditis) there was slight optic neuritis and a diffuse 
oedematous retinitis.J The face has also been affected on both sides 
in some of the cases due to exposure to cold, and also, usually in 
slight degree, in some toxtemic cases; it seems always to escape in 
cases due simply to alcohol. The sphincters almost always escape; 
a slight impairment of function has indeed been met with in a few 
very severe cases of probably pure polyneuritis, but their affection, 
as already stated, usually indicates an implication of the spinal cord. 
The Course of the affection is determined by the same conditions 
as influence its intensity, and by the extent to which the cause 
is under control. The more severe and acute the symptoms, the 
* Acute gout, it must be remembered, sometimes attacks the larger joints with 
or before the smaller ones, and may closely resemble an attack of rheumatic fever, 
f As in a case recorded by Taylor, ‘ Guy’s Hosp. Rep.,’ 1888. 
I The changes are described by Edmunds and Lawford, ‘ Trans. Oph. Soc.,’ ix, 137, 128 
MULTIPLE NEURITIS. 
wider is their range and the longer is their duration. Very com- 
monly the symptoms increase during three to six weeks, then become 
stationary (if the cause is stopped), and after one or two months 
slowly improve. The first sign of improvement is a diminution in 
the pain and hyperaesthesia, but the tenderness of the muscles and 
the nerve-pains on movement often continue long after the spon- 
taneous pains have ceased. If tingling, &c., ceased as the disease 
advanced their return may herald improvement. Power slowly returns, 
first in the muscles affected last and least, and afterwards in those 
paralysed and wasted in greater degree. In these the weakness lasts 
for many months, and shortening of the opponents of the most 
affected muscles is apt to occur. The contracture of the calf muscles, 
secondary to palsy of the flexors of the ankle, constitutes a grave 
hindrance to the use of the legs in standing and walking. The 
patient cannot get the sole and heel on the ground so as to afford 
a uniform base of support, and keep his body upright so as to balance 
it. But this contracture invariably yields to persistent efforts to 
walk. The palsy of the arms lasts longer than that of the legs, or 
vice versa, according as the one or other suffers most. The excess of 
impairment of the muscles most affected is often very conspicuous 
during recovery. Improvement goes on for a long time, generally 
until recovery is perfect, but very rarely there is some permanent 
loss of power. It is remarkable, however, how almost complete a 
recovery may take place, even after the paralysis has been consider- 
able for a year. The wasting lessens and power returns; latest where 
there is most loss of irritability, and usually later in the small muscles 
of the hand than in the muscles of the forearm. Relapses are apt to 
occur, but only when the cause of the neuritis is still in operation in 
some degree, or when the patient is again exposed to it or to some 
adjuvant cause, such as cold. 
But the malady sometimes runs a very acute course, especially in 
the cases due to toxaemia or to cold, so that all parts of the limbs 
have become weak and the extremities powerless by the end of seven 
or ten days, and the involvement of the nerves of the respiratory 
muscles may bring life to an end within a fortnight, sometimes 
even within a week. In this form there may be severe initial pain, 
not specially related to the regions afterwards affected. In one case 
it was severe in the back, in another across the abdomen. It is 
probably a direct effect of the blood-state, distinct from its influence 
on the peripheral nerves. Such cases bear considerable resemblance to 
those of “ acute ascending paralysis ” in their course—differing, how- 
ever, in the fact that the ascension is up the limbs rather than up the 
general frame. Sometimes, on the other hand, the disease presents a 
course far more chronic than that described above, and occupies many 
months in its development and progress. This is often the case 
with the limited alcoholic forms, especially the ataxic variety, “pseudo- 
tabes,” and with cases in which the toxic agent is absorbed from with- COMPLICATIONS. 
129 
out very slowly and its effect accumulates gradually, as in some cases 
of chronic arsenical poisoning. Slight cases, again, treated promptly 
have been known to recover in a month. 
The temperature, usually raised in an acute onset (see p. 120), may 
be normal in chronic cases, with or without an occasional rise, or may 
be slightly raised during the chief part of the course of the disease. 
A persistent considerable elevation suggests some complication, such 
as phthisis, and should lead to careful and repeated examination of 
the lungs. It may also indicate a persistence of toxsemia, other 
indications of which are mentioned among the complications of the 
disease. 
The Cause of Death in acute cases is often palsy of the respiratory 
muscles, sometimes aided by a catarrhal bronchitis, or paralysis 
of the heart when the vagus is affected ; in more chronic cases it may 
be caused bv exhaustion, due to chronic gastric derangement and the- 
wearying effects of prolonged suffering, or the effects of disease of the- 
spinal cord. Pneumonia frequently causes death in the acute forms,, 
and in alcoholic subjects the inflammation of the lung so often runs 
a low course, with extensive consolidation, sometimes bilateral and 
unusual in seat (as in the middle lobe and central portions of the 
lung), that it is difficult to avoid the suspicion that its form and course 
are determined by coincident neuritis of the pulmonary branches of 
the vagus, either primary or secondary to the inflammation of the 
lung. Death may result unexpectedly from cardiac failure when no- 
preceding symptoms have suggested an affection of the cardiac nerves,. 
and in such cases there is generally a coincident degeneration of fire- 
walls of the heart. Fatal neuritis of the vagus, however, may occur 
very early in relapses. Other coincident effects of chronic alcoholism 
are frequent causes of a fatal issue, such as cirrhosis of the liver, 
gastric troubles, and chronic cerebral meningitis in cases of alcoholism, 
or acetonaemia in cases of diabetic polyneuritis. Various morbid 
blood-states, causing the neuritis, may continue and cause death. 
Lastly, phthisis is a frequent cause of death, and probably varies in 
the relation it bears to the neuritis, sometimes being its consequence, 
and sometimes apparently a coincident effect of some obscure cause. 
Complications.—The chief of these have been just enumerated in 
the list of the causes of death. The most important in alcoholic cases 
are the effects of alcohol on various organs and tissues, especially on 
the liver, heart, and spinal cord. It is very common to find the liver 
enlarged, sometimes very large ; less commonly it is contracted. The 
enlarged liver may be either fatty or fibroid. Ascites and other effects 
of portal obstruction are much less frequent complications than might 
be expected, perhaps because it is rare to have much contraction of 
the new tissue in the liver. The kidneys also are often diseased. 
Gastric catarrh with its varied symptoms, morning vomiting, anorexia, 
and the like, is very common. So also are the several effects of 
gout due to the alcoholism or to metallic poisons when these have 
VOL. I. 130 
MULTIPLE XEURlTfS. 
been the cause of t-lie neuritis (as lead, or, as in one case under 
my notice, silver). On the part of the nervous system there may 
be various subacute and chronic forms of inflammation of the sub- 
stance of the spinal cord or of its membranes, the common manifesta- 
tions of which are to a large extent prevented by the affection of 
the nerves. The most important, the trunk girdle pains and the 
affection of the sphincters, are further considered in the section on 
diagnosis. Chronic cerebral meningitis is also common, and usually 
fails to produce its usual manifestation, pain, even when marked 
and extensive opacity and increase of fluid are found after death. It 
usually causes some chronic mental disturbance, often slight optic 
neuritis, and sometimes general convulsions. But mental change is 
also common as a direct effect of the alcohol on the brain; distinct 
delirium tremens often coincides .with the onset of the neuritis. In 
most alcoholic cases, indeed, the mental state is unnatural; the 
patient is irritable, intolerant of pain, and deficient in self-control. 
Various manifestations of hysteria occur in women, and a peculiar 
childish jocularity is sufficiently common to deserve special mention. 
The craving for withheld stimulants increases the irritability, and, in 
the case of women, previous training in duplicity in order to obtain 
alcohol has usually induced a general deterioration of the moral 
sense, which has results that startle those who have been success- 
fully deceived Mental change is for the most part absent in the 
cases due to cold (save in some in which there is an intense blood- 
change), and in those produced by metallic poisoning; but it occurs fre- 
quently in toxaemic cases, generally in the form of simple delirium, 
and is apparently due to a simultaneous action of the morbid agent 
in the cells of the brain. A persistent morbid blood-state may cause 
endocarditis and other consequences. 
Phthisis is also a very fiequent complication; its double relation 
to the neuritis has been already mentioned. The form of lung dis- 
ease met with in neuritis presents no special peculiarities, except that 
low pneumonic changes play a considerable part in the morbid pro- 
cess. Acute pneumonia is also common. 
Pathological Anatomy.—The changes in the nerves correspond to 
those already described in the account of neuritis, with the exception 
that the chief changes of isolated neuritis are in the connective tissue, 
and especially in the sheath; and those in the nerve-fibres are subor- 
dinate In most cases of polyneuritis the connective tissue suffers far 
less than do the nerve-fibres. Considerable variations are found, how- 
ever, in the extent to which the two elements suffer. In rare cases, 
and chiefly in those in which the distribution of the affection is not 
strictly symmetrical, the inflammation chiefly affects the sheath and 
interstitial tissue; in acute symmetrical cases both the connective 
tissue aud nerve-fibres are involved, as in Fig. 59, p. 132. This ivas 
also the condition in the case of fatal septicaemic neuritis recorded by 
Both (see p. 115). In the vast majority the fibres are affected chiefly PATHOLOGICAL ANATOMY. 
131 
or even exclusively; the changes are essentially parenchymatous. 
This is the rule when the affection is strictly symmetrical. It is 
remarkable, often, how slight is the affection of the connective tissue 
and sheath, even in nerve-trunks that have been extremely tender. 
Hence it is probable that this tenderness is often due to changes in 
the nerves of the sheath, the “nervi nervorum,” similar to that which 
the proper conducting fibres of the nerve undergo, rather than to an 
inflammation of the connective tissue itself. 
Naked-eye changes are present only when the connective tissue and 
sheath are inflamed in considerable degree. In recent and acute cases 
of this character the nerves may be found reddened, swollen, and 
sometimes small haemorrhages are visible. In older cases they may or 
may not be swollen, but are usually softened, and even pulpy. "When 
the changes are confined to the nerve-fibres, diminished consistence 
may be the only alteration that can be recognised on simple examina- 
tion ; and often this is absent, and the nerves appear normal on external 
examination, even when their fibres are extensively diseased. Some- 
times under a low magnifying power a section of the nerve has a 
mottled aspect, due to the irregular degeneration of the fibres. 
When the connective tissue is involved the microscope shows the 
sheath to be infiltrated with lymphoid cells (probably leucocytes), 
and in old cases many spindle-cells and fibres increase its bulk. The 
same changes may be traced in the septa between the fasciculi, and 
in the secondary sheaths that surround the latter. The walls of the 
vessels are also thickened (Fig. 59, a). When mere acuteness of 
parenchymatous neuritis causes the connective tissue to be inflamed, 
the interstitial tissue and inner part of the sheath are chiefly affected, 
and an amorphous “exudation” may be found in these situations. 
But the fibres themselves always suffer in conspicuous degree; and in 
the majority, as in the case from which Figs. 59 and 60 are drawn, 
they suffer chiefly, the interstitial tissue presenting comparatively little 
change. In this case the patient was a woman aged thirty-three, 
alcoholic; the course of the disease wras subacute ; the symptoms 
reached a considerable degree in a few weeks, and the patient died, 
chiefly from coincident liver disease, five months after the onset. The 
symptoms were charactei'istic, and continued up to the time of death. 
The condition found after death is a good illustration of the paren- 
chymatous or degenerative form, but in all forms of polyneuritis 
the process in the nerve-fibres is the same, whether the connective 
tissue is or is not affected. The fibres undergo acute degeneration, 
essentially the same as that -which occurs after an injury to a nerve. 
It has been represented in Figs. 33 and 34 (p. 50), and, associated 
with inflammation of the sheath, in Fig. 44 (p. 65). Examination 
in the recent state reveals abundant products of the degenera- 
tion of the fibres, granule corpuscles, &c. After hardening, a trans- 
verse section, stained with carmine and cleared in the usual way, 
presents the appearance shown in Fig. 59, a. There is a slight increase 132 
MULTIPLE NKUKITIS. 
in the connective tissue between the fasciculi; the area of these is- 
occupied by tracts of interstitial tissue, which under a higher mag- 
nifying power (b) have a branching form, enclosing spaces which have 
been occupied by nerve-fibres, and in some of which healthy fibres still 
Fig. 59—Multiple alcoholic neuritis: sections stained with carmine and cleared. 
A. Transverse section of p ,rt of sciatic nerve ; low power, b. Part of a fas- 
ciculus of same, more highly magnified, c. Part of a less affected fasciculus 
from a musculo-spiral nerve. 
G. 60.—Sections from the same sciatic nerve, stained with osmic acid and mounted 
in glycerine. A. Fasciculus under low power, b. Fart of a fasciculus more 
highly magnified, c. Longitudinal section of nerve-fibres. (From sections 
prepared by Dr. Beevor.) 
remain (c). The space between this tissue is occupied by the pro- 
ducts of degeneration of the fibres, but these are rendered invisible 
by the clearing process, and only faint indications of their outline can 
be seen (b). In sections stained with osmic acid and mounted in 
glycerine (Fig. 60) these products of degeneration, stained dark, are 
conspicuous. Under a low magnifying power (a) a fasciculus is seen 
to be studded with black granular spots, elongated where the fibres 
are divided obliquely; the increase in the tissue between these de- PATHOLOGICAL ANATOMY. 
133 
•generated fibres is distinct; aggregations of myelin are seen in the 
connective tissue between the fasciculi. Under higher powers (b) the 
dark spots are seen to be the sections of degenerated nerve-fibres, in 
some places two or more being blended into a larger mass. In a 
longitudinal section (c) the process of degeneration of the fibres is 
more distinctly seen, and from it the appearance of the transverse 
section can be better understood. The white substance is broken up 
and enlarges the fibres at some places, while at others it has been 
removed, and the sheath is left empty. Round masses of myelin lie 
(on the left) outside the fibres. The nuclei of the fibres are enlarged; 
one, of considerable size, is seen in the centre of the figure. Connec- 
tive-tissue fibres and cells lie between the nerve-elements, and near 
the sheath are round and spindle cells containing myelin granules and 
globules which they have taken up (b). 
The distribution of the changes in the nerves varies much in 
different cases. The signs of inflammation of the sheath may exist 
only on the larger and medium-sized nerves of the limbs, and in the 
smaller nerves the changes may be confined to the nerve-fibres. These 
may be traced down into the intra-muscular nerves and their endings. 
On the larger nerves the signs of inflammation of the sheath are most 
intense at certain spots, especially (as in simple neuritis) where a 
nerve turns round a bone, or passes through a fascia, or divides, 
or in the neighbourhood of joints, their situation being probably 
determined by mechanical influences. 
In all cases in which the affection is chiefly of the nerve-fibres 
themselves the changes are usually intense in the peripheral parts of 
the nerves, and as the nerves are examined farther from the periphery 
the alterations become progressively slighter, and the proportion of 
normal fibres larger, until the morbid appearance ceases. The centri- 
petal extent of the disease—that is, the degree in which the larger 
trunks are affected—varies according to the duration and severity of 
the case. If the nerve-fibres could be isolated and seen like the branches 
and twigs of a tree, as they separate in the peripheral ramifications, 
we should see the endings and twig-like branches withered, and 
as the branchlets become larger and larger by junction they would 
assume a more and more normal aspect until the larger branches 
appear perfectly natural. The size of branch to which the change 
extended would vary according to the severity of the ease. In some in- 
stances, even those of largest size would present some alteration, while 
in others the small twigs would be withered in a considerable part of 
the tree although the change did not extend beyond them. In a 
tree the leaves would drop off equally whether the twigs only were 
diseased or the branches also; and so the muscles sutler equally whether 
the nerve degeneration is limited to the periphery or extends to the 
nerve-trunks. In the case from which the illustrations are taken even 
the sciatic nerve presented few healthy fibres; but here, as usual, the 
anterior roots were healthy. This limitation to the peripheral ex- 134 
tremities of the nerves is met with in slight cases of considerable 
duration, but also in some severe cases of very brief duration. For 
instance, in a case accompanied by pneumonia, and fatal in seven days, 
the only change found was in the fibres themselves within the muscles 
it was a motor parenchymatous neuritis. The character of the 
changes is also influenced by that of the nerve-fibres involved. If the 
affection is partial, as in the ataxic or the purely motor forms, the 
mixed nerves contain many healthy fibres mingled with those that have 
undergone atrophy. When the symptoms are both motor and sensory 
almost all the nerve-fibres are found to have suffered. 
The nerves of the limbs alone present changes in the majority of 
cases. The corresponding nerves on the two sides are almost always 
affected. The musculo-spiral nerve in the arm and the anterior tibial 
nerve in the leg usually suffer first and in greatest degree, but often 
all the terminal nerves of the limbs are involved in some measure j 
in the lower leg the anterior tibial almost always presents more 
change than the other nerves of the same level, aud in the thigh the 
sciatic more than the anterior crural. In the arm, the median and 
musculo-spiral and ulnar all suffer, but the alteration in these nerves 
in the upper arm may be slight when it is considerable in their 
branches in the forearm. The changes occasionally met with in 
other nerves correspond to their implication, as described in the 
section on symptoms. 
The Muscles present changes of the same character as those which 
result from ordinary neuritis (see p. 43). They are paler than 
normal and smaller in bulk. The fibres are reduced in size, and pale; 
the transverse striation may be preserved, or they may be granular j 
normal fibres may be found side by side with those that are degene- 
rated. The nuclei of their sheaths and of the interstitial tissue may be 
increased in number, and often are arranged in groups ; and sometimes 
a quantity of such nuclei and leucocyte-like cells may separate widely 
the fibres, and granular and pigment masses may accumulate between 
them. In very acute cases the changes in the muscles may be great, 
and alike parenchymatous and interstitial; the fibres presenting 
loss of their striation with fatty and granular degeneration, while 
there may be a great increase in the amount of the interstitial tissue, 
especially of its nuclear elements. 
The Spinal Cord has been found healthy in most cases. Occasionally 
the grey substance has appeared pale and somewhat shrunken, so as 
to present a slighter difference from the white than normal. The 
ganglion-cells, in some instances, have presented abnormal appearances 
—a vitreous appearance or vacuolation, and this when the anterior 
nerve-roots were not diseased. In many alcoholic cases, however, 
changes more or less considerable have been found in the cord. 
Chronic myelitis in irregular disseminated areas is the chief, and there 
has been sometimes also chronic inflammation of the membranes, 
especially of the pia mater, involving also the peripheral layers of the 
MULTIPLE NEUIilTIS. PATHOLOGY. 
135 
cord ; an instance of this is figured in the chapter on chronic myelitis. 
In other cases there has been merely a general increase in the con- 
nective tissue throughout the cord, which has been in some instances 
greater in one region than elsewhere, and especially marked in the 
posterior columns. 
Other organs are often found diseased, and in alcoholism the lesions 
common in that disease are generally found in some degree, especially 
alterations in the liver and kidneys. The former may be large and 
either cirrhosed or fatty; the kidneys are generally large and opaque, 
sometimes with fatty striae in the cortex. Pneumonia is frequent 
both in these and in all cases due to causes that induce an intense 
change in the blood. In these there may also be enlargement of the 
spleen, such as is met with in typhoid fever and septicaemia. Phthisical 
changes in the lungs are also common in chronic cases, both in those 
tliatai’e due to alcohol and in others. No special peculiarity has been 
observed in the pulmonary lesion, but it is very desirable that more 
attention should be paid to the state of the nerves of the lungs 
entering the diseased parts. When not otherwise diseased, the 
lungs are generally found the seat of terminal congestion and 
oedema. The walls of the heart may be degenerated, and alterations 
may sometimes be found in its nerves. 
Pathology.—An outline of the chief facts in pathology of multiple 
neuritis has been given in the introductory section, and not much re- 
mains to be added. The relation of the motor symptoms to the 
lesion of the nerves has also been described in the general account of 
diseases of the nerves, and in the description of isolated neuritis ; all 
that has been said of the single form is true also of that which is 
multiple. The wasting that accompanies the loss of power, and the 
change in electrical irritability, are the same in each. In each it is 
true, moreover, that the position of the lesion in the course of the 
nerve-fibre makes no difference to the symptoms ; these are the same 
whether the disease is in the trunk of the nerve, the peripheral fibres, 
or the actual nerve-endings. The relation of the ataxy in the pseudo- 
tabetic form to a neuritis of the afferent muscular nerves is proved 
partly by exclusion, partly by analogy, since in true tabes the lesion 
may be confined to these ; the spinal cord may be free, and only the 
peripheral nerves diseased. The evidence for this will be described in 
the general account of the functions and symptoms of diseases of the 
spinal cord, and in the chapter on locomotor ataxy—a disease which 
sometimes not only resembles, but is almost identical with the pseudo- 
tabetic form of neuritis. The pains and hypersestliesia are explained 
by the fact that the disease of the nerves is one in which the nerve- 
fibres themselves suffer primarily, and that on them the cause must 
have a primary and direct action.* An influence which leads to the 
* In the first edition I suggested that the degeneration of some of the fibres 
might be secondary to their damage by the inflammation of the sheath and inter- 
stitial tissue at some higher spot. But this now seems very unlikely; it is far 136 
MULTIPLE NEURITIS. 
molecular destruction of the nerve-fibres must, in destroying their 
structure, disturb gravely their function ; and this disturbance of 
structure and of function proceeds in the parts still connected with 
the nerve-centres, so that the irritative influence of the molecular 
•changes can act on the centres by the normal upper parts of the 
nerves throughout the whole course of the malady. It induces in the 
centres, as all prolonged pain does, an undue readiness of action, a 
state of over-excitability ; and so we can understand the persistence 
of the pains and hyperaesthesia, and the fact that these continue 
until the process of restoration has become definitely established. 
The same considerations apply to the tenderness of the muscles, since 
the afferent muscular nerves correspond in the direction of their 
function to the sensory nerves of the skin. In both cases mechanical 
influences constitute the chief mode of their normal stimulation, and 
hence they may well be morbidly sensitive to such influences. The 
peripheral distribution of the changes indicates, moreover, that pro- 
bably the first to suffer are those in which functional susceptibility 
is most highly developed—the actual endings of the nerves, and the 
structures which are especially adapted for the reception of stimuli 
and the production of nerve-force. 
We have seen that two facts give us the key to the pathology of 
-the disease so far as this is yet understood. One is its symmetry, 
the other is the fact that it is commonly a disease of nerve-fibres — 
that these, and not the connective tissue, are the parts primaiily and 
specially diseased. In all structures, in proportion to the intensity 
and acuteness of the parenchymatous affection, the interstitial tissue 
participates in the changes, and escapes in proportion to its slowness 
and slightness. The extent to which this is true of multiple neuritis 
has been already pointed out. Further, in its relation to a morbid 
blood-state as its sole cause, we have the key to the symmetry of 
the affection as well as to its parenchymatous nature, and on this 
point there remains little to add to what has been already said. 
Such a limitation to the nerve-fibres as is seen in multiple neuritis 
is unknown in the isolated form, in which, as in gouty or syphilitic 
neuritis, the affection is chiefly one of the sheath and interstitial 
connective tissue; and the fibres suffer only secondarily in chronic 
cases, although, in accordance with the law already stated, they are 
involved in acute cases in proportion to the intensity of the process. 
It is not surprising that the symptoms of multiple neuritis should 
bear so close a resemblance to those of some affections of the spinal 
cord, since we must regard the peripheral nerves, at least the motor 
fibres, as essentially outlying parts of the cord, and it will be seen 
that one central disease, primary lateral sclerosis, presents many 
points of correspondence with the chronic form of polyneuritis, being 
more probable tbafc all the fibres suffer in the same way, and the more thoroughly 
cases are studied the more elearly does it appear that all symmetrical neuritis is 
peripheral and parenchymatous. PATHOLOGY. 
137 
an affection of the fibres proceeding from the motor cells of the brain 
analogous to that of the fibres proceeding from the motor cells of the 
cord. We can understand the peripheral distribution of the disease 
by the fact already pointed out—that the nerve-fibres are really the 
prolonged processes of the nerve-cells, sharing the life of the cell, and 
depending on it for their vitality. The influence on which their life 
depends must lessen with the distance from its source, and hence their 
vital power of resisting morbid agencies is least at the periphery. 
The conditions of life of the sensory fibres, it need hardly be pointed 
out, differ little from those of the motor, since the ganglia containing 
their cells are near the cord, and almost as far from the periphery as 
are the motor nerve-cells. This fact also has a relation to the paren- 
chymatous nature of the disease, since we can find no reason why 
the connective tissue of the nerves should suffer most at the extreme 
periphery. On the contrary, the inflammations that begin in the 
sheath are generally situated in the course of the nerves, at some spot 
exposed to the influence of an exciting cause such as pressure or motion. 
The same fact (that the cause is a blood-state) affords also an explana- 
tion of many facts of distribution. In addition to the points already 
mentioned it is only necessary to point out how common are instances 
of selective action of toxic agents upon various parts of the nervous 
system ; and analogy prevents ns feeling any difficulty in at least 
accepting the fact that a blood-state should act upon one set of nerve- 
fibres rather than upon another, or on the fibres of the extensors, or 
even first and chiefly on only some of the nerve-fibres of a certain set 
of muscles. We do not yet know what are the influences that deter- 
mine such susceptibility, but it is probable that a very slight difference 
in nature is sufficient to determine a very great difference in the result. 
The fact of symmetry excludes, as we have seen, any other causal 
influences than those which act through the blood, or consist in a 
vital tendency, and act on all structures with similar vital conditions. 
We know nothing as yet of the precise character of the morbid influ- 
ence which causes the malady, beyond the facts mentioned in the 
introductory section. The greatest difficulty is presented by the 
fact that a poison generated through exposure to cold, or possibly by 
a growth of organisms in the body, should have an influence similar 
to that which is exerted by metals or by alcohol. At the same time 
it is instructive to note that the most recent researches in bacteriology 
point to the production of chemical substances by the disease-causing 
organisms in the course of their growth, and suggest that these 
chemical products, rather than the organisms themselves, act upon 
the nerves.* Alcohol, it may be further noted, is itself the result of 
the growth of organisms, almost as low in the scale as those which 
are the causes of disease; the process of the growth of bacteria in the 
boly may be not unlike a process of fermentation, and the results of 
the one not unlike those of the other. The analogy is the more perti- 
A theory first suggested by Rosenheim, ‘Arch. f. Psych.,’ xviii, 3. 138 
MULTIPLE NEURITIS. 
nent, since multiple neuritis is not known to be excited by any other 
organic poison than that which is so produced. 
The forms of polyneuritis ascribed to anaemia and cachexia, &c., 
may be a simple failure of nutrition in those structures of the nervous 
system that are farthest removed from the centres ; but the possibility 
must not be forgotten that imperfect tissue changes may generate a 
toxic agent capable of acting on these nerves, analogous to that 
assumed to be effective in diabetes. 
The changes in nutrition are sufficiently explained by the alterations 
found in the nerves, in accordance with the general facts of trophic 
disturbance stated at pp. 22 and 61. That in the muscles corresponds 
in distribution to the changes in the motor nerves, that in the skin and 
joints to those in the sensory nerves. All trophic changes which 
result from ordinary nerve-lesions must be ascribed to the propagation 
downwards of the influence of the defective an'd abnormal nutrition; and 
hence it necessarily follows that such abnormal nutrition, beginning in 
the nerve-endings, should have a similar influence, since it is through 
those nerve-endings that the effects of higher lesions are transferred 
to the tissues. The law already stated holds good here also,—that 
changes in nutrition are in proportion to the intensity and acuteness of 
the disturbance in the nerves. All that has been said regarding such 
changes in the skin, in diseases of isolated nerves, is true also of the 
multiple form, and even more clearly in the case of the motor nerves 
and muscles. The more acute the process in the nerves, the more 
intense is the change in the muscular tissue. One special point, indeed, 
arises in this connection. Although, in very acute isolated neuritis, 
the muscles may undergo the same intense and destructive changes 
seen in the most acute forms of multiple neuritis, it is possible that 
the extreme changes in the latter are sometimes a result and evidence 
of a direct action of the blood-poison on the muscular tissue itself.* 
There are some facts of both physiology and pathology which suggest 
what may be called a certain degree of solidarity of relation between 
the substance of the nerve-endings and that of the muscular fibres on 
which they terminate. This may lead to a common susceptibility to 
suffer from the same morbid influence, so far less in the muscle that 
only when the influence is very intense does its nutrition suffer directly 
to a considerable extent. 
Diagnosis. —There are few diseases in which an early diagnosis is 
of greater importance. Prompt treatment would save many patients 
from months of suffering and disability, since the removal of the cause 
ensures with certainty, during a gradual onset, a quick removal of the 
symptoms, whereas its effect on the developed disease is manifested 
much more slowly. These remarks apply especially to the alcoholic 
cases, but in some of the others the patient may be saved further 
exposure to the cause if the disease is promptly recognised, or early 
* This suggestion has been made by Soemerling as an explanation of the verv 
intense changes found in the muscles in one acute case. DIAGNOSIS. 
139 
treatment of the blood-state may have a considerable influence in 
lessening its effects upon the nerves and ameliorating the course of the 
affection. 
The diagnosis of multiple neuritis depends on the motor and sensory 
symptoms above described, their correspondence in function and dis- 
tribution in the opposite limbs, their peculiar symmetrical localisation 
in the extremities m the first instance, and on the tenderness of the 
shin, nerve-trunks, and muscles. Symmetrical weakness of the extensor 
muscles situated in the forearm, and of the corresponding muscles in 
the lower leg, or of either of these, is the leading diagnostic motor sym- 
ptom. Bilateral wrist-drop or foot-drop suggests multiple neuritis, and 
hypersestliesia or deep tenderness gives strength to the opinion. It is, 
however, most important to remember how widely the symptoms vary 
both in different forms and in different cases of the same form. The 
acute rapidly fatal cases, with palsy quickly becoming general, are of a 
type quite unlike the chronic cases in which one group of muscles on 
each side suffers alone; while there is a positive contrast between the 
latter and a case of “pseudo-tabes,” in which ataxy and pains are almost 
the only symptoms. In chronic cases also the early pains are often 
mistaken for those of rheumatism, and in those of acute course and due 
to cold these pains suggest the onset of rheumatic fever rather than 
of any affection of the nerves. The seat of the pains, however, is not 
that of rheumatic pain, and their association with tingling in the 
extremities should excite a suspicion that they are of nerve origin 
even before muscular weakness renders their nature clear. The im- 
portance is great of ascertaining precisely the position of all pains in 
the limbs. Neglect to do so is a fertile source of error in diagnosis, 
and may easily put the observer on a wrong path, from which other 
symptoms fail to withdraw him. It must be again pointed out that 
pain near a joint, produced by movement of the joint, is easily mis- 
taken for pain in the joint, even when it depends entirely on tenderness 
of the adjacent nerves. In some cases the pain is regarded as 
neuralgic, especially when it is seated in the arms and hands, and 
its position is perceived to be that of nerve-trunks or branches. But 
the general elements of the diagnosis between the two diseases gene- 
rally (described partly in the section on neuritis, partly in that on 
neuralgia in vol. ii) usually suffice for the distinction, the most im- 
portant point being the persistence of tenderness and hypersesthesia in 
relative excess of the spontaneous pain, and the development of sym- 
ptoms that indicate damage to the conducting fibres. The bilateral 
symmetry of the pain should also help to prevent error; true neuralgia 
is essentially a unilateral disease. A gouty diathesis may increase 
the difficulty of the diagnosis, especially in alcoholic cases; but the 
pains of gout are unequivocally articular or muscular, and neuritis 
due to it is single and distinctly adventitial. 
The symptoms resemble most closely those of certain diseases of the 
spinal cord, especially acute and subacute inflammation of the grey 140 
MULTIPLE NEUEITIS. 
matter, polio-myelitis. Until recently, indeed, all cases of multiple 
neuritis were looked upon as of that nature. It is chiefly in the rheu- 
matic and toxaemic forms that the diagnosis is really difficult. In each 
disease there may be a febrile onset, muscular wasting with the reac- 
tion of degeneration, initial rheumatic pains, and a tendency to the 
spontaneous recovery of the least affected parts. The distinction rests 
on the symmetrical localisation of the neuritic palsy, while that of 
polio-myelitis is characteristically random in distribution ; on the 
persistence and severity of the neuritic pains; on the tenderness of 
the inflamed nerve-trunks; and on the changes in sensibility, a symptom 
never present in polio-myelitis. The electrical reactions are the same 
in both affections. It has been said the early extinction of voltaic 
irritability in the muscle (see p. 124) is met with only in disease of 
the nerves, but this is incorrect: I have more than once met with it 
in central affections. But we have seen that it is probable that 
the nerve-trunks are sometimes inflamed in polio-myelitis, and suffer 
as a simultaneous effect of the cause of the spinal lesion. In this con- 
dition, however, the spinal symptoms preponderate, and the distri- 
bution of the neui’itis is irregular. In all cases the presence of 
increased myotatic irritability, or of the spasm in the legs that accom- 
panies considerable excess of this, may be taken as proof of disease of 
the cord; all active muscular spasm, indeed, has this significance. 
Thus if the arms are paralysed, even though the paralysis closely 
resembles that of polyneuritis, and the legs are weak, with excessive 
knee-jerk and foot-clonus, the disease is of the cord, and not of the 
nerves. The greatest difficulty is presented by some sensory cases 
in which there are only tingling and numbness in the legs, and 
also by the problem of detecting cord disease in the presence of 
peripheral neuritis. The latter will be considered further on. The 
former is generally decided by the presence or absence of the knee- 
jerk, and by the fact that in peripheral neuritis the sensory symptoms 
are more peculiar and symmetrical than in cord disease ; there is 
tingling or anaesthesia, for instance, in the palms or soles, or both, 
and a careful examination of the nerves and muscles will generally 
reveal a condition that is characteristic. 
Pachymeningitis, damaging the nerve-roots, may cause paralysis, 
wasting, and anaesthesia, but in this all four limbs are not affected; 
the legs rarely suffer; the anaesthesia extends on to the upxper part 
of the limbs and to the trunk; there is no tenderness of nerve- 
trunks, and there is usually distinct evidence of damage to the spinal 
cord itself. The mysterious disease, “ acute ascending paralysis,” 
may resemble the most rapid form of multiple neuritis, but in it the 
symptoms ascend the trunk from the legs to the arms, and do not 
begin in the hands and feet at the same time or successively, and 
involve the trunk last, as does the usual form of multiple neuritis. 
Moreover there is no anesthesia in the spinal malady. Diphtheritic 
pxaralysis, when severe in degree, may also be attended by musculai 141 
wasting and anaesthesia, but there is no considerable pain, and the 
weakness in the limbs usually succeeds paralysis of the palate and 
ciliary muscle, never met with in other forms of polyneuritis. The 
distinction from other diseases (as, for instance, that from the sym- 
metrical paralysis of the extensors which may occur at the onset of 
progressive muscular atrophy) will be considered when these diseases 
are described. 
The distinction of the ataxic form, “ pseudo-tabes,” from true tabes 
is often beset with great difficulty. This is indeed natural, since the 
lesion in true tabes may be identical with that in the neuritic affec- 
tion ; not only is degeneration of the peripheral nerves a common 
lesion in tabes, having the same distribution at the peripheral ex- 
tremities of the nerves as in polyneuritis, but in the variety termed 
“neuro-tabes” the lesion consists only in this nerve-degeneration, and 
the spinal cord is free from disease. We have then affections iden- 
tical in pathological anatomy, and almost identical in symptoms- 
Tet we must class the neuro-tabes with the spinal form, from 
which polyneuritis, as here described, has to be distinguished; it 
is necessary to do so on account of the relations and etiology of the 
two maladies, as well as on account of practical considerations. The 
presence of actual paralysis, of distinct weakness of the extensors, in 
addition to inco-ordination, would of course decide the question, since 
there is no actual loss of power in tabes : hence a distinction in gait 
pointed out by Westphal and Charcot, that in pseudo-tabes the feet 
are raised too high on account of the difficulty of getting the toes off 
the ground (like a person stepping over low objects), is of little actual 
value; it only exists when there is distinct loss of power. But it is 
in the cases of neuritis in which there are only sensory symptoms 
that the difficulty especially exists. It occurs, moreover, chiefly 
when the ataxy is moderate in degree; when this is so great 
that the patient is not able to stand alone, in spite of the 
power of moving all joints of the legs with fair force, true tabes 
should alone be thought of. The cases of tabes in which there is 
moderate inco-ordination of movement, distinct unsteadiness on 
walking, whether increased by closure of the eyes or not, and distinct 
irregularity and uncertainty in the movement of the feet and legs, are 
those which are perfectly simulated by the pseudo-tabetic form of 
polyneuritis. Pains are common to the two diseases, and neither pro- 
longed acute pain nor dull rheumatoid pains afford the means of 
distinction. True “ lightning ” pains are seldom met with in neuritis ; 
they are therefore strong evidence that the case is one of tabes. 
Extreme hypermsthesia is much more common in neuritis than in 
tabes, but is of little service in the diagnosis because it is not 
often present in ataxic polyneuritis, but the muscular tenderness of 
neuritis is of considerable diagnostic value. A great excess of the 
reflex action from the skin is occasionally met with in tabes, the 
sensory impressions being painless; while in ataxic neuritis the reflex 
DIAGNOSIS. 142 
MULTIPLE NEURITIS. 
action is seldom excessive,and is generally diminished,while thesensory 
impression is commonly painful from the hyperaesthesia. Some other 
symptoms are also of value as indications of tabes rather than neuritis, 
—an affection of the sphincters; a sense of constriction round the 
trunk (which may be felt over a wide area as a band rather than as a 
cord) ; and lastly (but among the first in importance), the reflex action 
of the pupil to light is often lost; scarcely ever in neuritis. Since it may 
be normal in tabes, its loss is of more significance than its presence, but 
the cases of tabes in which it is preserved form only a small minority, 
so that its preservation is often at least corroborative evidence that 
the case is one of polyneuritis. Mental change is of little value in the 
diagnosis, unless it is in the form of definite delirium ; but the less 
common symptoms of tabes, if present, often afford proof of the 
nature of the malady, although generally in association with other 
symptoms rather than by themselves. Optic nerve atrophy, for 
instance, is almost unknown in the neuritic pseudo-tabes,” and so 
also are the various “ crises : ” care must be taken not to confound 
the vomiting of alcoholic gastric disturbance with the gastric crises of 
tabes. The trophic changes differ in the two, the tabetic enlargement 
of the bones and disease of the joints are unknown in neuritis ; and 
so, in the former affection, are the simple arthritic adhesions and the 
“ glossy skin ” of the latter. If all the symptoms are considered 
separately for their individual value, and conjointly for their asso- 
ciated significance, it is not often that the observer will remain in 
doubt. 
One other special diagnosis should be mentioned, that for hysterical 
palsy. This occurs chiefly in women when the symptoms are motor 
and are in the legs. When in the arms, the characteristic situation 
of the palsy usually attracts attention and prevents error. A defect in 
the power of extension of the wrist has probably never been met 
with as a consequence of hysteria. Slight ataxy may, however, be 
purely functional in nature, but the knee-jerk is not lost, and if there 
is anaesthesia it is much more extensive in the functional affec- 
tion. 
It is of great importance to know whether the spinal cord is suffer- 
ing as well as the nerves. The following symptoms are those that 
are the most common and important evidence of this complication:— 
(1) Any impairment of the functions of the bladder or rectum—in- 
continence of faeces, retention or incontinence of urine. It is not, 
indeed, improbable that their impairment may form part of the most 
intense form of polyneuritis ; but it is not part of the ordinary pheno- 
mena of the disease; hence, in such cases, these symptoms suggest 
that the disease involves the cord as well as the nerves. It is impor- 
tant to remember that when there is mental change, evacuations into 
the bed are frequently without significance as to the state of the 
sphincters, and are due solely to the inertia of the mind. This is a 
fertile source of error. (2) A distinct sense of constriction, “ girdle- DIAGNOSIS. 
143 
pain,” referred to any part of the trunk, probably always constitutes 
proof of damage to the cord. Of the same significance is sharp pain 
radiating around the trunk at a definite level and not elsewhere. (3) 
An important distinction in alcoholic cases is an unusual distribution 
of the affection, e. g. complete paralysis of all parts of the legs, or 
weakness of the muscles above the knee, and not of those below. Im- 
pairment of sensation up to a certain level on the legs or trunk has 
the same significance; disease of the nerves does not involve those of 
sensation up to a definite level. Bedsores also increase the proba- 
bility that the cord is affected. 
If a case is recognised as one of multiple neuritis there remains 
the question, what is its cause ? In many cases this question does 
not arise, because the cause is obtrusive, and has been recognised as 
one of the elements of the diagnosis; but in other cases the cause 
is not clear, the diagnosis has been made independently of it, and it 
remains to be discovered. For the most part it is only necessary to 
know the various causes in order to determine which is effective in 
the patient under observation, because one or another of them is to be 
discovered without difficulty, and the rest are absent. It may be 
useful, however, to remember that, as a rule, in chronic metallic 
poisoning the arms suffer before the legs, and that in lead 
poisoning the acute paralysis is limited to the arms; in arsenical 
poisoning the affection of the arms is soon followed by that of the 
legs, while in alcoholic cases the legs generally suffer first. In a 
case in which arms and legs are affected simultaneously metallic 
poisoning would be a very unlikely cause. An initial affection of the 
proximal parts of the limbs at the same time as the distal parts sug- 
gests some other cause than alcohol, especially cold or toxaemia. 
Early affection of the muscles of the trunk or of the bulbar nerves 
has the same significance, and so also has severe constitutional 
disturbance at the outset. It must be also remembered, however, 
that alcoholism often co-operates with other causes, especially with 
cold; and it must also be remembered that the inquiry needs to be 
exhaustive before the influence of alcohol can be excluded. This is 
especially true in the case of females, who often obstinately deny that 
which would bring shame upon them. Exposure to cold has gene- 
rally been severe; and if it has not, the co-operation of alcohol is ex- 
tremely probable. Neuralgic pains of irregular distribution in addi- 
tion to the symptoms of polyneuritis should suggest diabetes as a 
cause, but the examination of the urine for sugar should never he 
omitted. When polyneuritis is due to septicaemia this cause may be 
suggested by the fact that the patient is under treatment for some 
surgical ailment; while in all cases of obscure origin inquiry should 
be made for any acute specific disease to which the neuritis is known 
to be secondary, and the fact should be remembered that a consider- 
able interval may separate the two. Some form of toxaemia is always 
suggested by the fact that the onset of the neuritis is associated with 144 
MULTIPLE NEURITIS. 
such pyrexia and constitutional disturbance as indicate an acute 
morbid blood-state. But this diagnosis often rests chiefly on the 
exclusion of other causes ; if these are absent the fact that neuritis is 
known to result from obscure blood-poisons may be allowed weight, 
especially if the symptoms begin in the legs or in all parts of the 
limbs simultaneously, and do not affect exclusively at first the extensors 
of the extremities. Sensory symptoms in these cases at the early 
stage often take the form of tingling and “ numbness,” and the pains 
so characteristic of the alcoholic form are frequently absent, or are 
represented only by dull aching. In slight cases of this type sensa- 
tions of numbness and “pins and needles” in the legs, with readiness 
of fatigue and loss of the knee-jerk, may be the only symptoms. 
The facts that the nature of toxaemic causes is to a large extent un- 
known, and that the poison may probably be acquired from without, 
make it necessary to be prepared to find this cause of multiple neuritis 
under almost any circumstances. Residence abroad should suggest 
an inquiry for exposure to malarial influences. The possible signifi- 
cance of tubercle as a cause should lead to a careful examination of 
the lungs; but the possibility that phthisis may be an effect, and not 
a cause, of multiple neuritis, must be borne in mind. 
Prognosis.—The danger to life is in proportion to the acuteness 
of the malady, to its severity as measured by the extent of the para- 
lysis, and to the degree in which the strength of the patient is 
impaired by other maladies, or by the cause of the neuritis. It is 
important also to remember that when the affection has increased up to 
the time that the patient comes under treatment, it generally does not 
respond immediately to the arrest of its cause, such as the withdrawal 
of alcohol, but continues to increase for two or three weeks. It is 
this temporary progressive tendency that constitutes the graver 
element in the disease, and must be taken into account in every 
initial prognosis. Hence the forecast must be guarded in all cases 
that are severe when the patient comes under treatment, and most 
so if there has been a rapid increase in symptoms that had existed for 
a long time in slight degree. If the extensors of hands and feet are 
powerless, and the muscles connecting the limb with the trunk are 
distinctly enfeebled, unless the disease has clearly begun to lessen, 
there is danger that a further extension may involve the muscles 
of respiration; this is especially great when the muscles moving 
the shoulder are considerably weakened. It obviously follows that 
the danger is still greater if the muscles of the trunk, and especially 
of the chest, have already given evidence of changes in their nerves. 
Pain in the trunk of the same character as that in the limbs is also 
a grave symptom if the motor power of the limbs has become small, 
or the case is one unusually general in its distribution, because 
where the sensory fibres are suffering the motor fibres are in danger 
also. Paralysis of the diaphragm adds considerably to the danger, 
and its power should be carefully watched in the manner and with PROGNOSIS. 
145 
the precautions mentioned in the account of its paralysis (p. 27). 
It may become paralysed without the fact coming to the conscious- 
ness of a patient lying quietly in bed, but a slight weakness of the 
intercostals will then cause considerable difficulty of breathing and 
an accumulation of mucus in the lungs, a condition predisposing to 
definite bronchitis, by which the patient may be quickly suffocated. 
The importance of this point is great, since respiratory palsy is one of 
the most common immediate causes of death. It is probable also 
that deficient breathing power is one of the causes, perhaps even the 
chief cause, that leads to the development of the qhronic phthisical 
lung disease that comes on in so many prolonged c&ses. Especially 
important, also, is any indication that the nerves of the heart are 
suffering. In an acute increase due to continued use of alcohol, the 
vagus sometimes suffers severely before other nerves, and increasing 
frequency of the pulse is then of most serious significance. The 
prognosis should be guided by the motor rather than by the sensory 
symptoms. The latter may improve while the former increase, with- 
out lessening the gravity of the latter indication. Persistent oedema 
is of bad omen, and so also are other indications of considerable 
blood-change. 
When once the malady has become stationary, and its cause has 
definitely ceased, the danger to life is small, except in severe cases, 
in which the pains are intense, the patient helpless, or the heart is 
feeble, and the pulse persistently frequent, or there are signs of lung 
disease. In these, as in all cases, moreover, the danger is much 
increased by any indication that the spinal cord is involved. The 
tendency to recovery is far less in the cord than in the nerves; and 
retention of urine (with all its secondary consequences), bedsores, &c., 
are prone to occur, and to involve their own danger even if the 
disease in the cord does not increase. The prognosis as regards 
life in cases of moderate severity depends, indeed, as much on com- 
plications as on the state of the nerves. Signs of chronic cerebral 
meningitis, of degeneration of the walls of the heart, of disease of 
the liver and of the kidneys, also lessen the prospect of escape with 
life. 
The danger is, however, greatest, and the mortality highest in the 
acute cases that are due to some toxsemic state or to cold, and it must 
be estimated by the rapidity with which the paralysis develops and 
spreads. Whenever it becomes considerable in a few days, the danger 
of early extension to the mechanism for respiration is very great. In 
these cases, also, pneumonia frequently occurs, concomitant with the 
early symptoms, and few cases thus complicated recover. 
In cases that are not fatal, the full development of the symptoms is 
followed by a stationary period which lasts for one or two months 
before improvement begins, and for this the patient or friends should 
be prepared. The course of restoration is always extremely slow; the 
muscles least affected regain power in from two to four months, but 
YOL. I. 146 
MULTIPLE NEURITIS. 
it is usually six months or more from the onset of improvement before 
the extensors are fairly strong, if their palsy was considerable or com- 
plete. The intrinsic muscles of the hand are still longer in recovery. 
The improvement in the nutrition of the muscles follows that in 
their power, so that they remain smaller than normal, long after 
they have regained strength. It may indeed be years before the 
muscles whose size can be well seen, such as the abductor indicis, 
are of normal size. It is seldom that any permanent weakness is 
left unless the spinal cord is diseased, and when a patient is distinctly 
improving a good ultimate prognosis may be given, provided there are 
no complications to interfere with it. In no case with distinct spinal 
symptoms can we feel confident that restoration of power will be 
complete; and in cases in which there are indications of considerable 
damage to the cord, it is almost certain that some lasting weakness 
will be left. 
The electric irritability of the muscles and nerves may be expected 
to return to the normal more slowly than their capacity of response to 
the will, but sooner than their nutrition. The conditions that are 
observed in these cases are the same as in the isolated form of 
neuritis, in which, although the primary change is in the connective 
tissue, the symptoms depend on the secondary changes in the nerve- 
fibres. Hence the statements made on p. 69 are equally applicable to 
multiple neuritis. The reactions often furnish important infor- 
mation, especially soon after the onset; the more the irritability 
deviates from the normal the greater will be the subsequent wasting 
and the longer the duration of the palsy. When some faradic irrita- 
bility returns in both nerve and muscle, it may be regarded as 
a sure indication of advancing restoration of structure, which is certain 
to involve a progressive increase of conduction of voluntary impulse, 
and response to it. If the trunk nerves are not involved, the prog- 
nosis in severe cases is a little better when the arms are chiefly 
affected than when the legs have suffered most. 
The sensory disturbance may be expected to follow a course, on the 
whole, similar to that of the motor symptoms. A diminution in the 
spontaneous pain may be anticipated sooner than in the tenderness of 
the nerves and muscles, which usually lasts, in lessening degree, until 
the muscles have l'egained some power. The extreme tenderness, 
indeed, passes away with the spontaneous pain, but some degree of 
over-sensitiveness continues for a long time. Happily the tendency 
to persistent neuralgia, seen after the isolated form, need not be antici- 
pated after multiple neuritis. We find the explanation of this in 
the absence of the new formation of connective tissue from the 
inflammatory products, which in the isolated form perpetuate, by cica- 
tricial contraction, the irritation to which inflammation gave rise. 
There is little difference in the prognosis as regards recovery, in 
the different forms of neuritis. The anticipations that may be formed 
are governed in all by the rules just mentioned, and the risk to life TREATMENT. 
147 
lias been already considered. In all, however, it may be repeated 
the extent to which the cause is under control forms an essential 
element in the problem, and must influence the conclusion in every 
case. The prognosis, however, is better in the sensory than in the 
motor form, better when the arms escape than when all the limbs are 
involved, and better in cases of chronic than of acute onset, and 
better if an apparently acute onset is really such than if it succeeds 
slight symptoms of longer duration. When the malady follows an 
acute specific disease, the severity of the latter is no guide to the 
course of its sequel; severe neuritis may follow a mild attack of the 
acute specific. 
Treatment.—The different classes of multiple neuritis here con- 
sidered need treatment that in some respects varies, and in others is the 
same in all forms. In all it is essential to discover, if possible, the 
cause of the neuritis, and to remove it or arrest the continuance of its 
action. This obviously should be the first consideration in cases due 
to alcohol, in which it is sometimes of great difficulty. It is desirable, 
as a rule, that alcohol in all forms should be given up entirely, but often 
this has to be done by degrees, a great reduction in amount preceding 
entire abstinence from it. With patients who are “ their own masters ” 
the reduction is often most difficult to secure, and it is necessary 
to give a warning that not only will life be in danger, but that the 
pains will certainly increase, and continued indulgence will entail 
sufferings so great that any sacrifice would be made, or depri- 
vation endured, if their intensity could be realised. With every 
female drinker, deception should be considered not only possible but 
probable ; those who are under the control of relations or of a husband, 
have generally had a long training in duplicity in order to procure 
stimulants, and it is easy for them to continue it, even when kept in 
bed, if they are attended by their own servants. These are corrupted, 
and alcohol is taken in secret when the fact is being stoutly denied. 
If a case does not present the arrest or improvement that might 
reasonably be expected from the withdrawal of the cause, such con- 
tinued drinking should always be suspected. Hence it is of great 
importance that such patients should be, whenever practicable, under 
the immediate care of trustworthy trained nurses, rather than of their 
own servants or of relatives who may be improperly influenced or 
persuaded; if the patient’s means do not permit this, removal to a 
hospital or some public institution is desirable. When the heart is 
too weak to permit the entire withdrawal of stimulants, the amount 
taken must be regulated solely by the state of the pulse. In such cases 
total abstinence is attended with some danger of the cardiac failure 
which has been mentioned as one of the causes of death. When the 
disease is due to cold, the patient should be carefully preserved from 
risk of further exposure, which, during the early stages, may convert 
a slight into a severe attack. Even in alcoholic cases, a chill will cause 
a rapid increase in the symptoms, and both this and fatigue should 148 
MULTIPLE NEURITIS. 
be carefully guarded against. In other forms, also, these measures* 
adopted in the stage when pains and tenderness are the only or chief 
symptoms, would often prevent the further development of the disease. 
Physical rest is of great importance, and in all cases, except the 
slightest, rest in bed is desirable. The excitation of the nerves 
caused by movement tends to intensify the morbid process in them, 
and so does whatever produces pain. If the patient is in bed, local 
treatment can be more readily employed, and the restraint facilitates 
the necessary control over habits. The feeding of the patient is 
an important part of treatment, especially when the stomach has been 
deranged by alcohol. At the outset, warm fomentations should be 
applied over any tender nerves. Care must be taken in their use 
over the region supplied by the affected nerves, on account of the 
danger of vesication ; troublesome ulcers may be caused by even 
moderate degrees of heat, as in the case mentioned on p. 62. Such 
applications, and also counter-irritants, have less effect in the 
parenchymatous forms than when there is a tendency for the connec- 
tive tissue and sheath to suffer, and for their vessels to be involved 
in the process. A warm bath, for fifteen or twenty minutes daily, is 
often of service if the patient is able to bear the necessary pro- 
cedures. 
Care should be taken that the patient does not habitually assume a 
posture that will promote the occurrence of deformitn s. The drop- 
ping of the feet is the greatest danger, and should be prevented by a 
large and heavy sand-bag about nine inches in diameter, which may 
be adapted to the position of the feet, or by a board placed across the 
bed. Another danger is the habitual flexion of the knees, permitting 
a contraction of the hamstring muscles, and due to the discomfort 
that is caused by extension of the knees ; this should, however, be 
insisted on because the initial discomfort soon passes away if 
extension is adopted from the outset. The extension of the knees 
involves that of the hip-joint, and prevents contraction of its flexors. 
No drug has any very marked influence on the morbid process. It 
has been seen that multiple neuritis tends to lessen after its cause has 
ceased to act, and under such conditions it is easy to come to the con- 
clusion that drugs do good which merely do not hinder. Mercury, 
which is certainly useful in isolated perineuritis, has little influence 
on the parenchymatous form, but it may be tried in any ease in 
which it seems probable that the sheaths are primarily affected, and 
in which pain and tenderness of the larger nerve-trunks is a pro- 
minent symptom. Dui’ing an acute febrile onset the treatment 
should be that adapted to the general state, and must differ according 
to it* cause. In such an onset of an alcoholic neuritis, citrate of 
potash, nitrous ether, and compound tinct ure of cinchona are suitable, 
with a little digitalis if there is feebleness of the pulse. When due 
to cold, salicylate of soda may be given, or, if the attack has been 
predisposed to by alcohol, salicylate of potash may be substituted so TEEATMENT, 
149 
as to avoid the retention of uric acid in the system by the soda. The 
probability of a gouty state of the system should be remembered in 
all cases in which there is a history of alcoholism. In the toxaemia 
forms in which there is a suspicion of a blood-state allied to that of 
septicaemia, no drug affords such a prospect of influence as the tinc- 
ture of the perchloride of iron in full doses, 20—30 minims three or 
four times a day. Afterwards, when the actual onset is over, and 
from the first in the more chronic cases, tonics answer best—iron, 
quinine, or small doses of strychnine. Iodide of potassium, for some 
reason, seems to do good only in the chronic sensory form. In this 
also arsenic has been found useful, but arsenic should be given with 
caution, and in small doses; there is some danger that large doses 
may intensify the malady, since polyneuritis is one of the effects of 
chronic poisoning by arsenic, and has actually been produced by the 
medicinal use of the metal. Cod-liver oil is useful in the later stages, 
especially if there is impairment of general nutrition. In alcoholic 
cases, the addition of cocaine, to grain to each dose of whatever 
is taken, aids in lessening the craving for stimulant. When due to 
malarial poisoning, quinine may be given freely. The complications 
of multiple neuritis do not need other treatment than that suitable to 
them when they occur alone, nor do they indicate any special modi- 
fication in the treatment of the disease of the nerves. 
In most cases the pain is such as to render anodynes necessnrv. 
Of these, morphia, by hypodermic injection, is the most effective, but 
should be employed only as a last resource, and so regarded, will not 
often be found necessary. Its danger is the readiness with which 
those persons who were previously alcoholic become habituated to it. 
It may be given by the mouth with less risk, but in other drugs we 
may find a substitute that is effective in most cases. Injections of 
cocaine beneath the skin over the seat of pain often afford consider- 
able relief, and cocaine may thus be given instead of by the mouth, 
securing the double object of lessening at once the local pain and 
the craving for stimulant—which is relieved almost as effectually 
when cocaine is given by the skin as by the mouth Atropine may 
also be given hypodermically. In antipyrine and acetanilide we have 
drugs of another nature, that often give great relief to spontaneous 
pain. Indian hemp may also be given regularly without harm, and 
without interfering with the occasional administration of other ano- 
dynes ; while to procure sleep, if pain is slight, reliance may be placed 
on bromide, sulphonal, or chloralamide. Antipyrine also often gives 
a patient a good night in spite of some pain. When there is mental 
excitement, hyoscine is useful, especially by hypodermic injection in 
doses of to xio of a grain. 
The application of electricity to the paralysed muscles is important 
in order to maintain their nutrition in as good a state as possible 
during the process of recovery of the nerves. Only voltaisin has the 
power of doing this, and should be applied daily, large sponge-holders 150 
MULTIPLE NEURITIS. 
being employed so that the current may reach as much muscular 
tissue as possible; only such a strength should be employed as will 
produce visible contraction and cause no after-pain. Voluntary 
muscular action constitutes a more effective stimulus to nutrition ; 
but if, although the muscle can be put in action by the will, there is 
loss or great diminution of faradic irritability, or an excess of voltaic 
irritability shows that some fibres are in an abnormal state in conse- 
quence of the degeneration of their nerves, voltaism may still be 
applied with advantage. There is no evidence that the application of 
electricity to the nerves has any influence on their regeneration. 
Slight sensory loss is sometimes lessened in the chronic stage by the 
application of faradism by the wire brush. 
The tender limbs may be wrapped in cotton-wool, with or without 
a covering of oiled silk. Massage is of service in the later stages of 
the disorder, for its influence on the nutrition and circulation in the 
affected limbs. An upward movement of the pressing hand helps the 
circulation of fluid in the vessels and in the tissues. It cannot be 
borne during the acutely painful stage, and, indeed, as long as it gives 
pain, it probably has more capacity for harm than for good. In 
the later stages it helps to overcome the contracture of the muscles,, 
which should be gently extended at the same time as they are rubbed, 
—pressure, for instance, being made upon the ball of the foot at the 
same time as the calf muscles are rubbed. 
The very long course of all severe cases makes a heavy demand on 
the patience of the sufferer and the perseverance of the medical practi- 
tioner ; but the prolonged convalescence has the advantage, in alcoholic 
cases, of enabling a habit of abstinence to be formed. This, with the 
recollection of what has been endured, renders multiple neuritis more 
often a cure of intemperance than any other of the many maladies to 
which alcohol gives rise. During the slow recovery, the measures 
above indicated—tonics, electricity, and massage—should be con- 
tinued. As already stated, the power of standing is interfered with 
for a time after the muscles have regained adequate strength, bv the 
contraction of the gastroenemii, causing a degree of talipes equinus. 
This is often so considerable as to suggest the desirability of dividing 
the tendo Aehillis, but the operation is seldom if ever necessary. The 
attempt to stand and walk constitutes a powerful means of extension 
of the calf muscles, before which they soon yield sufficiently to permit 
the balance of the body to be maintained, and then progress becomes 
more rapid. The contraction at the knee and hip is more difficult to 
get rid of, but generally yields in time to persevering and gentle 
efforts. 
Endemic Neuritis. 
The clear evidence that has accumulated, showing the dependence 
of multiple neuritis on toxic blood-states, some connected with an 
organismal virus, might prepare us to find that it sometimes results MALARIAL NEURITIS. 
151 
from such poisons of endemic character. It is probable that many 
varieties of neuritis of this origin will yet be discovered; at present 
it is proved to be part of only three such diseases,—the malaria of 
remittent fever, leprosy, and the malady so widely prevalent in certain 
regions of the earth, the Kak-ke of Japan, Beri-beri of the Eastern 
Archipelago. 
Malarial Neuritis.—Several cases have come under my notice in 
which persons living in districts in which remittent fever is endemic 
have suffered from weakness in the legs, chiefly in the muscles of the 
foot, and far greater in the anterior tibial group of muscles—the 
flexors of the ankle and extensors of the toes—than in any others. 
In most cases the paralysis of these muscles was absolute, and they 
presented the reactions of degeneration. The hands were unaffected. 
Such palsy is typical of peripheral neuritis. In one case there was a 
suspicion of alcoholic excess, but in the others there was no history of 
this or of any other cause than the exposure to malaria. There was 
slight muscular tenderness in some, but the more acute symptoms had 
had an opportunity of passing away during the long sea voyage to 
England. In all the sphincters were unaffected. The symptoms 
steadily improved, quinine being given and the muscles stimulated 
by voltaism. Contraction of the calf muscles had, however, resulted 
from the foot-drop in all the cases, so that the foot could not be 
brought beyond or up to a right angle; but as soon as the patients 
were able to attempt to stand, this contracture, however great, gradu- 
ally yielded, and all made a good recovery. 
This outline embodies the chief symptoms of the disorder. It 
must be regarded as a peripheral neuritis, involving chiefly the motor 
nerves and confined to the legs, at least in cases of moderate severity. 
It is probably due to the malarial ageut that causes the endemic fever 
of tropical countries—which is presumed to be of organismal nature 
—or to some virus left behind by this. Its occurrence may be aided 
by alcoholism or excited by exposure to cold, but no case came from a 
non-malarial district. How frequent it is we cannot at present say. 
Its nature had not been recognised in any of the cases that have 
come under my own notice, the symptoms having been ascribed to 
disease of the spinal cord. But most physicians who have practised 
iu such districts as those in which it occurs (India, the East Indies, 
coast of Africa, &c.) have recollected such cases when the sym- 
ptoms were described to them, and it may perhaps turn out to be far 
from rare, and to occur also in a more acute and general form, the 
nature of which has also been misunderstood. Its symptoms and 
pathology are of especial interest in connection with the variety next 
to be described. 
Beri-beri, the Kak-kIs of Japan, is also known by other popular 
names in the various countries in which it is native.* Probably many 
* Beri-beri is probably a modification of the Cingalese name for the disease, balir 152 
MULTIPLE NEURITIS. 
names and localities remain to be discovered, or rather identified, for 
it is a mysteriously wide-spread disease, having apparently its chief 
homes in Japan, the Eastern Archipelago, India, New Zealand, 
Ceylon, the South Pacific Islands, and the coast of Brazil. 
It is especially prevalent in the Dutch East Indies, among the 
soldiers and in the prisons, and this has led to its systematic investi- 
gation under the direction of the Netherlands Government. Through 
this our knowledge of the malady has been much increased, especially 
by the investigations of Pekelharing and Winkler,* who had a large 
number of cases under their observation both during life and after 
death. Opinion as to its nature and cause has varied much, and still 
is far from uniform among those who have studied it; but there is a 
strong preponderance of evidence that it depends on a specific organ- 
ism, and that symmetrical peripheral neuritis is the common effect of 
the virus, and the mechanism by which its chief symptoms are pro- 
duced. The organisms found f are in the form of rods and cocci, but 
it is probable that these are only different stages in the development 
of the same species. They have been cultivated, and peripheral 
neuritis of nearly the same distribution as in beri-beri has been pro- 
duced by their inoculation. Repeated inoculations are, however, 
necessary for this result to be produced; and hence, from this and 
the phenomena of the disease, it is assumed to be not a simple infec- 
tious malady, capable of being induced by a single exposure to its 
cause, but one in which repeated opportunities for infection are neces- 
sary. In harmony with this are the facts that sufferers acquire the 
disease from residence in certain infected houses, or places in which 
it is supposed that the soil is saturated with the organisms; that they 
may rapidly recover on removal to a district that is free, and relapse 
only on returning to an infected place ; that it prevails where persons 
are gathered together, as in barracks and prisons; and that the air of 
these places is found to contain the organisms which, collected from 
it, will cause the disease in animals, from whom it is transmissible to 
bari = extreme weakness. Kak-ke is the old Chinese name for it, by which it is 
mentioned by their medical works since 200 B.C.; it is derived from two words, 
meaning "legs” and “disease.” The affection disappeared from China two cen- 
turies ago, remaining in Japan, where it continues a most serious endemic malady. 
* Pekelharing and Winkler, 4 Onderzoek naar den aarden de oorzaak der Beri- 
beri,’ Utrecht (sep. publication), 1889, analysed in the ‘Centralbl. f. Nervenkr.,’ 
1889; also ‘Weekblad f. Nederl. Geneesk.,’ 1888, and ‘Dent. med. Wochenschr.,’ 
1888, No. 30. Other important contributions to the subject are by Balz, 
* Zeitschr. f. kl. Med.,’ 1881; Scheube, ib., 1882; Weintraub, ‘Wien. med. 
Wochenschr.,’ 1888, Nos. 23—44; Van Eecke, * Tijdschr. v. Nederl. Indre,’1887, 
p. 71; Wernich, ‘Virchow’s Archiv,’ Bd. Ixxi; Minra, ‘Virchow’s Archiv,’ 
Bd. cxi and cxiv, whose conclusions, however, differ from those of most investi- 
gators; Segnin, ‘Phil. Med. and Surg. Rep.,’ 1888; and Springthorpe, ‘Australian 
Med. Journal,’ 18S9. Balz, in 1881, expressed the opinion that the disease was 
a specific "panneuritis.” 
t First described by Balz and Scheube, and since by Pekelharing aud Winkler, 
Eigkman, Weintraub, Springthorpe, and others. 153 
MALARIAL NECTRITIS. 
others by further inoculation. The serious extent to which it may 
spread among those who live together under conditions favouring its 
extension, is shown by the instance of a ship arriving in Japan from 
New Zealand after a voyage of 272 days. The disease spread on board 
so rapidly that altogether 169 cases occurred, with twenty-five deaths. 
In 1878 no less than 38 per cent, of Japanese soldiers were affected. 
It is probable that the inhalation of dried organisms floating in the 
air as part of “ dust,” is the chief way in which the disease is pro- 
pagated. By some it has been thought that a nitrogenous diet induces 
or predisposes to the disease, and facts apparently supporting the 
opinion have been adduced; an exclusive fish diet has been thought 
to cause it, and so also has a rice diet. A remarkable outbreak in 
Manila in 1880 followed a period of rice-eating during a cholera 
epidemic. These influences probably merely produce susceptibility. 
It is a remarkable fact that Europeans seldom suffer. Males are 
more liable to the disease than females, and it is chiefly prevalent 
during the hot season. 
Symptoms.—Peripheral symmetrical neuritis is a constant feature 
of the malady, which is usually chronic in course and gradual in 
onset, but prone to undergo acute exacerbations. These have been 
generally regarded as acute forms of the disease, but it is said by 
Pekelharing that the symptoms of neuritis may always be discovered 
before the onset of the definite symptoms, and this when the patient 
is ignorant of their existence and feels quite well. Most observers 
have failed to recognise this, and it is probably true only under 
certain conditions, and persons suddenly exposed to an intense infec- 
tion may suffer acutely from the very commencement. Occasionally 
the malady develops with extreme rapidity and severity. On the 
other hand, many cases are chronic throughout, and last for 
months. The leading symptoms are those of multiple neuritis (chiefly 
affecting the legs and the cardiac branches of the vagus), dropsy, 
and symptoms of cardiac failure. The amount of urine is generally 
lessened, and its secretion may be almost suppressed in acute cases. 
A “ critical ” increase in the secretion may mark the commencement 
of improvement. It is unchanged in character, and does not contain 
albumen. The dropsy is a very variable symptom, and this has led to 
the distinction of two forms, the dry and the dropsical. Pekelharing 
and Winkler, however, found some effusion of fluid almost invariably 
after death, and it is probable that its conspicuous presence or absence 
depends chiefly on the state of the heart (conditioned by that of its 
nerves), and partly on the tx*ophic and vaso-motor disturbances due to 
the local neuritis. 
The earliest symptoms are a change in the electrical excitability of 
the peroneal nerves and the flexors of the ankles (which suffer most 
throughout)—a slight degree of the reaction of degeneration, quantita- 
tive and often qualitative. These are often to be found before there 
are any subjective symptoms, which begin as a sense of heaviness of the 154 
MULTIPLE NEURITIS. 
legs, readiness of fatigue, dysaesthesiae and diminution of tactile sensi- 
bility in the lower legs, palpitation and undue excitability of the heart. 
The electrical changes may be met with in slight cases which pro- 
ceed no further,* and have shown that some patients, supposed to be 
shamming, were real sufferers. To these subjective symptoms are 
added other objective signs,—oedema along the edge of the tibiae, a 
peculiar pasty and stiff aspect in the face, an increase in the cardiac 
dulness to the right, roughness of the first and accentuation of the 
pulmonary second sound. These symptoms may increase slowly, or 
rapidly in the form of an acute stage. The degenerative reaction 
becomes complete in the muscles first affected, and they become para- 
lysed and undergo the characteristic atrophy, while other nerves and 
muscles progressively suffer in the same manner, the calf muscles, the 
extensors of the knee, the adductors of the thigh, and, lastly, the 
flexors of the thigh and the abductors of the hip. In the trunk the 
abdominal muscles and intercostals may be involved, and in severe 
cases the arms are paralysed, first the extensors of the wrist and fingers, 
later the flexors, and sometimes most of the muscles may be so atro- 
phied as almost to disappear. The face often suffers: the diaphragm 
may become paralysed, and also the larynx (the inferior before the 
superior laryngeal nerve) ; while grave cardiac weakness and increas- 
ing dilatation of the heart testify to the serious implication of the 
cardiac branches of the vagus. Simultaneously, sensory symptoms 
develop, corresponding in distribution to the more severe motor sym- 
ptoms ; sensibility to touch is lessened or lost (first on the inner side 
of the lower leg), while that 1o pain usually remains, and sometimes 
is augmented to the degree that constitutes what has been termed 
“anaesthesia dolorosa.” The temperature-sense may be diminished 
to either heat or cold or both in various parts, and there is often con- 
siderable loss of cutaneous sensitiveness to faradism. There may be 
tingling, formication, and other dysaesthesiae, together with tenderness 
of the nerves and muscles, but far less in degree than in most forms 
of polyneuritis, and chiefly marked in the early stage of the disease. 
The oedema that is so common begins in the legs, usually 
spreads widely, and involves not only the subcutaneous tissue but 
the cavities of the peritoneum, pleura, and pericardium : in the 
last it seriously impedes the action of the already dilated and feeble 
heart. It is to the cardiac failure that death is commonly due ; the 
other chief cause is failure of the respiratory muscles, aided generally 
by effusion into the pleural cavities, and accompanied by the 
indications of cardiac weakness, and of dilatation of the right side 
of the heart. From this cause the cardiac duluess sometimes increases 
rapidly, even in a few hours. The cedema is usually attended by 
increasing anaemia, which doubtless facilitates its occurrence. These 
symptoms are always later in development than are those due 
directly to the neuritis. In the most acute cases the definite symptoms 
Pekelliaring and Winkler, Eigkman (1889), &c. MALARIAL NEURITIS. 
155 
take commonly six or eight weeks to run their course, and the usual 
duration of the malady is several months. Death from the heart 
failure is usually prolonged, and accompanied by much distress. 
Occasionally a very acute form prevails, in which rapid failure of the 
heart and various effusions lead to death in about a fortnight, and 
cause a mortality of 60 and 70 per cent. 
Pathological Anatomy.—The only constant changes are in the 
nerves, but some serous effusion is almost invariable. Thus Pekel- 
haring and Winkler found an excess of fluid in the cellular tissue 
in 83 out of 85 cases—about 97 per cent. The pericardial fluid was 
increased in 67 per cent, of the cases, in about 23 per cent, there 
was hydrothorax, and ascites in 14 per cent. 
The changes in the nerves are often indistinct to the naked eye, 
although always conspicuous under the microscope. They are met 
with in both motor and sensory branches, and, in advanced cases, in 
the nerves of the vessels. They are always greatest at the terminal 
portions, lessening upwards, while the nerve-roots and spinal cord 
are always normal, with the doubtful exception of vacuolation of the 
motor cells,* and some degeneration,of the fibres of the posterior 
column in a few cases.f The first change is an increase in the seg- 
mental nuclei, shrinkage of the medullary sheath at the nodes, and a 
peculiar “ lumpy ” degeneration of the medulla, sometimes replaced 
by a “foam-like ” appearance in it, concealing the axis-cylinder. Both 
changes are often accompanied by the formation of granule corpuscles. 
These slighter changes are found chiefly where the lesion is commenc- 
ing, and especially in the vagus and phrenic nerves, in which, neces- 
sarily, a considerable degree of change is incompatible with life. 
They have been seen in the branches within the heart, in some of 
the fibres of the trunk, and in the lai'yngeal nerves. Where the 
change in the nerves is more advanced, the white substance is 
entirely broken up, and the axis-cylinder presents segmentation or 
irregular swellings, or has disappeared, and the increase in the nuclei 
of the neurilemma sheath is still greater than before. The blood- 
vessels of the nerves are but little changed in the early stage; after a 
time they may present some thickening of the wall, accompanied by 
a general increase in the amouut of the interstitial tissue; but, as 
a rule, there is an absence of any signs of interstitial inflammation— 
the changes are essentially parenchymatous. 
In the muscles there may be at first a cloudy opacity with indis- 
tinctness of the transverse striae, going on to granular degeneration; 
or the fibres may simply become narrow, preserving their striation. 
The nuclei of the fibre-sheath are always increased in number, but 
the interstitial tissue is generally but little altered. 
Pathology.—The characteristic organisms have been invariably found 
in the blood, and, what is a remarkable instance of their slow action, 
* Minra, loc. cit. 
f Van Eecke loc. cit 156 
MULTIPLE NEURITIS. 
and of the cumulative influence needed to generate the malady, 
Pekelharing and Winkler* found them in the blood of all the 
inhabitants of an intensely infected place, whether these had or 
had not symptoms of the disease, and failed to find them in the blood 
of persons living in places free from infection. Cultures from the 
blood reproduce the malady, and so do cultures from the animals 
thus infected. The organisms have not been found in special associa- 
tion with the morbid process in the nerves. It thus appears that the 
malady bears a close resemblance, in its essential features, to cases of 
multiple neuritis due to a chronic blood-poison such as alcohol, and 
still more to that which, as we shall see, is presented by chronic 
arsenical poisoning. There is a slow accumulation in the blood of a 
virus that has a specific action on the peripheral nerves, and like some 
others, first and chiefly on the nerves of the legs, but with a greater 
affinity for the vagus, especially for its cardiac branches, than most 
others. Although invariably associated with the presence in the blood 
of a special organism, the absence of this in the vicinity of the lesion, 
taken in conjunction with modern researches in bacteriology, makes 
it probable that the virus is a chemical substance produced bv the 
organism in its growth. This brings the disease into close affinity 
with some other forms of multiple neuritis, on which it throws suffi- 
cient light to justify this somewhat full account of a malady that is not 
likely practically to concern many readers. If we regard, as appa- 
rently we must, the cardiac failure as the result of the cardiac neuritis, 
and the dropsical effusion as the combined result of this and the local 
trophic and vaso-motor influence of the neuritis (to which, perhaps, 
the change in the blood should be added), we have a remarkable illus- 
tration of the extent, variety, and degree of the secondary processes of 
disease which multiple neuritis may produce. 
The Diagnosis can only be a matter of difficulty in a very early 
case, or in a patient who is not known to have been exposed to 
the infection, or in consequence of ignorance of the disease. Doubt 
may exist, however, whether in a given case the malady is alcoholic 
neuritis or beri-beri. The former is probable if the arms are involved 
at the same time as the legs, still more if they suffer first; also if 
pains are severe, oedema absent, and the heart unaffected. The con- 
verse would make the endemic malady probable. Beri-beri has cer- 
tainly been intensified by alcohol in some cases, and the symptoms 
then presented are a combination of the two,—pains, associated with 
the weakness and enlargement of the heart and the wide spread 
tendency to dropsical effusion met with in beri-beri. In most cases some 
other indication of the influence of alcohol, especially enlargement of the 
liver, will assist the diagnosis. From other forms of multiple 
neuritis it is unlikely that the diagnosis would have to be made. 
From affections of the spinal cord the distinction (chiefly needed in 
* Also Ogata (1888) and others. They have also been found sparingly in tho 
organs, even in the spinal cord, which is commonly free from disease. LEPROUS NEURITIS. 
157 
the chronic “ dry ” variety) depends on the points already mentioned 
in the account of multiple neuritis. Acute cases with much oedema 
and weakness of the heart, and enlargement of the right side, may be 
mistaken for primary heart disease ; but if the symptoms of beri-beri 
are known, the affection may be recognised by the absence of anv 
indications of primary valvular disease ; while an examination of the 
legs will reveal the weakness of the flexors of the foot and lessened 
tactile sensibility in the skin over them. 
Treatment.—Beri-beri is one of those diseases for which it is 
probable that a method of at least prophylactic inoculation will be 
discovered in the future. At present the destruction of the organisms 
bv disinfecting agents, or, better, the removal of a person to an unin- 
fected district, constitutes the only means of preserving him from the 
continued entrance of the poison—a measure essential for successful 
treatment, and, in many cases, all that is really necessary. The 
limits of disinfection are, however, reached with the dwelling-house; 
and the great difficulty presented by the disease is the manner in 
which whole districts are capable of giving rise to it, probably by 
the infection of the soil, which cannot be rendered innocuous. 
However, even within the narrow limits of personal use, disinfection 
has achieved some remarkable results, and in few diseases has the 
light of pathology given more useful guidance to the hand of the 
practitioner. 
In most respects the treatment of the symptoms of beri-beri does 
not differ from that of alcoholic neuritis. A special point, however, 
is that the strengthening of the heart by digitalis or strophanthus is 
more often of urgent importance, and requires greater care lest the 
feeble fibres be overtaxed. Small doses should therefore be given— 
three or at most five minims of the tincture of digitalis. Bodilv 
rest is of paramount importance to the weak organ, in order that 
there may not be any demand on its energies for other work than 
that involved in the maintenance of what may be termed static 
nutrition, and that it may be spared the increased work necessi- 
tated by muscular exertion. Strychnia, quinine, &c., may do good, 
but their use in this disease does not differ from that in the more 
common forms of multiple neuritis. 
Leprous Neuritis. 
Far removed as leprosy may seem to be from tbe malady last 
described, both by its general character and extremely chronic course, 
it is certainly also an endemic disease ; its cause must be sought 
in local influences; and it agrees with beri-beri in the nature of that 
influence. Since the researches of Carter, Hansen, and Neisser have 
proved the constant presence of a specific bacillus in all the new forma- 158 
MULTIPLE NEURITIS. 
tions met within the disease, their observations have received abundant 
corroboration; the disease was indeed one of the first to be proved to 
depend on living organisms. The virus resembles that of beri-beri in 
being transmissible from individual to individual, but differs in its 
capability of passage by inheritance, in the less readiness with which 
it passes from person to person, and in the extreme slowness with 
which it commonly develops to the degree necessary to cause 
symptoms. Tears may elapse after the last possible exposure, 
before distinct symptoms of leprosy appear. In the case from which 
Fig. 62 was taken the sufferer was a European of healthy parentage, 
who could not have been infected within ten years of the first sym- 
ptoms. In one case of infection from adult to adult, nine years 
elapsed after the death of the leper before the man who had lived 
with him began to suffer. When, indeed, a large quantity of the 
virus is received, the malady develops much more rapidly. But 
leprosy differs from beri-beri, and from most other forms of multiple 
neuritis, in the fact that although inflammation of many nerves is 
frequently a part of the disease, it is not an essential part or a 
constant feature of the affection. On the contrary, it is only one 
of an extensive series of lesions, inconstant, not only in its occur- 
rence, but in its seat and extent. It characterises a special variety 
of the disease, the “ anaesthetic leprosy ” in which not only areas of 
the skin become insensitive, but the ends of the fingers may suffer 
such an impairment of their nutrition that they are lost. Moreover, 
as we have seen in the introductory section, the want of strict sym- 
metry is associated with an important difference from the symmetrical 
forms—the neuritis is not a parenchymatous or degenerative form, 
but is a perineuritis and interstitial neuritis, and the damage to the 
fibres is secondary. This change in the connective tissue is asso- 
ciated with the actual presence of the organisms in it. The neuritis 
thus seems to be due to the direct action of the bacilli on the affected 
tissues, and not, as in beri-beri, to a virus circulating in the blood— 
not to a product of the organisms, but to the organisms themselves. 
This fact enables us to understand better its peculiar features, and 
especially its irregular distribution; the inflammation occurs where 
the organisms happen to fix themselves in the connective tissue, and 
although certain common conditions on the two sides may determine 
a partial correspondence in the nerves affected, there is not the sym- 
metry that results from an action on like structures on the two sides, 
equally accessible to the virus. In this, and in its connective-tissue 
seat, the neuritis of leprosy resembles the more isolated neuritis of 
syphilis, rather than the common varieties of the multiple form. 
The symptoms of the malady are extensive and various, but only those 
that consist in derangement of the functions of the nervous system 
concern us here, and it is alike needless.and impracticable to describe 
the others. The nervous symptoms of leprosy depend almost exclu- 
sively on inflammation of the nerves. These symptoms are muscular LEPROUS NEURITIS. 
159 
■wasting and anaesthesia, greatest in degree towards the extremities of 
the limbs, bnt more or less irregular in situation and in the region of 
the distribution of nerve-trunks, which, if accessible, are obviously 
diseased. The symptoms are not confined to the limbs, but are also 
met with in the face, where an affection of the fifth nerve may cause 
anaesthesia, and movement may suffer from involvement of the trunk 
of the facial nerve, so that the eyelids cannot be completely closed. 
The form of sensibility that is impaired also varies ; sometimes touch, 
sometimes pain is lessened in greater degree, but usually all forms are 
implicated to some extent. The legs often suffer before the arms, but 
a special order of affection cannot be distinguished. There may be 
unpleasant tingling sensations, but pains are usually trifling, perhaps 
because the process is extremely chronic. In some cases there may 
be severe pain in the position 
of the nerves or deeply seated in 
the limbs. The inequality of 
the affection of the fibres of the 
same nerve is shown by the fact 
that the knee-jerk may persist 
although the extensors of the 
knee are partially paralysed. 
Fig. 61 shows the distribution 
of anaesthesia in the hands in 
a well-marked example of this 
disease which came under my 
observation some years ago. 
The patient was a creole of 
Mauritius, who had come to 
England in early childhood, and 
presented the first distinct sym- 
ptoms at twelve years of age— 
changes in the pigmentation of 
the skin, anaesthesia, and mus- 
cular wasting. They steadily 
increased during the next four 
years, the anaesthesia extending 
each half-year from one finger to another. There was also scattered 
anaesthesia of the legs below the knee. As the figure shows, the loss 
of sensation does not correspond in area to nerve distribution. This 
depends on the fact that even when all the nerves, including those 
of the fingers, are diseased, all the fibres may not be destroyed in any 
one nerve, so that some sensibility exists in each nerve area. Various 
perversions of sensibility, spontaneous “ dysaesthesiae,” tingling, 
formication, and the like, may precede the loss. The latter usually 
occurs gradually, but sometimes so suddenly as to suggest some 
secondary vascular lesion, haemorrhage or thrombosis, in the vessels 
of the nerve that is the seat of the process—a possible result in its 
Fio. 61.—Distribution of anae«tbesia in a 
case of leprosy. The black areas indicate 
the loss. 160 
MULTIPLE NEURITIS. 
early and most active stage. It must be remembered that in all 
inflammations of the slieatb and interstitial tissues this proceeds to 
a considerable degree before tbe fibres of the nerve suffer, and thus 
sudden loss of sensibility does not show that the nerve was previously 
healthy. This occasionally sudden onset is of much practical import- 
ance ; one case was sent to me from a place in which the disease is 
endemic, by a doctor well acquainted with it, who had not suspected 
leprosy because the anaesthesia came on almost suddenly. 
Accompanying anaesthesia there is usually some muscular wasting, 
which may be great. In the case figured it was considerable, although 
only in the small muscles of the hands was it comparable to that of 
progressive muscular atrophy. The electrical excitability of the mus- 
cles was greatly lowered to each current, and this is perhaps the most 
common condition ; either the damage to the nerves is so chronic that 
the fibres undergo slow changes pari passu with those in the nerves and 
their endings, or the patient comes under observation at a late stage 
in the local affection, at which the changes present in the early stage 
have disappeared; sometimes, indeed, all irritability has vanished. 
In cases that are seen soon after the onset of the lesion of the nerves, 
there may be the reaction of degeneration in the muscles, either partial 
or complete, and there is often a conspicuous exaltation of the mechani- 
cal irritability of the nerve-trunks. When the facial nerves are affected 
this may be well seen, and may resemble that met with in tetany.* The 
thickening of the nerve may be felt when that which is affected is 
accessible. The state of mvotatic irritability varies according to the 
distribution of the neuritis ; it is lost at places where the sensory or 
motor fibres are involved, but those supplying the front of the thigh 
and its muscles often escape, and the knee-jerk is preserved. Anchy- 
losis of the joints may occur, as in other forms of neuritis. 
The “ mutilations ” of lepi-osy, by which the ends of the fingers and 
toes are lost, are also regarded by some as a consequence of the neuritis. 
The numerous other symptoms of the disease are independent of the 
nerves (except perhaps the pigmentation of the skin), and are beyond 
the province of this book. 
The neuritis of leprosy is typically adventitial (Fig. 62). The 
primary sheath and the secondary sheaths of the fasciculi are greatly 
increased in thickness, and consist of nucleated fibrous tissue arranged 
concentrically (a, b). From the sheath, tracts extend into the inte- 
rior of each fasciculus (b), isolating the groups of nerve-fibres. The 
increase of tissue even extends between the fibres themselves (c), aud 
these undergo slow wasting; many of the fibres in the figure are 
seen to be distinctly narrower than normal. The concentric growth of 
fibrous tissue may even invade the whole area of the fasciculus, all the 
nerve-fibres perishing before it (d). The characteristic bacillus of 
leprosy is found abundantly, in recent cases, in the neAv tissue of the 
nerves. Peculiar cells are met with, infiltrated with the organisms. 
* Scliultze, * Deufc. Arch. f. klin. Med./ 1888, 13d. xliii. LEP110US NEURITIS. 
161 
As the fibrous tissue develops and contracts, the bacilli seem to perish,, 
and ultimately can no longer be discovered. 
The diagnosis depends on the occurrence of irregular areas of anaes- 
thesia, generally associated with irregular patches of pigmentation 
and pallor in the skin, and 
often with muscular atro- 
phy, in a person who has 
been exposed to the risk 
of infection, generally by 
having lived in a district 
in which the disease is 
endemic. The irregularity 
of distribution and the 
limitation of considerable 
sensory changes suffi- 
ciently distinguish it from 
other forms of neuritis. 
The spinal affections with 
which the mixed anaes- 
thesia and wasting are 
most likely to be con- 
founded are, as Schultze 
has pointed out, cases of 
syringo-myelia in which 
the distension of the cen- 
tral cavity damages the 
grey matter, and may cause 
similar symptoms of irre- 
gular distribution. But 
these are limited to the 
arms; and if the legs 
suffer it is in a different 
way—as simple paraplegia 
with excess of mvotatic 
irritability that may go 
on to spasm. 
The prognosis of the disease in the simple anaesthetic form is grave 
only when the sufferer is still exposed to fresh infection, or in cases of 
considerable severity. But it must be remembered that, just as the 
disease may develop long after exposure to its cause, so it may slowly 
increase for a long time after this exposure has ceased. 
The treatment of the affection is beyond the scope of this work; in 
so far as the nerve symptoms require special measures, these are the 
same as in ordinary neuritis. A trial may be made of the stimula- 
tion of the muscles by whatever form of electricity they will respond 
to, and of the anaesthetic areas in the skin by the wire brush and 
faradism. 
Fig. 62.—Sections of nerves from a case of anaes- 
thetic leprosy, under the care of Dr. Buzzard, 
A, median nerve at wrist x 5; B, portion of 
same more highly magnified; c, part of a less- 
diseased fasciculus from the ulnar nerve; D, a 
small fasciculus from median in which the con- 
centric fibres have invaded the whole area of the 
fasciculus. 
VOL. I. PART III. 
DISEASES OF THE SPINAL CORD. 
INTRODUCTION. 
ANATOMY OF THE SPINAL CORD* 
The spinal cord, it will be remembered, is much shorter than the 
spinal canal, reaching only to the second lumbar vertebra. Hence the 
nerve-roots descend to their foramina of exit. The lower they arise, 
the longer is their intra-spinal course. All those below the second 
lumbar pair leave the canal below the lowest portion of the cord. It 
is customary to speak of the portion of the spinal cord from which 
each pair of nerves arise as the corresponding “ segment” of the cord. 
The segments are longest in the dorsal region, and shortest in the 
lumbar enlargement. They are also called “ metameres.” 
The only parts of the spinal column that we can usually feel are 
the vertebral spines. Many of these are not on a level with the 
bodies of their vertebrae. It is important, therefore, to know the 
relation of the spines to the bodies of the several vertebrae, and of 
these to the origin of the nerves. These relations are shown in the 
accompanying figure (Fig. 63). 
Of the Membranes, the pia mater closely invests the surface, and is 
continuous with the tracts of connective tissue that pass within the 
substance of the spinal cord. It is also prolonged along the nerve- 
roots as their sheaths. The arachnoid forms a much less close invest- 
ment. The dura mater is not in contact with the bones, as it is m the 
cranium, but a layer of fat and a plexus of large veins intervene 
* The following outline of the anatomy of the spinal cord is intended merely to 
place before the reader those points that are essential, or likely to become so, for 
understanding the functions of the organ and the symptoms of its disease. It does 
not profess to be exhaustive even in outline, and is designedly kept as free as 
possible from whatever, in either the substance or terminology of recent science, 
does not come within the scope of those objects. Many of the results reached 
by modern investigators are mutually incompatible, and where a choice has been 
necessary the observers have been followed who possess the greatest authority 
and whose conclusions best agree with facts previously ascertained. STRUCTURE. 
163 
between the two. It thu3 forms a loose sheath for the cord, 
and variations in the amount of blood in the plexuses outside it 
permit corresponding (but inverse) varia- 
tions of the amount of cerebro-spina 
fluid within it. An extension of the 
•dura mater passes along each nerve-root 
and blends with its sheath. 
Structure of the Spinal Cord.— 
The general form of the cord, the enlarge- 
ments it presents, and its constitution of 
white and grey substance, are too well 
known to need description here. The 
white substance surrounds the grey, ex- 
cept at the two points at which the 
posterior horns come to the surface 
(Fig. 64). It consists of medullated 
nerve-fibres, chiefly longitudinal. The 
posterior cornua isolate the posterior 
columns from the rest of the white sub- 
stance. These columns are separated by 
a “ posterior median septum ” of connec- 
tive tissue, and a little distance from this 
another incomplete septum, “posterior 
intermediate septum,” corresponding to 
a depression on the surface, marks off 
a portion next the median septum, the 
“ postero-median column,” or “column 
of Coll,” from the part next the pos- 
terior horn, “ postero-external column,” 
Fig. 63.—Diagram (framed from an original in- 
vestigation) showing the relation of the verte- 
bral spines to their bodies and to tbe origin of 
the several nerve-roots. It will be seen that 
the ends of the vertebral spines are opposite 
the middle of their own bodies only in the 
lumbar region; they correspond to the lower 
edge of their own bodies in the cervical and 
the last two dorsal vertebrae, and to the upper 
part of the body below in the rest of the 
dorsal region. Each cervical spine is nearly 
opposite the lower roots of the nerve below; 
the vertebra prorainens is opposite the first 
dorsal roots, and from the 3rd to the 10th 
dorsal the spines correspond to the second root 
below; the 11th spine corresponds to the 1st 
and 2nd lumbar nerves, the 12th to the 3rd, 
4th and 5th; the 1st lumbar to the 1st, 2nd 
and 3rd sacral nerves, while the top of the cord 
is opposite the upper part of the 2nd lumbar. 
or “ column of Burdach,” the part of which next the cornu 
is called the “ posterior root-zone,” because many fibres of the 164 
SPINAL CORD. 
posterior root pass through it. The rest of the white substance is 
divided, in the middle liue in front, by the anterior median fissure, 
Fig. 64.—Diagram of a section of the spinal cord in the cervical region. A. C.,. 
anterior commissure; P. C., posterior commissure; I. g. s., intermediate grey sub- 
stance; P. cor., posterior cornu; c. c. p., caput cornu posterioris; L. L. L., lateral 
limiting layer; A.-L. A. T., antero-lateral ascending tract, which extends along the 
periphery of the cord. 
down which the pia mater and blood-vessels pass, and at the bottom 
of which is the anterior or white commissure. Between the anterior 
median fissure and the posterior cornu the white substance is con- 
tinuous and undivided, extending round the front and side of the 
cord. It is artificially divided into an anterior and a lateral column, 
the line of division being the outermost of the anterior nerve-roots, 
which pass through the front of the cord; but there is no correspond- 
ing distinction of structure, and hence it is often termed the “ antero- 
lateral column.” 
The white substance varies in amount in different parts of the 
cord, but, as a whole, lessens gradually from above downwards (see 
Fig. 65). It is everywhere composed of medullated nerve-fibres, 
which, however, possess no neurilemma-sheath. In carmine-stained 
sections the axis-cylinder is seen within each fibre, not always in the 
centre, and around this are concentric cloudy lines due to the irregular 
refraction of the white substance. 
Between the fibres is a peculiar substance, the “ neuroglia ” or 
nerve-cement. It appears to consist of fine fibres, which form a net- 
work, embedded in a finely granular or homogeneous matrix. At 
their intersections are peculiar cells consisting of a nucleus and 
small cell body (“glia-cells,” “cells of Deiters ”). The fibres are 
generally regarded as their processes, but, according to Ranvier and STRUCTURE. 
165 
Weigert, the cells are flattened, without processes. This neuroglia 
is developed from the same (epithelial) embryological elements as the 
nerve-structures—an important 
fact, because it enables us to 
understand the fact that, in de- 
fective development of the nerve- 
structures, the neuroglial tissue is 
excessive in amount. But its differ- 
entiation in development involves 
also its chemical nature, since it 
consists of material like that of 
hair or horn, and hence called 
“neurokeratin.” 
The nerve-fibres, thus con- 
nected, lie in a coarser network, 
formed by branching processes 
of septa that proceed inwards 
from the pia mater. In these 
septa blood-vessels run, and some 
are occupied by nerve-fibres that 
have a horizontal course. The 
septa consist of fine fibres from 
the pia mater and of neuroglial 
material, which forms also a layer 
between the membrane and the 
nerve-fibres in the intervals be- 
tween the septa. This layer varies 
■considerably in thickness. Many 
of the septa pass through the 
white substance to join projec- 
tions from the grey substance, 
which cause the irregularity of 
the outline of the latter. These 
processes, outside the neck of the 
posterior cornu, are bi oad, and join 
each other so as to form a sort of 
network, the meshes of which en- 
close columns of nerve-fibres. This 
is called the “ lateral reticular for- 
mation ” (Fig. 64, right side; also 
65, c, 2—8). The substance of the 
horn behind the caput is sometimes 
broken up in the same way—the 
“posterior reticular formation.” 
The grey substance varies in 
shape and size in different parts 
o£ the cord, being largest in the 
Fig. G5.—Diagram showing the relative 
size and shape of the cord and grey 
matter at different levels. 166 
SPINAL COED. 
cervical and lumbar swellings, and corresponding to tbe number and 
size of the nerve-roots given off. The variations in shape and size 
are indicated in the accompanying figure (65), and will be readily 
understood by an examination of this. The division into anterior 
and posterior horns or cornua is familiar. The part on each side 
that intervenes between the two horns may be conveniently termed 
the “ intermediate grey substance ” (I. g. s. in Fig. 64). In the dorsal 
region a projection from this extends into the lateral column (Fig. 65,. 
r> 2, 5, and 8), and has been termed the “lateral horn”). It is customaiy 
to divide the grey matter into two varieties, “ spongy ” and “ gela- 
tinous.” The latter forms a cap on the posterior horn, and a layer 
immediately around the central canal, and is named on account of 
its naked-eye aspect. The spongy substance, which forms the rest of 
the two cornua, consists mainly of an excessively fine felty network 
of very narrow medullated nerve-fibres, naked axis-cylinders, and fine 
nerve-fibrillse which arise, in part at least, from the branching 
processes of the nerve-cells, and perhaps in part by a division of the 
axis-cylinders of the nerve-fibres. It also contains small cellular 
bodies, which vary in size and shape. Many are angular with pro- 
cesses, and are probably of nervous function. These structures are 
embedded in a supporting neuroglia. Through it course many larger 
medullated nerve-fibres, passing to or from the white columns and 
nerve-roots. In it also lie many nerve-cells of various sizes. Those 
in the anterior cornu are, for the most part, large “ ganglion-cells ;’r 
each contains a large nucleus, and usually a mass of pigment, and 
sends out several processes. One process is continuous with the axis- 
cylinder of a nerve fibre (Fig. 66), and can be sometimes traced into 
a fibre of an anterior root (Fig. 67). The other processes, after a 
Fig. 66. 
Fig. 67. 
G8. 
Fig. 66.—A nerve-cell from the anterior cornu of the 
spinal cord of man: o, unbranclied process becoming 
the axis-cylinder of a nerve-fibre; b, pigment mass. 
(After Gerlach.) 
Fig. 67.—Nerve-cells of tlie anterior cornu sending a pro- 
cess into the anterior root. (After Henle.) 
FiG. 68.—A fine nerve-fibre dividing into two parts, each 
of which joins the plexus of fibrillae formed by the 
branching processes of a nerve-cell. From the spinal cord of an ox. (After 
Gerlach.) STRUCTURE. 
167 
longer or shorter course, divide and subdivide, their ramifications 
being lost in the sponge-like matrix of the grey substance. In this 
they are probably connected with the terminal ramifications of nerve- 
fibres (Fig. 68). These cells lie in groups, between and through 
which course tracts of fibres, chiefly from the anterior roots. Other 
fibres come from the anterior commissure, white columns, and 
posterior horn. The ganglion-cells are certainly motor in nature, 
and give origin to at least most, and perhaps all, of the motor fibres 
of the spinal nerves. Birge, in a careful investigation, found that 
in each segment of the spinal cord of the frog the number of nerve- 
cells in the anterior cornu nearly corresponds to the number of fibres 
of the anterior roots arising from that segment. Each cell is traversed 
by many nerve-fibrillse, such as are discerned in a cell-process or in 
the axis-cylinder of a nerve-fibre. These cross and intermingle in the 
middle of the cell, but pass along the margin from one process to 
another. By this arrangement impulses entering the cell by one 
process may leave it by many.* 
The arrangement of the nerve-cells of the anterior cornu is of some 
practical importance, on account of the frequency with which this part 
is the seat of limited lesions. They form, as already stated, certain 
groups, but these groups vary in different regions of the cord, partly 
under the influence of the shape of the horn, partly irrespective of 
this, and they even vary in parts of the cord that are near together. 
They are influenced by the course of the tracts of fibres of the ante- 
rior roots, which may pass through a group and break it up into smaller 
groups, although in a neighbouring section it is undivided (see Fig. 
69, the cervical groups). Hence very different descriptions have been 
given of these groups, and the process of distinction has sometimes 
been carried too far. The grou ps that can most readily be recognised 
are the following:—In the inner anterior angle of the cornu is a small 
group, the inner or median group. This is one of the smallest, and is 
absent in some parts of the cord, especially in the lumbar region. A 
much larger group lies near the anterior edge of the horn, in the 
middle, or a little to the outer side of the middle, the anterior group. 
External to this, in the outer extremity of the front part of the horn, 
is another group, the antero-lateral group. These two groups are 
* Kronthal, ‘ Neur. Centralbl.,’ 1890, p. 40. Impulses may thus be diffused, even if 
there is no junctiou of fibrill® or passage of impulses from one fibril to another. 
These fibrillte are said to be composed of fusiform elements, united at their extremities 
by finer threads of the substance of which they consist. They break down, two or 
three hours after death, into rows of fine granules. This arrangement provides a 
mechanism by which the nerve-cells may couduct and diffuse impulses, but such a 
mechanism does not exclude (as has been assumed) the reinforcement or origination 
of such impulses, and their discovery leaves untouched the facts which demonstrate 
the trophic influence of the cells, and the manner in which they arrest secondary 
degeneration. These functions are indicated by facts of a totally different nature. 
Kronthal’s observations (by a new method) are of great importance, and appear 
trustworthy. 168 
SPINAL COED. 
often blended, so that the anterior group cannot be separately distin- 
guished, as in the right-hand mid-cervical figure. A fourth group, 
usually the largest, lies in the outermost part of the horn, behind its 
front, usually in the posterior outer angle; it may extend inwards, 
halfway across the horn. It is called the external or postero-lateral 
group (p.-l., Fig. 69). These three are the most important groups. 
U'poer Dorsal 
Mid. Lumbar. 
FlO. 69.—Diagrams of the groups of nerve-cells in the anterior cornu. Groups :— 
I., inner or medial; A., anterior; A.-L., antero-lateral; P.-L., postero-lateral; I. !■. p., 
intermediate lateral process; P. V. C., posterior vesicular column or tract. The two 
mid-cervical sections are only a few millimetres apart, and show how the anterior 
group, separate in the one, may be blended with the antero-lateral group in a 
neighbouring part of the cord. 
There is in some parts also a central group, occupying nearly the centre 
of the horn. In the small cornu of the dorsal region, often no well- 
defined groups can be made out, but when any can be recognised, they 
are generally the anterior and external. 
Similar cells, usually smaller in size, and isolated, are scattered 
through the intermediate grey matter, and a group of cells occupies a 
projection outwards into the lateral column in the lower cervical and 
upper dorsal regions. It was termed by Lockhart Clarke the inter- 
medio-lateral tract, but which is better designated the intermediate 
process (or lateral horn), and the cells the intermediate group (i. l. p., 
Fig. 69). Nerve-cells also lie in the grey matter of the reticular STRUCTURE. 
169 
formations, lateral and posterior, and are sometimes described as 
special groups. Many isolated cells, medium and small in size, also 
lie in the posterior horn. These are probably connected with some of 
the fibres of the posterior roots. They extend back into the caput 
eornu posterioris.* 
In the lower dorsal and upper lumbar cord, from the eighth dorsal to 
the second lumbar nerves, a group of nerve-cells lies in the inner part 
of the neck of the posterior horn, the posterior vesicular column of 
Lockhart Clarke (sometimes called “ Clarke’s column ”) (p. v. c., Fig. 
69 ; see also Fig. 78). Most of these cells are fusiform in shape, but 
are placed vertically, so that they appear round or oval in transverse 
section, and their processes are not seen. Some, however, present pro- 
cesses that run forwards or backwards. Nerve- fibres pass into and by it, 
which we shall consider subsequently. Although this tract is chiefly 
developed in the lower dorsal and upper lumbar cord, a few nerve- 
cells of similar character are met with in the same position in other 
parts, and are occasionally sufficiently numerous to form a small 
group. 
The “ gelatinous ” grey matter, grey substance of Rolando, which 
forms a cap on the posterior horn, caput cornu posterioris (c c. p., 
Fig. 64), differs considerably from the spongy substance. It lias 
been described as made up of granules, but, according to later 
researches, consists of a peculiar translucent material forming an 
excessively fine network, which, like the rest of the neuroglia, behaves 
to reagents like horny material. In the embryo it is continuous with 
that which surrounds the central canal,f but from this it becomes 
separated in the course of development. Its basis substance is thus 
of neuroglial nature. Numerous nerve-fibres pass through it from 
the posterior roots, and these, coursing forwards, seem to divide 
it into columns, as it is viewed in transverse section. A few small 
ganglion-cells lie in this gelatinous substance, chiefly on the inner 
side; it also contains many minute cells, some of which are thought 
to be nerve-cells, others to belong to the neuroglial tissue. Bundles 
of vertical fibres are also seen in transverse section, and these are 
often numerous just above the caput, especially on the inner side of 
the horn. Most of these are fibres of the posterior nerve-roots that 
have a vertical course for a short distance. In Fig. 78 the axis- 
cylinders of these fibres are seen to be changing from the horizontal 
to the vertical direction, and their relation to the posterior root. 
* It is generally believed that their branching processes enter into the plexus oi 
fibrillae in the grey matter, and thus connect these cells with those of the anterior 
cornua, and also with fibres that cross by the posterior commissure and form the 
ascending sensory path to the brain. It has been recently maintained that there is 
no actual union of the fibrillae in the grey substance, but that impulses pass from 
one to another by contiguity, or through a special intermediate conducting material 
(His and Fovel, ‘Cor.-bl. f. Schw. Aerz./ 1889, Oct. 1st). This observation needs 
confirmation. 
f Cf. Corning, ‘Arch f. mikros. Anat.,’ xxxi, 1888. 170 
SPINAL CORD. 
fibres can he distinctly traced. The hinder part of the gelatinous 
substance is less dense in structure than the rest, and is sometimes 
distinguished from it as the “ spongy zone.”* The gelatinous sub- 
stance contains many vessels, running for the most part vertically. 
White Substance.—We may now examine, in greater detail, the con- 
stitution of the white columns of the cord, and the probable course and 
function of the fibres they contain. Their analysis has been greatly 
aided by three facts : continuity of degeneration, difference in time of 
development, and the variation in the size of the fibres of the different 
tracts. 1. It was discovered by Turck that in certain tracts in the 
white substance the nerve-fibres undergo secondary degeneration when 
separated from their ceils of origin, a degeneration analogous to that 
which, as we have already seen, occurs in the nerve-fibres outside the 
cord. 2. In the developing cord the fibres of different tracts acquire 
their white substance at different periods, and the study of these 
differences (first by Flechsig and later by Bechterew and others) has 
not only confirmed, but also extended, the differential indications 
afforded by disease. It enables us to make a distinction between 
fibres that do not degenerate separately or not through a sufficiently 
long tract to enable us to distinguish them. The groups into which 
this method enables us to divide the fibres, and the order in which 
the medullation takes place, are as follow:— 
(1) Anterior and posterior root-fibres. 
(2) 
(3) 
(4) 
Ground-fibres of the 
- inner anterior column, 
postero-external column, 
outer anterior and lateral column. 
(5) Lateral limiting layer and antero-lateral ascending tract. 
(6) Posteromedian column. 
(7) Direct cerebellar tract. 
(8) Lateral and anterior pyramidal tracts (which in man are first 
medullated at the time of birth).f 
3. The size of the nerve-fibres varies in different tracts, but the 
full significance of the variations has still to be ascertained. Even in 
the same tract of the cord considerable variations are met with, which 
probably correspond to differences in function. When a tract dege- 
nerates it is common for the degeneration to be incomplete; fibres 
remain intact among those that perish : this indicates a difference in 
function, and with it the difference in size usually coincides. It is also 
possible that some of the small fibres seen among larger ones may be 
due to the division of the latter (Sherrington) ; hut such division 
has not been actually demonstrated, and is probably not frequent. 
The variation in size is from 1 to 25 /u (T-5^00 to yoVo inch). The 
variations are especially great in the fibres of the pyramidal tract. 
* So tliat in some descriptions the posterior horn is divided into (1) spongy sub- 
stance of the horn itself; (2) gelatinous zone of the “ caput,” and spongy zone 
at the tip of the horn. See Lissauer, ‘ Arch. f. Psych./ 1836. 
f See Obersteiuer, loc. cit., p. 192. STRUCTURE. 
171 
and it is in these that division has been thought to occur. Those of 
the direct cerebellar tract are uniformly large, while most of those 
that constitute the postero-median column are small. 
It will facilitate the detailed study of the tracts if we consider 
first those that undergo secondary degenei'ation for a considerable 
distance, as our knowledge regarding these is the most complete. 
These degenerations are both ascending and descending. Only one 
Fio. 70.—Diagram of the elements of the white substance at various levels 
of the spinal cord. (Modified from Flechsig.) The pyramidal tracts are 
shaded by short horizontal lines; the direct cerebellar tract by dots; the 
posterior median column by dots, as it degenerates in disease of the lowest 
part of the cord or of the nerves of the cauda equina; the small circles 
in the forepart of this column indicate the area which degenerates in 
disease of the cervical enlargement. The antero-lateral ascending tract 
is shown by crosses. It is not represented in the first cervical section 
because there are no facts, at present, to show its exact position here; 
it probably lies chiefly in front of, and between, the direct cerebellar and 
pyramidal tracts, as 0. 3. The anterior ground-fibres, lateral limiting 
layer, and postero-external column are left white. Fig. 62 should be 
compared with this. 172 
SPINAL CORD. 
important set of fibres degenerates downwards through a considerable 
extent—those that continue through the cord the anterior pyramids 
of the medulla. They commence still higher, in the motor region of 
the cortex of the cerebral hemisphere, passing thence by the “ internal 
capsule ” between the two parts of the corpus striatum, &c., to the 
crus and pons ; they are the chief, perhaps the sole conductors of 
voluntary impulses. They are termed the pyramidal tracts because 
they constitute the anterior pyramids of the medulla. They ai*e shaded 
by short horizontal lines in Fig. 70; compare also Fig. 64. 
At the decussation of the pyramids about three quarters of the 
fibres usually cross to the other side. These pass down the cord in 
the lateral column, and constitute the lateral (or crossed) pyramidal 
tract. Those which do not decussate, pass down their own side of the 
cord, in the inner part of the anterior column, at the side of the 
anterior median fissure, and constitute the anterior (or direct) pyra- 
midal tract. Flechsig has found that the decussation is subject to 
many variations. In the majority of cases the decussating fibres are 
between 70 and 80 per cent, of the whole. Sometimes they con- 
stitute a still larger proportion, and in one case (of 60 examined) all 
the fibres crossed. Sometimes fewer fibres decussate, only one half 
or even less than half; in one case 35 per cent., in another only 10. 
Xo case has yet been met with in which no fibres crossed. A few 
fibres seem to decussate, at least in some cases, within the pons, 
where the paths for the tongue, &c., cross the middle line, since 
slight degeneration from a cerebral lesion has been found in the 
opposite pyramid of the medulla oblongata.* 
The lateral pyramidal tract occupies the posterior half of the lateral 
column, outside the posterior cornu. It extends down to the end of the 
cord, even when it is originally small. Hence those fibres that do not 
cross at the medulla must do so lower down in the cord. Through the 
greater part of the cervical and dorsal regions this lateral tract is 
separated from the surface by a narrow layer of fibres, the direct cere- 
bellar tract. In the upper part of the cervical region (third cervical 
segment) this tract lies farther forwards, so that the pyramidal tract 
comes up to the surface close to the posterior cornu (Fig. 68, c. 3), 
and heie, if the tract is small, there may be a depression on the sur- 
face. In the lower part of the dorsal cord there is a similar move- 
ment forwards of the cerebellar tract, so that the pyramidal tract 
again comes in contact with the surface posteriorly (Fig. 68, d. 12), 
and, as the cerebellar tract ceases at the last dorsal nerve, the pyra- 
midal tract extends up to the surface throughout the lumbar enlarge- 
ment (Fig. 63, l 4). The inner side of the tract is in contact with the 
hinder part of the posterior cornu, near the surface, throughout the 
entire length of the cord, but further forwards it is separated from the 
neck of the cornu and intermediate grey substance by a layer of nerve- 
fibres, termed bv Flechsig the lateral limiting layer (L. l. l., Fig. 64). 
Hadden and Sherrington, ‘ Brain,’ viii, 502, pi., fig. 1. STRUCTURE. 
173 
Among the fibres of the pyramidal tract, in the dorsal and cervical 
regions, degeneration reveals a few other fibres that belong chiefly 
to the cerebellar tract. The lateral pyramidal tract diminishes in 
size from above downwards as its fibres end by entering the grey 
matter ; those that extend lowest (for the leg) occupy the posterior 
part of the tract in the cervical region. The fibres curve inwards 
along the septa that extend from the grey matter into the lateral 
column, and they enter the grey matter between the anterior and 
posterior cornua. They pass inwards and forwards in the anterior 
cornu, and are then lost in the complicated structure of the grey 
matter. Their probable termination will be considered presently. 
The anterior or direct pyramidal tract (called also the “ column of 
Tiirck”) descends the cord in the inner 
part of the anterior column, adjacent 
to the anterior median fissure. Its 
exact form and size vary; usually it 
bounds the fissure on each side : some- 
times it forms only a small tract at 
the posterior part of the fissure ; when 
large, it not only reaches forward to 
the front of the cord, but may cause a 
prominence on the surface bounded 
by a distinct sulcus. Its extent down 
the cord, always less than that of the 
lateral tract, varies according to its 
size. It steadily lessens in area, and, 
if originally small, may not extend 
beyond the middle of the cervical en- 
largement ; if originally large, it may 
be traced as far as the lumbar enlarge- 
ment (Pig. 71) ; when bearing the 
usual proportion to the lateral tract, 
it ceases about the inid-dorsal region. 
Most of the fibres pass through the 
anterior commissure to the oppo- 
site side, either entering at once 
the grey matter, or passing first to the lateral tract. The latter 
is probably the course of most of the fibres when the pyramidal 
decussation is small. Whether any fibres end in the grey matter on 
the same side of the cord we do not know. 
Disease of the brain destroying the motor cortex, or the fibres which 
descend from it to the pyramids, causes descending degeneration, 
usually limited (at least in conspicuous degree) to the related pyra- 
midal tracts,—anterior on the same side, lateral on the opposite side 
(Fig. 72). But in many cases slight degeneration has been also found 
in the lateral tract on the same side, extending into the lumbar region. 
Hence it is probable that some fibres of each anterior pyramid find 
Fig. 71.— Ascending and descend- 
ing degenerations from myelitis 
of the mid-dorsal reirion; the 
upper section is from the lower 
cervical, and shows the ascending 
degeneration of the post.-median 
column spreading out against the 
commissure. The other figure is 
from tlie lower dorsal, and shows 
degeneration of the pyramidal 
tracts, anterior and lateral. 174 
SPINAL CORD. 
their way to the lateral tract on the same side, and descend to the 
corresponding limbs, especially to 
the leg. This degeneration of the 
lateral tract on the same side as 
the lesion is sometimes very marked 
just below the decussation of the 
pyramids, and has therefore been 
thought not to be due to any 
lower re-deeussation in the cord.# 
Nevertheless facts suggesting that 
there is such a re-decussation in 
dogs and monkeys have been ascer- 
tained by Sherrington,f but the 
anatomical relation in man between 
each anterior pyramid of the me- 
dulla and the anterior roots of 
the same side must be regarded 
as still uncertain. That there is 
such a physiological relation is 
clearly indicated by clinical facts. 
We shall afterwards see that there 
is abundant evidence that each 
hemisphere of the brain is con- 
nected with both legs, although 
chiefly with that of the opposite 
side. There is also a similar and 
even more equal connection with the 
trunk muscles, and a slighter con- 
nection with certain muscles of the 
arm. Such muscles invariably re- 
gain some power on the paralysed 
side, even with a complete inter- 
ruption to the motor path, and they 
are weakened on the unparalysed 
side. The subject is considered 
further in vol. ii. On the whole, 
the facts hitherto ascertained 
suggest that the arrangements 
which subserve this relation vary 
in different persons, just as does 
the chief decussation of the pyra- 
mids. The fibres probably in some 
cases continue downwards on the 
Fig. 72.—Descending degeneration of 
the pyramidal tracts in a case of 
hemiplegia from disease of the right 
cerebral hemisphere. (From sec- 
tions prepared by Dr. Mott.) 
* Pitres, ‘Arch, de Physiologie,’ 1874; Hadden and Sherrington, ‘Brain,’ Jan., 
1886. An illustration of this bilateral degeneration will be found in the section on 
Diseases of the Brain, vol. ii. 
+ “Every unilateral lesion induces degeneration in both lateral pyramidal tracts, STRUCTURE. 
175 
came side until they reach the level of grey matter for which they are 
destined. In other cases most or many of them cross at the hulhar 
•decussation, to recross near the level at which they end. In this case, 
moreover, it is evident that the presence of visible degeneration in 
the lateral column, due to the decay of these fibres, will depend on 
the distance of their re-decussation above their ending. If they cross 
only when they have to enter the grey matter, they will have no 
recognisable place in the pyramidal tracts. Lastly, there is the pos- 
sibility that a connection between the motor cells or structures of 
the two sides may supplement the re-decussation.* 
How do the fibres of the pyramidal tract end ? They seem all to 
pass into the intermediate grey matter, and forwards into the anterior 
cornu, among the motor nerve-cells. There they are lost in the plexus 
of the spongy substance. There is strong indirect evidence that they 
divide and subdivide, and that their ramifications join the plexus of 
nerve-fibrillse constituted by the dividing processes of the ganglion- 
cells. The evidence of this is twofold. As far as is at present known, 
only one process of a ganglion-cell becomes an axis-cylinder; the 
others divide. The axis-cylinder process passes into an anterior root; 
it can be seen to do so in the case of some ganglion-cells (Fig. 60), 
and, as we have seen, the number of ganglion-cells and ante- 
rior root-fibres is nearly the same in the frog, and therefore, pre- 
sumably, in man also. Since some root-fibres are not motor, the 
number of motor cells may safely be assumed to be at least not 
smaller than that of the motor fibres ; thus each fibre will have at 
least one cell related to it. If so, since the pyramidal fibres are 
certainly connected with the ganglion-cells, the connection can 
only be by the ramifying processes of the cells, and this involves 
a division of the nerve-fibre. The dividing fibre isolated by Gerlach, 
and shown in Fig. 61, may have been a branch of a pyramidal fibre. 
The second point in evidence of division is the fact that the nerve- 
cells and root-fibres must be many times more numerous than the 
fibres of the pyramidal tract.f But all (or at least most) of the 
motor root-fibres may be stimulated through the pyramidal fibi-es, 
and therefore each of the latter must be connected with several gan- 
glion-cells. Physiological considerations suggest the same conclusion. 
the smaller degeneration (on the same side as the lesion) being most pronounced in 
the cervical and lumbar enlargements, immediately above which regions it is often 
absent. It follows, therefore, that the degeneration on the same side as the lesion 
is a ‘ recrossed ’ degeneration. Further, the lower regions may even contain more 
•degenerated fibres than the upper ones; and as degenerated fibres can often be 
traced for a long distance in pairs, it is inferred that the fibres of the pyramidal 
tracts divide into two ” (Sherrington). 
* Broadbent, Hadden. In a unilateral lesion of the cord the paralysed foot may 
•move with the other. Such a connection of nuclei was originally suggested by 
Broadbent to explain the association of bilateral movements. 
f The total area of the anterior roots of the cord is probably at least five times 
*s great as that of the pyramidal tracts in the upper cervical region. 176 
SPINAL COED. 
Let us now consider, for a moment, the whole 
motor path, from the cortex of the brain to the 
muscles. We mav regard it as composed of two 
segments, an upper and lower (Fig. 73). Each 
consists of a ganglion-cell above, a nerve-fibre, 
and the terminal ramification of the latter. The 
upper, “cerebrospinal” segment consists of the 
cortical gangliou-cell, and the “ pyramidal” fibre, 
which proceeds from the cell, passes through the 
brain and cord, and ends in the grey substance 
by division and terminal connection with several 
nerve-cells. The lower, “ spino-muscular ” seg- 
ment consists of the spinal motor cell, and the 
fibre proceeding from this, which passes through 
the anterior root and nerve-trunk to the muscle, 
where it divides and ramifies on the muscular 
fibre. Thus each segment has a similar consti- 
tution—cell, fibre, terminal distribution. The 
elements of the two segments do not correspond 
in number, since, as we have just seen, each 
cerebro-spinal element is connected with many 
spino-muscular elements. So, too, each motor 
fibre is connected with a considerable area of 
excitable muscle-tissue. It will be found that 
this conception of the motor path conduces to 
clearer ideas of many facts of disease, and it is 
important to grasp it firmly. We shall see, for 
instance, that diseases involving any part of a 
segment produce similar effects, however diverse 
their nature ; while there is a fundamental differ- 
ence between the effects of disease of the two 
segments.* 
Fibres that degenerate downwards through the 
greater part of the cord are also scattered 
through the antero-lateral column, in a zone that 
extends beneath the surface between the direct 
pyramidal tract and the direct cerebellar tract. 
Some are mingled with the fibres of the ascend- 
ing antero-lateral tract presently to be described; 
FlO. 73.—Diagram of an element of the motor path. ir. g.,. 
upper segment; L. 8., lower segment; C. C., cortical cell; 
S. C., si'inal cell; A. C., anterior cornu; M.. muscle; the 
dotted line, at the level of s., indicates the junction of 
the two segments; S., path from sen-orv nerve-roots. 
* I have found this conception of the motor path of so much practical value that 
it may be worth while to mention the curious coincidence that, a few months after its 
publication in the first edition of this book (in August, 188G), nearly the same STRUCTURE. 
177 
Fig. 73a.—Degeneration of the 
antero-lateral ascending tract iu 
a case of locomotor ataxy (q. v. 
figure), showing its position in 
the upper cervical region, where 
the direct cerebellar tract passes 
outside it into the restilorm body. 
Fig. 75.— Degeneration after 
injury to the cauda equina. 
C a, b, c, upper middle and 
lower cervical; Da, upper; 
b, c, lower dorsal ; L a, 
upper; and L b, middle lum- 
bar region. (After Scbultze.) 
Fig. 74.—Ascei'ding degene- 
ration in the postero-median 
column and antero-lateral 
ascending tract. Tlie cord 
was crushed at the first lum- 
bar segment. 
dra was stated (no doubt independently), and even the same terminology 
employed, by Dr. v. Renz in the ‘ Centralblatt f. Nervenkr.,’ Oct. 15th, 1886. 
VOL. I. 178 
SPINAL CORD. 
others lie beneath this. It is possible that they really belong to the 
crossed pyramidal tract. They have been termed by Foster the 
descending antero-lateral tract.* 
Fibres degenerate upwards in both the lateral and the posterior 
columns. We may consider the latter first. 
Each posterior column, as we have seen, is divided by the imperfect 
“ intermediate septum ” into two parts,—a narrow “ postero-median 
column,” and a wider “ postero-external column” (Fig. 64). Secon- 
dary degeneration confirms this distinction. It the posteriorcolumns are 
interrupted anywhere in their course, ascending degeneration results ; 
and this, a short distance above the lesion, is confined to the posterior 
median column (Figs. 71, 74, 75), in which the degeneration continues 
upwards to the medulla oblongata, and ends there as the grey matter 
of the “ post-pyramidal nucleus.” The fibres of these median columns 
Fig. 76. 
Fig. 77. 
Fig. 76.—Degenerations after a Tesion of the cord in the lower part of the cervical 
region. A, highest cervical ; B, middle cervical 1£ cm. above lesion. Degeneration 
of the posterior median columns, spreading slightly in A and widely in b into the 
post. ext. col. The nature of the circumferential degeneration is uncertain; it 
is probably a partial ascending degeneration set up by peripheral myelitis. 
C, upper dorsal 2 cm. below lesion. Degeneration of the lateral pyramidal tracts ; 
“ comma shaped ” degeneration in front of the post. ext. col.; slight degenera- 
tion of the anterior ground-tibres. (Schultze.) 
Fig. 77.—Ascending degeneration after injury to the lowest part of the spinal 
cord and sciatic nerve-roots arising from it. A, cervical; b, lower dorsal; C, junction 
of dorsal and lumbar regions; D, middle of lumber enlargement. (After Schultze.) 
degenerate in the same way when the lesion is not in the cord, bnt 
in the posterior nerve-roots (as of the cauda equina, Fig. 70). Hence 
* Foster, * Physiology,’ 1890, p.873. See also Hadden and Sherrington, ‘Brain,’ 
vol. viii; and Tooth, ‘Secondary Degeneration of the Spinal Cord,’ 18S9. STRUCTURE. 
179 
it is clear that these fibres are continued upwards from the posterior 
nerve-roots without interruption. The contrast between these dege- 
nerated columns and the undegenerated external columns through 
the greater part of the cord above the lesion (Fig. 74) is very striking. 
But just above the lesion the degeneration is not confined to the 
median columns; it spreads out into the external columns, espe- 
cially towards the hinder surface, and the more extensively the 
nearer to the lesion, until close above this the degenerated fibres 
occupy the whole extent of the posterior column, except a small area 
close to the posterior cornu. This is due to the fact that the fibres 
pass to the median column through the hinder part of the external 
column. It is the same whatever is the seat of the lesion, whether 
it is in the cervical (Fig. 76), dorsal, or lumbar (Fig. 77) parts of 
the cord ; and if it is in the cauda equina, the degeneration spreads 
out in the same way in the lumbar enlargement (Fig. 75). This 
shows clearly that all the way up the cord fibres pass to the median 
column from the external column, and that these are uncrossed fibres 
from the posterior roots. As the fibres ascend the cord in the median 
column, they come to lie posterioi-ly in proportion as their source is lower. 
Those from the sciatic nerves, for instance, in the lower cervical cord 
only occupy the posterior half of the columns (Fig. 77). Those from 
the whole lumbar enlargement, or whole cauda equina (Fig. 74), reach 
forward to the commissure in the lower cervical region, spreading 
out a little near the commissure, where, however, the degeneration is 
much less dense than it is behind. Above the middle of the cervical 
enlargement the degeneration from a lesion in the dorsal or lumbar 
regions does not extend forwards beyond the junction of the anterior 
and middle thii-d of these columns ; but if the lesion is in the cervical 
region the degeneration extends up to the commissure, even at the 
level of the second cervical segment (Figs. 76, A, 66), showing that 
the fibres from the cervical roots occupy the anterior portion of these 
columns. 
It is important to remember that the root-fibres that pass to the 
median column through the external column do not decussate. This 
is not, however, the only source of fibres to the median column. 
Fibres pass to it (1) from the neck of the posterior horn, across the 
anterior part of the external column, curving backwards (Fig. 78, x) ; 
many of them extend almost to the postero-median septum. They 
come from the layer of fibres that lies in the inner part of the neck 
of the cornu, on the inner side of the vesicular column where this 
exists. Some of them may be distinctly seen to turn backwards in 
the neck, as if they come either from the posterior roots or from cells 
near the caput cornu. It is possible that others may be fibres from 
the posterior commissure. (2) From the posterior commissure in 
the middle line (Fig. 78). These are very numerous and conspicuous 
in the lumbar enlargement. They course backwards in the septum 
and then pass outwards on each side into the adjacent column. 180 
SPINAL CORD. 
Flechsig believes that these are posterior root-fibres. They may 
easily decussate in the septum, but such decussation has not been 
proved. 
In the lower lumbar region there is a narrow tract of fibres close to 
the posterior median septum, that is apparently of different nature 
from the rest of the column. It is lenticular on transverse section, and 
is indicated by the clear area in l. 4, Fig. 70, and faintly in L b, 
Fig. ?5. It is distinguished by a difference in time of development 
(Flechsig), and by freedom from the secondary degeneration that 
involves the rest of the column. 
It is very doubtful whether all the fibres that enter the postero- 
median columns continue in these to the medulla. Some certainly do, 
but the upward increase in size of the columns seems to be far too 
small for the accommodation of all the fibres that seem to pass to them. 
At the same time we have, at present, no indication of the mode in 
which fibres leave these columns. 
At the medulla oblongata this column becomes filled with nerve- 
cells, the post-pyramidal nucleus, so called because the highest por- 
tion of this column has been termed the posterior pyramid of the 
medulla. It is also called the nucleus gracilis. The discovery that 
the fibres of this column are continuous with the nerve-roots invests 
the post-pjramidal nucleus with considerable importance, since its- 
Fio. 78. —Posterior cornu and column at the last dorsal segment, p. it. C., postero- 
median column ; p. E. C., postero-external column ; p. M. S., posterior median sep- 
tum ; P. C., posterior commissure ; v, commissure vein. p. V. C., posterior vesicular 
column ; C. C., caput cornu ; p. k., posterior root; a, an aitery ; d, d, d, adjacent 
to a strip of the lateral column, indicate the tracts of fibres passing from the 
vicin tv and interior of the posteiior vesicular column along the septa of the 
lateral column, to form the direct cerebellar tract; x, x, tracts of fibres passing 
from the neck of the horn, near the post, vesic. col., to the post-median column. STRUCTURE. 
181 
nerve-cells are the first witli which these root-fibres are connected, 
and they arrest secondary degeneration. The upward degeneration 
of the median fibres implies upward conduction; their probable 
function will be considered in the next section. 
Thejoostero-external column (“column of Burdach,” containing the 
■“ posterior root-zone ” of Charcot) consists chiefly of vertical 
fibres. Many of the posterior root-fibres pass through it, horizontally 
or obliquely (Fig. 64). These either curve inwards to the posterior 
horn (some first inclining upwards), or pass obliquely upwards and 
inwards to the median column and constitute the fibres of this column 
that are continued from the nerve-root. Across the anterior part 
fibres also pass, as just described, between the neck of the posterior 
horn and the median column. The vertical ground fibres of the 
external column have apparently only a short course, since they 
degenerate for only a few centimetres above or below a lesion. The 
longest descending degeneration is of a “comma-shaped tract,” in 
the middle of the anterior third of the column in the dorsal region, 
which degenerates downwards for four or five centimetres (Fig. 76). 
These vertical fibres, of short course, may connect the grey matter of 
the posterior horn at different (but adjacent) levels. This column is 
larger in the swellings than it is in the dorsal region, chiefly in con- 
sequence of the larger number of root-fibres that pass through it. 
Above, it also ends in a grey nucleus, the postero-external nucleus 
or cuneate nucleus. 
Both these posterior nuclei are connected directly with the cortex 
of the opposite hemisphere, and chiefly with the ascending parietal 
convolution. Fibres also pass from them to the cerebellar hemi- 
sphere of their own side, which is connected with the same region 
of the opposite cerebral cortex by the superior cerebellar peduncle.* 
The two nuclei (of both sides) are also found (by developmental 
researches) to send fibres through to the inferior cerebellar pe- 
duncle,f and fibres pass from the posterior median nucleus to the 
middle lobe of the cerebellum on the same side,J a fact of consider- 
able significance. 
The “ direct cerebellar tract” is another series of fibres that de- 
generate upwards. It forms a layer at the periphery of the lateral 
column, outside the pyramidal tract (Fig. 64), but does not extend 
through the whole length of the cord, ceasing below at the level of the 
first lumbar nerve (Fig. 70). The anterior part of the tract (as seen 
in section) does not extend forwards beyond the level of the lateral 
pyramidal tract, although it was formerly thought to do so because 
there are other fibres in front of it that also degenerate upwards, 
and these were not distinguished from those of the tract. But near 
its upper and lower extremities, at the level of the second cervical 
* See Flechsig and Hosel, ‘Neurol. Cent./ 1890, p. 417. 
f Darkscliewitscli and Freud, ib., 1886, p. 121. 
X Beebterew, ‘ Wjistnik Psych., &c.,’ 1886. 182 
SPINAL COHD. 
nerves, and also in the lowest part of the dorsal region, the tract lies a 
little anterior to its position in the rest of the cord, and hence at these 
places the pyramidal tract comes to the surface behind the cerebellar 
tract, close to the posterior nerve-roots, up to which elsewhere the 
cerebellar tract extends. The tract increases somewhat in size from 
below upwards, and hence receives fibres throughout its course, but 
most of its constituent fibres enter it at the level of the lowest dorsal 
and first lumbar nerves, i. e. at its lowest part. These fibres come 
from the grey substance, passing through the lateral column, along 
the septa that cross the pyramidal tract fi’om the grey matter. In 
the latter these fibres are conspicuous objects at this level 
(Fig. 78, d, d), passing transversely and obliquely from the front 
of the posterior vesicular column. Into this many of them can 
be traced ; others change their direction and become vertical, per- 
haps passing into the vesicular column at a different level. It is 
probable that the fibres come from this column; the cerebellar tract 
is chiefly formed at that part of the cord at which the column is most 
developed, and the cells of this column have been found atrophied 
when the cerebellar tract is degenerated.* Besides the fibres that are 
gathered into the compact cerebellar tract, others, apparently belong- 
ing to it, ascend among those of the adjacent pyramidal tract. 
The cerebellar tract only degenerates when a lesion of the cord is at, 
or above, its place of origin, the junction of the dorsal and lumbar 
regions. If the lesion is in the lumbar enlargement, as in the case 
shown in Fig. 74, the tract does not degenerate. 
At the level of the first cervical nerve (where the pyramidal tract 
leaves the lateral column to cross into the anterior pyramid of the 
medulla) the cerebellar tract lies in front of the “grey substance of 
Rolando ” (formed from the caput cornu posterioris), and passes up, in 
the restiform body, to the cerebellum. Since it degenerates upwards wo 
must conclude that it also conducts upwards.f 
We have seen that the lateral pyramidal tract, although in contact, 
behind, with the head of the posterior cornu, does not extend quite 
up to the neck of the horn or to the intermediate grey substance, 
the two being separated by a“ lateral limiting layer ” of vertical fibres, 
in part broken up by processes from the grey matter. In the upper 
cervical cord, and also to a less extent in the dorsal cord, this layer 
extends forwards outside the anterior horn, which, in these parts, is 
* E.g. by Minkowski, ‘ Deut. Arch. f. kl. Med.,’ Bd. xxxiv, p. 433. Slight degene- 
ration of the pyramidal tracts was the only other lesion. 
f In the absence of evidence of contrary character, the direction in which fibres 
conduct must be assumed to be that in which they degenerate. We know of no 
exceptions to it within the central nervous system. Wherever we can observe the 
relations this law obtains, except in the peripheral sensory nerves, in which the con- 
ditions are conspicuously exceptional. Hence the probability is very great that, the 
correspondence obtains where we have not yet been able to ptove it, and to ignore 
the probability because it is not a certainty is scarcely reasonable, although not 
uncommon. STRUCTURE. 
183 
narrow. It consists of fine fibres that seem to pass into and out of 
the grey matter. This course, and the fact that the tract does not 
degenerate through any considerable extent, suggest that its fibres 
have but a short course, and connect the grey matter of adjacent 
regions. 
There is a small tract of fibres, all of small size, at the junction of 
the tip of the posterior horn and lateral column known as Lissauer’s 
tract. The fibres come from the posterior roots ; they course upward 
for a short distance, forming the tract, and then enter the posterior 
horn. 
The rest of the lateral column, in front of the pyramidal and cerebellar 
tracts, consists of fibres that vary in 
size, course, and date of development. 
Secondary degeneration, however, as 
I pointed out some years ago,* enables 
us to distinguish an important tract 
which occupies an irregular area in 
front of the pyramidal and cerebellar 
tracts, and degenerates upwards 
throughout the cord. It extends 
across the lateral column, as a band 
which fills up the angle between the 
pyramidal and cerebellar tracts, and 
it reaches the surface of the cord in front of the latter tract, nearly 
on a level with the anterior commissure ; it then extends forward in 
the periphery of the anterior column, almost to the anterior median 
fissure, and up to the direct pyramidal tract when this exists. I 
have termed it the antero-lateral ascending tract (Figs. 64, 70, 
73a, 74, and 79). It has often been confounded with the cerebellar 
tract, and hence the impression arose that the cerebellar tract extends 
farther forwards than it really does. Posteriorly the tract extends 
across the lateral column towards the posterior commissure, from 
which its fibres probably come (Fig. 70, l. 4). In the cervical 
(ib., c. 3), especially in the upper part, where the direct cerebellar 
tract extends farther forward, the broadest part of the ascending tract 
lies just within the anterior part of the cerebcdlar tract, and extends, 
like a wedge, between the latter and the pyramidal tract. 
This tract has been found by Bechterew to undergo development at 
a different period from the rest of the lateral column. It apparently 
constitutes an upward path from the opposite posterior roots, since its 
degeneration, if unequal on the two sides, is greafer on the side oppo- 
site to that on which the uncrossed post.-median column is most 
degenerated. Its fibres do not degenerate when the nerve-roots are 
divided, and hence probably spring from cells in which the root- 
fibres end. Fibres apparently pass to it through the whole length of 
the cord, and these are mingled together, so that the degeneration 
Fig. 79.—Cervical section. As- 
cending degeneration in post- 
med. col. and ant.-lat. ascending 
tract, secondary to a lesion in 
tlie dorsal region. (From a 
section prepared by Dr. Mott.) 
* ‘ Diagnosis of Diseases of the Spinal Cord,’ first ed., 1879. 184 
SPINAL CORD. 
from a lesion of the lower part of the cord is not dense * The precise 
form of the tract seems subject to individual variations. Above, its 
fibres probably end in the lateral nucleus. 
Some fibres of the anterior part of the lateral column are large in 
size, and curve upwards and downwards into the anterior born. They 
must be of short course, and may be fibres of the anterior nerve-roots, 
which ascend and descend to nerve-cells on a different level from 
that of the roots by which they leave the cord. 
The fibres of the anterior column, excluding the anterior pyramidal 
tract, are termed by Flechsig the anterior ground-fibres (Fig. 57). 
They are not separable, structurally or by development, from those 
of the lateral limiting layer. The ground-fibres do not degenerate 
through any considerable extent of the cord, and some probably connect 
the anterior cornua at different levels. Moreover, some of the fibres 
pass to the anterior commissure, and thus, by the agency of the ante- 
rior columns, a connection may be established between the two anterior 
cornua at different levels. Whether any of the ground-fibres are of 
long course but do not degenerate at all we do not know. 
The Commissure of the spinal cord lies between the bottom of the 
anterior fissure and the posterior columns, and in it alone is there a 
passage of fibres from one half of the cord to the other. It consists 
of two parts, an anterior or white, and a posterior or grey commissure. 
The white commissure varies in thickness in different parts of the cord, 
and is largest in the lumbar region It is composed of medullated 
fibres, which cross in the commissure in such a manner that the 
anterior fibres on each side pass out in the posterior part of the 
commissure on the other side. The fibres in front pass into the 
anterior white column, those behind into the grey substance; hence 
they appear to establish a connection between the anterior column of 
one side and the anterior cornu of the other; but many of those 
entering the anterior column merely pass through this to the cornu, 
and this is probably true also of some of the fibres that turn upward 
in the column. Some seem to go to ganglion-cells of the grey matter 
or to the fibrillary plexus, others to the anterior nerve-roots. Through 
this commissure must also pass the fibres of the anterior pyramidal 
tract, and from it may come certain fibres that have been traced 
across the intermediate grey substance to the lateral column, where 
* Other illustrations of the degeneration of this tract will be found in the section 
on Locomotor Ataxy. For an example of its degeneration and references to previous 
ol)servations, see Tooth, ‘ St. Bartholomew’s Hospital Kcports,’ 1885, p. 137. See 
also his ‘Lectures on Secondary Degeneration in the Spinal Cord/ Lond , 1890. 
The degeneration found by Hadden and Sherrington (‘ Brain,’ Oct., 1888), and 
regarded as evidence that the tract passes to the cerebellum, is, I am convinced, the 
anterior extremity of the cerebellar tract. This is manifest on a comparison of 
fig. 5 in their plate with Fig. 79, p. 183. It is important, moreover, to note that, in 
many cases of transverse lesions, a superficial myelitis extending up for a short 
distance in the middle of each side of the cord has determined a secondary degene- 
ration of partial, and sometimes perhaps combined character. STRUCTURE. 
185 
they assume a vertical direction in the pyramidal tract, so that 
part of the anterior commissure is to be regarded as a continuation 
of the decussation of the pyramids. Other fibres may be redecus- 
sating fibres, subserving the connection of one anterior horn with 
the cerebral hemisphere of its own side. Lastly, a few fibres of the 
anterior commissure have been thought to come from the posterior 
nerve-roots. 
The grey commissure contains very fine medullated nerve-fibres, a 
large number of which pass backwards in the posterior horn of each 
side; some appear to be continuous with the fibres of the posterior 
roots, while others probably end in the nerve-cells of the posterior 
horn. It is highly probable that thus a considerable number of the 
posterior root-fibres (or fibres from 
cells in which the root-fibres end) 
cross to the other side, and that thus 
the decussation of the sensory path 
in the cord is effected, which is known 
to take place a short distance above 
the entrance of the nerves. Some of 
the fibres that thus cross may find 
their way to the antero-lateral ascend- 
ing tract in the opposite lateral 
column, since this tract seems to begin 
below close to the grey matter oppo- 
site the posterior commissure. Others 
leave the commissure in the middle 
line, and pass backwards to the pos- 
terior median column, but whether 
these decussate or not we do not know. 
They are very numerous, and the lower 
part of the cord within the grey com- 
missure is the central canal of the 
spinal cord, lined "with epithelium, 
and surrounded by granular material, 
said to be similar in nature to that 
which caps the posterior horn; the 
two are, indeed, as we have seen 
(p. 169), continuous in the embryo. 
The canal is often filled up by epi- 
thelial debris in adult cords,* or, 
sometimes, is much larger than normal. 
The latter state probably depends 
on an arrest of development, for the layer of neuroglial tissue around 
it is much larger than usual. 
Boot-fibres.—The course of the root-fibres has been already incident- 
Fig. 80.—Central canal in normal 
cords. It lias tlie form of a 
transverse slit in A, a vertical 
slit in C (from the conus medul- 
laris), while in B it is circular. 
In each it is lined by columnar 
epithelium and surrounded by 
cellular elements, rounded, or 
angular from compression, 
mingled with granules. In D, 
which is from the same spinal 
cord as C, the position of the 
canal is occupied by a mass of 
nuclear tissue. 
* This obliteration of the canal has no pathological significance, but has been 
repeatedly described as one of the morbid changes in disease. 186 
SPINAL COltD. 
ally alluded to, but remains to be considered in a more systematic 
manner. The anterior roots pass through the anterior columns in 
bundles which are distributed through an area of the column approxi- 
mately corresponding to the width of the anterior surface of the cornu. 
In the grey substance, the coarse fibres that constitute the chief part 
of each of these bundles pass in three different directions, outwards, 
inwards, and directly backwards in the middle of the horn, and thus 
cross each other and the fibres from the anterior commissure. Many 
of the fibres enter the groups of nerve-cells, and certainly end in these 
cells—or rather arise from them, each axis-cylinder being the pro- 
longed chief process of the cell. Such cells often lie among the 
bundles outside the limit of the grey matter, and their processes can 
easily be traced forwards to the nerve-root and backwards into the 
grey matter. Some processes that pass outwards enter the lateral 
white column (“ mixed zone ”), and probably, after a short course in 
this, re-enter the grey matter at a higher or lower level. Some of 
the fibres that pass inwards may go through the commissure to- 
the opposite anterior horn. These coarse fibres are probably all 
motor. Besides them, the nerve-roots contain fine fibres for the 
sympathetic which do not come from the cornual cells. 
The posterior root-fibres have been the subject of much investiga- 
tion on account of their complicated arrangement and the importance 
that attaches to them from their degeneration in locomotor ataxy. 
Although arranged in a continuous vertical series at their surface 
attachment, the fibres are divisible into three sets, one of which passes 
through the caput cornu posterioris (Fig. 78), a second into the 
adjacent part of the post-external column (Fig. 64), while a third set 
consists of fine fibres which at once change their direction, turning 
upwards, and keep together so as to form a zone (zone of Lissauer), 
which lies outside the extremity of the posterior horn in the cervical 
region, but lower down the cord between the caput and the surface 
of the cord. 
The fibres of these three sets have only two immediate destinations 
—to the postero-median column and the posterior grey cornu. 
(1) Many of the fibres that enter the post-external column (a) pass 
obliquely upwards and inwards to the post-median column. This 
course is through the hinder part of the post-external column, and 
in the lumbar region, where the roots enter at the bottom of their 
furrow, many fibres actually pass backwards into the adjacent angle 
of the column, and may be there seen to turn upward in their ascend- 
ing course to the median column. It is this arrangement that leads 
to the peculiar wedge-like shape of the ascending degeneration just 
above a lesion (Figs. 75 and 76) ; (b) other fibres entering the post- 
extei'nal column curve forwards and enter the posterior cornu, chieflv 
in front of its head. The curves they describe are largest in the 
lumbar region, where they almost reach the post-median column. 
(2) The fibres that enter the caput directly, pass through this to the STRUCTURE. 
187 
posterior horn, some on their level of entrance (and these, in the 
lumbar region, have a curved course like the meridian lines on a 
globe), while others turn upwards in compact bundles to pass forward 
into the cornu at a higher level. (3) The fibres of Lissauer’s group 
also enter the horn, either through or in front of the caput, after a 
short ascending course. 
Thus, except the fibres to the post-median column (which ascend 
in it without decussating), all the other posterior root-fibres enter the 
posterior horn, chiefly on its inner side or through the caput, a few 
(Lissauer’s) on its outer side.* 
In the posterior horn, fibres of each set pass to the posterior com- 
missure; others go to the posterior vesicular column (where this exists), 
while some pass forwards into the anterior cornu, chiefly towards 
the outer group of nerve-cells; a few pass towards the anterior com- 
missure, and a considerable number probably end in the nerve-cells 
of the horn. It is probable that the fibres that pass to the posterior 
vesicular columnt are connected with its cells, most likely indirectly 
through ti eir ramifying processes and the spongy plexus, because the 
fibres of the plexus have been found atrophied with those of the pos- 
terior root. Many of those that pass towards the posterior com- 
missure are probably also interrupted by nerve-cells in the posterior 
cornu. Thus the chief destination of the fibres that do not enter 
the postero-median column must be regarded as the anterior cornu 
of the same side and the opposite half of the cord; and this is 
probably true also of the numerous fibres that end in the nerve-cells 
of the cornu. The fibres from the vesicular tract to the direct 
cerebellar tract perhaps continue the path of the posterior root-fibres. 
Blood-supply to the Spinal Cord.—The arrangement of the 
arteries in the cord is not a matter, at present, of much practical 
importance. Nevertheless it is one on which some detailed facts are 
necessary, because it is a subject to which it is most desirable close 
attention should be given, on account of the probability that vascular 
lesions are more frequent than our present knowledge indicates, and 
the relation of lesions to arterial regions should be carefully noted. 
The chief general fact is that the blood-supply is in part central, in 
part peripheral: the central supply is derived from the branches in 
the anterior median fissure and embraces the grey matter, except the 
posterior horn; the peripheral supplies the posterior horn (except 
the neck) and the white substance. 
The arterial blood is brought to the cord by small branches, derived 
* The fibres that pass to the post-external column have been termed the 
“ median group,” and the rest of the root-fibres the “ lateral group,” those entering 
the caput being distinguished as an “ intermediate group.” But each investigator 
describes much the same facts in a different method, and adopts an original 
nomenclature, which renders it better at present to keep the facts more prominent 
in the mind than the names. 
f According to Mott the fibres divide and form a Cue plexus before joining the 
eehs of the vesicular column. 188 
SPINAb CORD. 
from the vertebrals, intercostals, and other arteries, which reach tlae 
cord by the anterior and posterior roots. The anterior pass for the 
most part inwards, to the anterior median fissure, where they are 
connected by vertical branches, continuous in direction, so as to form 
an anterior spinal artery. From this a series of branches pass back- 
wards in the anterior median fissure, which may be called anterior 
median arteries, and are of great importance, supplying most of the 
grey matter. At the bottom of the fissure, each divides into two 
branches, a right and left commissural artery, which passes outwards 
and backwards through the commissure, displacing its fibres (and 
hence, in section, the commissure often appears to be interrupted 
where the fibres are divided obliquely). At the end of the commis- 
sure each divides into an anterior central artery, which sup- 
plies most of the ante- 
rior horn, and a posterior 
central, which supplies 
the intermediate grey 
matter and the neck of 
the posterior horn, in- 
cluding the region of 
the posterior vesicular 
column. Each commis- 
sural artery, moreover, 
before dividing, gives off 
a branch which immedi- 
ately bifurcates into an 
upward and downward 
vessel, each continuous 
with a corresponding 
branch from the next 
commissural artery above 
and below — the anasto- 
motic artery. This effects 
a vertical continuity of 
anastomoses within the 
cord, like that of the 
anterior spinal artery 
outside the cord. 
The peripheral arteries 
pass inwards from the surface. A posterior medial artery courses in the 
median septum, giving branches to each side, and an intermediate 
■septal artery passes in the corresponding septum outside the post- 
median column. Midway between this and the root-furrow, a branch 
enters and passes through the post-external column to the posterior 
horn, which it enters in front of the caput and chiefly supplies—the 
posterior cornual artery ; while a posterior radicular artery passes in on 
the inner side of the posterior root, and is distributed to this and the 
Fig. 81.—Semi-diagrammatic representation of the 
arteries of the spinal cord; AS, anterior spinal. 
Central arteries.—A M, anterior medial; c a, be- 
tween the right and left comm ssural arteries; 
a, anastomotic arterv, divided transversely, to 
which a branch goes from the commissural artery, 
which then divides into a c, anterior cornual, and 
me, mid-cornual arteries. Peripheral arteries.— 
p in, poterior medial; p i, post-intermediate; pc, 
posterior cornual; p r, posterior radicular; p l, 
ml, a l, regions of the posterior, middle, and 
anterior lateral branches; a r, anterior radicular. 
In the r ght half of the figure the more deeply 
shaded part indicates the region supplied by the 
central arteries. FUNCTIONS. 
189 
caput. A series of anterior radicular arteries enter with the anterior 
roots, and between them and the posterior horn are anterior, middle, 
and posterior lateral arteries in corresponding parts of the lateral 
column. The branches into the lateral column do not reach the 
grey substance; the branches in the grey substance extend into the 
inner part of the lateral column. 
The veins of the cord correspond in the main to the arteries, but a 
larger proportion of the blood passes into the peripheral system. 
Some, especially those of the white substance, pass outwards along 
the septa, and those on the surface of the sides and back of the 
cord are gathered into a posterior spinal vein. Others, especially 
of the grey matter, pass inwards to a large vertical vein that lies 
in the grey commissure, a little distance from the central canal on 
each side (v. Fig 73 ; compare also Fig. 57), from which branches pass 
forwards to the anterior median fissure, and through this to an 
anterior spinal vein. The anterior and posterior spinal veins 
deliver their blood, through communicating veins, into the large 
venous plexuses that lie outside the dura mater, and which receive 
blood also from the bones, and from the structures and skin behind 
the spine. But the veins of the spinal cord cannot be injected from 
these plexuses, not because there are valves in the connecting branches, 
but apparently because they form so trifling a proportion of the total 
connections. From the plexuses blood passes to the various vertebral, 
cervical, and intercostal veins. 
Although there is a vertical continuity of the vessels of the cord, 
it is probable that the course of the circulation is, in the main, hori- 
zontal. From the very tortuous course of the path by which arterial 
blood enters the cord, it is evident that the pressure to which the 
arteries of the cord are exposed must be far lower than that in the 
arteries of the brain, and hence they are far less liable to degeneration 
and to rupture. On the other hand, the conditions that prevent an 
injection of the plexus of veins outside the dura mater from passing 
into the veins of the cord, must save the latter from the extreme over- 
distension to which they would otherwise be liable when there is a 
hindrance to the return of blood from the plexus. 
FUNCTIONS OF THE SPINAL COED. 
We are now in a position to consider tlie functions of fhe spinal 
cord, and the structures by which they are subserved. The functions 
are these: (1) The spinal cord conducts motor nerve impulses from 
the brain and sensory impulses to it. (2) It constitutes a series of 
centres for reflex action. (3) It contains certain centres that ulti- 
mately govern nervous action in structures under the immediate 190 
SPINAL COED. 
control of the sympathetic system, the bladder, rectum, blood-vessels, 
&c. (4) It influences the nutrition in all parts to which its nerves 
extend. 
Motor Conduction.—The chief facts regarding the physiology of 
the motor path have been necessarily considered in the account of 
its anatomy. We have already seen that the path of motor impulses 
is through the pyramidal fibres (in the anterior and lateral pyramidal 
tracts), the anterior cornua, and the anterior nerve-roots. The gan- 
glion-cells form part of the path, and so also probably does that part 
of the plexus of fibrillae in the cornu which intervenes between the 
pyramidal fibres and the ganglion-cells. We have seen that the 
crossed relation of the cerebral hemisphere with the limbs is subserved 
by the decussation—chiefly at the pyramids, partly along the cord 
from the one anterior to the opposite lateral tract, and apparently to 
a slight extent above the chief crossing, since some degenerated fibres 
have been seen in the anterior pyramid opposite to the lesion of the 
brain. We have seen also that we are still ignorant of the mode of 
connection of the motor cells with the cerebral hemisphere of the 
same side in the case of the muscles that habitually act with their 
fellows on the opposite side. These can be acted on by either hemi- 
sphere in degree that approaches equality in proportion as they act 
together, and is almost complete in muscles such as the intercosta,Is, 
which can only act together. It is great in the case of all the trunk 
muscles and of those of the leg, less in those of the arm. This relation 
is further considered in the account of hemiplegia in vol. ii, to which 
it specially pertains. The variations in the decussation of the chief 
set of fibres suggest that the variations in observed facts bearing on 
the question may merely represent variations that exist in nature. 
The connection may be subserved by fibres that never decussate, and 
by fibres that recross in the cord, in different degrees in different 
persons. 
The large fibres of the anterior, motor, nerve-roots ai'e far more 
numerous than the fibres of the pyramidal tracts, and so also are the 
cells of the anterior horn, from which the large root-fibres proceed. 
Nevertheless, it is probable that all these cells and root-fibres can b« 
excited through these tracts. Hence many cells must be related to 
each of the pyramidal fibres. We do not know precisely how the 
latter end, but it is probably a complex mechanism, constituted by 
minute nerve-cells and fibrillary network. This mechanism is such 
that the stimulation of certain pyramidal fibres excites to action a 
much greater number of nerve-cells, so connected and arranged as to 
produce, through the related nerve-roots, a complex movement, in 
which many muscles may take part. The nerve-cells thus connected 
may not all be at precisely the same level, and only some of those at a 
given level may be thus associated. The simpler the movements, and 
the fewer their possible variations, the fewer pyramidal fibres may 
suffice for the production of the movements. Thus it is conceivable FUNCTIONS. 
191 
that tor such movements as those of the intercostal muscles, which 
are simple and constant, very few pyramidal fibres may suffice, 
whereas a much larger number must be necessary for the highly vari- 
able movements of the hand. It is also possible that the pyramidal 
impulses pass not only through their own end-structures, but also 
through part at least of the muscle-reflex centre, and that this enters 
into the mechanism that enables these impulses to effect a more 
complex and varying movement than could otherwise be produced. 
Representation of Movements in the Spinal Cord.—It is 
important to inquire how far we can identify these various motor 
mechanisms of the anterior grey matter. There are several sources of 
information on this subject. We have already seen that the arrange- 
ment of fibres in the anterior roots is such as to associate certain move- 
ments with certain nerve-roots, and it is a reasonable assumption that 
this corresponds, to some extent at least, with the arrangement in the 
grey matter. The sources of our information ou this point are the 
limited facts of anatomy, rare cases of restricted disease of the nerve- 
roots in man, and especially the experiments of Eerrier and Yeo on 
monkeys. We have already considered the indications that these 
experiments afford, and their suggestiveness, and we have seen that 
their value is relative rather than absolute. As regards the grey matter, 
we must remember also that there may not be a strict horizontal corre- 
spondence between the nerve-roots and the nerve-cells, because it is 
probable that some root-fibres enter the antero-lateral white columns, 
and are connected Avith nerve-cells at a higher or lower level than that 
at which they leave the cord. Another source of inflammation is the 
degeneration of nerve-cells that follows slowly on an amputation of a 
limb, and the condition of the spinal cord in congenital absence of 
part of a limb. The last and most important source of information is 
supplied by cases of limited disease of the anterior cornua, in which 
the position of the lesion and the distribution of the resulting palsy 
can he compared. Destruction of nerve-cells causes degeneration of 
the motor fibres proceeding from them, and wasting of the muscles to 
which those motor fibres proceed. This alone affords us certain know- 
ledge. Cases of clear significance are, however, rare, and it will be 
long before our knowledge can he complete. Meanwhile, we may 
learn something of the central association of muscles by observing 
what muscles are most frequently paralysed together by such disease. 
This subject has been carefully studied by E. Remak,* and hv 
Tkorburn.t and many valuable isolated observations have been pub- 
lished. It is only the associations which are frequent that can be 
* * Arcliiv f. Psychiatrie,’ vol. ix. 
f * Brain,’ January 7th, 1887, and October, 1888 The facts were observed on 
cases of injury. He associates each muscle with a single spinal nerve, but these 
nerves are only collections of roots that are severally continuous, as are the groups 
of nerve-cells within the cord, and it is certain that the roots related to many of 
the muscles go into adjacent spinal nerves. 192 
SPINAL CORD. 
allowed significance, because it is not uncommon to have more than 
one focus of disease in the grey matter. The following summary 
presents the conclusions that seem probable from the evidence at 
present available * 
The various facts for the most part fully confirm the conclusion of 
Remak, corroborated by the experiments of Perrier and Yeo, that 
most movements and muscles are represented in vertical tracts, and the 
whole anterior grey matter, at any one nerve-segment, contains cells 
that are concerned with different movements. An extensive lesion of 
small vertical extent may thus weaken many movements, but abolish 
none. The special representation of the muscular functions, i. e. 
of definite movements, is no doubt related to special groups of nerve- 
cells, but a single group may be concerned in more than one associated 
movement. Different groups are probably intimately connected, 
because we know that the contraction of any muscle is accompanied 
by a slighter but proportioned contraction of its antagonists. Anato- 
mical connections in both spinal cord and braiu doubtless underlie 
this association. 
Cervical Reqion.—The highest cervical region apparently contains centres 
for the small rotators of the head, and the depressors of the hyoid bone were 
found by Beevor and Horsley to be related to the first two pairs of nerves, the 
sterno-hyoid and sterno-thyroid chiefly to the first and the omohyoid to the 
second.f The upper part also contains centres for the muscles of the neck, 
especially for the sterno-mastoid and upper part of the trapezius. The dia- 
phragm is probably represented in the grey matter at the level of the roots of 
the phrenic nerve, the fourth cervical. In the brachial l-egion of the cervical 
enlargement, the muscles of the shoulder are represented chiefly in the upper 
part; the intrinsic muscles of the hand in the lower part. The flexors of the 
elbow are represented above its extensors, and the supinators and extensors 
of the wrist above the flexors of the wrist. 
Deltoid, scapular muscles, pectoralis, and serratus.—The fifth and sixth 
segments, for the most part the sixth, and probably the outer group of nerve- 
cells. J The centres for the two parts of the pectoralis are separate, and are 
associated—the clavicular with that of the serratus magnus, the costal with 
that of the latissimus dorsi (see p. 30). These associated muscles are represented 
near together, but not at the same spot; the association is often reproduced in 
disease of the anterior cornu, the clavicular part being affected together with 
the serratus, but one muscle may suffer without that which is commonly 
associated with it. 
The Flexors of the elbow and supinators probably correspond nearly in level 
# A useful summary of the evidence up to the middle of 1884 was given by Dr. 
Allen Starr, in the‘American Journal of Neurology,’ Aug. aud Nov., 1884. The 
subject is a tempting one for theory, but it is very important to keep to the solid 
ground of facts, however limited it may be in extent. 
f Chiefly the posterior belly of the muscle, by a branch joining the glosso- 
pharyngeal. The other muscles named (including sl'ghtly the anterior belly of the 
omohyoid) are innervated from the first cervical by a branch joining the hypoglossal. 
J Thorburn (loc. cit.) refers the infra- aud supra-spinata with much probability to 
the fourth pair of nerves. FUNCTIONS. 
193 
with the deltoid. The whole of this series of muscles may be affected alone by 
disease of the nerve-roots (see p. 91) or of the grey matter, and then we have 
the “upper arm type” of palsy, described first by Erb. 
Extensor of the elbow (triceps): probably tbe middle of the brachial region, 
chiefly the seventh segment, extending down to the eighth, and perhaps up to 
the sixth, possibly chiefly in the outer group of nerve-cells. 
The Extensors of the wrist are represented above those of the elbow; probably 
chiefly at the sixth or sixth and seventh segments, and not from the postero- 
external, but from the other groups. Flexors of the wrist: below the extensors, 
nearly on the same level as the extensors of the elbow, at the seventh and eighth 
segments, and probably also from one of the outer groups of cells. 
nators have nearly the same representation as the flexors of the wrist. 
Long Extensors of the fingers: upper part of the brachial region, about the 
level of the sixth or between it and the seventh segment; probably from one 
of tbe anterior groups (not from the postero-lateral group). Long Flexors of 
the fingers: below the extensors ; probably seventh or eighth segment. 
Intrinsic muscles of the hand: lowest part of the brachial region, and the 
thenar muscles a little higher than the interossei; the latter being represented 
in the first dorsal segment.* The intrinsic muscles (like the long extensors) 
are probably related less to the outer than to the inner and anterior groups. 
The two sets of muscles are related both in action and in central connection, as 
was illustrated by a case of concussion-lesion under my care, in which the two 
outer interossei were paralysed and wasted, and also the part of the long 
extensor supplying the two outer fingers, but no other muscles. 
Lumbar Enlargement.—Our knowledge of the representation of muscles in 
the lumbar enlargement is very slight, and we have scarcely any definite facts 
concerning their relation to the cell-groups. The postero-external group 
preponderates over the others in size, even more than in the cervical cord, and 
doubtless also in importance. The few pathological observations of changes in 
the several groups are not altogether consistent. The chief facts available 
relate to the probable segmental level and association of the centres, and are as 
follows: 
Cremaster, second lumbar segment. Psoas, second, iliacus, third, lumbar; 
the two muscles (one in function) are probably related to a group of cells ex- 
tending through botli segments. Adductors, fourth lumbar segment. Gluteal 
muscles (extensors of hip), fourth and fifth lumbar segments. 
Extensors of knee, third and fourth lumbar segments, probably from the 
same group as the flexors of the hip ; the two sets of muscles are often affected 
together, and sometimes the adductors suffer xvith them. Tbe Sartorius is 
probably related to the third segment, but not to the same cell-group as the 
extensors of the knee (to which, indeed, it does not belong; seep. 40). It usually 
escapes in atrophic palsy of the extensors. Flexors of knee, fifth lumbar and 
first sacral segments. Their centre is thus below and certainly distinct from 
that of the extensors. 
The muscles of the lower leg, moving the foot and toes, are related to the 
* This is the indication of the majority of cases. Nevertheless Sahli has recorded 
a case of atrophy of all the intrinsic muscles of the hand, in which the lesion did not 
extend below the seventh segment: the eighth and first dorsal were perfectly 
normal. I have seen a case of atrophy limited to the deltoid and intrinsic muscles 
of the hand, due to an acute process, probably haemorrhage, hut in this case there 
may have been two lesions. 
VOL. I. 194 
SPINAL COED. 
fourth and fifth lumhar and the first sacral segments. The calf muscles, the 
tibialis anticus, and the peroneus longus have certainly separate centres, and 
are often affected separately. The tibialis anticus may suffer alone, or may 
alone escape when the other muscles in front of the leg are paralysed. The 
muscles of the calf may be affected when those in front of the leg are not. It 
is probable that the peroneus longus is the highest in central representation, 
and is related to the fourth lumbar segment. 
The inlrins13 muscles of the foot, especially the interossei, are the lowest in 
central relations, being connected with the second sacral segment. The position 
of their centres, in the lowest part of the lumbar enlargement, thus corresponds 
to that of the analogous muscles of the hand, in the lowest part of the cervical 
enlargement. 
Sensory Conduction.—Our knowledge of the sensory path in the 
cord is far less definite than that of the motor path, in spite of the 
fact that it has been the subject of a large number of experimental 
investigations. The subject is a very difficult one for experimental 
solution, on account of the difficulty of ascertaining the condition of 
sensation in animals. The indications afforded by disease are equivocal 
for another reason. We have seeu (p. 60) that, in the sensory nerves, 
a lesion which permanently interrupts motor conduction may scarcely 
affect sensory conduction, and the same thing is apparently true of 
the spinal cord. If loss of feeling results from an acute lesion, it 
often quickly passes away, although motor palsy remains complete 
and absolute, and this when all the elements of the cord seem equally 
implicated in the morbid process. In cases of such chronic disease 
as compression, which when slow must act on all the structures in 
nearly equal degree, the same escape of sensory conduction is often 
observed. Difficulties are encountered whatever mode of interpretation 
of the phenomena we adopt, and the fact of importance to our present 
problem is that we are not yet able strictly to compare structural and 
functional damage when the former is moderate. When the damage has 
been slowly produced it may be apparently great, and yet function may 
not be much impaired, especially the lower function of conduction of 
nerve-force. The significance of these facts as regards the problem of 
sensory conduction in the cord is that we must be cautious in drawing 
any conclusion from the persistence of sensation. We cannot infer, 
because supposed sensory tracts are visibly diseased in a case in which 
there was no loss of sensibility, that these tracts have not the function 
assigned to them, unless we can feel sure that all the axis-cylinders 
are destroyed. This we can seldom do; a,nd for this reason, and 
because morbid processes are ofteu wide in distribution, the evidence 
that can be obtained by comparing the position of lesions with the 
sensory symptoms they produce is limited and uncertain. Other 
sources of information are the effect of partial lesions of the cord, 
intense in degree, but limited in area, especially traumatic lesions 
affecting one half of the cord or part of one half. Cases of this kind 
are of high value, but in few, at present, have the extent of lesion and 
the range of symptoms been accurately ascertained. FUNCTIONS. 
195 
Hence physiologists have relied chiefly on the results of experiments on 
animals. Unfortunately the help these can give is also reduced to a literal 
minimum hv the difficulties of experimentation and of interpretation; the 
physical difficulties on the one hand, the functional perplexities on the other. 
Some clear facts have been ascertained, and other results have been obtained 
that still wait certain interpretation. The earlier experiments of Brown- 
Sequard established one important fact, which has been fully confirmed by 
pathology, that the chief part of the sensory path crosses the middle line soon 
after it enters the cord, and passes up to the brain on the other side. The experi- 
ments by others which seem to deserve the greatest weight are those of SchifE 
and Woroschiloff. The latter employed, as a test of upward conduction, the 
effect of stimulation of the sensory nerves on the vaso-motor centre, availing 
himself also, in some experiments, of confirmatory evidence of pain. Woro- 
schiloff’s experiments have also been repeated by Sherrington with conclusive 
corroboration. These various experiments are far from certain in their indica- 
tions, and the degree of uncertainty is also the subject of much difference of 
opinion. Taken together, they point to the white substance as containing the 
sensory path—the posterior and the antero-lateral columns. In these two 
regions there are fibres which, degenerating above a lesion, must be presumed 
to conduct upwards, and extend through the spinal cord to the medulla. These 
are the fibres of the posterior median columns and the antero-lateral ascending 
tract. But the posterior median fibres may be extensively degenerated when 
sensation is unimpaired. We shall presently see the probable meaning of this 
fact. The experimental evidence that there is sensory conduction in the lateral 
columns is not opposed in the same way by pathological or anatomical facts, 
and, indeed, presents some harmonies with them which should be allowed 
weight,—although no scientific evidence is more easily undervalued and even 
ignored than that which consists in the agreement of facts in different regions 
of investigation. 
The subject, however, at the present time is too far from even the semblance 
of settlement to make a discussion of the evidence worth the space it would 
need, especially in a work dealing with practical medicine. It is only desirable, 
therefore, to point out certain leading facts and leading considerations. 
Experiments suggest that the lateral columns conduct the impressions that 
are felt as pain, and that act on the vaso-motor centre—conduct them in 
animals chiefly on the side of the-cord opposite to that on which they are 
produced, slightly on the same side. They suggest also that sensations of touch 
are conducted in the posterior columns of the cord. In man the paths for both 
sensations are on the opposite side of the cord. We may accept as certain 
the fact that the tactile or painful impulse we feel crosses the middle line 
soon after entering the cord ; it is probable that some impulses that we do not 
feel do not cross. We must never forget that there is strong reason to believe 
that only a minority of the impulses that traverse afferent nerves affect our 
consciousness. 
But how few fibres there are, in either situation, that can subserve the func- 
tion. The fibres of the posterior median column pass up the same side of the 
cord, and in the posterior columns elsewhere we have, besides the remaining 
root-fibres and the “ comma tract,” an apparently insignificant number of fibres, 
and these do not degenerate through any considerable extent of the cord. 
Nevertheless the front of the post-external column contains a very large 
number of exceedingly small nerve-fibres, which have attracted less notice than 
they deserve. In the lateral column, moreover, we must, in like manner, 196 
SPINAL COED. 
dismiss the pyramidal and cerebellar tracts—the latter because disease has 
proved to us that the patli of these sensations is by the pons and not the cere- 
bellum. Still, we have here the antero-lateral ascending tract, and we have 
also the ground bundles, and the question presents itself which seems to have 
been tacitly taken as a greater difficulty than it really is—does the absence 
of the continuity which would cause continuous degeneration, exclude such con- 
duction as we need ? The fibres that do not degenerate through long courses 
may degenerate through short tracts, passing into the grey matter to nutrient 
cells. Prof. Foster has suggested such an “ in and out” path as probable for 
this sensory conduction. But there are many difficulties in the conception of 
such very frequent interruption by nerve-cells as this theory involves. A 
special obstacle, moreover, to the opinion that any part of the path involves the 
grey matter is the invariable escape of sensation in anterior polio-myelitis, 
which must often involve at least the intermediate grey substance. But it is 
possible that there may be many fibres which undergo no secondary degenera- 
tion, and yet habitually conduct in one direction. Because we admit, as we 
probably ought to admit, that degeneration in a given direction means habitual 
conduction in that direction, it does not follow that the absence of degeneration 
means the absence of such habitual conduction, although the assumption seems 
to underlie a good deal of current reasoning on the subject. There are many 
fibres of unknown function, which do not degenerate, scattered even among 
those of the posterior median column, and there are still more in the post.- 
external column, while they are comparatively abundant in the anterior column. 
Still, they are not numerous enough to save us from the second difficulty, 
that the fibres we can look to are, taken altogether, insufficient in number to 
subserve the marvellous differentiation of sensation in the periphery—differ- 
entiation in quality of feeling and especially in locality of feeling. But a 
difficulty may become inoperative, without ceasing to exist, by being absorbed 
in a still larger difficulty of tbe same kind. If we avail ourselves of all the 
structures of the spinal cord that can conceivably subserve upward conduction, 
we fail to find room for the separate conduction of impulses which, nevertheless, 
the spinal cord must separately convey. 
On only one hypothesis is it possible to conceive such conduction. The in- 
creased power of the microscope has shown us that each axis-cylinder, so called, 
is apparently not a simple body, but a compound structure, composed of fibrillae, 
and comparable, in point of fact, to a bundle of nerve-fibres. The sensory 
axis-cylinders divide at their peripheral distribution in the skin, and we can 
scarcely conceive them dividing except by their fibrillm. It seems to follow of 
necessity that each sensory area of distinct perception must be subserved by one 
of these fibrillse. It is conceivable that the impulses may keep each to its own 
fibrillary path, even if an axis-cylinder contain as many fibrillse as a nerve 
does fibres. We have, indeed, seen that such fibrillse seem to keep separate 
even in traversing a nerve-cell. It is only by such an arrangement that it 
seems possible for the sensory impressions from skin and tissue, of touch, 
pain, and temperature, to be carried to the brain so as separately to excite 
certain nerve-cells of the cortex. 
If these considerations have weight we cannot exclude the lateral 
and posterior columns from the function of sensory conduction on 
account of the scanty fibres we can discern to subserve the function, 
and may consider what evidence on the point disease and injury 
afford in man. FUNCTIONS. 
197 
Unilateral lesions of the spinal cord, which cause loss of sensibility 
of the skin, do so on the side opposite to the lesion. This is true of 
all forms of sensibility. They thus prove, beyond doubt, the decussa- 
tion in the spinal cord of the path from the cutaneous nerves of pain 
(i. e. common sensibility), of touch, and of temperature. An analysis of 
the cases in which both effect and lesion have been exactly ascertained 
—which will be considered more fully when these lesions are described 
—suggests certain other conclusions regarding the position of these 
paths. The facts suggest, first, that the paths for sensations v,£ pain 
and of touch are not near together. Sensibility to pain has been lost in 
almost all recorded cases, but that to touch in only two thirds. They 
suggest, secondly, that the two paths for tactile sensibility are nearer 
together than are the two paths for common sensibility. In no case 
of chiefly unilateral lesion has sensibility to pain been lost on both 
sides, whereas in two recorded cases sensibility to pain was lost on the 
side opposite to the lesion, while that to touch was lost on both sides.* 
Both these conclusions harmonise with the suggestion of experiment, 
that painful sensations are conducted in the lateral column, those of 
touch in the posterior column. These conclusions, moreover, are sup- 
ported by the facts of two important cases of injury to the cord 
which afford direct localising indica- 
tions. One is a case, recorded by 
myself,f in which the spinal cord 
in the upper cervical region was 
damaged by a small spiculum of bone 
being driven against it by a bullet, 
which, entering the mouth, lodged 
in the body of the third cervical 
vertebra. The extent of the lesion of 
the cord is shown in Fig. 82. The 
chief injury is clearly to the latei'al 
column and grey matter, the posterior 
column being merely swollen, appa- 
rently bv oedema. The affected part was the seat of hemorrhage and 
hemorrhagic infiltration. The effect was entire loss of sensibility to 
pain on the opposite side without any impairment of tactile sensi- 
bility. To this the other case, recorded by Muller,J is almost a com- 
plement. A stab-wound divided the whole of one half of the cord, 
including the posterior column, and also the posterior column of the 
Fig. 82.— Section of spinal cord be- 
tween the second and third cervical 
nerves, contused by gunshot inj ury. 
* It is possible that tactile sensibility may have been lost, in other cases, on the 
second side, i. e. on the side of the lesion, and the loss may have escaped notice in 
•consequence of the exaltation of sensibility which is commonly present, and which 
is presumably due to the nerves of common sensibility, 
f ‘ Clinical Society’s Trans.,’ vol. xi, 1878, p. 21. 
J * Beitrage zur Path. Anat. und Phvs. der Ruckenm.,’ Leipzig, 1871. Abstracts, 
which supplement each other, and, together, give a full account of the case, will be 
found in Kobner’s article on unilateral lesions, * Deut. Arch. f. klin. Med.,’ 1877, 
Bd. xix, p. 190; and in ‘Virchow’s Jahresbericht,’ 1871, Bd. i, p. 152. 198 
SPINAL COED. 
other side almost up to tbe nerve-roots. The whole of both postero* 
median columns was thus divided. Tbe effect was loss of sensibility to 
pain on the side opposite to the lesion, and of that to touch on both 
sides. 
Thus there is strong reason to regard the antero-lateral ascending 
tract as containing tbe patb for sensibility to pain. As to the path of 
tactile sensibility we must wait for further evidence. The fibres that 
degenerate upwards in the median columns, passing to them from tbe 
external posterior columns, and constituting so large a proportion of 
their mass, apparently come from the muscles. We may, however, 
remember that many fibres pass to the posterior columns from the 
grey matter, and also from the posterior commissure in the middle 
line; some of the former may also come from the posterior commis- 
sure, and both these sets of fibres may have crossed in the middle line. 
It is possible that these fibres conduct tactile sensibility, and that 
they are mingled with those that conduct muscular sensibility. This 
theory, however, can only be regarded as a suggestion for future 
observations. 
The conduction of impulses from the muscles is certainly in the 
posterior median columns. This is clearly shown by the tacts of the 
pathology of tabes. The function of the direct cerebellar tract has 
still to be demonstrated. There are certain resemblances between its 
fibre-relations and those of the posterior median columns which give 
countenance to Flechsig’s theory that it conveys impressions from the 
muscles of the lower part of the trunk and between the trunk and 
lower limbs. But the probable origin of its fibres from the cells of the 
posterior vesicular column, and the mystery attaching to the latter, 
give additional obscurity to this structure. The fine nerve-plexus 
between its cells seems connected with fibres of the posterior roots, 
and this plexus is said to atrophy early in locomotor ataxy.# Tho 
obscurity will, indeed, be dispelled if we can accept the speculation of 
Sherrington that this cylinder is really part of the series of ganglia 
on the posterior nerve-roots, which occupies a position within the 
spinal cord, and is continuous instead of broken into ganglia. 
The path for sensations of temperature is still unknown. The fact 
that this sense is frequently impaired with sensibility to pain suggests 
that the two paths may be near together in the lateral columns. More 
than this cannot be said. 
But we have to consider another problem in our study of the 
sensory path. The same impression that is felt may excite a reflex 
action. For this, afferent root-fibres must end in the grey matter of 
the cord. Are the two functions subserved by the same or by different 
fibres? A similar question presents itself with regard to the muscle- 
nerves. If the ascending degeneration in the postero-median column, 
when the cauda equina is diseased, is admitted, as it must be, as 
* Lissauer, Oppenlieim, &c. See Mott, “ Bipolar Ceils of the Spinal Cord,”- 
, Brain,’ part lii, 1890. FUNCTIONS. 
199 
proof that these root-fibres pass up without interruption, the muscle- 
reflex action must be subserved by other fibres. For it, however, 
comparatively few may suffice. With regard to the other sensory 
fibres, the evidence at present suggests that all undergo inter- 
ruption in the spinal cord, since no other paths have yet been 
found degenerated when a lesion has been confined to the nerve-roots. 
If so, the same fibres probably subserve sensation and reflex action, 
the nerve-cells or fibrillary plexus providing a mechanism for the 
division of the path and diversion of the impulses. No impression, 
in health, causes a true reflex action that does not also produce a 
conscious sensation. 
We know very little of the serial representation of cutaneous 
sensibility in the spinal cord. It is probable, however, that there 
is a progressive representation of the skin in the posterior nerve-cells 
without relation to the nerve-trunks and with only a slight relation to 
the nerve-roots. Correspondence with the latter must not be assumed. 
In the roots the serial representation is along the axis of the limb, not 
across it, as it probably is in the nerve-cells. In the dorsal cord, 
ascending disease often causes an affection of sensation which extends 
around the trunk at higher and higher levels. In the limbs we have 
indications of the same arrangement: the soles and palms may be 
affected alone, and anaesthesia may extend on the limb to a certain 
level, irrespective of nerve distribution. This is often seen in the legs. 
I have known anaesthesia in the arms, due to disease of the cord, to 
cease midway between shoulder and elbow, at the same level around 
each arm. Disease of the cord may affect sensation on the tips of the 
fingers only. It is probable that the ascending course of many of 
the root-fibres subserves a rearrangement of representation in the 
cells, and provides also for a special connection of the tactile nerves 
from each part of the skin with the motor cells for the muscles beneath 
—so conspicuous in many of the cutaneous reflexes. 
Reflex Action.—The grey matter of the spinal cord constitutes a 
series of reflex centres, some of which must be of considerable ver- 
tical extent and much complexity, and are subserved possibly not 
only by the grey matter, but by the short fibres that in the several 
white columns seem to connect the grey matter at different levels. 
The passage of the root-fibres upwards and downwards in the cord, 
before they turn into the grey matter (conspicuous in the posterior 
roots), also, as we have noted, constitutes an arrangement for spreading 
the afferent impulses through a considerable vertical extent of the cord. 
We have already seen (p. 14) that we must distinguish two 
forms of reflex action—the cutaneous reflex action and the muscle- 
reflex action, the latter producing the “ myotatic irritability ” which, 
as we assume, determines the so-called “tendon-reflex contractions.” 
The first form of reflex action is not, however, limited to impres- 
sions on the cutaneous nerves. It may be produced by stimulation of 
the nerves supplying the deeper structures, including those of the 200 
SPINAL CORD. 
tendons and muscles. The attempt to obtain the knee-jerk mav cause 
a true reflex action as well as its special effect, the two being separated 
by an appreciable interval of time (see “Locomotor Ataxy ”). Reflex 
action from the skin is apparently subserved by all the sensory 
nerves, since it may continue, although the nerves for either pain or 
touch have ceased to act, in consequence of those degenerative pro- 
cesses by which function is sometimes abolished in as complete 
degree and with as pirecise limitation as the physiological inquirer 
could desire. 
The central process concerned in reflex action must take place 
between the posterior nerve-roots, by which the sensory impulses reach 
the cord, and the anterior roots by which the motor impulses leave it. 
The motor ganglion-cells form part of the reflex centre, and the rest 
of the centre is doubtless constituted by part of the fibrillary plexus, 
the minute nerve-cells within it, and also by the sensory nerve-cells. 
The whole path between and including the in- and out bearing nerves 
may be spoken of as the “ reflex arcthe grey matter concerned 
being called the “reflex centre.” In this “centre” the sensory 
impulse is transformed into—or rather gives rise to—a motor impulse, 
usually much greater in the degree of its energy. Within the centre 
there are paths established by the connections between the nerve- 
structures, of which only a few are in functional use. It is easy 
to conceive that the functional action takes place more readily in 
some lines than in others, and these lines of easiest action are often 
spoken of as “ lines of least resistance,” and are said to determine the 
form of the reflex action. 
The stronger (within limits) the afferent stimulus, the more widely 
does the process spread in the centre, and the more extensive is the 
movement produced. Thus a slight touch on the sole may cause only 
a movement of the foot, while a prick may cause a movement of the 
whole limb. At the same time there is much more than degree involved 
in the difference between these two stimuli. The impression that is felt 
as pain causes a quick simple movement of the part, in which chiefly 
the flexors are involved. It is a movement obviously to withdraw from 
harm, and it is proportioned, in energy and extent, to the intensity 
of the stimulation. To this, however, there is one limitation:—a 
strong impression of pain may prevent all reflex movement by 
exerting an inhibitory influence on the centres. On the other hand, 
a tactile impression causes a much more complex movement, which 
does not bear a simple relation, in extent and energy, to the degree 
of the sensory impulse, but is also influenced by the quality of the 
impression at the place at which it is produced. Thus the reflex move- 
ment produced from the palm or sole is especially elaborate; it may 
present an indication of the central relations by which the purposed use 
of the extremities is facilitated. The effect of all painful impressions 
is similar, whether these are produced through the nerves of the skin 
or those of deeper structures. The reflex action caused by pinching FUNCTIONS. 
201 
a tendon is just tlie same as that caused by a pinch of the shin over 
the tendon. Even impressions from the afferent muscle-nerves cause 
a similar reflex movement. Thus there is no real distinction between 
the deep and superficial true reflex action. 
The muscle-reflex action which is assumed to exist between the 
afferent and efferent nerves of a muscle (and to underlie the myo- 
tatic irritability which permits the knee-jerk, &c.) has been already 
considered in discussing the theory of this irritability. It is appa- 
rently a uniformly simple relation between the two sets of nerves 
for the same part of a muscle; the reflex action is confined to these, 
and does not spread through a wider extent of the grey matter, as 
that from the skin frequently does. When a muscle is made tense, 
or its tendon is tapped, the mechanical stimulation influences all the 
afferent nerves or all the muscular fibres, and the whole muscle neces- 
sarily responds. The motor ganglion-cells of the anterior horn must 
form part of the centre for each form of reflex action, but that 
portion of the centre which intervenes between the afferent nerves 
in the posterior root and the motor cells must be distinct in part 
or altogether. Beyond this we can say nothing of the relation of 
the two centres. 
These reflex centres are subject to control by higher centres, as are all 
lower centres in the nervous system. All true reflex action, e. g. that 
from the skin excited by a touch or prick, is controlled and kept mode- 
rate by an influence from the brain, for it becomes excessive when the 
influence of the brain is stopped, as by a lesion interrupting the spinal 
cord; it is increased in all parts that are connected with the cord 
below the lesion. We have no precise knowledge of the seat of the 
controlling centre or of the path by which the control is exerted. 
In frogs, however, the restraint seems to be exerted by the optic 
lobes ; in man it is less likely to be exerted by the homologous corpora 
quadrigemina than by the optic thalamus. The mechanism must, 
however, be complex, since the restraining influence may be increased 
by disease in some parts of the brain ; many cerebral lesions which 
cause hemiplegia, cause also a diminution of cutaneous reflex action 
on the paralysed side. The effect seems to indicate that the cerebral 
centre which controls reflex action is itself habitually controlled by a 
higher centre, perhaps in the cortex. When this is destroyed, or the 
path from it is interrupted, the controlling centre passes into a 
condition of increased activity, and the reflex action is lessened. 
This is a theory only, but it seems impossible otherwise to explain 
the facts. 
The muscle reflex centres seem also to be under the control of other 
centres, because, if there is disease of the cord higher up, they also pass 
into a condition of increased activity. But the phenomena of their 
disturbance present three important points of difference from those 
of common (e. g. cutaneous) reflex action. (1) We know with cer- 
tainty the path disease of which determines their excess : it is the 202 
pyramidal tract. (2) Disease of the brain does not cause a permanent 
diminution in the action of the muscle-reflex centres, as it so frequently 
does in the case of the centres for cutaneous reflex action.* On the 
contrary, disease of the pyramidal fibres in the brain causes the same 
excess of this form of reflex action as does disease of the pyramidal fibres 
in the cord. (3) The excess does not, as a rule, quickly follow au inter- 
ruption of the path from the brain, as does the excess of superficial 
reflex action. There may, indeed, be an immediate, usually temporary, 
excess, coinciding with “early rigidity” from the irritation of the 
pyramidal fibres, but the permanent excess comes on at the end of a 
week or ten days, and gradually increases. 
The explanations may be these. The slowness with which the reflex 
action usually becomes excessive is conspicuous, and its significance 
must be considerable. The lesion of the pyramidal fibres causes their 
degeneration below the lesion, and this must involve their termination 
in the grey matter. The excess of action of the centres may be the 
result of the degeneration of the terminal structures, which may 
constitute a controlling mechanism that normally restrains the activity 
of the muscle-reflex centres. The interval which elapses before the 
excess is manifested may be due to the fact that there is little 
tendency to increased activity; that hut slight control is habitually 
exercised or needed; and that the capacity for over-action is gradually 
developed and gradually increases—increasing capacity being deve- 
loped by the increased activity. 
It is probable that the voluntary impulses pass from the termina- 
tion of the pyramidal fibres to the motor cells through structures 
of which this muscle-reflex centre forms part, and that therefore 
its elements must be in part excited to action by pyramidal impulses 
—a conclusion quite compatible with a restraining influence exerted 
by these fibres or their endings when no volitional impulses descend 
them. 
The chief local forms of superficial and muscle-reflex action have 
been already described (see p. 14 et seq.). Their centi*es are found 
in the corresponding segments of the cord shown in the table at 
p, 210. 
Adaptation to Posture.—Every difference in posture involves a 
difference in the distance between the attachments of the muscles of 
the part. When the muscles are at rest they present always a certain 
state of “ tone,” which, being equal in every posture, must vary auto- 
matically with every change of posture, however brought about. In 
passive movements the muscles that are elongated and those that are 
SPINAL CORD. 
* A very rare exception to this rule will be mentioned when the functions of the 
brain are considered Moreover the knee-jerk is abolished in some cases of tumour 
of the cerebellum, a phenomenon to be remembered in connection with the fact that, 
while one part of the afferent impulses from the muscles act on the cord, another 
part apparently pass up to the cerebellum. See the account of co-ordination of move- 
ment on the next page. 203 
FUNCTIONS. 
shortened adapt themselves to the change as it proceeds. Apparently 
the increased tension on the former makes them yield to the move- 
ment, and the lessened tension on the latter makes them contract, each 
set thus preserving its proper tone. The tone of a muscle seems to be 
produced by a reflex process, due to a certain state of the motor cells 
regulated by the impressions from the afferent muscle-nerves. These, 
as we have seen, are produced by two mechanical influences, the 
lateral pressure of the fibi’es (as in the pain of cramp) and the tension 
on the muscle. An increase of the latter, in passive movement, 
seems to lessen the activity of the cells and permit the fibres to 
elongate ; a diminution increases the activity of the cells and causes 
the fibres to shorten. Whether any other afferent impressions 
influence the process we do not know. 
Co-ordination of Movement.—The co-ordination of muscular 
contractions, which results in the ordination or ordering or arrange- 
ment of movement, has been already described (p. 7), so far as its 
general features are concerned. We cannot ascribe to the spinal cord 
any process that can be designated the arrangement of movement; 
siuce the muscular contractions correspond to the activity of the motor 
cells of the cerebral cortex and to the corresponding impulses along the 
pyramidal fibres. These determine the initial activity of the motor 
cells of the cord both for the muscles that move a part, and for those 
that oppose the action of the others and give steadiness and uni- 
formity to the movement. But these impulses from the brain descend 
on spinal cells that are not in a passive, inactive, functionless state. 
Such a state probably never exists, for even when there is no volun- 
tary activity, there must be the activity on which the tone depends, 
that, as we have just seen, must exist in all postures of the limbs. 
This state of the cells preceding voluntary activity is determined by 
the afferent impulses, chiefly by those from the muscles. Through these 
the muscles are adapted to posture, and in the mechanism for adapta- 
tion to posture we may trace also a mechanism for part at least of the 
co-ordination effected in the spinal cord. This seems to consist of 
two pai'ts. (1) An automatic variation in the state of muscles, per- 
mitting the ordered performance of intended movements. The state 
of the afferent impulses acting from the muscle on the motor cells 
must be at once altered by the effect of the voluntary activity 
of the muscles, since this will alter the impulses in the muscle- 
nerves by the changed and changing pressure and tension on 
the tissues in which these nerves end—the pressure of the con- 
tracting and widening fibres and the tension in the antagonists 
that oppose the motion, but do not prevent it, and are made 
more tense by the muscles they are opposing. These impulses 
pass to the cord, and there act on the motor cells, and influence 
their state in a way that we can at present only guess at, but 
which must be of the utmost importance. There must of necessity 
be a definite relation between certain states of the muscle and the 204 
SPINAL CORD. 
strength of afferent impulse produced thereby. If we conceive that 
an increase in the impulse (making it greater than corresponds to 
the degree of activity of the motor cells), such as must result from 
the increased tension on the muscle, lowers the activity of those 
cells, we can understand the way in' which the contracting antagonists 
relax to permit movement which tends to occur. As soon as the 
resistance begins to yield, the tension-stimulus will be increased, and 
the total afferent impulse become disproportionately great in relation 
to the degree of activity of the cells ; as a result, this activity is 
lessened and the muscles yield. This involves a constant regulation 
of the activity of the various motor cells by the afferent impulses. 
A like but opposite effect must be produced on the cells of the 
muscles producing the movement. This effect on the cells will, of 
course, blend with that of the voluntary impulse from the brain that 
is causing the movement. Thus the spinal muscle-reflex process 
permits the desired movement to take place, as it could not do if the 
state of the cells were not thus automatically regulated. (2) Rela- 
tions between the various reflex processes are doubtless established 
by the repetition of movements, and thus planned mechanisms, as it 
were, are established in the cord ; within their range the various 
movements occur. The state of the muscles in standing, for instance, 
is almost perfectly reproduced by the extensor spasm that occurs 
when the muscle-reflex processes are in great excess. Thus we have 
a mechanism by which a relatively simple voluntary impulse may 
produce an extensive co-ordinated movement. But what we can 
discern shows that we must regard spinal co-ordination as essentially 
a reflex process, chiefly due to the impulses from the muscles. The 
correctness of this view can hardly be doubted when we come to see 
its perfect harmony with the phenomena and the conditions of spinal 
inco-ordination. 
Still, it must be always remembered that this spinal process is of 
the nature of a subordinate mechanism, determining the precision of 
form rather than the actual arrangement and order of the muscular 
contraction. This is done by a higher process, a co-ordination which 
consists in the form of action of the motor cells of the cerebral 
cortex that is produced by still higher volitional processes. These, 
however, as we shall see, are themselves subject to a like influence and 
the seat of an analogous regulation, chiefly, it is probable, by impulses 
proceeding from the cerebellum, which are also due to the varying 
excitation of the muscle-nerves. That the nerve-fibres which pass up 
the posterior median columns conduct impulses from the muscles that 
determine cerebral co-ordination scarcely admits of doubt. Interrup- 
tion of this path in any part of its course causes a defect of co- 
ordination, which resembles that due to cerebellar disease with sufficient 
closeness, to add weight to other facts suggesting that it is through 
the cerebellum that the impulses carried by this path act on the 
cortex, regulating and determining the activity of its cells and the FUNCTIONS. 
205 
resulting movement.* The impulses may reach the cerebellum, as 
we have seen, from the grey matter of the post-pvramidal nucleus in 
which these fibres end.f But this primary co-ordination is not a 
function of the cord, although it may be lost in consequence of 
disease of the cord. The direct cerebellar tract may constitute a 
similar path, hut of this we have only the evidence of destination and 
analogy. 
It is probable that the mechanisms just alluded to, as constituted 
by the functional relations between the motor and sensory structures 
in the cord, very much facilitate the execution of many movements, 
and especially of those that are the more simple in their character. 
The less variation a movement is capable of, or needs, the more largely 
may the spinal mechanism be concerned in its arrangement; and hence 
such actions as standing and walking may be effected through a 
comparatively small number of the pyramidal fibres, and, as we shall 
see, they may still be performed when there is disease that would 
prevent a more elaborate action. It is also probable that in animals 
such spinal mechanisms are developed to a greater extent than in 
man, and care must be taken in drawing inferences from one to the 
other. 
The impulses from the muscles that determine the muscle-reflex 
action and the spinal co-ordination, must pass by nerves that end in 
the grey matter and are connected with nerve-cells, at or near the 
level at which they enter the cord. We do not know whether it is 
through these fibres, or through those that pass upAvards without 
interruption, that the impulses are conveyed which, when excessive in 
degree, give rise to muscular sensations. But attention may again be 
called to the important evidence, afforded by such sensations, of the 
abundance of upward impulses of which we are normally unconscious. 
These nerves, it will be remembered, begin in the connective tissue 
of the muscles, and the acute pain of cramp, and the muscular 
tenderness in such affections as multiple neuritis, afford indirect 
evidence of impulses which we do not usually observe, and might 
almost doubt; while the manner in which such pain is excited is very 
clear evidence of the sensitiveness of the nerves to the modes of stimu- 
lation that have been assumed as effective. We have already seen 
(p. 9) that it is through such unfelt impulses that we probably derive 
the chief part of our conceptions of posture, a subject that must again 
be considered in connection with the brain. 
Influence on Nutrition —The nutrition of the muscles is under 
the control of the anterior grey matter, and probably of the motor 
* This has been experimentally confirmed by Bechterew, who finds that section 
of the posterior columns, in various animals, above the lumbar enlargement causes 
a defect of co-ordinatiou similar to that produced by loss of the cerebellum 
(Ifechterew, * Wjestnik psich. i. nevropat./ 1889, vii, 1; and ‘Near. Centralbl.,’ 
1890, p. 82). 
+ A connection recently confirmed by Brosset, ‘ Des Connexions du Ccrvelet,’ 
Paris, 1891 206 
SPINAL CORD. 
nerve-cells. The influence is exerted through the motor nerves, and 
indeed consists in the normal integrity of the fibres (see p. 24). 
The nutrition of the bones and joints is also under the control of the 
cord, and probably is exerted through the posterior roots. It is true, 
the growth of the bones is hindered when the anterior cornua are 
diseased, but no atrophic change seems then to occur in the osseous 
structure, and the influence of the paralysis may be indirect. A true 
trophic change, and an alteration in the joints, may occur in locomotor 
ataxy, in which the disease is of the posterior nerve-fibres. 
The nutrition of the slcin seems also to depend on nerves that have 
their course in the posterior roots. The clearest fact is that irritation 
of the nerve-structures has far more effect than simple loss of function. 
It is when the cord or nerve-roots are the seat of irritative inflam- 
mation that the most acute trophic changes occur, while mere degene- 
ration of these nerves induces slower and slighter changes (see p. 22). 
Visceral Control.—Although the viscera are under the immediate 
control of the sympathetic system of nerves, they are related to centres 
in the spinal cord, and it is from these centres that the controlling 
influence is really derived, probably by means of the finer fibres of 
the anterior roots. The relation is the most direct and important, 
so far as concerns the diseases of the spinal cord, in the case of 
the organs over which the will has an influence, the rectum and the 
bladder. The centres for these are in the lumbar enlargement, but we 
do not know their exact position. They are probably complex reflex 
centres. We can best understand their action by studying them when 
voluntary influence is lost. 
The centre for the sphincter ani is the more simple, but the system 
of action of each is probably similar. In the wall of each viscus we have 
muscular fibres to expel the contents, and at the mouth a sphincter 
arrangement to prevent continuous evacuation. Faeces or air in the 
rectum, and urine in the bladder, may excite the lumbar centre, 
and cause two effects—contraction in the wall and relaxation of the 
sphincter. This process can be controlled by the will to a consider- 
able extent, although we are still ignorant of the precise mode in which 
the voluntary influence is exerted. But if the volitional path in the 
cord is interrupted above the lumbar centres, the will can no longer 
control the reflex processes ; as soon as faeces irritate the rectum, they 
are expelled by the reflex mechanism ; as soon as a sufficient quantity 
of urine accumulates in the bladder, a reflex contraction of the detrusor 
and relaxation of the sphincter cause its escape. The affection of the 
voluntary path for the sphincter is not always proportioned to that 
for the legs. If the damage to the cord involves also the sensoi'v tract, 
the patient is unconscious of the action of the bladder or bowel. If 
the sensory tract is unaffected, the patient is aware of the process, but 
cannot control it. It is often said that there is permanent relaxation 
of the sphincters, but this is true only when the lumbar centres are 
inactive or destroyed. In this condition evacuation occurs as soon FUNCTIONS. 
207 
as fseces or urine enter the bowel or rectum. The urine escapes 
continuously, instead of being expelled at intervals. The condition is 
less obvious in the case of the rectum, because there is no such con- 
tinuous passage of faeces into the rectum as there is of urine into the 
bladder. We may, however, distinguish between the two states of the 
rectum by the introduction of the finger. If the lumbar centre is 
inactive, there is a momentary contraction, due to local stimulation of 
the sphincter, and then permanent relaxation. If, however, the reflex 
centre and motor nerves from it are intact, the introduction of the 
finger is followed, first by relaxation, and then by gentle, firm, tonic 
contraction. I have verified this by introducing an india-rubber 
cylinder instead of the finger, and registering the pressure on the 
cylinder by connecting it with a recording apparatus. The relaxation 
is then found to be preceded by a very slight brief contraction, and 
to be followed by unbroken tonic contraction. The relaxation may 
also be readily produced by any impression on the mucous membrane 
above the sphincter. Fig. 83 shows some of the tracings obtained. 
Fig. 83.—Tracings or the Action op the Sphincter Ani. 
The vertical lines represent seconds of time. 
1. Effect on contraction of sphincter of the injection into the rectum of a small 
quantity of air at *. a, fall in pressure due to the inhibition of the contrac- 
tion ; b, rise due to the slowly returning contraction. 2. Effect of the intro- 
duction of the instrument, a, sudden rise of lever at moment of introduction, 
due to the exposure of the instrument to the pressure of the sphincter (the top 
of this line represents the decree of previous contraction); b, initial rise due to 
increased contraction; c, fall from partial inhibition; d, subsequent contrac- 
tion, rising to a greater degree than the initial contraction, and subsequently 
falling slightly. 3. Effect of cough, a, pressure of tonic contraction of 
sphincter (the slight irregularities are due to pulse-waves); b, fall in pressure, 
due to the movement of the instrument by the cough ; c, initial contraction; 
d, relaxation of inhibited sphincter ; e, e, e, rhythmical variations in subsequent 
rise. (From the ' Proc. Royal Society,' 1877.) 
The action of the bladder mechanism can be best understood by 
assuming that the motor centre really consists of two parts, one (ms, 
Fig. 84) maintaining the contraction of the sphincter, the other (md) 
exciting the contraction of the detrusor fibres, and that these two 
parts are antagonistic; when one acts the other is inhibited. Thus, 208 
SPINAL CORD. 
in normal rest, the sphincter centre is active, the detrusor at rest. 
Action is produced by an afferent impulse from the bladder and a 
voluntary impulse from the brain. Then the detrusor centre acts, and 
the sphincter centre ceases to act. If voluntary power is impaired, 
the afferent impulse from the bladder may be insufficient, and then 
there is retention, or in other cases the motor centre may yield too 
readily to the afferent impulse, and there is reflex incontinence. 
Although no other part of the alimentary canal is under voluntary 
influence, all parts are probably related to the spinal cord, by means 
of the connection between the sympa- 
thetic system and the nerve-roots. Con- 
stipation is extremely common in disease 
of the spinal cord, and is often greater 
than can be accounted for by the mere 
loss of power of the abdominal muscles. 
The pain in the back that is so common 
in disease of the stomach has been re- 
garded as a reflected pain, due to this 
connection. 
The uterine functions are probably in- 
dependent of the cord in greater degree 
than those of any other organs under 
the influence of the sympathetic. The 
function of menstruation goes on inde- 
pendently of cord disease, and may be 
regular although there is absolute arrest 
of all conduction, sensory and motor. 
Pregnancy and labour may proceed in 
normal course, in spite of such disease 
of the cord as causes complete motor 
paraplegia. 
Sexual Functions.—The activity of 
the sexual organs depends on the in- 
tegrity of the reflex loop to and from 
a special centre, also situated in the 
lumbar enlargement, but the due action 
of this centre depends on cerebral 
(psychical) as well as on reflex influences. 
Disease of the centre, or of the nerves 
leading to or from it, abolishes sexual 
action. The sexual reflex is, however, 
one of the cutaneous reflexes, and it shares the condition of these 
rather than of the muscle-reflex processes. 
The centre is probably double, and its action is impaired by inter- 
ference with either half. When, by disease higher up, the connection 
with the psychical centres is interrupted, the sexual act cannot be 
perfectly performed. If the path from the controlling centre (p. 20) 
Fig. 84-.—Diagram showing 
Probable Plan of the 
Centre for Micturition. 
MT, motor tract; ST, sensory 
tract in the spinal cord ; MS, 
centre, and ms, motor nerve 
for sphincter; MD, centre, 
and nid, motor nerve for de- 
trusor ; s, afferent nerve from 
mucous membrane to S, sen- 
sory portion of centre: B, 
bladder. At r the condition 
during rest is indicated, the 
sphincter centre in action, 
the detrusor centre not act- 
ing. At a the condit'on 
during action is indicated, 
the sphincter centre inhibited, 
the detrusor centre acting. FUNCTIONS. 
209 
is unimpaired, the reflex sexual processes are not in excess, and may 
even be diminished ; but if the path from this controlling centre is also 
interrupted, the reflex sexual processes are in excess like the other 
superficial reflexes, and priapism results. If the reflex centre, or 
connecting paths, are partially diseased, the sexual process may be 
impaired and imperfect, but not abolished. 
Vaso-motor Centres.—The sympathetic nerves to the vessels are influ- 
enced from the spinal cord. It is probable that the path is by the 
fine fibres of the anterior roots, and that most of the dilator fibres leave 
the cord between the third dorsal and the second lumbar, and most of 
the constrictor fibres from the seventh dorsal to the first lumbar. Some 
facts of disease suggest that the centres are situated in the inter- 
mediate grey matter ; and this conclusion is supported by the import- 
ant researches of Gf ask ell, which refer the function to the small cells 
of the intermedio-lateral tract, which he traces upwards to the vaso- 
motor centre in the medulla. The action of the vaso-motor nerves 
may be deranged by disease of the cord. It is probable that such a 
relation exists between all parts of the vaso-motor system of nerves 
and the cord, and that the relation obtains between each segment of 
the cord and the vascular nerves to the corresponding part of the 
trunk and limbs. This derangement in disease may take a part in 
the production of the changes in nutrition, but it is probably not the 
sole mechanism by which these changes are produced. 
There is a special connection between the sympathetic and the cer- 
vical region of the spinal cord. This region contains the path to the 
visceral nerves that control the sugar-forming functions of the liver. 
The lower part of the cervical enlargement contains also an important 
centre which controls the sympathetic nerves for the vessels of the head 
and face. The path of central influence for the radiating fibres of the 
ins passes also from the region of the third nerve nucleus, down the 
cervical cord, by the lowest cervical or first dorsal nerve, to the 
sympathetic, and then ascends the cervical trunk, and passes along the 
fibres which accompany the internal carotid artery to the ciliary 
ganglion. Fibres also pass from the cervical cord to the sympathetic, 
through which the action of the heart is accelerated. 
Mutual Relation of the Functions of the Spinal Coed.— 
It may be well to present, in the form of a table, the relation of the 
several functions of the cord, motor, sensory, and reflex, as far as our 
knowledge of these relations extends. Many points are still uncertain; 
these have been, for the most part, omitted. The table does not need 
any detailed explanation. It is merely a comparative collection of 
the facts that have been stated in the preceding pages. We shall find 
the value of this collocation of functions when we consider the effects 
of transverse lesions of the cord at different levels. 
YOL. I. 210 
SPINAL COED. 
Table showing the approximate relation to the spinal nerves of the 
various motor, sensory, and reflex functions of the spinal cord. 
MOTOB. (NEBVES 
•) 
MOTOB. 
SENSOEY. 
BEELEX. 
St.-mastoid, 
C 1 
" 2. 
Small rotators of hea( 
> Depressors of hyoid 
1 s 
ah 
1 
calp. 
1 
2 
Upper neck 
muscles, 
Upper part 
of 
Trapezius 
3 
Lev. ang. scapulae 
3J 
Neck 
and uppei 
3 
4 
. 6- 
s Diaphragm ''j g » 
4 
5 
- 
■ 
part of chest 
Shoulder 
4 
5' 
Serratus }>r3 Si 
|> Flex, of elbow _= g 
► Arm, outer side 
" 6- 
Supinators J m 
6 
Radial side, 
6 
> Ext. wrist & fingers 
forearm and 
Lower neck 
7< 
Ext. elbow 
7 
• 
hand; thumb 
7 
>• Scapular 
muscles, 
Middle parts 
of 
S< 
> Flex, wrist & fingers 
Pronators 
8 
Arm,inner side; 
ulnar side of 
s forearm and 
8 
Trapezius 
- Muscles of hand 
U 
hand ; tips of 
D U 
1 
fingers 
1^ 
L 
2 
2 
2 
3 
3 
3 
4 
4 
4T 
5 
5 
-Front of thorax 
5 
-1 
ntercostals 
- Epigastric 
Lower part 
of 
Trapezius 
6 
• 
6 
► Ensiform area 
G 
7 
*> 
7 
7. 
and Dorsal 
muscles 
8 
8 
81 
9 
9 
J 
9 
lO- 
Abdomen 
- Abdominal muscles 
10 
- (Umbilicus 
10 
10th) 
i> Abdomina1 
ll 
11 
11 
. 12 
12 
' 
_ Buttock, 
12 
upper part 
LI 
- 
1. 
Groin 
- 
a 
nd scrotum 
* 
r 2 
Cremaster 
2-; 
r 
(front) 
2 
Cremasteric 
Flexors of hip 
"outer side 
j 
’] 
Lumbar j 
3i 
3 
3J 
> Knee-j eric 
muscles 
r 
Extensors of knee 
-Thigh 
* 
front 
4 
Adductors of hip 
4 
4. 
J 
Peroneus, 1. 
Ext. & abduct, of hip 
inner side 
Gluteal 
* \Foot- 
Flex, of J 
. 5 { 
h 
Leg, inner side 
5 
ankle, Ext. | 
Flexors of knee 
of ankle ( 
Si 
Intrinsic muscles of 
1 
| i>uttocK, lower 
part 
1 
f clonus 
J 
4J 
foot 
2 
n 
i 
Back of thigh 
Leg 1 except 
2 
»Plantar 
J 
1 & foot 
J inner pait 
Q J 
3 1 
Perinseal and anal 
o 
4 j 
muscles 
-Perinseum and anus 
4 
5 
5: 
Skin from coccyx to 
5 
Co. 
Co.‘ 
anus 
Co. SYMPTOMS. 
211 
SYMPTOMS OF DISEASE OF THE SPINAL CORD: INDICATIONS 
OF THE SEAT OF THE LESION: ANATOMICAL DIAGNOSIS. 
The symptoms of disease of tlie spinal cord consist in derangement 
of its various functions; the loss of some, the exaltation and perver- 
sion of others. We have already considered these functions, and the 
parts of the cord by which they are subserved. We may now briefly 
consider the general character of their derangement, and its signifi- 
cance in regard to the position of the disease. The combination of 
symptoms indicates the seat of the lesion; we infer its nature from 
their mode of development, and other considerations, which will be 
subsequently discussed. It is always important to keep these two 
elements of the diagnosis distinct in the mind. 
A common feature of the symptoms of disease of the spinal cord is 
their bilateral character. This depends on two causes, of which, 
however, only the first is peculiar to the cord and can be regarded as 
the special cause of this feature of its diseases. The structures in 
each half of the spinal cord are in such close proximity, that any 
random process, such as haemorrhage or inflammation or pressure, 
readily affects both halves—can, indeed, hardly fail to do so in some 
degree, and usually to such an extent as to cause the bilateral cha- 
racter of the symptoms to be obtrusive. Secondly, morbid processes 
that commence in the nerve-elements and affect them according to 
their function (“ system diseases ”) usually involve the corresponding 
structures of the two sides, and the spinal cord contains many struc- 
tures that are liable to such processes. Hence a large proportion of 
the diseases of the spinal cord involve both sides and cause symptoms 
that have a corresponding range. The leading fact that results from 
this is that the characteristic type of palsy is “ paraplegia.” The word 
means literally paralysis of the parts beneath or beyond a certain 
locality, and involves the distinction of a motionless part of the frame, 
which no doubt arose from the variable extent of this, in comparison 
with the uniformity of the region affected in “hemiplegia.” But 
the second condition causing the bilateral character of the symptoms 
is shared equally with those outlying parts of the spinal cord—the 
peripheral nerves ; and as this condition obviously determines a stricter 
symmetry than does the first, it follows that this character is not, 
alone, of much significance, and is indeed least significant when most 
complete. In the affections that are strictly symmetrical, therefore, 
other features must also be taken into account. 
Another character of spinal symptoms, not shared by those of the 
nerves, consists in their variation in vertical extent according to the 
position or extent of the lesion. But we must distinguish two classes' 
of symptoms within the region in which they exist. (1) Those which 
depend on the interruption of the conducting path to or from the brain, 
and involve the whole region below the disease. (2) Those which depend on damage to the central structures in the cord and nerve-roots, 
which are present only at the level of that damage, i. e. in the parts 
functionally related to that part of the cord. The two sets of sym- 
ptoms may be distinguished as “conducting” and “central;” but in 
many diseases those at the level of the lesion are chiefly due to the 
irritation of the nerve-roots, and these are most usefully designated 
“ root symptoms.” 
Disease of the cord does not always cause bilateral symptoms. 
A little consideration will show that this must be so. A random 
process, of small extent, may damage one side only. It may affect 
one or several structures on one side or all of them. Nevertheless it 
is very rare for such a process to spare the other side altogether, and 
practically no lesion affects all parts of one side without damaging, in 
some degree, the other side, at any rate for a time. In very rare forms 
of traumatic lesion, however, the damage to the other side is almost 
imperceptible. Again, “ system diseases,” in quite exceptional cases 
and for unknown reasons, are limited to one side; much more fre- 
quently they may affect one side earlier and more than the other. 
Such unilateral symptoms have been awkwardly termed “ hemi- 
paraplegia.” 
Motok Symptoms.—Loss of motor power results from interference 
with the motor path in any part of its intia-spinal course,—pyramidal 
tracts, anterior grey matter, anterior nerve-roots. We have seen that 
the path may be divided into two segments, upper and lower (see 
p. 11G). The spinal cord contains a considerable portion of the nerve- 
fibres of the upper segment, and their lower termination in the grey 
matter, but only the commencement of the lower segment, the motor 
ganglion-cells, and root-fibres proceeding from them. The chief part of 
the lower segment is outside the spine, in the nerve-trunks. So far as 
the loss of power is concerned the effect is the same, in whatever part 
of the motor path the interruption is situated ; but the other symptoms 
that accompany the loss of power differ very much according as the 
interruption is in the upper or lower segment. The lower segment 
influences muscular nutrition, and forms part of the path of reflex 
action. Hence, as we shall presently see, the muscles waste, and 
reflex action is lost, when this is diseased; but when the upper 
segment is damaged there is no muscular wasting, and reflex action, 
instead of being lost, is commonly increased. The symptoms produced 
by disease of either segment are essentially the same, whatever part of 
the segment is diseased, whether the cell at the upper extremity, the 
fibre, or the ramification at the lower extremity of the fibre. If, for 
instance, the intra-muscular nerve-endings are paralysed by curara the 
symptoms produced are the same as if the fibres in the nerve-trunks 
are divided or these cells in the cord are destroyed. Disease of the 
termination of the upper segment in the grey matter of the cord 
must, of necessity, produce the same effect as disease of the pyramidal 
fibre itself, or the cell in the cerebral cortex from which the fibre springs. 
212 
SPINAL CORD. SYMPTOMS. 
213 
We shall afterwards see that this consideration has very important 
applications. 
If a fibre of either segment is seriously damaged, it degenerates 
below the division, since its nutrition depends on the influence of the 
•cell from which it has sprung. If damaged only by pressure., how- 
ever complete may be the evidence of degeneration, regeneration is 
possible, even after one or two years. It is possible that such regene- 
ration also occurs when the damage is by inflammation. The nutri- 
tional stability of the fibre, or rather of its essential element, the 
axis-cylinder, becomes less, and more easily deranged, the greater 
the distance from the parent cell, and it is least in the terminal 
ramification of each segment. This is probably the reason why 
curara acts chiefly on the intra-muscular nerves, and it explains the 
influence of many poisons on the peripheral nerve-endings, and the . 
facts of nerve-degeneration in tabes and “multiple neuritis,” &c. 
The law is probably also true of the upper segment; and if so, many 
facts of pathology become clearer to us, as will be seen in the chapter 
on “spastic paraplegia.” It may thus be taken as a general law of 
the utmost importance that the vitality of a nerve-fibre and its power 
of resisting morbid influences are less the greater the distance from the 
cell from which it springs and of which it is really part. 
A lesion of the pyramidal tract causes loss of power in all parts 
below the level of the disease—that is to say, of all parts the fibres 
for which are interrupted. A lesion of the grey matter, or of the 
anterior roots, causes paralysis only of those parts which are func- 
tionally on the level of the lesion. The two mechanisms often coin- 
cide. A transverse lesion in the cervical enlargement, for instance, 
may cause paralysis of the arms from the damage to the grey matter 
and nerve-roots, and paralysis of the legs from damage to the pyramidal 
fibres. The disease involves, primarily in the former case, the com- 
mencement of the second segment of the motor path for the arms; in 
the latter, the middle of the upper segment. The associations of the 
paralysis differ accordingly. The parts affected by a lesion at any 
level will be readily ascertained by an examination of the table of 
functions on p. 210. 
It is important to note that the affection of motor power is often 
incomplete. It may then involve one set of muscles more than 
another. The flexors or the extensors may be chiefly paralysed. In 
disease of the dorsal cord, it is very common for the flexor muscles 
of the hip and knee to suffer more than the extensors. Why this 
should be we do not know, but the fact is important, because consider- 
able weakness of the flexors of the knee is readily overlooked. In exa- 
mining motor power, each set of muscles should be separately tested. 
Motor over-action; ■Spasm is frequent in disease of the spinal cord 
and its membranes. It may present the form of tonic spasm, which 
when persistent is termed rigidity, or of clonic spasm, which is usually 
transient and paroxysmal. Tonic spasm, persistent, and involving 214 
SPINAL CORD. 
only a certain group of muscles, causes distortion of the parts to 
which they are attached, and is often termed contracture. Tonic 
spasm, paroxysmal or persistent, is far more frequent than clonic 
spasm, which occurs chiefly in association with tonic spasm as the 
muscular clonus described at p. 222, or as a consequence of certain 
functional derangements. Tonic spasm may be the result of direct 
irritation of the motor structures, or may depend on over-action of 
the reflex centres, due, not to irritation, but to deficient control. 
Either form may be acute or chronic. The acute irritation which 
causes spasm is generally inflammation of the membranes, rarely an 
acute lesion of the substance of the cord. The chronic irritation is 
chiefly due to compression of the motor fibres—either of the pyramidal 
tracts, when there may be persistent unvarying spasm in the parts 
below the disease, related to the fibres irritated,—or of the nerve- 
roots, when similar spasm is produced in the parts at the level of the 
lesion. The spasm that depends on reflex action is seen chiefly in the 
legs and trunk, but especially in the former. It may preponderate 
in either the flexors or extensors, so that the legs, when rigid, may be 
drawn up or straight out. The flexor spasm seems to be due to an 
over-action of the centres for cutaneous reflex action, the extensor 
spasm chiefly to that of the centres for muscle-reflex action, although 
it may also be excited indirectly by a cutaneous impression. This form 
will be considered in connection with the reflex over-action. 
Muscular Contraction.—The actual shortening of muscles, by which 
they cannot be passively extended to their normal length, is due to- 
tissue changes fixing the active persistent tonic spasm or contracture 
just mentioned. The rapidity with which it occurs depends on the 
uniformity of the spasm, and we may distinguish three modes in which 
it arises, which differ in the time required and degree attained. (1) 
When one set of muscles is paralysed, their opponents, never being 
extended, quickly become fixed in the contracted condition which they 
assume in virtue of their power of adaptation to posture. Thus in 
palsy of the flexors of the ankle, the calf muscles quickly become 
contracted, so that the foot cannot be flexed on the leg even up to a 
right angle. The same thing happens by a similar mechanism, when 
one posture is unceasingly maintained and one set of muscles are 
never extended, e. g. persistent flexion of the knee leads quickly to- 
structural shortening of the hamstring muscles. (2) Where there is 
unchanging active contracture from chronic irritation of the motor 
fibres by a growth, or permanent reflex contracture, as when reflex 
flexor spasm keeps the hip and knee permanently flexed, similar 
structural changes occur, so that passive elongation soon becomes 
impossible. (3) In paroxysmal tonic spasm of intense degree, if 
one set of muscles is stronger than their opponents, their action may 
so preponderate as to lead to a greater active contracture than their 
opponents present, and permanent shortening may occur; although it 
does so slowly and to a slighter degree than in the other forms, because SYMPTOMS. 
215 
the muscular action is more or less paroxysmal and varying, and the 
muscles are at times extended by their opponents. Thus in parox- 
ysmal extensor spasm in the legs, no shortening occurs in the muscles 
moving the knee, because they are equally balanced, but the calf 
muscles, being stronger than the flexors of the ankle, contract the 
more, and extend this joint, whenever a paroxysm of spasm comes on, 
and, after a time, may undergo slight structural shortening, so that 
the foot cannot be flexed on the leg beyond a right angle. 
It is of great importance to distinguish the shortening of muscles 
due to tissue changes in them, from the active contracture that may 
closely simulate it. In the latter, gentle extension, kept up for a few 
minutes, restores the muscle to its normal length. The importance 
of the distinction is due to the fact that the structural shortening can 
be removed by tenotomy or forced extension, while these measures are 
useless in the case of active contracture, which would subsequently 
reassert itself. 
Inco-ordination of movement, although motor, depends usually on 
disease of afferent fibres. Its characters have been already described 
in outline (p. 7). 
It occurs in three forms, of which the third differs entirely from 
the others in aspect and nature, and alone is a true motor symptom. 
The two chief forms are the following :—(1) Simple disorder of volun- 
tary muscular contractions, which, when considerable, amounts to a 
wild irregularity of movement, and when slight is only manifested by 
slight irregularity ivhen the guidance of vision is withdrawn—as in 
the inability to maintain the muscular contractions in the perfect 
uniformity needed for equilibrium when the base of support is ren- 
dered small by the juxtaposition of the feet. The delicacy of the 
test is increased by the removal of the firm base afforded by the boot, 
and by closure of the eyes. The increase in unsteadiness when the 
eyes are closed is sometimes termed “ Romberg’s symptom.” This 
condition results from interruption of the afferent path from the 
muscles to the spinal cord, including the fibres that ascend the cord 
and those that subserve the muscle-reflex process at the level of 
entrance. The effect of the loss of the latter is a cessation of the chief 
part of spinal co-ordination, which, as we have seen, depends on those 
processes, co-operating with the voluntary impulse. Hence it is asso- 
ciated with loss of the knee-jerk. The loss of other forms of reflex 
action does not seem capable of causing inco-ordination. Incomplete 
interruption of the root-fibres from the muscles the mechanism of the 
next form is necessarily conjoined. (2) Inco-ordination resembling 
the slighter degrees of that just described, and consisting especially 
in such a defect of equilibrium as results from disease of the middle 
lobe of the cerebellum, is produced by disease of the posterior median 
columns above the lumbar enlargement, or, if it extends into the 
latter, leaving the root-zones free so as not to impair muscle-reflex 
action. This is apparently produced by interruption of the path by 216 
SPINAL COED. 
■which impressions from the muscles are conveyed to the posterior nuclei 
©f the medulla and pi-obably thence to the cerebellum (p. 205). The 
effect is to deprive the motor cortex of the guidance afforded by these 
impulses. The difference between this form and the slighter degrees 
©f the first is that the muscle-reflex action is not lost, the knee-jerk 
being preserved. (3) Irregular compression of the motor fibres in the 
cord apparently causes the peculiar jei’ky inco-ordination seen in dis- 
seminated sclerosis, which is supposed to depend on unequal and 
irregular conduction along the fibres, due to their compression. This 
form, however, needs further study. 
Sensory Symptoms.—Loss of sensation is a very common effect of 
disease of the spinal cord. It may be total, and involve all forms, of 
sensibility, or partial, and affect only some forms. The statements 
made on pp. 8—10 regarding impairment of sensation generally, and 
the method of ascertaining it, apply to that wdiicli results from cord 
disease, and need not be here repeated. It has been also pointed out 
(p. 60) that loss of sensation occurs less readily than loss of motor 
power. In cord disease it is common for muscular paralysis to exist 
with intact sensibility. This may partly depend on the fact, ascer- 
tained by experiments on the effect of local anaemia of the cord, that 
the sensory fibres, of the nerve-roots at least, seem to have more 
resisting power than the motor fibres. Sensation may be impaired by 
disease of any part of the sensory path,—posterior roots, probably 
also the posterior cornua and commissure, or the conducting tracts up 
the cord. A division of the sensory path into upper and lower seg- 
ments is conceivable, analogous to that of the motor path, although 
we have not the same clear ground for the distinction into simple 
segments of similar composition. 
Disease of the posterior nerve-roots causes loss of reflex action as 
well as impairment of sensation, just as disease of the anterior roots 
interferes with reflex action as well as with motor power. Interrup- 
tion of the sensory conducting tracts higher up leaves reflex action 
unaffected. But a focal lesion, such as transverse myelitis, may 
damage both the conducting tracts and the nerve-roots at the level of 
the lesion, or may affect only one of these. Disease outside the cord, 
compressing it, may have the same double effect. Hence.it is impor- 
tant to test sensation at the level of the lesion, as well as in the parts 
below, and to remember that the “ level of the lesion ” may involve 
the limbs or the trunk. Areas of anaesthesia may thus be found on 
the trunk when there is none on the legs, and may be of considerable 
diagnostic importance, e. g. in spinal caries. 
Random disease of the nerve-roots outside the cord usually impairs 
all forms of sensibility, although slight damage may arrest the 
conduction of tactile impressions, and not those of pain, which are 
probably more energetic. Disease of the roots within the cord often 
causes only partial loss, because the fibres which conduct different 
impressions have a different course. But loss of one form of sensi- SYMPTOMS. 
217 
"bility from disease of the root-fibres or nerve-fibres usually depends 
on the kind of disease, and is especially due to degenerative changes, 
the result of some present or past local influence. Disease higher up 
the cord still more frequently causes partial loss ; either sensibility to 
pain or to touch may be impaired. That to temperature is rarely 
affected without that to pain. We do not yet know precisely the 
significance of this special form of loss, because, as we have seen, we 
are still uncertain as to the path for each form of sensibility. It is 
highly probable, however, that loss of sensibility to pain is produced 
by disease of the antero-lateral ascending tract. 
Disease of the posterior median column, and possibly that of the 
cerebellar tract, certainly impairs the conduction of impressions from 
the muscles. It probably abolishes the “ muscular sense” of posture 
and movement, although this does not entail'a distinct sensory loss. 
But there may be also a greater loss of muscular sensibility, so that 
the normal sensitiveness to pressure and passive extension (and even 
at last to electrical stimulation) may be impaired or lost. The 
“common sensibility” of muscles is probably lost only when the 
disease of the nerves is greater than suffices to abolish what is termed 
the “ muscular sense.” Interference with this path in the nerves or 
roots outside the cord abolishes muscle-reflex action, and also causes 
more pronounced symptoms (ataxy, &c.) than disease higher up the 
path within the cord. 
Increased sensitiveness, hyperaesthesia and hyperalgesia, are also 
common in disease of the spinal cord, and usually depend on irritation 
of the conducting fibres in some part of their course. Probably the 
irritation produces the effect by intensifying the impulse as it passes, 
since the phenomena of stimulation of nerves show that their axis- 
cylinders have some power of transforming other forms of energy into 
nerve-force, i. e. of evolving nerve-force, and therefore of increasing 
the strength of that which passes along them. 
The term “ hypersesthesia ” is commonly used in the sense of 
“hyperalgesia.” In the strict sense of the word, hypersesthesia is 
seldom observed or even searched for. 
When the sensibility to touch is “ increased ” there is some 
perversion of the sensation, not a simple increase. The sensation 
may be felt as “ thrilling ” or “ shock-like sensations.” When there 
is an exti-eme increase, pain may be produced by a touch, but it is more 
probable that the touch stimulates the over-sensitive nerves of common 
sensibility, than that actual pain is produced through the tactile 
nerves. A touch may cause pain when it is not felt as a touch, as in 
the condition termed “ anaesthesia dolorosa.” Other forms of altered 
sensibility have been already described. 
Pain, referred to the spine, occasionally present in organic disease 
of the cord, is more frequent in disease originating in the meninges 
or bones. But the frequency with which spinal pain is present in 
abdominal, especially gastric, disease, and in neui’algic affections, 218 
SPINAL COED. 
lessens its significance when it exists alone. In meningitis, acute 
or chronic, and in meningeal growths, spinal pain is frequent, and 
in organic disease of the bones of the vertebral column it is an 
almost constant symptom, and is combined with local tenderness. 
The same combination of local pain and tenderness frequently occurs 
in cases of neuralgic pain, “ rachialgia,”—a condition that is often 
loosely termed “ spinal irritation,” especially when it succeeds, as 
it often does, concussion of the spine. Such pain is usually felt through 
a considerable extent of the vertebral column, or has more than one 
place of chief intensity and tenderness. That which is due to organic 
disease is usually fixed and unchanging. In organic disease of the cord 
itself, pain is more often referred to the neighbourhood of the spine, 
to the loins or the sacrum, than to the spinal column itself. 
Still more important are the pains that are referred to the parts 
to which the sensory nerves are distributed, and have hence been 
termed “ excentric ” or “ radiating ” pains. They are of two kinds: 
(1) those due to the irritation of the posterior nerve-roots in their 
passage through the intervertebral foramina, through the mem- 
branes, or through the posterior columns of the cord ; (2) those pro- 
duced by irritation of the sensory conducting tracts. The pains of the 
first class are called “ root-pains,” and are often intense. They corre- 
spon.d in level to the disease. Those of the second class are sometimes 
acute, especially in lesions that irritate the conducting tracts by pres- 
sure, e. g. growths. More often they are dull pains, closely resembling 
rheumatism, and frequently mistaken for rheumatism by the patients 
themselves and their medical attendants. The mistake is the more 
easily made, because other symptoms suggestive of spinal disease 
may be inconspicuous, and the rheumatoid pains in chronic cases may 
be influenced by weather, being much more troublesome in damp and 
cold than in fine and dry weather. In all cases, persistent rheumatic 
pains in the limbs should suggest the possibility of spinal disease, aud 
watch should be kept for such symptoms as local loss of power, or 
alterations in reflex action. There is a third class of pains—resem- 
bling root-pains, which depend on degenerative changes in the nerve- 
fibres ; the molecular alterations that result give rise to upward 
impulses of considerable intensity. They are met with in locomotor 
ataxy and in multiple neuritis, and may be dull as well as acute. The 
position in which these various radiating pains are felt—legs, trunk, 
or arms—depends upon the seat of the disease. Although often 
produced in the root-fibres, these pains may also be due to the peri- 
pheral nerves. 
It is especially important to note that the root-pains are frequently 
felt as a sense of constriction, a painful sense of tightness, as if a band 
were tied tightly around the part—the “ girdle-pam,” as it is called. 
When there is transverse damage to the cord, at the lowest part of 
the healthy region there is a state of irritation of the sensory nerves, 
aud this irritation (referred to the nerve-endings) causes the girdle- SYMPTOMS. 
219 
pain. It is named from its frequency at the level at which a girdle 
is worn, the middle of the trunk, which depends on the dorsal region 
being the most common seat of disease ; hut it may be felt lower down, 
about the groins or even the legs, or higher up, in the arms. In the 
limbs it is a mere sense of tightness. 
The girdle-pain is a symptom chiefly of inflammatory and degene- 
rative processes within the cord. Pressure on the nerve-roots usually 
causes acute pain, but the most severe root-pains are those met with 
in disease of the bones of the spine. These have also, more than any 
other kind, the characteristic that they are increased by movement, 
and in growths commencing in the bones (which are usually malignant) 
this feature is of considerable diagnostic importance. The suffering in 
such cases is so great as to have gained for the resulting symptoms 
the ominous designation of paraplegia dolorosa. 
Spontaneous sensations, other than pain, are very common in disease 
of the spinal cord, and are often of considerable diagnostic importance, 
but suggestive rather of the presence of a morbid state than of its 
nature. They may present many varieties of character, but the 
familiar sensation produced by pressure on a nerve-trunk, when the 
part is said to be “ asleep,” or to have “ pins and needles,” is the 
most common and the most significant. It may occur in func- 
tional disturbance of the cord as well as in organic disease, and 
also is very common in peripheral neuritis. It depends on over- 
action of the sensory structures, but it has at present no special 
significance as to the locality of disease. It may be excited by contact 
when it is not spontaneous, and probably represents the highest 
degree of excess of impressions conveyed by the nerves of tactile sen- 
sibility. The still vaguer feeling called “ numbness ” is also common, 
and may occur, in slight degree, in diseases of which all other 
symptoms are purely motor. But this word is used in so many 
different senses that the meaning in which the individual uses it 
should always be ascei’tained as far as possible. Sometimes it signi- 
fies distinct loss of sensibility. More often a feeling as if there ought 
to be loss when there is not. Our sensations altogether transcend 
our vocabulary, but the observer must try (without leading) to ascer- 
tain the character of the sensation experienced. 
Reflex Action.—Loss of reflex action indicates an interruption of 
the reflex arc concerned. This interruption may be anywhere between 
the peripheral endings of the motor and sensory nerves, and thus is 
not necessarily within the spinal cord, or even within the spinal canal. 
It is as constant in peripheral neuritis as in any spinal disease. The 
position of the interruption must be determined by the associated 
svmptoms; if it is in the centripetal portion of the reflex arc, there is 
impairment of sensation, since the interruption will equally arrest 
conduction to the brain. If it is in the centrifugal portion of the arc, 
there is a corresponding interruption in the path of the voluntary im- 
pulse, and loss of motor power. Moreover, disease of the motor centre 220 
SPINAL COED. 
or motor nerves causes also degeneration of tlie nerves, and wasting 
of the muscles. Any considerable disease of the nerves abolishes all 
reflex action from, the part they supply, but disease limited to the 
motor structures may permit a reflex movement to take place at a 
distance, although preventing it at the part stimulated. 
Disease of the motor centre or nerves causes loss of all forms 
of reflex action, the simple form and the muscle-reflex that underlies 
myotatic irritability. Partial disease of the afferent path may 
impair one and not the other, may abolish the muscle-reflex action 
(myotatic irritability) and not the superficial reflex action, since the 
afferent nerves for the two are distinct, coming in the one case from 
the muscles, in the other from the skin. When one only is lost it is 
generally the muscle-reflex action; the nerves for this seem more 
susceptible and to have less power of resisting morbid influences. 
Loss of all reflex action may occur as a transient symptom, imme- 
diately after the onset of an acute lesion of the cord, apparently from 
irritative inhibition of the centres. Cutaneous reflex action may be 
lessened permanently in some cases of brain disease on the side of the 
motor palsy, even when the muscle-reflex action is increased. Indeed, 
this opposite change in the two forms of reflex action co-existing on the 
same side always suggests intra-cerebral disease. It may be well 
again to remind the reader how difficult it often is to be sure whether 
the knee-jerk is present or is lost, on account of the readiness with 
which its occurrence may be prevented by inability to relax the muscles, 
and its presence may be simulated by a true reflex action (see p. 200). 
Excess of reflex action implies, of necessity, the integrity of the 
reflex arc concerned, and shows that organic disease, if it exists, is 
higher up the cord. Each form of reflex action is often increased. 
In some acute diseases, a,s acute meningitis, and probably also in some 
chronic diseases, the increase may be due to an irritation of the centres, 
but in most forms of chronic disease it is apparently the result of a 
loss of control, and indicates disease between the centre concerned 
and the brain. We have already considered (p. 202) the probable 
mechanism, and have seen that the excess of the muscle-reflex action 
is related to disease of the pyramidal fibres, and especially to the loss 
of the terminal part of these fibres, within the grey matter, adjacent 
to the centres concerned.* This is the significance of considerable 
excess. Degeneration of the terminal portions of the fibres is com- 
monly due to a descending degeneration of the fibres themselves. It 
is possible, however, that the degeneration of the endings of the 
pyramidal fibres may be primary, as,is that of the nerve-fibres. (See 
Primary Spastic Paraplegia.) The increase of reflex action is chiefly 
* It is interesting to note the analogy between the effects of degeneration of the 
termination of the two segments of the motor path. The increased activity of the 
muscle-reflex centres, which results from degeneration of the termination of the 
upper segment, presents some similarity to the increased voltaic irritability of the 
muscular fibres which results from degeneration of the termination of the lower 
segment. SYMPTOMS. 
221 
manifested in the legs, in which reflex action is normally more active 
and important than in the arms, The increase in the cutaneous reflex 
action is shown by its occuri*ence on a slighter stimulation of the skin, 
and by a greater degree and extent of the muscular contractions 
produced. In these the flexors usually predominate, so that the leg 
is drawn up in a strong movement. As the action of the sexual 
organs depends, in part, on superficial reflex processes, priapism is 
common when the reflex excess is great. The increase of the muscle- 
reflex action is shown by an increase of myotatic irritability, and 
therefore of the so-called “ tendon-reflex contractions,”—the increased 
knee-jerk, rectus-clonus, foot-clonus, wrist-jerk, elbow-jerk, chin-jerk 
(jaw-jerk), &c. These have been already described. As already 
stated, the excess of this irritability is at first moderate, and slowly 
increases. A high degree of over-action is never suddenly attained, 
as it may be in the case of cutaneous reflex action. It would seem as 
though, in the centres liberated from control, a capacity for excessive 
action is slowly developed, which ultimately results in tonic spasm. 
Not only is the common cause of this excess damage to the pyra- 
midal tracts higher up the cord, entailing their secondary degenera- 
tion, but if such disease higher up—as, for instance, primary myelitis or 
injury to the cord—is followed by abolition of the muscle-reflex action 
in the parts below, it is the result of inflammatory damage to the 
lower part of the cord in which the centres are situated, generally 
by a descending myelitis. Sometimes the original myelitis involved 
the whole or a considerable part of the cord below, and the indications 
of a transverse lesion were merely those of the upper limit of the 
disease. It is not uncommon for the secondary myelitis below an 
original transverse lesion to succeed it, and abolish the reflex action 
which was at first unimpaired. I have several times met with such a 
sequence. A primary dorsal myelitis has left reflex action in the legs 
unimpaired and tending to excess, with the sphincter ani in its condi- 
tion of uncontrolled automatic action, when after a few days, a week' 
or more, indications of a recurrence of myelitis have been attended 
by abolition of all reflex action, including the knee-jerk, by flaccidity 
of the muscles, with rapid development of the reaction of degeneration 
in them, and by complete relaxation of the sphincter ani. This is the 
state from the first in the cases in which the primary myelitis involves 
the whole lower part of the cord. Sometimes, indeed, such descending 
inflammation is limited to the grey matter or to the posterior columns, 
with corresponding limitation of the symptoms but with a similar 
abolition of reflex action. Of course, such descending inflammation is 
a very different thing from the secondary descending degeneration of 
the pyramidal tracts.* 
* In consequence of the occurrence of this inflammation in the lower part of the 
cord having been overlooked, it has been thought that a transverse lesion higher up 
has the power of abolishing reflex action below, where the cord is iot damaged except 
by descending degeneration. See, however, p. 229, note. 222 
SPINAL CORD. 
Over-action may perhaps be also produced by a state of irritation 
propagated fi'om above, as in the “ early rigidity” of hemiplegia; we 
have seen that the motor impulses probably pass from the pyramidal 
fibres through part at least of the muscle-reflex mechanism. Primary 
over-action seems also to occur, although apparently it only attains a 
slight degree. It is probably the cause of the trifling excess met with 
in cases of defective nutrition of the spinal cord or of the nervous 
system generally. 
Reflex Spasm.—We bave seen (p. 16) that the muscular state on 
which myotatic irritability depends, assumed to be due to a muscle- 
reflex action, is probably identical with physiological tone. When- 
ever there is a considerable increase in the irritability, there is a 
tendency to tonic spasm, in which there is a balanced contraction 
of the muscles, fixing the limbs in the position of extension. At 
first there is merely slight stiffness of the legs, especially felt on 
waking from sleep; afterwards the legs, when extended, become 
distinctly stiff, although they may be quite supple when flexed. If 
gradually extended, when near full extension, the spasm suddenly 
comes on and completes the movemeut, as the blade of a pocket knife 
moves under the influence of the spring. Hence this has been termed 
“clasp-knife rigidity.” Ultimately the extensor spasm may be so 
great that, when it occurs, both legs are rigid, and are so firmly con- 
nected with the pelvis that if one is lifted from the bed the other is 
moved also. This is only met with in organic disease, and is an im- 
portant diagnostic indication. Paroxysms of spasm may be brought 
on by any impression on the sensory nerves, a prick on the skin, or an 
attempt to obtain the clonus. The extreme spasm prevents any clonus 
being obtained, and it may be necessary to flex the limb before an 
attempt to obtain it is successful. As violent spasm is passing 
off, moreover, the tension of the muscles may alone set up a clonus, 
so that the paroxysm of tonic spasm passes into clonic spasm, a 
phenomenon that was termed by Brown-Sequard “ spinal epilepsy,” 
on account of the superficial resemblance to the sequence of spasm in 
an epileptic fit. This clonic spasm may often be arrested by any 
strong painful impression on the sensory nerves, a pinch of the skin, 
or painful flexion of the big toe ; the strong stimulation of the nerves 
of common sensation inhibits the reflex centre concerned in the clonus. 
There is always much weakness of the legs when there is much 
spasm, and there may be almost complete paralysis. Hence the condi- 
tion has been termed “ spastic paraplegia.” It is probable that the 
central reflex mechanisms concerned in the production of this extensor 
spasm are those that subserve the act of standing. The spasm often 
enables a paraplegic patient to stand, when his voluntary power is 
quite insufficient for the act. In advanced cases the extensor spasm 
may be varied by attacks of flexor spasm, which at first come on 
chiefly during sleep, but after a time preponderate, and may ulti- 
mately be permanent; this is always an unfavorable symptom, since, SYMPTOMS. 
223 
for some reason not yet understood, this flexor spasm indicates a 
condition of the spinal cord from which recovery is rare. 
Vaso-motor and Trophic Disturbance.— Changes in Nutrition.— 
Considerable wasting of the muscles indicates disease of the motor 
nerve-cells, or of the nerve-fibres proceeding from these cells. If the 
disease is acute, there is rapid degeneration of the nerves, with the 
reaction of degeneration in the muscles (see p. 56). The wasting in 
these cases is always great, and there is always loss of reflex action. 
Occasionally some fibres of the nerve and muscle suffer and others do 
not, causing the “ middle ” or “ mixed ” form of reaction (see p. 26). 
In rare cases, in which the nerve degeneration set up is of an intensely 
irritative character, the muscles may rapidly lose all irritability in 
consequence of true degeneration of the fibres. I have observed 
this, for instance, in a growth in the lumbar region. In other cases of 
disease, however, there is a slighter degree of wasting of the 
muscles; there is no loss of irritability in the nerves; the irrita- 
bility may be slightly increased or lessened, but is changed in the 
same way to each form of electricity. In this condition reflex action 
is not lost, but, on the contrary, is often increased. The change is 
apparently the result of a peculiar alteration in the nutrition of the 
nerve-cells. It is usually the effect of an irritative degeneration of the 
pyramidal fibres, which influences in a peculiar manner the nutrition 
of the motor cells. 
The changes in the nutrition of the skin, if slight and chronic, 
resemble those produced by disease of the nerves (see p. 61), and are 
probably produced through the agency of the posterior roots. Some- 
times, however, these changes are most acute. Very slight pressure, 
continued for a few hours, causes vesication, and even sloughing of 
the skin. Sometimes bullae form where there has been no pressure. 
Occasionally there is inflammation of the joints. Such intense 
changes are only met with when the morbid process in the cord is 
irritative in its character, especially in haemorrhage, and in spreading 
or disseminated myelitis. The points on which sloughing occurs with 
greatest readiness are the heel, over the malleoli, the trochanters, and 
the sacrum. The position of the bedsores in paraplegia, usually over 
the sacrum, is different from that in hemiplegia, generally over the 
gluteal region on the paralysed side. The tendency to trophic dis- 
turbance probably favours the occurrence of cystitis from retention 
of urine, and the readiness with which the inflammation invades the 
kidneys. I have seen a low form of suppurating subperitoneal pelvic 
cellulitis, in a case of disseminated myelitis with cutaneous sloughs, 
in which no other cause for the cellulitis could be found. 
Vaso-motor disturbance is common in slight degree, irrespective of 
the seat of the disease, but, like the trophic changes, which probably 
depend, in some degree, upon it, it is always most intense in irritative 
lesions of the cord. The slighter and common degree consists merely 
in increased warmth of the limbs in which the vessels dilate too 224 
SPINAL COltD. 
readilv, while, at a later period, the limbs are colder, paler, and often 
livid at the extremities. In rare cases intense flushing of the skin 
has been observed, or copious and long-continued perspiration. When 
the disease is in the lower cervical region, flushing and perspiration 
may occur on the face and head. 
Disease of the cervical cord or nerves is sometimes attended by a 
change in the pupil, on one side only. It is due to the fact that the 
dilator is innervated from the cervical sympathetic through the last 
cervical nerves. There may be contraction, from paralysis of these 
radiating fibres, or there may be persistent dilatation from their 
irritation. The cause of the double myosis, so common in some 
degenerative diseases of the cord, is uncertain; it is associated with 
loss of the light-reflex, and also of the reflex dilatation produced by 
stimulating the skin of the neck. 
The frequency of the heart’s action is often permanently increased 
in locomotor aiaxy, but we do not know by what mechanism. In 
disease of the cervical cord (perhaps also in that of the cervical 
nerve-roots) the heart may be slowed to forty, thirty, or twenty beats 
per minute, usually only for a time. The effect may perhaps be due 
to a loss of the influence of the nerves which, when stimulated, quicken 
the heart. In acute disease of the upper dorsal region the heart’s 
action may be persistently frequent. 
Visceral Disturbance.—Various disturbances in the alimentary canal 
occur in disease of the spinal cord, and are no doubt due to the fact 
that the sympathetic nerves immediately controlling the canal are 
under the influence of the cord, and may be excited to abnormal 
action by its irritation, or may underact when its influence is lessened. 
Difficulty of deglutition is observed in some cases of acute disease 
of the upper cervical region. Vomiting occurs also in disease of the 
same part, especially in fracture of the cervical vertebrae. Constipa- 
tion is extremely common in disease of the cord above the lumbar 
enlargement. 
Paralysis of the Sphincters.—Incontinence of urine and faeces may 
be due to disease of the centres that control the action of the 
sphincter ani and the muscular mechanism of the bladder respectively, 
or it may be due merely to disease of the path (probably the pyra- 
midal tract) through which voluntary control is exerted. In the 
latter case the sphincter ani acts in an automatic reflex manner as 
already explained. If the finger is introduced within it, the initial 
relaxation is felt to be succeeded by a firm tonic contraction. This 
proves that the anal centre in the lumbar enlargement, and the 
nerves proceeding from it, are intact. If this centre is destroyed, or 
the nerves interrupted, no tonic contraction can be felt; there is 
complete and persistent relaxation. I have more than once observed 
a dorsal transverse myelitis to arrest the voluntary influence and 
leave the sphincter in its condition of simple reflex action, and, a 
week or ten days later, the extension of the myelitis into the lumbar SYMPTOMS. 
225 
region to be attended by (among other signs) perfect inaction of the 
sphincter. A rectal examination will then often give important in- 
formation regarding the extent of the disease downwards. 
The sphincter of the bladder is not accessible to such direct 
examination, and the mechanism seems to be more complex, but we 
may distinguish conditions corresponding to those of the rectum. If 
the lumbar centre is destroyed the sphincter is permanently relaxed; 
urine dribbles out of the bladder as fast as it enters it; there is 
simple incontinence. If there is an interruption of the voluntary 
path above the centre, the sphincter may act automatically; when a 
certain amount of urine has collected in the bladder it excites the 
muscular fibres in the wall to contract; the sphincter relaxes, and the 
urine escapes; there is intermittent incontinence. In this condition 
the mechanism is excited to action by any pressure on the bladder ; 
a movement, or the act of coughing, will make the urine come away. 
But the muscle of the wall of the bladder is indirectly under the 
influence of the will; when the sphincter is voluntarily relaxed the 
detrusor fibres in the wall contract. Loss of voluntary power seems 
to lead to weakness in the wall of the bladder, so that the bladder is 
never perfectly emptied, and ultimately the detrusor cannot contract 
to expel the urine, even when the sphincter is relaxed. Hence reten- 
tion of urine occurs. When a certain degree of distension of the 
bladder is attained, the pressure becomes sufficient to force the urine 
out whenever the sphincter relaxes, and such relaxation is continually 
occurring under the high pressure that is repeatedly renewed in 
consequence of the flow from the kidneys. Hence incontinence 
results—“ overflow incontinence.” The retention often develops very 
gradually and insidiously when the voluntary power is only lessened; 
the residual urine is at first small in amount, but gradually increases 
as the detrusor fails to contract adequately against the resistance. 
It is important, if the urine comes away involuntarily, to ascertain 
which form of incontinence exists; since overflow incontinence, and 
the retention it indicates, have much graver consequences than 
simple incontinence. The permanent distension of the bladder con- 
stitutes a permanent hindrance to the flow of urine from the kidneys, 
and serious kidney disease may result. This is a not uncommon cause 
of death in spinal disease. Moreover, whenever the bladder is habitu- 
ally emptied imperfectly, decomposition is apt to occur in the residual 
urine. The decomposition is often aided by the lessened acidity, or 
even actual alkalinity, of the urine. This change in the composition 
of the urine excites inflammation of the bladder; pus is formed by 
the mucous membrane, and this, in its turn, increases the decompo- 
sition of the urine. The damage to the kidneys, by the hindrance to 
the flow of urine from them, may be increased by inflammation 
ascending the ureters from the bladder. 
Pyrexia.—The initial elevation of temperature in some spinal 
lesions may be due to them directly, but sometimes it is due to a. 
YOL. I. 226 
SPINAL COED. 
blood-state of which the cord disease is a result. This is probably the 
case in polio-myelitis. The temperature is sometimes raised in dis- 
ease of the cord apart from the influence of morbid process. Disease 
of the upper cervical cord, like that of the medulla, may cause hyper- 
pyrexia, and this may also result from acute central lesions that occupy 
a considerable vertical extent, such as a central haemorrhage, although 
by what mechanism these act we do not know. Slight variable eleva- 
tion of temperature sometimes occurs in disease of the dorsal cord, 
and is probably due, in some way, to the disturbance of its functions 
rather than to any influence of the morbid process. For instance, in 
one case of haemorrhagic myelitis with damage from the third dorsal to 
the second lumbar segments, every application of electricity to the 
legs was followed by slight pyrexia. 
Convulsions.—Lastly, convulsive attacks have been known to attend 
the onset of acute lesions in various parts of the cord, in adults as 
well as in children. They are most frequent in disease of the cervical 
cord, but I have known a convulsion to occur in an adult at the onset 
of myelitis in the lower dorsal region. The convulsions are general. 
Their mechanism is unknown, and in some cases, especially of infan- 
tile polio-myelitis, they may, like the mitral pyrexia, be the result of 
general disturbance of the system by an acute morbid blood-state. 
Combination of Symptoms.—Certain symptoms are frequently 
combined, and their combination has a definite localising significance. 
Loss of motor power occurs in two different associations, according to 
the position of its cause in the motor path. It may be combined 
with muscular wasting, loss of electric irritability, and loss of all 
reflex action. In this case the disease is in the anterior cornua or 
nerve-roots, the lower segment of the motor path. (But the same 
symptoms are produced by disease of the nerves themselves—in 
multiple neuritis.) On the other hand, there may be no wasting, no 
change in irritability, and, instead of a loss of reflex action, the myo- 
tatic irritability is increased. The interruption of the motor path is 
then in the upper segment, usually in the pyramidal tracts. It may 
be a focal lesion of the cord, or a primary degeneration of the tracts. 
The distinction is that, in the latter case, there is nothing more than 
the muscular weakness and increased myotatic irritability. In the 
former case there are, or have been, indications that the lesion has 
extended beyond the purely motor elements. 
The symptoms caused by disease of the several elements of the cord 
have now been described, but it is necessary to consider further the 
combination of symptoms that results from a total transverse lesion of 
the cord, and from a unilateral lesion. 
A total transverse lesion, however limited in vertical extent, sepa- 
rates from the brain all parts below it, and hence, so far as will and 
feeling are concerned, it produces the same effect as if the whole of 
the cord below the lesion were destroyed. Compression of the cord 
in the middle of the cervical enlargement, for instance, abolishes SYMPTOMS. 
227 
motion and sensation in all parts below the distribution of the 
cervical plexus. A transverse lesion at the second dorsal nerve 
causes motor and sensory palsy of the trunk and legs, leaving the 
arms unaffected. But the same loss, motion and sensory, results 
from disease which damages the whole cord up to the level indicated. 
Hence the extent of the motor and sensory paralysis indicates only 
the upward limit of the lesion ; how far it extends downwards is 
shown by the interference with the central and especially the reflex 
functions of the cord. The upward level is indicated not only by the 
loss of conduction, but also by the position of the girdle-pain, and 
radiating pains, or zone of hypersesthesia, which are due to the irrita- 
tion of the lowest sensory nerves in the upper portion. 
It is desirable to know the symptoms of impaired conduction 
that occur when a transverse lesion is at different levels in the spinal 
cord. They may readily be ascertained by an examination of the 
table given at p. 210. There is, however, some uncertainty as to the 
effect on sensation in the limbs produced by disease at different parts 
of the lumbar and cervical enlargements, since, as we have seen, the 
exact representation of sensation in the cord is still uncertain. 
The upper limit of the lesion is shown by the upward extent 
of the motor and sensory loss, according to the first three columns. 
The lowest nerves supply the anus and perinseum. Those that 
supply the skin and muscles of the leg and foot arise from the 
fourth lumbar to the third sacral segments, and are damaged by 
a lesion involving the lower part of the lumbar enlargement. We 
must, however, remember that the skin of the inner part of the 
leg is not supplied from the sacral nerves, and so may escape 
when the outer part of the leg and back of the thigh have lost 
sensation. In the middle of the lumbar enlargement the nerves 
arise which enter the lumbo-sacral cord,’and these are probably 
destined for the flexors of the knee, and for the hip-muscles supplied 
by the sacral plexus, the glutei, quadratus, and gemelli, and for the 
skin of the lower part of the gluteal region. These parts then will be 
paralysed by disease in the middle of the lumbar enlargement, while 
the muscles and skin in front of the thigh are unaffected. The latter 
suffer when the disease affects the upper part of the lumbar enlarge- 
ment, the origin of the anterior crural (rectus, &c.), and obturator 
(adductors). The skin on the upper and outer parts of the thigh loses 
sensibility, with the part adjacent to the scrotum, and in the groin, 
only when the disease damages the highest part of the lumbar enlarge- 
ment, from which the second and third lumbar nerves arise, and then 
the flexors of the hip become paralysed. In proportion as the disease 
is higher in the dorsal region, we have the symptoms ascending higher 
up the trunk, and marking accurately the height of the lesion by the 
loss of cutaneous sensibility, and by the impairment—first, of the ab- 
dominal muscles, and then of the intercostal muscles. The umbilicus 
corresponds to the tenth dorsal nerves, and the ensiform area to the 228 
SPINAL COED. 
sixth and seventh. "When the disease reaches the lowest part of the 
cervical enlargement (the first dorsal nerves), we have the first sym- 
ptoms in the upper extremity; but these are not, as might be expected, 
in the muscles moving the shoulder-joint, but in the hand. The first 
numbness is complained of in the little finger, and the first weakness 
is in the intrinsic muscles of the hand. Ascending higher, the sym- 
ptoms pass up the arm with some uniformity, and without respect to 
nerve distribution. When the middle of the cervical enlargement is 
reached (the fifth, sixth, seventh cervical) the shoulder-muscles and 
the serratus magnus become paralysed, and there is general loss of 
power and sensation. (For details see table, p. 210, and also p. 192.) 
Above the level of the sixth pair, the trapezius and sterno-mastoid 
become somewhat weakened, for the fibres of the spinal accessory 
which supply them undoubtedly arise in part from this region of 
the cord. At the fourth and fifth cervical the lowcpart of the 
neck becomes anaesthetic, and the diaphragm ceases to act. Here 
our localisation might cease, for total transverse lesions at this spot 
necessarily cause death. For a little time the sterno-mastoids and 
scaleni can still get some air into the chest, rarely in sufficient 
amount to maintain life for more than a few days. Eut limited 
lesions may occur higher up, and then we have complete power- 
lessness of the muscles moving the head, upper part of trapezius and 
sterno-mastoid, and other muscles attached to the occipital bone, and 
interference with sensation in the neck and parts of the head, which 
are not supplied by the fifth nerve. 
The extent downwards of the lesion, its vertical extent, is thus not 
indicated by the impairment of the conducting functions, by the motor 
or sensory paralysis ; to ascertain it we have to examine the functions 
of the cord as a central organ, and to ascertain how far they are 
impaired in the paralysed region—to examine especially muscular 
nutrition and reflex action. The state of muscular nutrition and 
irritability indicates how far the anterior cornua are injured. The 
relation of the several groups of muscles to the cord is shown in the 
first column of the table. The integrity of reflex action indicates the 
integrity of the reflex loops, and the study of the superficial reflexes of 
the trunk is especially instructive in this respect. The series of reflexes, 
and the relation of each to the cord, are shown in the third column of 
the table; the muscle-reflex contractions are printed in italics in the 
position which corresponds to the centres and nerve-roots which are 
essential for their production. Excess of superficial reflex action indi- 
cates loss of the cerebral control exerted on the reflex centres, and con- 
siderable excess of the muscle-reflexes implies impaired function of the 
lowest part of the pyramidal tracts, and generally shows the existence 
of a descending degeneration in the lateral columns. Reflex action 
in the legs may be abolished for a few hours by acute disease or 
injury above the lumbar enlargement, in consequence of inhibitory 
shock, but soon returns if the lumbar centres are intact. As already 229 
SYMPTOMS. 
explained (p. 220), if there is no return of reflex action or myotatic 
irritability, tbeir absence shows that the lumbar region is involved in 
the primary lesion; secondary extension to this is indicated by loss 
of reflex action distinctly subsequent to tbe onset. If such loss 
occurs without wasting and loss of faradic irritability in the muscles 
it shows that the disease in the lumbar region is limited to the poste- 
rior columns or cornua.* 
The fact of chief importance is that dorsal cord disease, the most 
common form, causes no persistent loss of reflex action in the legs, 
and that for such loss special causes must be sought. 
Unilateral lesions interrupt the motor path to the muscles on the 
same side as the lesion, causing one-sided palsy, termed “ spinal hemi- 
plegia ” when the disease is so high as to alfect both arm and leg, 
“ hemi-paraplegia ” when it is lower, and affects one leg only. There 
is often some loss of power on the opposite side, which may be due 
either to slighter damage to the other side of the cord (since few lesions 
are strictly unilateral) or to damage to non-decussating or re-decussat- 
ing fibres. Conversely, the paralysis of the leg may be incomplete when 
that of the arm is complete, owing to the escape of the fibres for the 
leg which cross lower down the cord. Sensation is affected on the 
opposite side, but not quite up to the level of the lesion, because the 
decussation of the sensory tract is not immediate, but occurs some- 
what above the entrance of the nerves. The upper level may vary for 
different forms of sensibility, in consequence probably of the level of 
crossing (in relation to entrance) being different for the several paths. 
A lesion in one side of the lumbar enlargement often affects sensation 
on the same side as motion, because it damages the sensory path 
before it has crossed. In all cases of crossed motor and sensory para- 
lysis, the sensibility of the muscles differs from the other forms of 
sensibility, and if it is affected on one side, this is the side of the motor 
palsy and not of the cutaneous anaesthesia, f 
# A few cases have been met with in which a transverse lesion of the dorsal 
cord, especially a transverse concussion-myelitis, without post-mortem signs of 
lumbar inflammation, has caused a persistent loss of reflex action in the legs. In 
these cases, however, there has been not only loss of the muscle-reflex action, but 
also of the skin reflexes, a clear indication of an exceptional condition. Moreover, 
there has also been loss of f'aradic irritability and rapid muscular wasting—in short, 
there have been all the indications of a lumbar myelitis. The most probable 
explanation of these cases is that the descending degeneration of the pyramidal 
tract has been more than usually irritative in nature, so as practically to amount to 
a parenchymatous inflammation, and that this has invaded the motor structures as 
a nutritional change, sufficient to abolish their function, without, however, destroy- 
ing their form. In one such case it was noted that the lumbar nerve elements 
were extremely granular in aspect. For a different explanation of these cases, see 
Bastian, ‘ Med.-Cliir. Trans.,’ 1890. 
f This was first pointed out by Brown-Sequard in his important study of these 
cases. Scepticism has been expressed as to the fact, based on a denial that the 
test commonly employed, recognition of posture, is significant. Experiments on 
animals, even monkeys, are inconclusive, but the evidence from cases in man is very 230 
SPINAL COED. 
The crossed affection of cutaneous sensibility may involve all forms 
of sensation or only some of them. Sensibility to pain is almost 
invariably impaired. The temperature sense is usually affected with 
that for pain; in only two of twenty recorded cases (in which the 
affection of sensibility was carefully noted) was the sense of tempera- 
ture normal, and that of pain impaired, and in neither of these cases 
was the sensibility to pain actually lost. On the other hand, in one 
third of the cases tactile sensibility was unaffected, and in about 
one tenth of the cases it was impaired on both sides. 
Cutaneous sensibility is sometimes impaired in a zone at the level of 
the lesion, and on the same side, in consequence of the damage to the 
nerve-roots entering the cord, and above this there may be a narrow 
band of hyperaesthesia from irritation of the roots at the upper part 
of the lesion. On the side of the lesion, below the anaesthetic zone,, 
there is, in most cases, a remarkable hyperaesthesia, corresponding in 
distribution with the anaesthesia on the opposite side. Painful impres- 
sions are felt most acutely, and even a touch on the skin, or warm or 
cold bodies, produce pain. The cause of this hyperaesthesia is obscure. 
Both it and the opposite loss of sensibility may last for twenty years,, 
and it cannot be ascribed therefore to any irritation by the morbid 
process. It is perhaps due to an altered action of the cerebral centres 
on the opposite side of the brain. There is much evidence of an inti- 
mate connection between the sensory centres on the two sides, and it is- 
conceivable that the altered functional state of the centre on the side 
of the lesion, to which impressions cease to come, may induce in the 
opposite hemisphere a condition expressed as hyperaesthesia. The con- 
dition may be thought of in relation to the peculiar phenomena of 
transfer in hysterical hemianaesthesia. 
Reflex action is increased in all its forms on the side of the lesion,, 
but the increase only occurs after some days. At first it is lessened or 
even abolished, no doubt from the inhibitory influence of the irrita- 
tion of the morbid j>rocess. 
The side below the lesion is at first, for some days or even weeks, 
warmer than the other, the difference being usually about a degree 
Fahrenheit. In the course of time this difference passes away, and 
the side may even be colder than the other. 
These symptoms may be shown in the form of a table: 
strong, not only of the occurrence of the loss, hut of the significance of the test. Ii* 
some cases, moreover, the muscles were insensitive to pressure. One recorded 
instance is the following :—A stab in the dorsal region caused loss of cutaneous sen- 
sibility in the right leg and motor palsy in the left. On this left side, on which 
cutaneous sensibility was normal, the sense of posture was absolutely lost, while it 
was present on the right side on which cutaneous sensibility was impaired. The 
patient often thought the left leg was flexed when it was extended. Ultimately this 
leg presented distinct ataxy. (Gilbert, ‘Arch, de Neurologie,’ 1882, p. 275.) PATHOLOGICAL DIAGNOSIS. 
231 
Zone of cut. hyperaestbesia 
anaesthesia. 
LESION. 
Motor palsy. 
Hyperaesthesia of skin. 
Muscular sense impaired. 
Reflex action first lessened, then 
increased. 
Temperature raised. 
Muscular power normal. 
Loss of sensibility of skin. 
Muscular sense normal. 
Reflex action normal. 
Temperature same as that 
above lesion. 
The vertical distribution of the symptoms varies according to the 
vertical position of tbe lesion. Their relations are best marked when 
the lesion is in the dorsal region of the spinal cord. When it is in 
the cervical or lumbar enlargement the upper limit is less distinct 
because of the complex representation of skin and muscle in the 
nerve-roots. 
GENERAL PATHOLOGY AND ETIOLOGY: INDICATIONS OF THE 
NATURE OF THE LESION: PATHOLOGICAL DIAGNOSIS. 
The kinds of disease to which the spinal cord is liable are not 
specifically numerous, but those which are common present several 
varieties. The processes are congestion and anaemia, haemorrhage, 
inflammation, degeneration, and growths. Haemorrhage and growths 
are, on the whole, rare. Congestion and anaemia play an uncertain 
part in the production of symptoms ; their influence has been certainly 
overrated by some writers, and perhaps under-estimated by others. 
The most frequent lesions are inflammation and degeneration. These 
two processes, distinct in their typical forms, blend in their inter- 
mediate varieties. Inflammation varies much in character and course. 
Its effects are, in some cases, produced with great rapidity, in other 
cases with extreme slowness. It probably commences in most instances 
outside the nerve-elements, which are secondarily involved. Perhaps 
some acute processes in the nerve-elements themselves are most 
accurately regarded as a parenchymatous inflammation, analogous 
to that which we know occurs in the fibres of the peripheral nerves. 
Degeneration consists of two processes, a wasting of the nerve-struc- 
tures, cells and fibres, and an overgrowth of the connective-tissue 
elements. The latter leads to the condition termed sclerosis. The 
name has been given to it, apparently, because the process is one that, 
in other organs, increases their consistence. In the cord it has not 
often this effect. The newlv-formed connective tissue is rarely of 
greater firmness, and is often less firm, than the nerve-elements it 
replaces. In sclerosis, however, we must distinguish two types. In 232 
SPINAL CORD. 
one the process is limited to structures that have the same function ; 
the process begins as a degeneration of the nerve-elements, and the 
overgrowth of the connective tissue is a consequence of their wasting, 
the affection is essentially “ parenchymatous.” The so-called “ se- 
condary degenerations ” are of this character; but similar changes 
are often primary, and affect the structures that have the same 
function, often through a considerable extent of the cord. Hence 
they are termed “ system diseases.” In the other type the morbid 
changes are not distributed according to function. They are appa- 
rently random in incidence, and involve adjacent structures in con- 
sequence of contiguity. These begin in the connective tissue and not 
in the nerve-elements, which suffer secondarily. They are essentially 
interstitial processes. Insular sclerosis is an example of this type. 
The position of the islets of sclerosis has no relation to the function of the 
parts, and may involve parts of adjacent structures that have no common func- 
tion. Areas of diffuse sclerosis are also met with which have not the sharp 
limitation of the insular form, and are regarded by some as of the nature of 
chronic sclerotic inflammation. If such a lesion is so situated as to involve fibres 
that undergo secondary degeneration, this necessarily results when the damage 
to the fibres is sufficiently great. We have then a combination of the random 
and systemic forms of sclerosis, but one that has no real pathological signifi- 
cance. 
There are, however, other relations between the two types that deserve 
attention. These will be considered in connection with the special morbid 
processes that present them, but a brief mention of them here may make some 
facts of other diseases more intelligible. The process of secondary degeneration 
and secondary sclerosis varies in its character, presenting in some cases a 
greater amount of vascular disturbance than in others. It seems to partake of 
the character of the lesion causing it, as we have seen (p. 55) the process 
of secondary degeneration in the nerves may do. The same difference is seen 
in the primary degenerations, such as occur in tabes. This difference is 
analogous to that which, as already described, occurs in some varieties of 
multiple neuritis. We can indeed see the difference in the eye: tabetic 
optic nerve atrophy, in most cases, presents no sign of inflammation, while in 
others the early stage may be accompanied by distinct slight neuritis, to be 
seen with the ophthalmoscope. Secondly, the chronic inflammations, with the 
diffuse limitation, extending to adjacent structures irrespective of function, 
have yet sometimes a mai'ked tendency to be localised in structures of definite 
function. Thus there is sometimes diffuse sclerosis of the lateral pyramidal 
tracts and posterior median columns, not sharply limited to these, and yet with 
a correspondence and symmetry not to be overlooked. Thus the two processes 
tend to meet; the systemic degeneration or sclerosis to be diffuse; the 
diffuse inflammation or sclerosis to be systemic; and it is sometimes not 
easy to say, from mere microscopic examination, to which class a lesion 
belongs. Lastly, there is a curious fact, which has been strangely overlooked 
although attention was first called to it by Charcot—that inflammation 
may extend from a primary lesion along a tract that undergoes secondary 
degeneration, hut in the opposite direction to that of the degeneration. It is 
very common for the inflammation at a given place in the cord, especially that PATHOLOGICAL DIAGNOSIS. 
233 
due to compression, to extend farthest along certain tracts, irrespective of their 
secondary degeneration, and in some cases this extension occurs through a con- 
siderable extent of the cord. An ascending inflammation limited to the pyra- 
midal tracts may, for instance, be traced through several segments. The fact 
suggests that the neuroglial elements may share to some extent a difference 
that obtains between the fibres of different tracts, and it may easily lead, and 
probably has led, to erroneous conclusions. 
Softening of the spinal cord is very common. Whenever the nerve- 
fibres are broken up into disconnected globules of myelin, separated 
by serum in a sort of emulsion, the consistence of the part is neces- 
sarily lessened. Acute inflammation always causes such a breaking 
up of the nerve-fibres, and hence inflammation always causes softening 
as its first effect. The separate particles are augmented by leucocytes, 
which escape abundantly into the tissue. Ultimately, connective-tissue 
elements are formed, which increase the consistence, it may be up to, 
and even beyond, the normal degree. In a very chronic inflammation 
the formation of new tissue may proceed pari passu with the destruc- 
tive process, and there may be at no time much diminution of 
consistence. It is in these cases that it is difficult to draw the line 
between inflammation and degeneration. 
Does such softening of the cord occur apart from inflammation ? 
The question is not easy to answer. In the brain, necrotic softening 
is very common as a consequence of arterial obstruction—is indeed 
the common form of softening. But in the spinal cord we have no 
evidence of the occurrence of necrotic softening. If embolism occurs, 
it is excessively rare. The course of the vessels does not favour the 
passage of a plug into them, while the vertical connection in the 
anterior spinal and anastomotic arteries (see p. 188) will prevent 
damage from obstruction in the central system unless this is situated 
in the terminal vessels of the grey matter. Arterial thrombosis, due 
to athei'oma of the walls of the vessels, such as is so common in the 
brain, probably does not occur in the cord. The arteries are smaller 
than those in which atheroma is met with in the brain, and the low- 
ness of the blood-pressure within them involves the absence of the 
chief cause of atheroma. It is possible that spontaneous thrombosis 
may sometimes set up the changes that are now regarded as those of 
primary inflammation ; and such a lesion has actually been met with, 
but only in isolated form, and we have no evidence of its frequency. 
Besides the morbid processes to which the cord itself is liable, it 
suffers also in consequence of disease outside it. It may be com- 
pressed by growths springing from the membranes or bones, and by 
products of inflammation within the spinal canal. Compression not 
only causes degeneration of the nerve-elements, but usually excites 
actual inflammation. This “compression-myelitis” may attain a 
degree and an acuteness out of all proportion to the causal compres- 
sion. The membranes may be the seat of haemorrhage which com- 234 
SPINAL CORD. 
presses the cord, or inflammation which irritates it, even when the 
organ is not invaded in appreciable degree. 
The series of recognised lesions of the spinal cord, obvious or micro- 
scopic, does not by any means exhaust the list of its morbid states. 
Changes may occur in the nutrition of its elements interfering with 
their function, which are, and are likely to remain, altogether beyond 
our means of detection. Such morbid states are often called “ func- 
tional diseases,” but when prolonged they are probably more accurately 
conceived as nutritional diseases (see p. 1). Derangements of 
function that we can regard as purely such are few and rare. But 
disturbances of function may be due to organic disease in some other 
part of the nervous system, and they may also be the result of toxic 
agents. 
Lastly, functional action in all organs is attended with increased 
blood-supply; and when excessive, the vascular disturbance may go 
on to a condition indistinguishable from inflammation, with escape of 
leucocytes, &c. The prolonged experimental stimulation of sensory 
nerves has actually produced myelitis in the related portion of the 
cord. 
In connection with the general pathology of diseases of the spinal 
cord, it is important to note certain general facts of their causation:—■ 
(1) Neuropathic disposition.—An inherited tendency to disease of the 
nerve-elements, manifested by such affections as epilepsy and insanity. 
This cause is chiefly influential in producing the structural and 
nutritional diseases, beginning in the nerve-elements, and especially, 
among structural diseases, the “ system-degenerations,” as they are 
called. (2) Prolonged mental distress sometimes sets up degenera- 
tive changes in some elements of the cord, especially in persons who are 
predisposed by (1). (3) Injury.—A severe concussion of the cord 
may cause (a) instant grave damage, usually haemorrhage. Or (b) it 
may cause no immediate effect, but symptoms may come on at the 
end of a few days and progress slowly or rapidly. Such symptoms 
are usually due to inflammation, secondary to minute spots of injury, 
too small to cause direct symptoms. Lastly (c), the concussion 
sometimes seems to pervert the process of nutrition in the nerve- 
elements. Slow symptoms of impaired function may result, and 
these may progress, until, after months or years, there is actual 
structural disease. (4) Exposure to cold.—Wet cold is especially 
effective. The most frequent effect of a severe exposure is acute 
inflammation, but habitual exposure may pi’oduce chronic inflamma- 
tion, or degenerative disease. The exposure that is effective may be 
general, or chiefly of the feet and legs, occasionally of the back. (5) 
Toxic agents that can act on the cord are numerous and are seen in 
alcoholism and lathvrism. (6) Other diseases may also induce 
morbid changes in the spinal cord. The primary malady may be an 
acute specific disease, or some more obscure blood-state, the precise PATHOLOGICAL DIAGNOSIS. 
235 
nature and relations of which are still undecided. It is probable that 
certain blood-states, due to an organised virus, excite some forms 
of inflammation of the cord and of its membranes, just as it may 
cause inflammation of the peripheral nerves. Septicaemia may excite 
meningitis, or even abscess of the cord itself. Tubercle is common 
on the membranes, but seldom produces inflammation. Diphtheria 
may cause acute changes in the nerve-cells and nerve-roots. Syphilis 
is a very frequent cause of disease, and may act in several ways. 
The demonstrated mechanisms are (a) by a syphilitic growth, 
compressing or invading the cord, and (b) by chronic syphi- 
litic meningitis, damaging the cord and the nerve-roots. But (c) 
acute and chronic inflammations of the cord are often met with in 
syphilitic subjects, and have been thought to be, in many instances, 
of syphilitic origin. It is doubtful whether they present any syphi- 
litic characters, i. e. any histological features by which they differ 
from non-syphilitic inflammations. The evidence of dependence on 
syphilis is stronger in the case of chronic and subacute disseminated 
inflammation than in the case of acute myelitis. Lastly (d), certain 
degenerative diseases of the cord are very commonly preceded bv 
syphilis; one of them, locomotor ataxy, so frequently that a causal 
relation between the two can scai'cely be doubted. But these de- 
generative diseases are certainly not syphilitic in nature; they differ 
in no respect from the similar morbid processes that occur in 
individuals who have not had syphilis, and are probably the conse- 
quence of some virus left behind by the morbid agency to which the 
constitutional malady is due. 
The outline just given of the general pathology and etiology of 
diseases of the spinal cord will enable us to consider the last element 
in diagnosis, the nature of the lesion. The seat of the disease is 
indicated by the combination of symptoms; its nature can only be 
determined by considering, separately and together, several other 
points:—(1) The way in which the symptoms came on. (2) The 
causes that can be traced, taken in conjunction with the known effects 
of those causes. (3) The seat of the disease, taken in conjunction 
with the known liability of certain structures to certain lesions. The 
most important of these elements is the mode of onset, and the other 
indications should only be used in strict subordination to this. 
The time occupied by the onset of the disease is thus the first 
element in the pathological diagnosis. By “time of onset” is meant 
the period that elapses between the actual commencement of the 
symptoms and their attainment of a considerable degree of intensity. 
We may divide the chief modes of onset into five classes, and 
classify the most common lesions in relation to them, in the following 
table: 236 
SPINAL CORD. 
Disease. 
Onset. 
Disease. 
Sudden 1 
(few minutes) 1 T7- , , . 
, v , y > Vascular lesion?. 
Acute 
(lew hours or days) J 
”Subacute 
(one to six weeks) 
-Inflammation. 
Pressure and 
Subchronic 
growths 
(six weeks to six months)J ] 
Chronic 
s- Degeneration. 
(more than six months) 
J 
A lesion of sudden occurrence, the symptoms developing in the 
course of a few minutes, is almost always vascular, commonly haemor- 
rhage, sometimes perhaps vascular obstruction. But a vascular lesion 
may occupy a somewhat longer time in development—a few hours or 
days. In acute and subacute inflammation the symptoms come on in 
the coui’se of a few hours, a few days, or a few weeks. Subacute and 
chronic inflammation occupies from a few weeks to a few months. 
Degeneration, in which there is no adequate evidence of any inflam- 
matory process, occupies many months, or it may be years. The sym- 
ptoms produced by tumours which invade or compress, and by simple 
pressure (traumatic causes excluded) are never sudden or very acute, 
and rarely very chronic, the time occupied by the development of the 
symptoms varying, according to the nature of the cause, from a fort- 
night to six months. 
It is necessary to consider, however, not merely the whole time 
occupied by the development of the disease, but also the uniformity 
of its course. Two or more morbid processes may concur. An initial 
myelitis, for instance, may lead to a secondary degeneration ; and, on 
the other hand, in degenerated tissues, sudden vascular lesions 
occasionally occur. Pressure produces local myelitis, which may be 
independent of the pressure in its development, and have an acute or 
subacute onset. The whole course of the disease must be ascertained 
before an inference is drawn, and the possibility of a double process 
must always be kept in view. 
The onset and course of the symptoms thus sometimes enable us to 
decide at once that a lesion is of a given character, as that one which 
occurs instantly is vascular, or that one which takes years for its 
development is degenerative. More frequently they enable us to 
exclude certain morbid processes, and to restrict the possible lesion 
to two or three forms. For instance, a lesion which comes on in the 
course of a few hours must be either vascular or inflammatory. 
Between these we have to decide by attention to other indications. 
In actual diagnosis it is convenient to consider next the indication 
afforded by the position and distribution of the disease. We consider 
what diseases occur in this situation, and then which of them, have 
the mode of onset that has been ascertained. This indication involves 
a knowledge of the various diseases and their seat. The most important 
consideration is that a wide range of symptoms of uniform character PATHOLOGICAL DIAGNOSIS. 
237 
indicates the affection of a definite system of structure, and in most 
instances a disease commencing in the nerve-elements, and if the 
onset be chronic we may feel sure that it is a degeneration. On the 
other hand, the involvement of many functions suggests a random 
process, such as inflammation or pressure. But this indication is 
always to be subordinated to the mode of onset. Thus the limitation 
to a single structure does not exclude inflammation: this may affect, 
for instance, the anterior grey matter only, and cause corresponding 
symptoms. 
The symptoms may indicate a morbid process limited to one half 
of the cord, but this does not materially modify the diagnostic method. 
Almost any process may, in rare cases, be thus limited. System 
degenerations and acute inflammations are least frequently unilateral, 
and they never reach a considerable degree of intensity on one side 
without some affection of the other side. On the other hand, tumours 
and foci of chronic myelitis are often one-sided, and still more often 
affect one half of the cord first and then the other. 
Indication of disease outside the cord, irritation of certain nerve- 
roots, causing severe local pain, often precedes the symptoms of com- 
pression, and is an important aid to diagnosis. It shows the existence 
of a morbid process outside the cord before the cord is involved. But 
we cannot use even this indication except in dependence on the mode 
of onset. A disease, as a growth outside the cord, may, as we have 
seen, not only compress the cord, and cause slow loss of power; it 
may excite inflammation and cause rapid palsy. 
The last element in the pathological diagnosis is the detection of 
any influence which can be regarded as the cause of the disease in the 
spinal cord, or any associated condition which may Indicate an active 
morbid process. We have seen that the mode of onset may help us 
to limit the disease to certain possible forms of lesion ; the distribu- 
tion of the affection may render it probable that it is one or other of 
these forms; and the detection of a cause and the knowledge of the 
lesion that cause produces may help us to carry the diagnosis still 
further. The most important general causes of disease of the cord, 
and the processes to which they chiefly give rise, have been already 
mentioned. The causal element in diagnosis is chiefly an application 
of those facts. 
The morbid process outside the spinal cord that most closely simu- 
lates its disease is, unquestionably, parenchymatous multiple neuritis. 
The diagnosis depends on a thorough knowledge of the varied sym- 
ptoms of the latter, since its elements vary according to the different 
manifestations of the disease of the nerves. For these, and for any 
general diagnostic principles, the reader is referred to the account of 
that disease. 
The only sure ground for diagnosis is a thorough knowledge of the 
various morbid processes and their symptoms; and the only safe plan 
is to work by these, from symptom to seat and onset to nature, 238 
SPINAL CORD. 
treating every case as a problem to be worked out to a definite 
diagnosis, and only then comparing tbe result with the types of 
disease. To one of these the case may or may not conform ; if it does 
not, the comparison with types as a means of diagnosis will only 
leave the observer stranded and powerless. 
The distinction of functional and nutritional disease from organic 
lesions may conveniently be postponed until the symptoms of the 
former are specially described. 
SPECIAL DISEASES OF THE SPINAL CORD. 
DISEASES OF THE VERTEBRAL COLUMN. 
Diseases of the bones of the spine fall for the most part within the 
province of surgery. But there are few of these diseases that do not, 
among their most frequent effects, interfere with the functions of the 
spinal cord. Hence an account of the diseases of the cord would be 
incomplete without some mention of the morbid states that begin in 
its bony case. 
INJURIES OF THE SPINE. 
Injuries to the spinal column may consist of punctured wounds 
(which need not be considered here), concussion (the effects of which 
on the cord will be considered later), and fracture or dislocation of 
the vertebrae. It may, however, be useful briefly to describe the more 
salient features of the last two conditions, their relation to the damage 
the cord sustains, and the symptoms thus produced. 
Dislocation. 
Simple dislocation occurs in tlie cervical region, most frequently at 
the fifth and sixth vertebrae. It may take place gradually or suddenly: 
gradual displacement is always secondary to disease of the bones; 
sudden displacement may occur in disease or from injury. The 
damage to the cord is always greatest in traumatic displacement of 
healthy bones, because the force needed to produce the dislocation is 
much greater, the displacement is more considerable, and the effect 
on the canal and the contained cord is greater. Displacement may 
occur in any direction : it usually involves both vertebral articulations, 
but, in rare cases, it is oblique, involving one articulation only. The 
common causes are violent blows or falls on the head, rarely sudden INJURIES OF THE SPINE. 
239 
rotation of the Head while a weight is carried upon it. The symptoms 
are a lateral or forward or backward displacement of the head, so 
that the chin is in contact with the shoulder or the cbest, or the 
occiput with the nape of the neck. There is also irregularity of the 
vertebral spines, usually readily detected. The cord is damaged in 
most cases, and the symptoms are those of a total transverse lesion 
in the situation of the luxation. It may be merely compressed, 
especially in cases of disease, in which the displacement has occurred 
with little force. The symptoms of pai’alysis have been known to 
pass away, in such a case, on the reduction of the dislocation. More 
commonly the cord is also bruised, with extravasation of blood, and 
secondary myelitis occurs later. In such cases, if the patients live, 
there may be anesthesia or hvpei’sesthesia below the lesion, with total 
paralysis of the limbs, and excess of reflex action. In rare instances 
the cord has been completely divided. In still rarer instances of 
.slight displacement it has not been injured. 
Rupture of the transverse ligament which retains the odontoid 
process may permit the latter to compress the cord, and thus to cause 
instaut death. This often results from sudden suspension by the 
head, as in criminal executions. One of the curiosities of surgical 
literature is a case related by Petit in which a man, playing with a 
neighbour’s child, lifted it up by the head, and caused instant death 
by rupturing the transverse ligament. The father of the child, 
entering at the moment, stabbed the man with a knife, the blade 
of which passed in between the first and second cervical vertebrae, 
divided the spinal cord, and the man also fell dead. Rupture of the 
ligament has also resulted from raising a heavy weight with the 
head. The treatment of dislocation is too purely surgical to be de- 
scribed here. 
Fracture. 
All organic diseases of the bones, weakening them, predispose to 
fracture. Among these, one is of special medical interest; the ver- 
tebrae, especially in the lumbar region, may share the rarefaction and 
weakening of the osseous tissues occasionally produced in tabes, and 
then a very slight traumatic influence, a blow or wrench, may cause 
fracture. The force needed is often so slight as to fail to cause dis- 
placement or other symptoms except local pain, and symptoms may 
only supervene at a somewhat later date. Apart from disease, the 
accident is most common in adults, the greater elasticity of the verte- 
bral column in children giving to them a comparative immunity. Its 
cause is a blow or fall on the spine, or sudden forcible flexion. In 
extremely rare cases a fracture, usually slight, has resulted from a 
severe muscular exertion. This is an important fact, showing that 
muscular exertion may injure the spine, and may lead to symptoms 240 
SPINAL CORD. 
at a later date. Symptoms of such injury, in slight degree, are not 
uncommon. 
Fracture may occur at any part of the spine, but is most frequent 
at the fifth or sixth cervical, and at the last dorsal or first lumbar 
vertebrae. In the dorsal and lumbar regions, the bodies are broken 
in two thirds of the cases, but in the cervical region, the arches alone 
are fractured in one half. Usually there is a displacement of the 
vertebral column at the seat of fracture. Rarely the bodies may be 
crushed without displacement. The displacement of the bone involves 
a narrowing of the canal and, usually, compression of the cord. This 
may also result when the arches only are driven in. But the cord 
may be seriously damaged when there is no permanent narrowing of 
the canal, as in Figs. 85 and 86. The dura mater is rarely torn except 
Fig. 85.—Fracture of the first lumbar vertebra. D M. Dura mater. There 
was no permanent narrowing of the canal, but, nevertheless, the spinal 
cord was greatly damaged at the spot; see next figure. 
hv a splinter. Blood is almost always extravasated outside the dura 
mater, often in considerable quantity, from the rupture of the large 
veins in this situation. There are usually only small extravasations 
in the pia mater. The cord is, in most cases, bruised and compressed 
by the lower fragment (Fig. 87). Sometimes it is flattened, and it 
may even be divided, all nerve-substance being squeezed out of the 
pia-matral sheath at the spot. In the case shown in Figs. 85 and 86 
the cord appeared to have been split longitudinally at the spot, per- 
haps by the nerve-force of the concussion. It is very common to have 
local myelitis, opposite the fracture, without any permanent narrowing 
of the canal or compression of the cord, the inflammation seems to be 
the direct result of the concussion. Blood may be extravasated into 
the bruised part, sometimes in minute spots, sometimes in larger 
hemorrhages, and even into the central canal. These changes are 
usually limited to the spot directly damaged, but secondary myelitis 
may be set up, and sometimes extends beyond the contused area. It 241 
INJURIES OF THE SPINE. 
Fig. 86. 
Fig. 87. 
Fig. 86.—Spinal cord damaged by the fracture shown in Fig. 85. The elements 
of the cord itself are changed beyond the possibility of identification. The ascending 
degeneration is shown in Fig. 74. 
Fig. 87. —Fracture of the body of the fifth dorsal vertebra and of its processes. 
(After Gurlt.) 
may even extend through the whole length of the cord below the in- 
jury, and then its central functions are abolished (see p. 228). In cases 
of some duration the usual ascending and descending secondary de- 
generations are also found. It is important to note, moreover, that 
the secondary degenerations have sometimes the irritative character 
already described (p. 229, note), and that an ascending inflammation 
may for a short distance above the lesion be limited to a tract that 
degenerates downwards (see p. 232). Fig. 74, p. 177, represents 
sections of the cord from the case of fracture figured above. Occa- 
sionally the injury leads to secondary caries of the bone, with all its 
consequences. 
Symptoms.—Three classes of symptoms result. (1) The local indica- 
tions of the injury to the spine. (2) There may be certain nervous 
symptoms not distinctly due to the damage to the cord. One of these 
is general shock, which may be so great as to entail transient loss of 
consciousness. Vomiting occasionally occurs. There is great pain in 
the position of the fracture, rendered very intense by pressure, and 
often radiating along the nerves which come from this part, the roots 
of which are compressed. In rare cases epileptiform convulsions have 
followed fracture, usually at an interval of some days. 
(3) Symptoms which result from the damage to the cord, and con- 
sist in paralysis of the parts below the injury. Its character depends 
on the amount of damage. If this is considerable, there is both 
motor and sensory paralysis up to the level of the lesion, with loss of 
power over the sphincters. Reflex action is lost at the level of the 
lesion, and the examination of the trunk-reflexes often gives important 
VOL. I. 242 
SPINAL CORD. 
information regarding the extent of the damage, when this is in the 
dorsal region. Below, reflex action is commonly in excess, unless the 
centres are impaired by descending myelitis. Spasmodic twitcliings 
sometimes occur in the limbs immediately after the injury, accom- 
panied by priapism. The pains ai*e severe in the arms when the 
fracture is opposite the cervical enlargement, and in the legs when at 
or below the lumbar enlargement, so as to damage the nerve-roots. In 
these cases there may be rapid wasting of the muscles, with loss of 
electric irritability. There is usually at first incontinence, afterwards 
retention of urine, but the former is persistent if the lumbar centres 
are damaged. Cystitis, bedsores, &c., may supervene. Ultimately, 
if the damage is above the lumbar enlargement and the patient lives, 
there may be increased myotatic irritability in the limbs, progressing 
to spasm, so that spastic paraplegia results. 
Special symptoms result when the injury is in certain parts of the 
spine. Fracture of tbo first two cervical vertebrae causes instant death, 
unless the displacement is very slight, and even then there is imminent 
danger of further displacement, with the most serious consequences, 
on any incautious voluntary movement. With slight displacement 
persons have been known to live for weeks, and then die from secon- 
dary myelitis; they have even recovered altogether. How and then 
there is no compression of the cord, although there is distinct displace- 
ment, even sufficient to be recognised in the pharynx (Leyden). In 
such a case death has resulted at a later period from caries. The 
characteristic symptoms are local pain, increased by all movements 
(which are rendered almost impossible), displacement, and spinal 
symptoms. The latter may be slight—merely difficulty in breathing 
or swallowing—or considerable, and involving the trunk and limbs. 
Sometimes there is hyperpyrexia.' Hot more than one case in fifty 
recovers. 
Middle Cervical Vertebrae.—The third, fourth, and fifth vertebrae are 
most frequently fractured. When the injury to the cord is consider- 
able, death usually occurs very rapidly, because the roots of the 
phrenic nerve are involved, the intercostals being necessarily paralysed 
with the parts below. In some cases there is little immediate displace- 
ment, and the symptoms are slight until further displacement occurs 
in some movement. Thus a man who had met with an injury of this 
kind went to be shaved ; during the proceeding, his head was turned on 
one side by the barber, with the unexpected result of causing displace- 
ment of the fracture, and immediate death. When the fracture is at 
the cervico-dorsal region, opposite the lower part of the cervical en- 
largement, the arms frequently escape at first, the early paralysis 
being confined to the legs and muscles of the trunk. Respiration is 
diaplmagmatic only. After a few days the arms become involved, but 
their paralysis is often partial, affecting, for instance, only certain 
muscles, as the extensors of the hand, and it-is often accompanied bv 
local spasmodic movements. Movements and pressure cause pain, 243 
CARIES. 
and there is local muscular rigidity. The head may be in normal or 
in abnormal position. Vaso-motor disturbance in the face and general 
hyperpyrexia have been observed. 
In fracture of the dorsal vertebrae (2—11) the arms escape, the legs 
are paralysed, and the trunk-muscles up to the height of the lesion. 
The pain in the trunk may be very severe. There is hypersesthesia or 
anaesthesia in the parts below. The reflex action in the legs is exces- 
sive ; that in the trunk is abolished at the level of the lesion. The 
last dorsal and first lumbar vertebrae are fractured more frequently 
than the others, and there result paralysis of the legs, complete or 
irregular, severe pains, tingling, &c., sometimes followed by hvper- 
aesthesia or loss of sensibility, and by rapid disturbance of nutrition, 
in both the muscles and the skin. In fracture of the lower lumbar 
vertebrae the symptoms are often slight; below the extremity of the 
cord the nerves occupy a smaller space in the canal, and so may escape 
compression by a moderate displacement. If they suffer, the fractured 
vertebrae unite very slowly. A false joint is occasionally formed. 
Secondary myelitis and its consequences are frequent causes of death 
at a variable period after the injury. 
CARIES OF THE SPINE. 
Caries of the bones of the spine is a frequent cause of paraplegia. 
It is often termed “ Pott’s disease,” from the English surgeon, Percival 
Pott, who first described it (in 1779) as a cause of paralysis. 
Causes.—Males are said to be rather more liable than females, but 
the difference in sexual incidence is not great. It is more common in 
childhood (after three), and next in early adult life, but it may occur 
at any age, and is perhaps more common in the second half of life than 
any other scrofulous lesion. I have known it commence at fifty, and 
it has been met with as late as seventy. It is distinctly a manifesta- 
tion of the tubercular and scrofulous diathesis, and evidence of such 
inheritance is to be traced in most cases. Occasionally the sufferer 
himself presents such indications, lung disease, &c., or caries of other 
bones. It occasionally develops simultaneously with other signs of 
acute general tuberculosis. Injuries seem frequently to excite the 
bone mischief in the spine, as they certainly do analogous bone dis- 
ease elsewhere, in those who are predisposed; possibly, sometimes, in 
healthy persons. Falls, blows on the back, and severe strains are the 
most frequent traumatic antecedents. The last may act by straining 
the ligaments and settingup inflammation, which spreads to the bones 
directly or through the invertebral cartilages. There is usually an 
interval, sometimes of many months, between the injury and the 
definite symptoms of bone disease. 244 
DISEASES OP THE SPINE. 
Other causes besides scrofulous disease have occasionally been 
known to cause breaking down of the bodies of the vertebrae with 
angular curvature and all its consequences. Soft growths in the 
spine, and, in rare cases, syphilitic formations have had the same 
effect. Osteitis, due to extension from adjacent inflammation, is 
a rare cause; thus caries of the cervical spine has been secon- 
dary to a primary retro pharyngeal abscess. The disease sometimes 
follows septicaemia, probably in consequence of a secondary septicaemic 
abscess in the bone. This was the case in a surgeon about sixty 
years of age, in whom symptoms of blood-poisoning followed an 
injury to the ankle. They were succeeded by paraplegia of rapid 
onset, and this by the development of angular curvature in the 
lower dorsal region. In a large number of cases no exciting cause can 
be traced. 
Pathological Anatomt.—The changes in the bones need not 
detain us, since they belong to surgical pathology, except in so far as 
they lead to damage to the cord. There is inflammation of the bodies 
of the vertebrae, and of the intervertebral substance, often at first with 
enlargement, afterwards with breaking down of the substance of the 
bone, which gives way under the pressure to which it is exposed, so 
that deformity of the spine results. Products of inflammation and 
destruction of tissue, more or less purulent in character, accumulate 
either inside the canal or outside the vertebral column. In the latter 
situation they are increased in quantity by the inflammation they 
excite and the well-known forms of abscess result. 
Within the canal the inflammatory products have a firmer con- 
sistence. Although the inflammation extends to the loose cellular and 
adipose tissue between the bone and the dura mater, and often to the 
dura mater itself, it has little tendency to spread as a purulent menin- 
gitis, or even to penetrate the dura mater, the outer layer of which 
becomes irregularly thickened in the neighbourhood of the disease 
(see Fig. 89), while the inner surface of the membrane remains normal. 
The firm consistence of the inflammatory products, often caseous in 
character, is an important pathological feature, because this material 
is so often the agent by which the cord is compressed. 
The displacement that results from the disease varies according to 
the extent and character of the disease. Occasionally there is simply 
a lateral displacement—one spine is a little to one side of that above 
it. More commonly the collapse of the bodies leads to “ angular 
curvature,” the spinal column is bent forwards at an acute angle, and 
one or two vertebral spines are much more prominent than the others. 
There is often, however, a less abrupt bend; the curvature may ex- 
tend over four or five vertebrae. Less commonly one spine projects 
more than the others within any curvature. 
The nerves, as they pass through the membranes and intervertebral 
foramina, are irritated by the inflammation, and often compressed by 
the thickening of the dura mater which sheaths them by the bone, CARIES. 
245 
and those passing by the seat of compression may also suffer from 
the narrowing of the canal. They may be found red and swollen, 01 
shrunken and grey. They may be damaged when the cord is 
normal, or but little affected when this is compressed. 
The damage to the spinal cord depends on the secondary conse- 
quences or the caries, and is variable and uncertain in both occurrence 
and character. The mechanism of the damage is twofold—compression 
and inflammation. The relation between the two is considered more 
fully in a subsequent chapter (“Compression of the Spinal Cord”). 
Slow compression may be attended by chronic inflammation, secon- 
dary not only in character but in course, or by an acute inflammation 
out of proportion to the com- 
pression, alike in degree of 
severity and in rapidity of 
development. It is important 
to recognise these differences. 
The mechanism of compression 
varies. The most frequent is 
the collection of inflammatory 
products outside the dura mater 
and the thickening of this mem- 
brane. Less commonly the cord 
is compressed by the displace- 
ment of the bone, or by frag- 
ments of bone that are pushed 
into the canal. Often both these 
causes are influential, as in the 
ease shown in Fig. 88, in which 
the compression (at s) is between 
displaced bone in front and in- 
flammatory products (e) behind. 
Probably an inflammatory swell- 
ing or abscess of the bone is 
sometimes the mechanism of 
compression, since the signs of 
pressure have disappeared when 
an abscess has formed outside 
the spine, or even when deformity 
has come on—the breaking down 
of' the bodies having relieved the compression produced by their 
enlargement. 
Symptoms.—Caries of the spine causes symptoms of three classes : 
(1) those of the bone disease; (2) the effects of damage to the nerve- 
roots ; (3) those due to the changes in the cord itself. Only the 
symptoms due to the damage to nerves and cord come within the 
special province of this book, but the bone symptoms are of much im- 
portance, as on them the diagnosis of the cause of the nervous symptoms 
Fig. 88.—Caries of the spine, mid-dorsal 
region. The spinal cord is much nar- 
rowed and discoloured at S from com- 
pression between the displaced bone and 
a mass of inflammatory product*, E, 
outside the dura mater, D M, the inner 
surface of which is normal. (After 
Leyden.) 246 
DISEASES OP THE SPINE. 
often depends. It is this which gives the subject its high medical 
importance, and brings the symptoms and recognition of bone disease 
into the province of practical medicine. 
Symptoms of Bone Disease.—The first is pain in the spine, chiefly 
felt at the affected spot, increased by movement, and especially 
by pressure on the bone. The local tenderness is a very important 
sign. It is elicited both by direct pressure on the spine and by lateral 
pressure ; if they are grasped and pressed to one side considerable- 
pain is usually produced. Nevertheless tenderness is occasionally 
absent,not only in cases of slight character and doubtful nature, but also 
in which paraplegia has come on some time after local curvature. The 
increase of pain by movement is greatest when the disease is in the 
more mobile parts of the vertebral column, especially when it is in 
the cervical region. Movement of the head occasions pain, and there 
is an instinctive fixation of the head, which is sometimes inclined to 
right or left, less commonly backwards. It may thus produce the 
aspect of torticollis, which differs from that due to muscular contrac- 
tion, in that the sterno-mastoid is teuse on the side towards which the 
head is turned, the muscle being simply stretched by the deviation of 
the head. 
The deformity of the spine is a later symptom than the tenderness, 
and usually comes on gradually. Its characters have been already 
described. It is often absent when the disease is in the cervical 
region. In this part there is usually another symptom—thickening of 
the tissues about the spine, which is rare in other parts. In any 
region an abscess may form in the neighbourhood of the disease. 
Those which come backwards, or descend to the groin by the psoas 
muscle, can be recognised externally. Those that form in front of the 
diseased vertebrae may give rise to symptoms that are puzzling, if the 
existence of spinal caries is not known. Thus a retro-pharyngeal 
abscess may cause difficulty of deglutition, and one in the dorsal 
region may cause symptoms of oesophageal obstruction. 
Increased pain and tenderness in the vertebral column often 
precede the indications of damage to its contents. The symptoms due 
to interference with the nerve-roots are very variable, and may be severe 
or absent; usually they are moderate in degree, and consist of motor pain 
along the course and in the distribution of the nerves that emerge at the 
affected region, often hypersesthesia of corresponding extent, sometimes 
with spots of anaesthesia. There is also muscular weakness and some- 
times muscular wasting. These symptoms are more fully described in 
the chapter on “ Slow Compression.” Here it may suffice to say that 
they are conspicuous only in the minority of the cases, and chiefly occur 
when there is pachymeningitis. The motor symptoms are most marked 
when the disease is in the cervical region, and the nerve-roots for the 
muscles of the arms are damaged, since slight and limited impairment 
is more readily recognised in the arms than in the trunk. If the disease 
is in the highest part of this region, the pains may be referred ro the CARIES. 
247 
occiput. Herpes zoster has been occasionally met with along the 
course of the irritated nerves. Spasmodic contraction in the muscles 
supplied by the affected roots is extremely rare in cases of caries. 
Reflex action is abolished in the affected parts, and the change in the 
superficial reflexes of the trunk sometimes gives important diagnostic 
information. Disease of the lower cervical roots may cause symptoms 
of deranged action of the sympathetic on that side of the head, occa- 
sionally shown in the pupil, more often in the vessels. I have seen 
persistent sweating on one half of the forehead from this cause. 
The symptoms of interference with the functions of the spinal cord 
itself are chiefly due to impairment of its conducting power, causing 
paralysis below the lesion. As the disease is most frequently in 
some part of the dorsal region, paralysis of the Rgs is the common 
effect. But the symptoms vary in their characters, according not only 
to the position of the disease, but also to the immediate process of 
damage to the cord. The signs of caries may have existed for years 
before paralysis comes on. Angular curvature may even come on in 
early childhood, and paralysis not till adult life. More commonly the 
interval between the two is not long, varying from a few months to one 
or two years, but either may first be conspicuous. The cases are 
numerous in which caries is not suspected until the paralysis leads to 
an examination of the spine, and it is not uncommon for the signs of 
bone disease to remain equivocal for some time after paraplegia has 
developed. 
The cord symptoms vary much in their mode of onset. Usually 
there is no exciting cause, but sometimes a strain of the back or ex- 
posure to cold seems to excite a change in the condition of the bones, 
in consequence of which the cord suffers. It is easy to conceive that, 
when the conditions are favorable, a very slight strain may be effec- 
tive, even as slight as the sneezing in the case mentioned below. 
When the cord symptoms have commenced, they may develop quickly 
or slowly. As instances of chronic onset may be mentioned cases in 
which the symptoms reached a considerable degree of intensity at the 
end of nine months, four months, and two months, after their com- 
mencement. But the onset is sometimes much more rapid; in one 
case there was complete paraplegia at the end of three weeks. Some- 
times it is still more acute, and in such cases, when there is no corre- 
sponding change in the bone, acute myelitis set up by slight pres- 
sure is probably the mechanism by which the cord suffers. Thus, 
in one patient, a child of three, slight weakness existed for three 
weeks, and then the power of standing was lost in a single night. In 
another child, aged eight, who had presented for two years indications 
of disease of the cervical vertebrae, the power of moving the legs was 
lost in the course of twenty-four hours ; during the second day the 
left arm became paralysed, and, at the end of a week, the right arm. 
Very rarely the onset is instantaneous, probably from sudden dis- 
placement. A child with angular curvature was walking across the 248 
DISEASES OP THE SPINE. 
room, when she fell, and on being lifted up the legs were powerless. 
The more rapidly compression occurs, the slighter is the amount 
necessary to abolish conduction. 
Both legs usually suffer together; rarely one is paralysed before 
the other ; very rarely one leg suffers much and the other little or not 
at all. Thus in one case angular curvature developed in childhood ; 
at sixteen there was an attack of weakness in the legs, which passed 
away at the end of three weeks. At 17\ the patient sprained his back ; 
pain in it followed, and six weeks later the right leg gradually became 
weak, and a year afterwards presented intense spastic paralysis, the 
left leg being very little affected. He ultimately recovered. An 
instance in which one leg became affected before the other is that of 
a woman, forty-five years of age, who suffered from pain in the spine, 
and one day, when walking, sneezed violently three times, and imme- 
diately felt “ pins and needles ” about the right knee, and presently in 
the foot. The leg became almost powerless during the next three 
days. A fortnight afterwards she felt similar tingling in the left knee, 
and at the end of another week in the foot, and during the next 
three weeks this also lost power, so that at the end of six weeks from 
the onset both legs were motionless. The diagnosis was verified on 
her death, six mouths later. 
The characters of the paralysis in relation to the seat of the disease 
are described in the chapter on “ Compression.” In the most frequent 
cases the dorsal cord is damaged, and whenever the compression is 
above the lumbar enlargement the condition of the legs is that of 
“ spastic paraplegia.” If it is situated in the cervical region there 
may be muscular atrophy in the arms, sometimes combined with 
palsy without atrophy, according to the seat of the disease. When, 
as is commonly the case, the arms suffer from damage to the nerve- 
roots, they suffer before the legs, but if the disease is so high up 
that the arms suffer from the damage to the cord, the legs may be 
paralysed before the arms, as in the case of the child mentioned above. 
In this case the muscles of the shoulder were wasted, the disease 
being at the level of their nerves, while the forearm muscles were not 
wasted. In this case, as in others of similar seat, the diaphragm was 
paralysed. The muscular part of the spinal accessory may be in- 
volved, and the power of supporting the head may be almost lost. 
Very rarely, from the disease of the highest cervical vertebrae, other 
nerves of the medulla are implicated, especially the hypoglossal and 
the fibres of the spinal accessory for the palate. 
Sensory symptoms due to the disease of the cord are less common than 
motor palsy. The onset of paraplegia may be preceded by subjective 
sensations in the legs. Dull aching pain in them is also not uncommon. 
Often there is no loss of sensation; in other cases there are 
various degrees of loss. Touch or pain may be impaired alone, or 
there may be absolute loss of sensibility up to the level of the lesiou. 
Partial loss is more common. Reflex action in all forms is excessive CARIES. 
249 
(unless the disease involves the lumbar enlargement), and great excess 
of the superficial reflex action is a common and important feature. 
The legs are often cold, and sometimes perspire continually. The 
sphincters are often affected, sometimes early, but they may escape 
even where there is complete motor palsy of the legs. 
Complications.—Among common complications are bedsores, cystitis, 
various secondary effects of the bone disease, such as abscess, local 
scrofulous disease elsewhere, and general tuberculosis. Tubercular 
tumours in the brain occasionally coincide with the caries. In 
very severe cases peculiar secondary mischief has occurred in the 
spinal cord, and has run an independent course, giving rise to very 
anomalous symptoms.* Thus a descending myelitis may invade the 
lumbar enlargement in its entirety and abolish its central and reflex 
functions, causing rapid wasting of the muscles and acute trophic 
changes in the skin. Inflammation may ascend the pyramidal tracts 
and thus paralyse the arms—an instance of the strange limitation 
of inflammation to functional tracts when it pusses in a direction 
opposite to secondary degeneration. Ascending degeneration of 
the posterior median columns may spread to the postero-external 
columns, and cause symptoms of ataxy by invading root-fibres at a 
higher level. Ataxy may come on as the power returns, when the 
disease is in the dorsal region, probably by damage to the path from 
the muscles to the cerebellum. Lastly, myelitis may occur in dis- 
seminated foci in various parts of the cord, and even in the medulla, 
giving rise to scattered symptoms of anomalous character. 
Course.—The bone disease may heal, union occurring between the 
altered tissue, or it may persist with continued formation of pus, or 
may become quiescent with occasional periods of renewed activity. 
The cord mischief is influenced by the state of the bone disease, al- 
though its progress may be to some extent independent. Thus in- 
flammation in the cord, in excess of the compression, may subside in 
spite of the continuance of the bone mischief. Pressure on the cord 
inay be relieved, although the bone disease continues, and even some- 
times as a result of the increased breaking down of bone and exit of 
pus by another channel. A case is mentioned below in which para- 
plegia passed away as angular curvature developed. Hence, there is 
no strict correspondence between the course of the bone mischief and 
that of the cord disease. In some cases the paralysis, motor and 
sensory, persists. More often the sensory loss passes away, while 
motor paralysis remains, usually as spastic paraplegia, and, in severe 
eases, flexor spasm comes on with muscular contractions. Life may 
be prolonged in that condition for years, but often, in such cases, 
bedsores form, or cystitis leads to kidney disease, or other tubercular 
disease develops and leads to death, or the lessened respiratory power 
renders an attack of bronchitis fatal. In many cases, again, the para- 
lysis gradually passes away even when the compression continues, aud 
See Charcot, ‘ Leijons sur les Mai. du Sjst. Nerv.,’ tom. ii. 250 
DISEASES OF THE SPINE. 
the cord is found considerably narrowed if the patient dies from some 
other cause. It is possible that such compression is sometimes pro- 
duced slowly without impairment of conduction. In children re- 
covery occurs far more readily than in adults. Even in adults, 
however, recovery may occur from palsy that hasjasted for more than 
a year, with all the signs of descending degeneration in the cord, 
amounting to severe spastic paraplegia. Usually rest on the back or 
mechanical supports are necessary to secure recovery, but it occasion- 
ally occurs without these measures. A youth acquired angular 
curvature at sixteen; at twenty paraplegia came on slowly, and pro- 
gressed, with some variations, during the next seven years. There 
was then absolute motor palsy in the legs, and sensation was lessened. 
He refused to rest, and continued to follow his occupation, which was 
however a restful one, that of a tailor ; he took cod-liver oil and iron, 
and gradually regained useful power, so as to be able to walk about. 
Such a case, however, is exceptional. 
Relapses sometimes occur in cases that improve, although they are 
certainly not nearly so frequent as might be expected from the nature 
of the disease. In the majority of cases recovery, once obtained, is 
permanent. In a minority the paralysis returns when some exciting 
cause renews activity in the bone disease. The tendency to relapse 
and possibility of repeated recovery are very strikingly shown by the 
following case. In a girl of fifteen, paraplegia developed during nine 
months, slowly at first, more rapidiy towards the end of that time. 
She came under my care six months later, having been unable even 
to move her legs for that time. Bone disease had not been previously 
suspected, but there was slight tenderness and enough lateral irregu- 
larity of the lower dorsal spines to show the nature of the case. 
Rest in bed and tonics were soon followed by improvement; in six 
weeks she could stand, and in four months was able to walk well. Aa 
she gained power, angular curvature came on, prominence of the 
seventh and eighth dorsal spines. Five months after her discharge, 
she fell and struck her back ; the curvature increased, and her legs 
gradually became weak again. Seven months after the fall she was 
readmitted, unable to stand, although the paralysis was not absolute. 
There was foot-clonus on each side. Sensibility was lessened below 
the ensiform cartilage. Rest on the back was again followed by slow 
improvement. In three months she could just walk. She was then 
suspended, and encased in plaster of Paris. At the end of another 
month she could walk about the room, and no clonus could be 
obtained. She was soon afterwards discharged, and her progress 
continued, so that, at the end of nine months, she could walk five 
miles, and there was no trace of clonus, although there was still some 
excess of the knee-jerk. She soon afterwards married, and bore a 
child, which died two years and a half after her discharge. She 
caught cold at the funeral, and a fortnight later again began to lose 
power; in six weeks the legs were almost motionless, with marked CARIES. 
251 
foot-clonus ; sensation to toucli was lost up to the umbilicus, that of 
pain being preserved. Neither rest nor encasement caused any 
improvement. After some months sulphide of calcium was given, 
and in a few clays power began to return ; in a month she could take 
a few steps, and in four months she could walk about the ward with- 
out difficulty. She made another good recovery. Some years later, 
however, paralysis again came on, and this attack proved permanent. 
Several cases have come under my notice in which the subjects of 
caries in early life, which healed without damaging the cord, have 
at some period in adult life presented the symptoms of primary 
lateral sclerosis—simple spastic paraplegia, without any root symptoms 
or evidence of renewed activity of the bone disease. If there is a 
connection between the two, it is probable that the cord has suffered 
compression so slowly that its functions have not been interfered 
with, but, nevertheless, the vitality of the pyramidal fibres has been 
rendered less enduring 
It is important to remember that the deviation is often lateral,* 
and the chief difficulty is due to the fact that a slight lateral devia- 
tion or slight prominence is not unusual in normal spines. Hence it 
is important for the student to make himself familiar with the degrees 
of deviation that occur in health. At the same time it must not be 
forgotten that a deviation not greater than occurs in health may be 
due to disease. If it coincides with distinct tenderness, and especially 
also with the position of root symptoms, it may be accepted as evidence 
of disease, probable or certain, according to the character of the sym- 
ptoms. 
The pathology of the affection only concerns us so far as it relates 
to the effect on the spinal cord, and this is considered in the chapter 
on Compression. 
Diagnosis.—When clear indications of caries precede the paralysis, 
the nature of the case can hardly be mistaken. The obvious infer- 
ence, that the affection of the cord is secondary to that of the bone, is 
scarcely ever wrong. When the two develop together, mistakes in 
diagnosis are often made, but are usually due to the want of repeated 
examinations of the spinal column It is when the root or cord sym- 
ptoms precede distinct evidence of bone disease, and when the latter 
is so slight as to be equivocal, that the chief real difficulty in dia- 
gnosis occurs ; the affection is apt to be mistaken for a primary disease 
of the cord or its membranes—a transverse myelitis when the dorsal 
region is affected, a progressive muscular atrophy, or primary pachy- 
meningitis, when the disease is in the cervical region. A correct dia- 
gnosis can only be made in these cases by recognising the significance 
of the slight bone symptoms that are always present, the deep tender- 
ness, and often slight irregularity. Even slight irregularity derives 
* To discover lateral deviation it is well to make an ink-dot on the skin over the 
middle of the tip of each spine, care taken that the skin is not stretched to 
one side. The ink-dots may be copied on tracing-paper. 252 
DISEASES OF THE SPINE. 
significance from tenderness, limited in extent and corresponding in 
position to the deviation. The irregularity may he absent at first, 
and then its development is doubly significant. An observed increase 
in the amount of displacement gives significance to even a slight 
irregularity. 
The early excess of the cutaneous reflex action (from the sole, for 
instance), while not conclusive, adds weight to the other symptoms of 
bone disease. It may be very marked even while the patient is able 
to walk about. Distinct root pains are always of great significance, 
and this is increased by the detection of spots of anaesthesia along 
their course. All these symptoms derive additional weight from their 
■coincidence in level with the spinal irregularity. 
It is this which enables the pains to be distinguished from the condi- 
tion for which they are most frequently mistaken—a trunk neuralgia. 
This error is especially common when the pain is chiefly unilateral. 
In all such cases the spine should be carefully examined, and any 
tenderness of the bone at the level of the pain should excite suspicion. 
I have also known unilateral abdominal pain due to caries to be 
mistaken for that of renal calculus. 
When damage to the cei’vical roots causes muscular wasting in the 
arms,the case may be mistaken for one of progressive muscular atrophy, 
but differs in the distribution of the wasting, in the pains, and the 
impairment of sensation. These occur in primary cervical pachy- 
meningitis, which is distinguished by the absence of the signs of hone 
disease, and in the wider extent through which the root symptoms 
extend. 
In the first half of life the recognition of bone disease is practically 
tantamount to the recognition of caries. In the second half, however, 
the relative infrequency of caries, the greater frequency of growths in 
the bone, and the occurrence of eroding aneurisms, introduce a fresh 
diagnostic problem. The absence of any other indication of a tumour 
or an aneurism is the first distinction ; aud the second is the fact that 
in both these diseases the root pains commonly reach a degree of 
severity scarcely ever attained in caries, and are especially increased 
by movement. 
When there are merely tenderness of the spine and slight weakness 
of the legs, the question may arise whether there is organic disease, or 
merely the condition termed “ spinal irritation,” or mere functional 
pain and tenderness and weakness of the legs. In these cases the 
tenderness is usually found over a considerable area of the spinal 
column, with more than one point of special intensity ; it is superficial 
as well as deep, and may change its seat; there are no root pains or 
spots of anaesthesia. There is more danger that caries of the spine in 
a young woman may be passed as hysterical paraplegia than of the 
opposite error. Especially when the subjects of caries present 
distinct symptoms of hysteria, there is risk, as experience shows, that 
unequivocal symptoms of caries may be overlooked. Some other CARIES. 
253 
diagnostic indications are mentioned in the chapter on Slow Com- 
pression. 
Prognosis—Our ignorance of the precise character of the morbid 
process which is damaging the cord renders the prognosis, in every 
case of caries, a matter of much uncertainty. Nevertheless there is 
no disease of the cord in which symptoms of equal gravity so often 
pass away. The cases are few, therefore, in which hope is unjustified, 
hut they are equally few in which we are warranted in a confident 
expectation of recovery. In childhood the prospects of recovery are 
certainly better than in adult life, and they are least in declining 
years. Damage to the cord between the enlargements is less serious 
than when these are affected, because the strong tendency to trophic 
changes constitutes a grave danger when the lumbar enlargement is 
diseased, and the diminished breathing power an equally serious 
danger in disease of the cervical enlargement, especially when this is 
high enough to entail the additional danger of paralysis of the 
diaphragm. 
But how perilous a condition may be recovered from is shown by 
the fact that the child mentioned on p. 247 had paralysis of all four 
limbs, the diaphragm, and weakening of the intercostals, and yet 
recovered. Still more striking is a case narrated by Dr. Buzzard, in 
which disease in the region of the third cervical vertebra caused 
almost complete palsy of arms, legs, intercostals, and diaphragm, 
respiration being carried on by the accessory muscles of the neck. 
Yet the child recovered in spite of the occurrence of an attack of pneu- 
monia when the paralysis was at its height. A girl of thirteen, whose 
cervical caries was accompanied by all the symptoms of cerebellar 
tubercle, recovered. All these, it will be noted, were children. 
Neither rapidity nor slowness of onset affords any guide to prognosis,, 
nor does the relative order of paralysis and curvature, or the degree 
of palsy. Severe spastic paraplegia may pass away entirely, provided 
it remains extensor in character. The prognosis is perhaps a little 
better when there is no loss of sensation, since this proves that the 
damage to the cord is moderate in degree ; but eveu complete anaes- 
thesia does not preclude recovery, as the cases mentioned show. The 
danger to life is dependent in considerable degree on the evidence that 
the scrofulous or tubercular tendency is active elsewhere, and also on 
any difficulty in securing proper treatment. The prognosis is, more- 
over, at present in a transitional state on account of the uncertainty 
regarding the range of successful surgical treatment. 
Treatment.—The first and chief element in the treatment of 
paralysis is that of the bone disease which causes it, and for full 
details of this the reader is referred to treatises on Surgery. It 
includes both the older means of securing an arrest of the morbid 
process, and, secondly, the still recent measures of operative treat- 
ment. If the bone disease heals, the spinal cord, in most cases, will 
recover. The two most potent therapeutic agents are persistent 254 
DISEASES OF THE SPINE. 
recumbency and tonics, especially cod-liver oil and iron. In the cases 
that have done best, these, and these alone, have been the effective 
agents. Rest should be maintained for months. The posture that 
answers best is upon the back, on account of the greater ease with 
which immobility of the bone is secured and maintained, and the 
great importance of this element in treatment; this position is also 
the most comfortable, and local pain probably interferes with the sub- 
sidence of local inflammation. If no improvement occurs after some 
months’ rest, suspension may be tried. It is said to be sometimes 
attended by instant improvement- especially in children ; but this 
result is rare, and can only occur in the cases, not very common, in 
which displaced bone compresses the cord. In cases in which there is 
reason to suspect that this is the cause of paralysis, it may be well to 
see the effect of suspension before rest is commenced. The moulded 
jacket is an inefficient substitute for rest, and an unnecessary con- 
comitant—to be adopted only when rest cannot be secured, or after 
rest alone has apparently done all that it can achieve. If, for instance, 
power gradually returns during rest, but the improvement after a time 
ceases, and the bone disease seems inactive, the patient may be sus- 
pended, encased, and then permitted to stand and walk; improvement 
may be renewed and power may rapidly increase. In caries of the 
mobile cervical spine, even during the period of rest, fixation of the head 
is necessary. Extension of the spine in the recumbent posture has also 
been employed, sometimes with apparent benefit. The head of the 
patient is fastened to the head of the bed by an elastic band attached 
to a strap passing beneath the occipital protuberance and round the 
patient’s head. A weight of from 4 to 12, or even 20 lbs. is fastened 
to a band passing round the patient above the hips. Continuous ex- 
tension is thus obtained.* 
The influence of cod-liver oil and iron is as marked in this as in 
other scrofulous diseases. They constitute an indispensable adjunct 
to rest, and may be effective even alone, as is shown by the case men- 
tioned on p. 250. But rest should always be secured if possible. 
Counter-irritation, opposite the seat of caries, has sometimes 
appeared to do good, perhaps acting especially on the process of mye- 
litis which attends compression. The actual cautery, in mild form, is 
that which has been most frequently found useful. Instances of 
speedy improvement are on record, but it is not always effective, nor 
can indications for its use be laid down. Sulphide of calcium, which 
is said to influence scrofulous processes, deserves further trial, although 
I have not found it so apparently effective in any other case than that 
mentioned on p. 251. Benefit can only be expected from its use when, 
as is often the case, inflammatory products constitute the compressing 
agent. Extreme care in general management, to avoid bedsores, 
bladder trouble, and bronchitis, are of great importance. In many 
cases there is a tendency to improvement after a time, especially when 
* Fleming, ‘ Lancet,’ April 27th, 1889. 255 
CARIES. 
the bone disease is stationary, or the cord has been inflamed, and in 
these the mere maintenance of life may result in recovery of strength. 
When power has returned, but the use of the limbs is restrained by 
the muscular contractions which came on during the paralysis, the 
ability to stand and walk may be quickly restored by tenotomy, and 
more slowly by the use of extending splints, &c. Electricity is useful 
only to maintain the nutrition of the muscles when these are wasting, 
in consequence of damage to their nerves. 
The belief expressed in the first edition of this work, that the cases 
are numerous in which relief to the compression may be afforded by 
the surgeon, has been fully realised. The path was, indeed, being then 
opened up by McEwen of Glasgow, who has shown, with Horsley and 
others, how safe and successful the operative treatment is in properly 
selected cases; and these, indeed, include a large proportion of the 
eases in which other measures have failed to give relief and must 
probably have remained unsuccessful. The operation is contra-indi- 
cated in cases of rapidly advancing general tuberculosis (to which 
most deaths after operation have been due). When the indirect con- 
sequences of the disease have greatly reduced the patient’s strength, 
the question of an operation may still be entertained if it is a dis- 
tinct alternative to a speedy death, provided the peril is such as a 
restoration of the functions of the cord might possibly relieve. On 
the other hand, the operation ought not to be regarded as the first 
resort in the majority of cases. The large number of cases that re- 
cover under the treatment described above, make it certain that, in 
most cases, these measures should first be tried ; and this conclusion 
is the clearer, since the duration of paraplegia, for a year or more, 
seems to interpose no appreciable barrier either to recovery or to the 
relief that can be given to the pressure. On the contrary, indeed, the 
prospect of recovery is better if the bone disease has become quiescent, 
or the caries has actually healed, processes that must be furthered by 
the preliminary rest. The operation has the best prospect of success 
in the cases, fortunately very numerous, in which the products of in- 
flammation outside the dura mater compress the cord. These, 
whether caseous material or a mass of connective tissue into which 
the inflammatory products have been changed, can be readily removed 
without opening the dura mater. Even if displaced bone is the source 
of pressure, the removal of the arches affords relief to it. The chief 
obstacle to success is the extent to which myelitis has proceeded 
out of proportion to the compression. This, necessarily, no removal 
of the pressure can relieve. In proportion as the inflammation has 
been acute without rapid compression, relief is unlikely. But this is 
not the only cause of a rapid onset, and a difficult question arises in 
such cases, whether the mechanism is not such that an immediate 
operation is justified. It may be due to sudden displacement or to 
sudden escape of pus into the canal, as well as to myelitis, and in the 
two former cases it is possible that relief may sometimes be given, and 256 
DISEASES OF THE SPINE. 
an immediate operation may be wiser than delay. An operation is 
suggested whenever a sudden increase in the curvature or severe root 
pains coincide with the onset. Without these symptoms, the rapid 
onset is probably due to acute myelitis, and then an operation cannot 
be expected to lessen the interference with the conducting fibres. To 
justify surgical interference, however, the existence of caries must be 
beyond doubt. The operation involves some danger to life, although 
it may not be great, and this fact must always receive due considera- 
tion in regard to the certainty of diagnosis as well as the prospect of 
relief. 
TUMOURS AND OTHER DISEASES OF THE SPINE. 
Growths in the Spinal Column. 
The bones of the spine are sometimes the seat of primary or secon- 
dary growths, and less commonly are invaded by tumours springing 
from the various structures and even organs in front of the spine. 
Cancer (scirrhous and encephaloid) and sarcoma are the most common 
forms of growth ; myxoma has been also met with. Cancer is some- 
times secondary to a primary growth elsewhere, in the breast, stomach, 
&c. A primary growth usually begins in the bodies of the vertebrae, 
and spreads from one to another. The bodies may collapse, because 
the soft tissue which replaces the bone yields under the weight it has 
to bear, and thus angular curvature may occur, or some other abrupt 
deviation from the normal line. From the bodies the growth may 
extend into the lateral processes, enlarging them, and narrowing the 
intervertebral foramina through which the nerves pass. It may extend 
into the arches, and even into the spines, and may also grow into the 
muscles and tissues beside and behind the vertebral column. The 
nerve-roots suffer (1) by pressure, (2) by simple inflammation, (3) 
sometimes by cancerous infiltration. They may thus be found red- 
dened, swollen and soft, or grey and atrophied, or enlarged and hard- 
ened. The growth, cancer especially, is apt to spread in the adipose 
tissue between the bone and the dura mater, and may even entirely 
surround the dura mater and cord. The cord may suffer compression, 
but this is less frequent than in caries, even when curvature occurs. 
On the other hand, it is often inflamed, sometimes acutely ; consider- 
able inflammation without compression is far more frequent than in 
caries. The myelitis occurs without any perforation of the dura mater 
by the growth. The cause of this tendency to acute local inflamma- 
tion is not known ; once excited, it may spread in the cord upwards 
and downwards. The growth never invades the cord itself. GROWTHS IN THE STINE. 
257 
Etiology.—The general causes are the same as those of similar 
growths elsewhere. Males suffer, however, more frequently than 
females, and the morbid growths, taken together, are most common 
between forty and fifty years of age. An injury has been supposed 
sometimes to be the exciting cause in this as in other situations. 
Symptoms.—There may be direct symptoms of the presence of the 
growth—pain in the spine, sometimes severe, sometimes absent; local 
tenderness, and occasional interference with movement of the vertebral 
column apart from pain. A palpable tumour is never an early sym- 
ptom, but ultimately a deep-seated hard swelling may be felt on one 
side of the spine, most readily and earliest when the disease is in the 
cervical region, where it is occasionally perceptible in the posterior 
triangle of the neck. The angular curvature which sometimes occurs 
does not differ from that of caries in its external characters, except 
that it is more frequently a rounded prominence than a sharp angle, 
and it may be accompanied by the indications of a tumour, never by 
those of an abscess. 
The affection of the nerves is almost invariable in spinal growths, 
and gives rise to the symptoms that are the most distressing, and 
also the earliest and most constant,—radiating pain in the course of 
the nerves that emerge at the part, and due to their irritation by pres- 
sure or inflammation. Such pains are far more prominent symptoms 
in this disease than in caries. At first slight, they gradually increase 
to extreme intensity. It was this feature that led Cruveilhier to call 
the disease paraplegia dolorosa, a name it has since commonly borne. 
The pain at first intermits, but subsequently is constant, with 
paroxysms of greater suffering from time to time. It is usually a 
sharp and lancinating pain, and its special characteristic is the degree 
in which it is increased by movement. Even slight movements of 
the trunk induce the paroxysms. The distribution in the arms, 
trunk, legs, depends on the seat of the disease. It is extremely rare 
for these pains to be absent, but they occasionally occur late instead 
of early.* On the other hand, they may precede other symptoms for 
months. Cutaneous hyperaesthesia usually accompanies them, and 
spots of anaesthesia often develop, after a time, in the areas to which 
the fixed pains are referred. Corresponding damage to the motor 
roots may cause painful muscular contracture (Figs. 56 and 57, 
p. 91), paralysis, and wasting. Contractures may also occur in the 
parts below the disease, produced by the persistent pressure on the 
motor tract in the cord. Paroxysms of spasm often attend the pains, 
especially in the abdominal muscles when the disease is in the dorsal 
region, and are apparently reflex in nature. 
The damage to the cord causes symptoms similar to those in caries, 
and described more fully in the chapter on “ Compression.” The 
chief difference from caries is the greater frequency of a rapid onset 
* The pains succeeded curvature in a case described by L. Humphry (‘ Lancet,’ 
1881, i, p. 15). 
VOL. I. 258 
DISEAS US OP THE SPINE. 
of the paraplegic symptoms, due to the invasion of the cord by acute 
inflammation. All power in the legs is often lost in twelve or twenty- 
four hours, and this when no curvature has taken place. Such acute 
paraplegia is not uncommonly preceded for a week or so by retention 
of urine, probably indicative of slight pressure in the cord. Displace- 
ment of bone has also been known to cause rapid paralysis.* On the 
other hand, especially in very slowly growing tumours, the onset of 
the palsy may be gradual. 1 have known it to occupy several years 
in reaching a considerable degree. Probably in these cases the 
mechanism is a simple slow compression. Thus, compared with caries, 
the onset is more often rapid, and occasionally much more deliberate. 
The characters of the resulting paralysis are, as a rule, similar to 
those in caries, but are more frequently modified by the spread of 
inflammation, immediate or subsequent. Hence the central and 
reflex functions of the lumbar enlargement, although the bone disease 
is some distance above it, may be lost at the onset, or they may be at 
first, normal or excessive, and afterwards lost. In a man with a growth 
in the mid-dorsal region, paraplegia came on rapidly, evidently from 
myelitis, and was followed by foot-clonus, &c. But a few weeks later 
the clonus suddenly ceased, the muscles became toneless, with loss of 
fai’adic irritability, and the skin began to slough. The inflammation 
had spread down into the lumbar enlargement. In many cases, how- 
ever, there is no descending inflammation, and the reflex actions are 
in persistent excess, so that spastic paraplegia results. Sensation is 
lost rather more frequently than in caries. Other symptoms are the 
same as in compression from any cause. The course of the disease is 
from its nature progressive ; occasionally, however, some improve- 
ment succeeds a rapid development of palsy, and is due to the 
partial recovery of a cord damaged disproportionately by inflammation. 
It is seldom, however, that life is prolonged for a sufficient length of 
time. Much more rarely the pains lessen, although the growth 
spreads—perhaps from destruction of irritated nerves. 
The duration of the disease varies according to the nature of the 
growth. In cancer it is to be measured by months. In slowly 
growing tumours the symptoms may last for years. Death may be 
due to bedsores, &c., to cystitis and kidney disease, to growths else- 
where, or the patient may be simply worn out by the prolonged 
agony. In one curious case a growth from an intervertebral cartilage 
caused characteristic symptoms for thirteen years, and then death by 
meningeal haemorrhage.f 
Diagnosis.—The recognition of the disease is only a matter of cer- 
tainty when signs of a tumour are present, but the probability almost 
amounts to certainty when such symptoms as those mentioned follow a 
primary growth elsewhere. Such pain as that above described, occur- 
ring in a person from whom a malignant tumour has been removed, 
* Humphry, loc. cit. 
+ Boivert, ‘ Arch, de Phys.,’ 1887, No. 8. GROWTHS IN THE SPINE. 
259 
should always be regarded with grave suspicion, and the grounds for 
this are not lessened by either an interval of several years since the 
removal of the tumour, or by the completeness with which this was 
effected. Especially is this true of cases of mammary cancer. The 
pains should lead to careful and repeated examination of the spine and 
a search for any abrupt deviation, in any kind, and in any part of the 
vertebral column; while the cervical spine should be examined at the 
sides and from the posterior triangle of the neck, the character of the 
bony prominences on the two sides being minutely compared. Indi- 
cations of a growth may often be thus discovered long before they are 
obtrusive. It is also important to remember the fact that acute 
transverse myelitis may be an early effect of the disease, and if this 
lesion, in such a subject, coincides with marked local tenderness, the 
probability of secondary growth in the bone is very great; it is 
rendered still greater by preceding pains, and certain by coincident 
deformity. 
It must be remembered that similar root symptoms are sometimes 
due to an aneurism or to a growth in front of the vertebral column, 
commencing, for instance, in the glands, irritating the nerves as they 
emerge from the intervertebral foramina. 
From intercostal neuralgia, the influence of movement on the pain 
is usually a sufficient distinction, even when cord symptoms are 
absent. The commonly bilateral character of the pain is a further 
difference. The symptoms of a growth in the lower cervical region 
are sometimes very closely simulated by symptoms which, from their 
character and course, are probably due to radicular neuritis. There 
are severe root-pains, referred to one arm (or less commonly, to both 
arms), increased by movement and without marked tenderness of the 
plexus of nerve-trunks. The subjects are also in the later period 
of life. The distinction rests on the absence of the signs of a growth, 
on the slighter effect of motion on the pains, on the absence of any 
progressive tendency, and on the common presence of a history of 
gout, and especially on the absence of any symptoms of compression 
of the cord even after the nerve-roots have suffered for some months. 
Sometimes it is necessary to wait and watch the course of the sym- 
ptoms. It is necessary to be very careful in assessing the value of 
slight irregularities; the vertebra prominens is apt to be thought to 
project too much even for its designation, and a deep bilateral swelling 
is readily perceived under normal conditions, when the head is bent 
forward. 
The chief difficulty in diagnosis is the distinction from caries 
when distinct evidence of a growth is absent. In the first half 
of life caries would alone be thought of in such a case, but in 
the second half the two diseases are about equally frequent. 
One distinction, suggestive, not absolute, is the intensity of the pain 
in tumour, taken in conjunction with its great increase when the 
patient moves. It is true that the root-pains of caries are said to be 260 
DISEASES OF THE SPINE. 
sometimes most severe, but such severity is not frequent enough to 
destroy the significance of intensity. 1 have not, for instance, seen a 
single case of caries (of a large number) in which the pain was com- 
parable to that in most of the cases of growth that have come under 
my observation. Therefore, while absence of pain is of slighter diag- 
nostic value (in favour of caries), great severity, and agonising 
increase by movement, are strongly in favour of vertebral growth. 
In each disease there may be angular curvature, but this, in growths,, 
is usually soon succeeded by other signs of tumour. In caries these 
signs are absent, and an abscess often develops. A history or indica- 
tion of tubercle is almost conclusive evidence of caries. These points 
will, I believe, avail for the distinction in most cases. In a few it is 
necessary to wait and watch before an opinion can be formed. 
Among other diseases with which these growths may be confounded 
is the dorsal form of tabes, in which severe radiating pains occur in the 
trunk and not in the legs. But the wide extent of the root symptoms, 
the slight effect of movement, and the fact that the knee-jerk is lost, 
suffice for the distinction. The distinction from tumours of the spinal 
cord and membranes is considered in a later chapter. 
Prognosis.—The prognosis scarcely requires formulating. The 
chief differences are in the time that life is likely to last. The pains 
usually persist, in spite of the progress of the disease, although there 
is a bai-e possibility of their subsidence. The chance of any return of 
power in the paralysed part is small, although not quite absent if the 
palsy develops in a manner to suggest a secondary myelitis, and the 
progress of the growth itself is slow. 
Treatment.—Possibly in a few cases a growth may be so placed as 
to be removed, and an exploratory operation would be justifiable in 
any case that might prove suitable; otherwise treatment must neces- 
sarily be confined to the relief of pain, and to the avoidance of bed- 
sores and other results of the cord disease. Morphia is alone powerful 
for the relief of pain, but unhappily the dose has to be quickly 
increased, and the power of the drug is lessened by custom. It 
becomes a race between dose and pain, in which, if life lasts long, the 
pain not uncommonly gets in front of the narcotic. Cocain, however, 
affords some relief in many cases, and may, with other anodynes, at 
least prolong the influence of moderate doses of morphia. 
Vertebral Exostoses. 
Exostoses sometimes grow from the bodies of tlie vertebrae into tbe 
spinal canal, and may compress tbe cord or nerves. They are, how- 
ever, exceedingly rare. The symptoms may be those of- slow compres- 
sion of tbe cord, or of irritation, expressed chiefly by pain. They 
usually resemble those of a tumour of the cord or membranes rather 
than of the bones, but the pain is occasionally much increased by move- 
ment. Their chief characteristic is extreme chronicity. In one case GROWTHS IN THE SPINE. 
261 
the patient suffered frequent intense paroxysms of pain in the right 
groin, which had occurred for two years, with occasional intervals of 
freedom. There was some weakness of the legs, but no considerable 
paralysis. Ten years before, he had had some loss of sensibility in 
each thigh, which had passed away. An intra-spinal tumour was 
diagnosed ; the post-mortem examination revealed exostoses from the 
bodies of the ninth and tenth dorsal vertebrae, slightly compressing 
the cord. Although extreme chronicity may raise a suspicion of 
exostosis, it is doubtful whether a confident diagnosis is ever justified 
except in the cases in which there are similar exostoses elsewhere. 
This rare indication existed in a patient, under the care of my col- 
league Dr. Barlow, who presented multiple exostoses, and paraplegia 
of gradual onset, which was supposed during life, and found after 
death, to be due to a similar exostosis within the spinal canal. It had 
sprung from one of the lumbar vertebrae, and had compressed the 
nerves of the cauda equina. 
Exostoses constitute a more promising field for the surgeon than 
other kinds of vertebral tumour. Many of them are so placed that 
their removal is feasible. If situated in front of the cord, the 
division of some nerve-roots, at least in the dorsal region, might 
permit access to the growth. 
Syphilitic Disease. 
Syphilitic caries of the bodies of the vertebrae is a rare variety, the 
symptoms of which do not differ from those of the scrofulous form. 
It has been observed in the cervical region, secondary to deep syphilitic 
ulceration of the pharynx. Nodes of the vertebrae, within the canal, 
are occasionally presumed to exist and to compress the cord, but I do 
not know of any pathological observation confirming the assumption, 
and it is probable that most of the supposed instances have been cases 
of syphilitic gummata in the meninges. Deep-seated thickening of 
the tissues about the cervical vertebrae sometimes occurs in syphilitic 
subjects. It may develop on one side or both, and is apparently due 
to a syphilitic cellulitis. The swelling may be felt either on each side 
and behind the upper cervical spine, or deep in the posterior triangle 
of the neck. It may damage the nerves before they enter the brachial 
plexus, causing a defined palsy, as in one case of the lower arm 
muscles. Movements of the neck may be interfered with, and irrita- 
tion of the nerves may cause neuralgia-like pain, generally felt down 
the arm, and often very severe. Except by the absence of modula- 
tion, it is scarcely to be distinguished from a deep-seated growth. 
The spinal cord does not usually suffer. All the symptoms pass away 
under anti syphilitic treatment. In one case, however, iodide had no 
infiuence, although mercury quickly cured. 262 
DISEASES OE THE SPINE 
Erosion by Aneurism 
Bones, like other structures, may atrophy and waste before the 
pressure of an aneurism, and the bodies of the dorsal, or rarely of 
the lumbar vertebrae may be thus eroded by aneurisms of the aorta. 
The pressure and absorption take place from the 1 f: side. Two or 
three vertebrae usually suffer, and the bodies more than the inter- 
vertebral cartilages. The periosteum becomes thickened, and may 
resist the pressure and to some extent protect the cord. Sometimes, 
however, the cord becomes compressed, or the periosteum may come 
to form part of the wall of the aneurism, and may give wav before 
the blood-pressure, so that rupture occurs into the spinal canal. 
The symptoms vary much. Pain along the nerve-roots is usually 
severe, but this may attend aneurisms that merely compress the nerves 
after their emergence, and do not damage the bone. The process of 
erosion is usually attended by severe pain in the spine. When the 
cord is reached, compression causes the usual paraplegic symptoms, of 
slow or rapid onset. Rupture into the canal is attended by sudden 
complete paraplegia and death, either immediate, or in the course of a. 
few hours, from ascending paralysis, due to the hsemorrhage around 
the spinal cord. 
The diagnosis is scarcely possible unless other indications of 
aneurism are detected, since the symptoms olosely resemble those of a 
growth in the bone. The nature of the disease may, however, be 
suspected if such symptoms as have been described are succeeded by 
sudden paraplegia followed quickly by ascending paralysis. 
Hydatid Disease. 
Hydatid cysts sometimes develop in the loose adipose tissue 
between the dura mater and the bone, and it is believed that they 
sometimes form in the substance of the bones themselves. About 
a dozen cases have been collected bv Levden.# As the cyst grows, 
the bone of the arches sometimes becomes atrophied by pressure, and 
the cyst may develop outside the canal, so that there is a double 
cyst, outside and inside, connected by a narrower part. Occasionally 
the cyst develops also in front of the spine, in the thorax or abdomen. 
The internal cyst necessarily compresses the spinal cord, which often 
also becomes inflamed. The usual paraplegic symptoms develop, bot h 
motion and sensation being usually lost. Radiating pains along the 
nerve-roots are frequent. The symptoms, in themselves, resemble too 
closely those caused by other diseases of the spinal column to permit 
a diagnosis to be made, unless similar disease elsewhere suggests the 
nature of the spinal lesion, or unless the cyst can be felt in the back, 
when a puncture may prove its nature. All the cases hitherto recorded 
have terminated fatally, but it has been conjectured that, if puncture 
‘Klinik der Rxickenm. Krankh.,’ Band i. VERTEBRAL ARTHRITIS. 
263 
can be effected, a cure may sometimes be possible. In one such case, 
however, a girl, aged twenty-two, in which a small tumour beside the 
last dorsal and first lumbar spines was opened (on account of 
complete palsy of legs, bladder, and rectum), a continuous discharge 
of echinococcus cysts occurred, more than a hundred escaping in the 
course of four months, when the patient died in consequence of 
ascending damage to the cord. The tumour has been noticed for 
eight years before death, during four of which it produced symptoms 
of irritation of the nerves, and finally prominence of the vertebral 
spines developed.* 
Humei'ous small cysticercal vesicles have also been occasionally 
found within the, dura-matral sheath. In one case, several such 
vesicles were attached to nerve roots, one to each, in the lumbar 
region, while a considerable number on the cervical enlargement were 
beneath the pia arachnoid.f Such cysts may compress the cord, 
producing paraplegia, and even death. As in other forms of com- 
pression, the paraplegia may come on suddenly.J 
Diseases of the Articulations. 
Lateral Curvature of the Spine seldom affects tlie functions 
of the cord. Even when slight compression has occurred, the slow- 
ness of its production has apparently prevented interference with 
function. In very rare cases some weakness of the legs has been 
present, possibly, but not certainly, the result of the curvature. Occa- 
sionally the intervertebral foramina have been narrowed, and the 
pressure on the nerves has caused radiating neuralgic pains. 
Vertebral Arthritis.—In chronic rheumatoid arthritis the 
intervertebral articulations are sometimes involved. The symptoms 
are local pain, tenderness, and limitation of movement, which may 
go on to absolute fixation, especially in the cervical region, if anchy- 
losis occurs. I have known the whole neck to be rigid from this 
cause, in a case in which also the movement of the lower jaw was 
much reduced. More frequently, movement is restricted by pain 
before the mechanical limit is reached. Sometimes an occasional 
clicking sound occurs. Enlargement of the ends of the bones may 
occur, and, in thin persons, may even be felt. The pain is increased 
by movement, and often by changes in the weather, and by fatigue. 
It is often felt through a considerable extent of the spine, and may 
extend to the back of the head. The cord is scarcely ever compressed, 
but the narrowing of the foramina may damage the nerve-roots. The 
articular processes, it will be remembered, form one side of the intcr- 
* Pedjkow, ‘ Med. Obos.’ (Russ.), xxviii; and ‘Cent. f. Nerv.,’ xii, 271. 
+ Hirt, ‘ Berl. kl. Wochenschr.,’ 1887, No. 3. The relation of the symptoms to 
the parasitic disease is doubtful in a degree that makes it useless to mention them. 
+ As in a case recorded by Wiegand (‘Warsaw Med. Ob.;’ and ‘Cent. f. Nerv.,* 
1888, 665). 264 
vertebral foramina, which are thus encroached on by any enlargement 
of the bones. The nerves may thus be compressed and irritated, and 
radiating pains are produced, sometimes even a descending neuritis. 
The nerve-trunks in the limbs may then become tender as well as 
painful; muscular atrophy may even occur, and, when the disease is 
in the cervical region, there may be symptoms of disturbance of the 
sympathetic. Spasmodic torticollis is said to have been caused by 
this disease in the cervical region. The atlo-occipital articulation 
has been affected alone, or with the adjacent vertebra*, and peculiar 
interference with the movement of the head has resulted. Sometimes 
the foramen magnum is narrowed, or the odontoid process projects 
into the canal. Symptoms of damage to the nerves of the medulla 
have also been produced (Solbrig). In the dorsa'l region the sym- 
ptoms produced are slighter in degree, but similar in general cha- 
racter, although the local symptoms usually preponderate over those 
of irritation of the nerves. 
The degree in which the morbid process causes symptoms varies, 
however, very much in different cases, and it has occasionally been 
found out at the post-mortem examination without being suspected 
during life. It is usually associated with distinct evidence of a rheu- 
matic diathesis, and commonly with obvious arthritis elsewhere. 
This is the most important diagnostic indication as to the cause of 
the spinal symptoms, but it must be remembered that the vertebral 
affection sometimes exists alone, and it may cause symptoms during 
many years, often when their nature is unsuspected. It occurs in both 
sexes, and is not rare in young women, in whom the symptoms are 
often ascribed to hysteria. The treatment is the same as that of 
the general disease, nerve-symptoms alone needing special treatment, 
such as is described in the section on diseases of the nerves. The 
most important point in regard to the malady is its diagnosis, because 
distant nerve-pain is liable to be regarded as unconnected with local 
disease, or the disease to be thought far more serious than it really is, 
and especially to be mistaken for chronic meningitis or malignant 
disease. 
DISEASES OF THE SPINE. 265 
SPINAL MENINGITIS. 
DISEASES OF THE MEMBRANES OF THE SPINAL CORD. 
The general arrangement of the membranes of the spinal cord has 
been already mentioned (p. 162). The pia mater closely invests the 
cord, while the arachnoid forms a loose sheath around it, and the two 
membranes are connected by trabeculae and membranous expansions of 
fine connective tissue, which occupy the “subarachnoid space.” Each 
surface of the dura mater is covered by a layer of epithelium. The 
outer sheaths of the nerves are continuous with this membrane; the 
connective tissue, within the outer sheath, is continuous with both the 
pia mater and arachnoid. The blood-vessels of the cord ramify, as we 
have seen, in the pia mater, and the lymphatic canals of the two are 
continuous. Most of the cerebro-spinal fluid within the vertebral 
canal is contained in the subarachhoid space, but there is a little fluid 
between the dura mater and the arachnoid. Both membranes are 
supplied with nerves, but those of the pia mater are the more abundant. 
The morbid processes that involve the membranes are chiefly three, 
—growths, haemorrhages, and inflammation. Tumours of the mem- 
branes may be conveniently considered in connection with those of the 
spinal cord. Inflammation and haemorrhage will be here described. 
SPINAL MENINGITIS: INFLAMMATION OF THE 
MEMBRANES OF THE SPINAL CORD. 
Inflammation of tlie membranes may be acute or chronic, and may 
begin, and affect chiefly, the dura mater (pachymeningitis, i. e. inflam- 
mation of the firmer membrane), or the pia mater (leptomeningitis, 
inflammation of the softer membrane). The arachnoid usually 
suffers with the pia mater, but is sometimes the seat of inflammation 
that affects the pia mater but little, a form that has been termed 
arachnitis. Acute inflammation, beginning in one membrane, usually 
spreads to the others. Chronic inflammation may remain limited to 
one membrane, dura mater or pia mater. 
All forms of acute inflammation, wherever they begin, cause similar 
symptoms. It is only when the inflammation is chronic that the 
symptoms may differ sufficiently to allow of a precise diagnosis. 
Spinal meningitis may be conveniently divided into two forms, 
which depend on the situation of the inflammation in regard to the 
dura mater: (1) that which begins outside this membrane, and some- 
times arises by extension from some adjacent focus of inflammation, 
—external meningitis ; (2) that which begins within the dura-matral 
sheath, and is often primary,—internal meningitis. 266 
SPINAL MEMBRANES. 
EXTERNAL MENINGITIS. 
External meningitis is thus an inflammation of the dura mater. It 
has heen termed external pachymeningitis, peripachymeningitis, and 
perimeningitis. The inflammation involves not only the membrane, 
but also the connective tissue outside it, in which are the venous 
plexuses and adipose tissue. This connective tissue may be inflamed 
before the membrane itself. The morbid process usually remains, 
limited to the outer surface of the dura mater, even when the inflam- 
mation is acute and intense, passing thx-ough it only in rare cases. 
Causes.—External meningitis is generally due to extension from 
some contiguous disease, especially of the bones of the spine, caries of 
which is the most frequent cause of the affection. It results also from 
other forms of bone disease, and a syphilitic inflammation is probably, 
in rare cases, associated with syphilitic disease of the vertebrae. Such 
secondary external meningitis is generally limited in extent and 
chronic in cause. Deep sacral bedsores, however, sometimes cause an 
acute inflammation, which may spread widely. An ascending neuritis 
has been supposed in some cases to set up local inflammation. Sup- 
puration adjacent to the vertebral column is sometimes associated 
with a general acute purulent meningitis, and has generally been 
regarded as the cause of the latter; but careful observations have- 
rendered it probable that in most cases the external suppuration has- 
been the consequence, and not the cause, of the meningitis. It is 
certain that acute general external meningitis occurs as a primary 
disease, and may run an intensely rapid course with profuse suppura- 
tion between the membrane and the bone. The subjects have gene- 
rally been young, ill-nourished adults, and when any exciting cause 
has been traced, this has usually been exposure to cold In some 
cases the pus has worked its way backwards between the vertebral 
arches (sometimes through the foramina), and has spread among the 
muscles of the back, sometimes forming also collections at one or 
more spots, either at the back, or in front of the spine,—under the 
pleura, for instance, or behind the peritoneum. Such local collec- 
tions of pus were also formerly regarded as the cause of the menin- 
gitis. It is still possible that this mechanism is effective in some 
instances, as when a retro-pharyngeal abscess is followed by the 
meningeal affection ; but it is certain that in many cases the actual rela- 
tion is the reverse, and that the external suppuration, in acute cases, 
is often secondary.* Hence it is probable that this is true of all cases 
in which the evidence of primary external disease is not conclusive. 
At the same time further observations are needed to decide the point. 
Pathological Anatomy.—The inflammation is sometimes simple, 
but much more frequently purulent or semi-purulent. If simple, the 
* Two instructive cases are recorded by Dr. W. H. Spencer, ‘ Lancet,’ 1879, i, 
and Dr. Maguire, ib., 1888, ii. EXTERNAL MENINGITIS. 
267 
dura mater may be merely reddened and opaque, witb a little lymph 
on the surface ; when purulent, the surface is covered by a layer of 
pus. In the more common semi-purulent form, such as is common in 
caries of the spine, a layer of inflammatory products covers the outer 
surface of the dura mater, soft, semi-caseous or firm caseous material, 
sometimes with liquid pus here and there in the firmer substance. 
Often the inflammatory products undergo 
development into fibroid tissue, a mass of 
which then lies between the dura mater and 
the bones. Such a layer, caseous or fibroid, may 
sometimes be half an inch thick (see Fig. 88, 
p. 245). It may either surround the dura 
mater, or be chiefly on one side. Sometimes 
there is an irregular nodular thickening of the 
outer layer of the membrane (Fig. 89). In 
most cases the inner surface is normal, even 
when the cord itself is inflamed. Occasionally 
the inner surface of the dura mater is also 
inflamed, and then the internal membranes 
are involved and adhesions form between 
them. 
In all forms of external inflammation, the 
fat outside the dura mater quickly becomes 
absorbed, and the membrane may ultimately 
become adherent to the bone, or connected 
with it by intervening fibrous tissue of in- 
flammatory origin. 
The vertical extent of the disease varies 
much; when secondary to caries, the inflam- 
mation is usually limited to the neighbour- 
hood of the bone disease. When acute and 
general, as in the primary form, the space 
between the membrane and the bone is 
filled with pus through the whole length 
of the canal. Occasionally the pus only lies 
behind the membrane, between it and the 
arches of the vertebrae, apparently determined in position by 
gravitation. It ceases in the upper cervical region, where the 
dura mater is in closer contact with the bone, its ascent being 
perhaps also hindered by gravitation as the patient lies with the head 
raised. As already stated, pus is often found among the muscles of 
the back (having escaped between the arches), and sometimes collec- 
tions are found in front of the spine. The amount outside is no 
doubt increased rapidly by the local suppuration excited by the 
presence of the pus. In these cases the membrane itself is swollen, 
and has a soddened aspect, resembling a piece of wash-leather, being 
softened in proportion to the duration of the affection. The inner 
Fig. 89.— External pachy- 
meningitis ; nodular 
thickening of outer 
layer of dura mater in 
caries of the spine. 268 
SPINAL MEMBRANES. 
surface is usually normal, and the pia mater is either unchanged oi 
merely congested. 
Symptoms.—In different cases of external meningitis the symptoms 
vary much, and they are usually complicated with those of the cause 
of the inflammation. Those that occur in caries have been already 
described. In most acute cases the symptoms are nearly the same 
as those of internal meningitis, although they are subject to greater 
variations, and more frequently have unusual and anomalous manifes- 
tations, presently to be described. The chief symptoms are pain in 
the back, often referred to the loins, increased by movement, accom- 
panied by stiffness of the muscles of the spine, severe root-pains, and 
cutaneous hypersesthesia. The pains are usually associated with 
spasm ; the hypersesthesia may be followed by anaesthesia, and some- 
times by paralysis of the muscles supplied by the irritated and 
damaged nerves. When there is a rapid formation of pus, the func- 
tions of the cord itself are rapidly interfered with in consequence of 
its compression, and the symptoms of irritation are to a large extent 
replaced by those of paralysis, beginning in the legs and ascending. 
The motor palsy is accompanied by fiaccidity of the muscles and loss 
of all reflex actions. Sensation may also be lost, or may be preserved 
or changed. The sphincters are usually paralysed. Bedsores form 
rapidly if life is sufficiently prolonged. A peculiar lividity of the 
skin has been sometimes noted. In these acute cases there is much 
constitutional disturbance, rigors, profuse sweating, and high fever, in 
one case amounting to 110° (Maguire). 
In local secondary forms the symptoms differ in character according 
to the acuteness of the inflammation, and in distribution according to 
its seat. Although, as a rule, pain is considerable, other signs of 
irritation, stiffness and muscular spasm, are generally inconspicuous, 
and the symptoms resemble, and are merged in, those due to the 
disease by which the meningitis is produced. 
Diagnosis.—The most important indications of the chronic form 
are the vertebral pain and the radiating pains, with other symptoms 
of irritation of the nerve-roots, combined with the signs of pressure 
on the cord. These symptoms are seldom distinct from those of the 
cause of the external inflammation; the meningitis is indeed the 
chief mechanism by which the local disease causes its nerve-manifes- 
tations. 
The acute form causes symptoms that have much in common Avith 
those of internal meningitis. It is indeed doubtful Avhether the 
diagnosis can be made from the character of the nerve-symptoms 
alone. The special indication of the seat of the process is furnished 
by evidence of its extension to or from the structures outside the 
spine. If such acute symptoms are secondary to external disease 
that clearly preceded the meningeal inflammation, this may safely be 
assumed to be outside the dura mater. In a case of apparently 
primary meningitis a careful watch should be kept on the tissues of 269 
INTERNAL MENINGITIS. 
the back; any sign of deep oedema among the muscles beside the 
vertebral column, in such a case, is probable evidence of commencing 
purulent inflammation extending from within, and the development of 
acute local inflammation in either the pleura, posterior mediastinum, 
back of the abdomen, or behind the pharynx, has the same signifi- 
cance. It is important that the nature of such symptoms should be 
kept in mind, as otherwise their occurrence increases the perplexing 
character of the case. It is probable that the nature of many cases, 
which remain undecided during life, would be rendered clear by 
repeated careful observation. 
Prognosis. —The acute affection is exceedingly grave. Recorded 
cases have ended in death, but this termination has been a condition 
of the diagnosis; and it is possible that some cases which have 
recovered, in which the exact seat of the inflammation was uncertain, 
may have been instances of this form, and that the fatality of the 
disease may not be so great as published facts suggest. But on this 
point only future observations can throw light. Chronic external 
meningitis which results from caries is only serious in the compres- 
sion it exerts on the cord. 
Treatment.—The local form alone affords an opportunity for 
effective treatment. The first and most important element is the 
treatment of the original cause of the disease, the caries, &c.,to which 
the meningitis is secondary. Any accessible collection of pus should 
be opened, and if acute local symptoms, in a case of bone disease, 
suggest the passage of pus into the vertebral canal, the propriety of 
immediate trephining should be considered. Rest, counter-irritation 
to the spine, especially the actual cautery, sedatives to relieve the 
pain, and tonics are the most important measures in chronic cases. 
So far as the acute form is open to treatment, the measures suitable 
are those for the internal variety. In a subacute case, a free exit 
should be afforded to the pus. An opportunity for this very seldom 
presents itself, but may perhaps be furnished by sufficiently frequent 
examination more often than has hitherto been the case. 
INTERNAL MENINGITIS. 
Internal meningitis, inflammation beginning within the dura-matral 
sheath, may be either acute or chronic. The acute form usually com- 
mences in the pia mater and arachnoid; the chronic forms may begin 
in these membranes, or in the inner surface of the dura mater. Little 
is known practically of any separate affection of the arachnoid. 270 
SPINAL MEMBRANES. 
Acute Internal Meningitis. 
Internal meningitis, for the reason already mentioned, has been 
termed “ leptomeningitis.” but the acute form only remains limited 
to those membranes when of slight degree. In some cases the inner 
surface of the dura mater is also inflamed. Frequently the inflam- 
mation extends rapidly to the cord, and to such cases the term 
“ meningo-myelitis ” is often applied; in other cases, strange to say, 
no extension to the coi’d tabes place. The inflammation may be 
either simple or purulent, or it may be secondary to tubercle. It 
also occurs in conjunction with cerebral meningitis in the epidemic 
form. Acute simple spinal meningitis is a rare disease. 
The immediate causes that have been traced are in part such as 
have a local action ; in part they are general morbid influences, such as 
give rise to other internal inflammations, and have been effective in 
causing meningitis in consequence either of some personal predisposi- 
tion, or in consequence of a peculiarity in the agent, which led to a 
specific action on these structures. 
(a) The local causes maybe—(1) Injuries to the spine, severe or slight, 
from fracture to simple dislocation; concussion ; surgical procedures, 
such as an operation on the vertebral column, or the puncture of the sac 
in spina bifida. (2) The exposure of the back to cold has been the appa- 
rent cause in rare cases ; and still more rarely the prolonged exposure of 
the spine to the sun, “ spinal insolation,” has seemed to be effective. (3) 
Adjaet nt inflammation has sometimes caused internal meningitis, but 
m such cases external meningitis has of necessity been first produced, 
and the inflammation has passed through the dura mater. Hence, all 
the causes of acute external meningitis are also occasional causes of 
the internal form. But, as already stated, such extension through the 
sheath is very rare, and there is some doubt as to the precise nature of 
many of the cases in which it has been supposed to occur. We have 
seen that in many of the instances in which external meningitis has 
been ascribed to adjacent suppuration, the latter has been secondary, 
and the meningitis has been the result of a primary blood-state. 
When in such cases there has been both internal and external menin- 
gitis, it is probable that the former has not been due to actual exten- 
sion through the dura mater, but that both have been the simultaneous 
result of a general cause. 
(b) In a few cases acute internal meningitis is due to the extension 
of inflammation from the cerebral membranes. Such extension is 
rarely traced, however, except in two classes of cases :—(1) Those in 
which slight meningitis is found in the upper cervical region, as far 
as gravitation favours the descent of solid particles in the cerebro- 
spinal fluid as the patient lies in bed. The inflammation ceases when 
the spine becomes horizontal; for the most part symptoms are slight 
or absent in such cases. (2) In cases in which a general spinal INTERNAL MENINGITIS. 
271 
meningitis has been secondary in point of time to inflammation of the 
cerebral membranes the affection has generally been due to some 
cause capable of acting upon both, such as the local presence of 
tubercles or a morbid blood-state of the character to be immediately 
mentioned. 
(c) The most acute and severe forms of internal meningitis are 
■due to a morbid blood-state, either septicaemia or a virus allied to that 
which causes the cerebro-spinal form. Purulent meningitis occurs in 
cases of surgical and puerperal septicaemia, both with and apart from 
a similar affection of the cerebral membranes. Acute inflammation, 
purulent when intense and prolonged, occurs also as an isolated 
malady, sometimes without apparent exciting cause, sometimes after 
exposure to cold. In such cases organisms have been found in the 
spinal fluids, analogous to those of the cerebro-spinal form, in connec- 
tion with which the pathological relations will be more fully con- 
sidered. It probably results from a blood-state not far removed 
from those which cause some other forms of internal inflammation, 
and which give rise to acute articular rheumatism. General exposure 
to cold must be assumed to cause so special an effect only through 
the agency of toxaemia, such as that which has been already con- 
sidered as underlying the rheumatic form of acute polyneuritis. Such 
exposure has been apparently rendered effective in some instances by 
coincident menstruation, which may have produced a special suscepti- 
bility to the attack, or favorable conditions for the development of 
some organised virus, such as seems to be the essential factor in the 
causation of these forms. The exposure to cold that has been effec- 
tive has presented all the variations that are met with in the case of 
other diseases thus produced, variations which are common to so 
many maladies that they can have no special relation to any one of 
them. Lastly, as a crucial example of this origin of the disease, is 
the important fact that, it may follow, or occur in the course of 
certain acute specific diseases, as one consequence of the virus that 
produces them. 
Pathological Anatomy.—Internal meningitis is usually of wide 
extent, since the inflammation spreads readily in the loose tissue of 
the arachnoid. Probably also the movement of the cerebro-spinal 
fluid aids in the extension of local forms and in the descent, of intra- 
cranial inflammation by conveying irritant material. In the case of a 
patient who had been in bed for some time the precise level at 
which such slight descending meningitis ceases may be that at which 
the vertebral column becomes horizontal. In the earliest stage the 
only change is congestion in the pia mater, which is reddened from 
vascularity, and may be dotted with ecchymoses. The inner sur- 
face of the dura mater, and the substance of the spinal cord, may be 
similarly congested. When the inflammation is further advanced, 
in the stage in which the condition most often comes under observa- 
tion, the pia mater and arachnoid are opaque and thickened, and an 272 
SPINAL MEMBRANES. 
“ exudation ” of inflammatory products, greyish yellow in tint, may 
cover the pia mater and occupy the meshes of the arachnoid, forming 
a layer over the cord. This exudation varies in its consistence, and 
may be semi-purulent in aspect; in the suppurative form the mem- 
branes are infiltrated with pus, which also covers their surface. The 
inner surface of the dura mater usually presents similar changes, 
and the inflammatory products may fill up the whole space between 
the dura and pia mater, thus connecting the two membranes and 
surrounding the nerve-roots (Fig. 90). The microscope shows 
abundant leucocytal elements, and the larger round and spindle cells 
that are common in all inflammatory products. The former corpuscles, 
Fig. 90. 
Fig. 91. 
Fig. 90.—Purulent meningitis; portion of spinal cord and membranes; the space 
between the pia mater and dura mater is occupied by inflammatory products, pus, 
&c., in which the nerve-roots, n n, are embedded, a a. Cavities which bad 
apparently been filled with liquid pus. From a case of septic origin, secondary to 
caries of the jaw. 
Fig. 91.— From the same; meshes of arachnoid infiltrated with pus-corpuscles. 
A nerve-root, n. r., although surrounded by pus, is perfectly normal; and so also are 
the pia mater, p. m., and the peripheral layer of the spinal cord, s. c. 
which resemble, and are probably identical with pus-corpuscles, may 
be abundant, even when the exudation has not a distinctly purulent 
aspect; when it has, they constitute almost the whole of the material, 
lying among the fibres of the arachnoid (Fig. 91). The vessels are 
dilated,* and their sheaths distended with cells. The spinal fluid is 
increased in quantity, and turbid from flocculi, or even purulent in 
aspect. The nerve-roots are covered with exudation, and are often 
swollen and reddened from invasion by the inflammation. But they do 
not always suffer, even in purulent meningitis, as Fig. 91 shows, in 
which a nerre-root is almost normal in aspect, and its sheath is 
unaffected, although it is surrounded by pus-cells. The spinal cord INTERNA.L MENINGITIS. 
273 
is often invaded by the inflammation ; it is then reddened, pale, and 
softened, and the microscope shows the tissue-changes common in 
other forms of myelitis. The change is always most marked in the 
periphery of the cord, and may occur in wedge-shaped areas, having 
the apex directed inwards, and coalescing at the surface. The 
peripheral arterioles come from the pia mater (see “ Vessels ”), and the 
continuation of their perivascular spaces with the lymphatic interstices 
of the membranes renders it easy to understand the invasion of the 
cord. Nevertheless, in some cases, especially of purulent meningitis, 
the pia mater itself is little affected, even when the arachnoid is filled 
with pus, and in these cases the spinal cord may be normal, as in the 
example shown in Fig. 90. If recovery takes place, the inflammatory 
products may undergo cicatricial changes, the membranes remaining 
opaque and adherent, and there may be a permanent excess of arach- 
noid fluid. The changes in the cord may lead to sclerosis, widely 
spread, or limited to certain spots, and from these secondary degenera- 
tions, ascending and descending, may develop. 
The area affected varies in different cases ; the membranes are 
involved in their whole extent in most acute forms. Usually the 
affection is greater on the posterior than on the anterior surface 
probably on account of the influence of the recumbent posture, which 
determines the passage backwards of the lymphatic fluids containing 
material capable of exciting and increasing the inflammation. 
In tubercular inflammation the amount of exudation is usually 
small, and it may be absent. It is often grey and gelatinous in 
appearance, and in it are scattered the greyish or whitish tubercular 
granulations. Similar granulations may usually be found in abundance 
upon the inner surface of the dura mater. Such grey granulations 
are often found upon the spinal membranes in cases of tuberculosis 
when there is no inflammation, even when the cerebral membranes 
are intensely inflamed. The arachnoid, especially that covering the 
cauda equina, may appear as if dusted over with grey particles, so 
abundant are the granulations. 
In many cases, the signs of spinal meningitis are associated with 
those of inflammation of the membranes of the brain, especially of 
those about the base and posterior part of the brain. The continuity 
of the spinal and cerebral inflammation may be obvious or indistinct. 
In the latter case, the connecting inflammation has apparently been 
much slighter than that in the base of the brain or around the cord, 
so slight, indeed, as to have left no distinct traces, the inflamma- 
tion having apparently extended in consequence of the passage of 
morbid material by the cerebro-spinal fluid. In cases of slight cere- 
bral meningitis, in which the patient has been recumbent, signs of 
spinal meningitis, opacity of the arachnoid and its distension with 
slightly turbid fluid, may exist only in the cervical region, ceasing 
opposite the upper dorsal vertebrae, and thus extending as far as 
gravitation (the head being slightly raised on a pillow) favoured. 
VOL. I, 274 
SPINAL MEMBRANES. 
the descent of inflammatory products. But in the violent purulent 
cerebro-spinal meningitis, which is occasionally produced by a septic 
influence, pus around the cord is often continuous with that which 
bathes the base of the brain. In a case of this kind, in which the 
meningitis was secondary to acute double purulent otitis, Leyden 
found abundant active micrococci, very similar to those associated 
with erysipelas. In other acute cases, organisms have been found 
similar to these of pneumonia, and met with also in the epidemic 
cerebro-spinal form. 
Symptoms.—Slight pain in the back, and malaise, may precede the 
acute onset of the symptoms. This is usually marked by a rigor, by 
pyi'exia, and by severe pain in the back. The latter varies in posi- 
tion, according to the locality of the inflammation, but is often felt 
along the whole extent of the spine. Pain also radiates along the 
distribution of the nerves, round the trunk or to the extremities. 
This excentric pain is paroxysmal and intense ; sharp, darting, burning, 
or constricting. The pam in the back is usually constant, with 
exacerbations. It is often increased by movement, usually also by 
pressure, and by the application of a hot sponge to the skin. It is no 
doubt due to the irritation of the inflamed meninges, while the radi- 
ating pain is produced by the irritation of the sensory nerve-roots. 
Muscular spasm usually comes on at the same time as the paiu. 
It shows itself first in rigidity of the muscles of the back, most 
marked, if the inflammation is local, in the neighbourhood of the 
inflamed part. This rigidity is an important and characteristic 
symptom. It is often first observed in the neck, probably on account 
of the mobility of the part. When slight it may merely cause 
retraction of the head, or stiffness of the back, or may be so general 
and so severe as to cause opisthotonos, resembling that of tetanus. 
The spasm usually involves also other trunk-muscles, especially 
those of the abdomen, which become hard and cramped. The limbs 
also become rigid, and painful cramp-like spasms occur in them, 
especially on attempts to move. The spasm is probably partly due to 
the irritation of the motor nerve-roots, and is partly reflex, from the 
irritation of the sensory roots and the nerves of the pia mater. There is 
usually great hypersesthesia of the skin to all forms of stimulation, and 
also increased sensitiveness of the muscles, especially in the lower 
limbs. Pressure on the arms may cause no uneasiness, while a 
similar pressure on the legs occasions great pain. Reflex action is 
usually increased at the beginning. Constipation is common, and so 
is retention of urine, in spite of irritable attempts to empty the 
bladder—the result, apparently, of spasm of its muscles, including 
the sphincter, which resists the action of the detrusor. Dyspnoea 
may result from the spasm of the thoracic muscles, and may be 
almost suffocating in its severity. The pulse may be frequent or 
retarded. The temperature is raised, sometimes, however, to only a 
slight degree. Cerebral symptoms, headache, delirium, coma, occur INTEENAL MENINGITIS. 
275 
•when inflammation Las extended within the skull. The“Cheyne- 
Stokes breathing ” may be present, from implication of the medulla- 
The function of the vaso-motor nerves (which leave the cord by many 
of the anterior roots) is also deranged; the dilatation of the vessels, 
that follows a stroke on the skin of the trunk, is excessive and pro- 
longed (meningeal streak, tache spinale). 
As the disease progresses, the symptoms of irritation give place to 
those of paralysis, which may be most marked where the rigidity was 
greatest. The limbs become relaxed, and feeble or powerless. Sensi- 
bility becomes lessened or lost. Reflex action disappears, the mus- 
cular power in the limbs becomes so reduced that the patient is 
scarcely able to move; the heart shares the universal prostration, and 
death may occur from asthenia, or from paralysis of the respiratory 
muscles. Towards the end there is sometimes considerable rise of 
temperature. In some cases the symptoms become less progressive 
and the disease passes into a less acute stage ; the pains persist, the 
loss of power continues and may even slowly increase. Death may 
■occur, after weeks of suffering, from the effects of bedsoi'es or from 
secondary kidney disease, due to the retention of urine, and facilitated 
by trophic derangement. On the other hand, in slight cases, the signs 
of irritation may lessen and pass awav, while those of structural 
damage, paralysis and anaesthesia, may remain, and to these may be 
added muscular atrophy and contractures, from the secondary conse- 
quences of the lesions of the nerve-roots. Such persistent symptoms 
vary much in extent and degree, according to the position and intensity 
of the morbid process. Ultimately the symptoms of damage to the 
cord may either slowly increase, in consequence of the spread of 
chronic myelitis set up by the acute mischief, or, on the other hand, 
the symptoms of the meningitis may pass entirely away. 
The symptoms above described vary in their distribution, according 
to the position of the disease. When the membranes over the lumbar 
■enlargement are chiefly affected, the pains, hyperaesthesia, and cramps 
are confined to the legs and loins. When the disease is in the dorsal 
region there may be similar hyperaesthesia and spasm in the legs, but 
the pain and cramp extend higher, and involve the trunk. If the 
eervical region is affected, the symptoms extend to the upper extremi- 
ties, the dyspnoea may be great, and there is often difficulty in 
swallowing. The action of the heart is sometimes deranged, and con- 
traction or dilatation of one or both pupils may occur. Extension 
to the brain is marked by vomiting, general headache, delirium, and 
paralysis of cranial nerves, of which the first to suffer are the spinal 
accessory and hypoglossal. If such symptoms preceded those of 
spinal meningitis, we may conclude that the inflammation commenced 
within the skull. 
The symptoms vary somewhat according to the nature of the inflam- 
mation. In purulent meningitis, as already pointed out, the sym- 
ptoms of irritation are sometimes very slight, apparently because 276 
SPINAL M15MB It AXES. 
there is little tendency to invade the nerve-roots. In the case from 
which Figs. 90 and 91 were taken, there were hardly any symptoms to 
suggest meningitis, and, although there was paraplegia, it was probably 
produced by the mere pressure of a large collection of pus on the 
spinal cord ; there were no pains or spasm. The case was one of 
septic origin. It was apparently a pure arachnitis, and the tissue of 
the pia mater was able to resist invasion so completely as to protect 
the structures beneath it even from disturbance of function. 
The duration of the acute symptoms varies from a day or two, in 
severe cases, which end in death, to two or three weeks, in cases of less 
severity, which may end in either death or recovery. The duration 
of the subacute and chronic symptoms that supervene is to be 
measured by months, and sometimes by years. 
The symptoms of tubercular spinal meningitis resemble those which 
have been described, but are usually less intense. There is pain in 
the back and loins, with stilf uess of the spine and retraction of the neck, 
so that it may be difficult to bend the head forwards. There are also 
variable rigidity, hyperaesthesia, and tingling in the limbs, followed by 
lessened sensibility and paraplegic weakness. These symptoms occa- 
sionally come on in the later stage of cerebral tubercular meningitis. 
Diagnosis.—The diagnosis of the disease rests on the pain in the 
back, the retraction and rigidity of the neck and spine, the hyperaes- 
thesia and spasm in the limbs, excited especially by attempts to move 
them, on the acute onset of the symptoms and on their association with 
pyrexia. This grouping of the symptoms is sufficiently characteristic, 
as is shown by the fact that it is extremely rare for them to be simulated, 
even remotely. The chief difficulty in actually acute cases is presented 
by the forms that run an almost latent course, especially by the secondary 
purulent form, which has so little tendency to invade the nerve struc- 
tures, and a correspondingly slight tendency to derange their func- 
tions, and even to irritate them. In pure myelitis, on the other 
hand, pain in the back is absent or trifling ; paralysis occurs early and is 
the leading symptom, and there is little or no spasm in the limbs 
in the early stage of the affection. Often, however, some meningitis 
occurs at the onset of acute myelitis, and then some pain in the back 
and slight rigidity in the limbs may precede or accompany the onset 
of the paralysis. In such cases the predominance of the meningeal 
or cord symptoms must determine the category in which the case is to 
be placed. Meningeal haemorrhage most nearly resembles meningitis 
in its manifestations, and does so necessarily, because it produces 
inflammation ; the distinction chiefly depends on the onset, and 
will be considered in the next section. Haemorrhage into the spinal 
cord can scarcely be coufused with inflammation of the membranes, 
because the only common symptom, pain in the back, is confined to a 
definite spot. 
Tetanus is attended by rigidity of the back, and by spasm, and 
presents a closer initial resemblance to meningitis than most other INTERNAL MENINGITIS. 
277 
affections with which it may be confounded; but there is no fever at 
the onset, trismus is an early and obtrusive symptom, and the 
paroxysms of muscular spasm are excited by peripheral impressions 
much more readily than in meningitis, in which they occur chiefly on 
attempts to move. Only the “rheumatic” form of tetanus would 
give rise to difficulty ; the onset of the traumatic form after an injury 
should prevent any doubt, iRheumatism of the muscles may cause 
pain in the back on movement, and the resulting rigidity may 
prevent movement; but there is not the spontaneous pain which attends 
meningitis, nor is there distant spasm. Some difficulty may be 
caused by rheumatism of the cervical muscles in young children ; this 
may lead to retraction of the head, and if it comes on acutely, after 
exposure to cold, considerable doubt as to its nature may at first be 
felt. But it remains stationary, and the freedom of the patient from 
spontaneous or radiating pains, and from any affection of the nerves, 
soon enables a reassuring opinion to be formed. 
The diagnosis of the form of meningitis depends on the recognition 
of the cause of the inflammation. When spontaneous and acute the 
case is probably of the “ primary ” form, which depends on some 
toxic agency, probably often an organised virus, and is really a partial 
“ epidemic ” form. If it occurs under the conditions that give rise to 
surgical septicaemia, or after childbirth, purulent meningitis is almost 
certain, and the inflammation may be far more intense than the severity 
of the symptoms suggest. The diagnosis of tubercular spinal menin- 
gitis depends on the combination with cerebral meningitis, which 
usually precedes the spinal symptoms, and on the gradual and 
insidious onset. Indications of the tubercular or scrofulous dia- 
thesis are commonly present in the state of other organs, or to be 
ascertained from the family history of the patient. 
Prognosis.—The prognosis is grave in all cases. It is worse the 
more severe and acute the symptoms, the higher the temperature, and 
the sooner the symptoms of irritation give place to those of paralysis. 
It is worse also when the disease is due to serious lesions of the spine 
or to tuberculosis, than when due to cold, and worse in the so-called 
“ spontaneous ” cases than in those which result from traumatic causes. 
Recovery is more probable in middle life than in early or advanced 
age. The previous health of the patient also influences the prognosis. 
It must always be remembered that even if the patient survives the 
period of acute inflammation, serious permanent damage may remain. 
Treatment.—Perfect rest and quiet are of the greatest importance 
throughout the course of the disease. All sounds should be, as far as 
possible, excluded; the light should be subdued, and all bodily move- 
ment and mental exertion as far as possible avoided. The vascular 
disturbance of inflammation is intensified by all functional excitement 
of the too irritable structures, and continuous freedom from such 
excitement, as far as it is possible to obtain the freedom, is of 
paramount importance. Every attack of spasm means greater vascular 278 
SPINAL MEMBRANES. 
disturbance, and the circulatory derangement entails leucocytal infil- 
tration and other structural consequences. 
Although it is undesirable that the spine should be the lowest part 
of the body, yet, in acute meningitis, it is scarcely possible for the 
patient to lie in any other posture. The prone position interferes 
with respiration, and both it and a lateral posture entail, directly or 
indirectly, greater muscular exertion, and hence more frequent and 
more severe attacks of spasm, with secondary harm out of proportion 
to that which the posture could prevent. Here, as so often in thera- 
peutics, skill is shown and success secured, if it is within reach, by 
knowing when to permit no compromise, and when to adopt one. 
The dorsal position must be permitted if in it the spasm is much 
less than in others. Dry, or, in robust patients, wet cupping, or 
leeching, along the spine may be employed at the onset, and be 
followed by the local application of cold in traumatic or haemorrhagic 
cases, and of heat in others—the principles being the same as in 
myelitis. Counter-irritation, by blisters or repeated sinapisms, is 
more useful when the disease is subsiding than at the onset. In 
cases that are due to cold, free diaphoresis often does good; a hot 
air or vapour bath should be employed at the onset of the treat- 
ment. A warm bath may be followed by moist packing for several 
hours. The relief thus given is sometimes very great. The bowels 
should also be freely opened. 
The only internal remedy which has been held, for long, in general 
repute, as capable of influencing the inflammatory process, is 
mercury. The confidence placed in it of old is not altogether 
unwarranted. It should be given until there is a slight affection of 
the gums (the only evidence that enough is in the system to act on 
the tissues), and inunction is unquestionably the best way of adminis- 
tration. We know that it must then enter the blood before it can 
escape by the bowel; we can regulate its dose as we need, for we 
estimate it by the influence on the gums ; and by rubbing it in over 
the part affected we can combine some counter-irritant influence (as 
by an irritating agent added to the ointment used), and we neces- 
sarily secure the simultaneous action of the two agents, for the largest 
quantity of mercury in the blood will coincide with the most consider- 
able reflex action on the vessels. Lastly, the disturbance of the 
stomach and bowels is certainly less than when their mucous mem- 
brane is chosen as the path into the body. The oleate of mercury 
may be rubbed in along the spine. Iodide of potassium seems to 
have little influence over acute inflammation. 
It is necessary to give sedatives for the relief of the pain and 
spasm, if the application of cold does not suffice. Of these, morphia, 
given by the skin or the mouth, is the most effective, but vomiting 
lrom its use is a grave drawback; fortunately it does not readily 
occur under the circumstances. Sometimes inhalations of chloroform 
are necessary to relieve the suffering, and may be even more effective- INTERNAL MENINGITIS. 
279 
than morphia. In slight cases relief may be afforded by belladonna, 
or by atropia injected beneath the skin. Chloral, or chloral and 
bromide, or any of the milder sedatives, may be given if there is 
insomnia. Bromide alone, unfortunately, has very little power to 
lessen the spinal reflex action. Frequently, the spinal ice-bag is the 
most effective and least injurious. 
When the disease has passed into a chronic stage, iodides have been 
thought useful. Counter-irritation may be employed freely with 
advantage. Tonics, iron, quinine, and even strychnia are beneficial. 
Warm baths, as those of Bath and Aix-les-Bains, seem sometimes of 
service, especially employed as hot douches to the spine. But the 
acute form is followed by a tendency to the slow subsidence of its 
effects, which makes the influence of such measures difficult to estimate. 
The local consequences, muscular atrophy, contracture, &c., need 
special local treatment by electricity, rubbing, and the like. 
Epidemic cerebro-spinal meningitis is described in the section on 
diseases of the cerebral membranes. 
Chronic Internal Meningitis. 
Chronic inflammation of the membranes of the cord, within the 
dura-matral sheath, is divided into two forms, according as it begins 
in, and chiefly affects, the dura mater, chronic internal pachymeningitis, 
or the pia mater and arachnoid, chronic leptomeningitis. Although 
these forms sometimes present distinct clinical and pathological 
features, they have, when of considerable degree, many characters in 
common; they own the same causes, and need the same treatment. 
Hence it is most convenient to describe them together as forms of 
internal meningitis. The condition termed lisematoma of the dura 
mater depends on a form of haemorrhagic inflammation. 
Chronic meningitis is seldom fatal, and is rare as a general and 
primary malady. As such, therefore, our knowledge of it is still scanty, 
and the opinions formerly current have had to be largely curtailed. 
It was inferred that chronic symptoms, analogous to those which, 
when acute, are due to acute meningitis, were evidence of a chronic 
form. This was, therefore, assumed to be the cause of a group of 
symptoms, of which spasm is the prominent and dominant feature, 
which are now known to be due solely to a morbid state of the spinal 
cord itself, and to be consistent with a perfectly normal state of the 
membranes. Hence “ chronic meningitis,” as it was recognised 
twenty years ago, as a “ clinical entity,” has ceased to exist, or 
rather has passed into the pathological conception of “ primary 
lateral sclerosis.” The definite knowledge we now have of general 
primary chronic meningitis is limited. The important fact regarding 
it is that its symptoms differ from those of the acute form more widely, 
perhaps, than do those of any other chronic inflammation. Yet this 280 
SPINAL MEMBRANES. 
difference depends on a comparatively small element—on the fact that 
only acute inflammation causes acute irritation of the motor and reflex 
structures. The chi*onic form may irritate the sensory nerve-roots, 
hut its motor manifestations are chiefly the result of pressure, and 
even to this much, of the pain may he due. The pressure may cause 
spasm, hut it is a slow tonic contraction, wholly unlike that of the 
acute form. The difference in the effect of the two forms of inflam- 
mation suggests many problems that deserve investigation, hut their 
consideration would he out of place here. 
Causes.—Chronic internal meningitis, in every form,is most frequent 
in adult age, and, like acute inflammation, affects men more frequently 
than women. In its general and primary form, it has been thought 
to occur more readily in persons with neurotic heredity, although 
the influence of this is doubtful. Debilitating influences of various 
kinds predispose to the disease, and prolonged over-exertion has 
been thought sometimes to pi’oduce it. Among exciting causes the 
most important is severe and repeated exjmsure to cold. Traumatic 
lesions, concussion, &c., are occasional causes. It may result by 
extension from inflammation outside the dura mater and from chronic 
inflammation of the substance of the cord itself. But their iufluence 
in producing chronic internal inflammation (except as a sequel to the 
acute form) is a subject on which the opinions of the past have still 
to be subjected to careful comparison with ascertained facts. It is 
probable, however, that the condition does sometimes follow con- 
cussion of the spine that has no immediate or acute consequences, 
and the chronic stage into which an acute traumatic meningitis 
subsides may last so long as to throw its initial form into the shade, 
and may not only persist with independent pertinacity, but may 
extend without relation to the original seat. Thus we must dis- 
tinguish as effects of injury, the local and the general forms. The 
latter are predisposed to by the influences that seem to facilitate the 
occurrence of the primary form, and in these cases the influence of 
the injury often seems to be trifling, and the existence of the morbid 
state is not always beyond doubt. 
Local chronic meningitis may also result from any chronic disease 
either of the membranes themselves, the bones, or the spinal cord. 
These need not be enumerated in detail. It occurs in all cases of 
compression, and especially in all forms of chronic myelitis that 
involve the superficial layers of the cord. 
Lastly, certain general morbid states are frequent causes. The 
first is alcoholism, which may give rise to general inflammation, in- 
volving both the pia arachnoid and the superficial layers of the cord 
in various degrees. A second and also common cause is syphilis, 
which may produce either pachymeningitis, surrounding the cord in 
the way presently to be described, or local leptomeningitis, irregular 
in position and in effects. Lastly, in very i'are cases, tubercle has 
given rise to a chronic inflammation, chiefly of the inner surface of the INTERNAL MENINGITIS. 
281 
dura mater. Haemorrhagic pachymeningitis occurs especially in the 
insane, but has been met with as a consequence of chronic alcoholism 
and after injuries. 
Pathological Anatomy.—In slight and moderate degree, there is 
merely opacity and thickening of the membranes affected, sometimes 
with distension of vessels or minute spots of extravasation. The 
opacity of the arachnoid may be such that the spinal cord cannot be 
seen through it. The inner surface of the dura mater may be 
granular when it is not otherwise changed. The spinal ffuid is 
increased in quantity and is turbid. When the changes are greater 
in degree, the dura mater and pia mater may be connected together 
by a layer of inflammatory tissue of considerable thickness, so that it 
may be impossible to say in which membrane the disease commenced. 
The microscope shows the ordinary elements which result from 
inflammation, cells of various kinds, many lymphoid and pus-like 
corpuscles, and distended vessels, often incrusted by similar cells. 
Frequently also the pia mater is transformed into a thick irregular 
layer of homogeneous tissue in which no distinct cell-elements can be 
Fro. 92.—Chronic alcoholic meningitis. Section of edge of anterior column and of 
a large nerve-root; earn ine preparation, p.m., pia mater irregularly thickened 
and transformed into amorphous-looking tissue, from which wedge-shaped 
branching tracts (xx) extend into the white substance; f.f., fasciculi of nerve- 
fibres entering the cord; a., an artery in the nerve-root, enlarged and with 
thickened walls; t. t., tracts of amorphous connective tissue; e., a small 
extravasation. 
perceived, and only faint indications of a fibrous structure (Fig. 92). 
The walls of its vessels may be greatly thickened by similar material. 
The nerve-roots passing through the diseased membranes very 
seldom escape, as they may in the acute form, but are inflamed, 282 
SPINAL MEMBRANES. 
reddened, and swollen in the active stage, and afterwards com- 
pressed and atrophied, if the amount of new tissue formed about 
them is considerable. The fibres suffer especially when the inflam- 
mation involves the dura mater, on account of the unyielding 
character of the fibrous sheaths which the nerves receive from that 
membrane. When the pia mater is thickened, scattered tracts of 
connective tissue may be seen in the substance of the nerve-roots, 
between the fibres (Tig. 92, t). 
The spinal cord presents the same variations in the degree in which 
it suffers. It may be little affected, but is frequently damaged by the 
extension to it of the inflammation of the pia mater, which causes 
softening, vascularity, loss of distinction between grey and white 
substance, breaking down of nerve-elements, and infiltration by 
lymphoid and other inflammatory cells. Ultimately indurating 
tissue remains, constituting an irregular zone of peripheral sclerosis. 
From the thickened pia mater tracts of similar tissue may extend 
into the cord, becoming narrower as they pass inwards and sending 
out branching trabeculae (Fig. 92, *). Between these tracts the nerve- 
fibres are more or less damaged, partly by the inflammation, and 
partly by the compression produced by the newly-formed tissue. 
This peripheral sclerosis associated with chronic meningitis, espe- 
cially in the neighbourhood of injuries, frequently damages tracts 
that undergo secondary ascending degeneration—post-median column, 
direct cerebellar tract, and ascending antero-lateral tract. The result 
is to produce a mixed lesion, the precise nature of which is not always 
easily distinguished and has certainly often been mistaken. The 
equivocal aspect of the process is probably increased by the fact 
that, as we have seen, secondary degeneration entails an interstitial 
process that is prone to assume an inflammatory character, espe- 
cially when set up by an irritative lesion. Hence the peripheral 
sclerosis set up by the meningitis is apt to carry with it a certain 
amount of inflammation in the pia mater far beyond the region to- 
which this would otherwise be limited. A similar thickening of the 
pia mater is, however, met with over areas of the cord that are the 
seat of other forms of sclerosis, both those that are systemic, as in 
tabes, and those that are random, as the insular form. It is probably 
secondary in all cases, but it formerly gave rise to some erroneous 
conceptions of the nature of such degenerations (see Locomotor Ataxy). 
A still more considerable implication of the pia mater is met with 
over regions that are the seat of focal chronic myelitis. 
In the ordinary form of chronic meningitis, the membrane in which 
the inflammation, begins may be much more affected than the other, 
although the latter is very rarely healthy, except in the slightest cases. 
Inflammation beginning in the pia mater and arachnoid is often 
extensive in range, and may be considerable or slight in degree. That 
which commences on the inner surface of the dura mater is frequently 
limited in extent, but is accompanied by the formation of a large 283 
INTERNAL MENINGITIS. 
amount of new tissue, and hence has been termed hypertrophic internal 
pachymeningitis. It constitutes a very important variety, giving 
rise to peculiar and grave symptoms which were first carefully studied 
by Charcot and Joffroy. It is most commonly the cervical region, 
hut sometimes occurs at the lower part of the cord. On opening the 
spinal canal a fusiform tumour is seen, the outer surface of which is 
the unaltered outer surface of the dura mater, and on section the 
enlargement is seen to depend chiefly on a great thickening of tho 
inner part of this membrane, sometimes amounting to a quarter of an 
inch; several layers of new tissue can often be distinguished. The 
pia mater may be normal, but is more commonly thickened, and it is 
often united by the thickened arachnoid to the tissue proceeding from 
the dura mater. The cord is compressed and commonly softened at 
the spot, and it presents signs of inflammation. The nerve-roots are 
also damaged and compressed by the newly-formed tissue. Some- 
times at the spot most affected, the cord may be surrounded by a ring 
of new tissue of cartilaginous hardness. In other cases the thickening 
of the dura mater is slighter and more diffuse, affecting occasionally 
a wide extent of the membrane. In rare cases the membranes about 
the cauda equina may alone be affected—the dura and pia mater 
adherent, and the nerves united in a fibi'ous mass. 
The white fibroid or cartilaginous plates found so ofteu in the 
arachnoid after death are probably not connected with preceding 
inflammation. In most cases in which they are found, no symptoms 
have existed during life. It is said, however, that when they are 
numerous and extensive they may give rise to symptoms closely 
resembling those of chronic meningitis (Vulpian). But fibroid plates 
in the dura mater have been seen in a case in which previous 
svmptoms suggested that they resulted from chronic inflammation 
(Jaccoud). 
The rare condition termed internal hsemorrhagic pachymeningitis, or 
hsematoma of the spinal dura mater, is similar to, and commonly 
associated with, that which affects the cranial membrane, and will 
be afterwards described. In this, a reddish-brown exudation covers 
the surface of the membrane, and is composed of fibrin and extrava- 
sated blood ; the latter may be encysted in small cavities, or may be 
in various stages of transformation. The change commonly extends 
over a great part of the dura mater, and is apparently the result of 
haemorrhage into inflammatory tissue. 
The local form of syphilitic meningitis presents an irregular thick- 
ening of the pia mater and arachnoid, with the extensive production 
of new tissue in the affected region characteristic of this variety, so 
that it often resembles a diffuse growth as much as a chi’onic inflam- 
mation. The new tissue has a peculiar gluey aspect, and presents a 
tendency to caseous degeneration and fibroid change, so that scattered 
or coalescing cheesy spots are ultimately met with in tracts of mixed 
fibrous and gelatinous aspect, the later predominating in the more 284 
SPINAL MEMBRANES. 
recent parts. This process of growth may attain such a development 
at some spot as to constitute a distinct “gumma,” which may invade 
the substance of the cord, growing inwards from the pia mater. A 
similar process of cell-growth may be sometimes traced with the 
microscope into the substance of the cord, along the tracts of neuroglial 
tissue and peri-arterial spaces, when there is no invasion distinct to 
the naked eye.* A more limited affection of the walls of the 
arteries of the pia mater, extending into the cord, has also been 
thought to be syphilitic in nature ; the whole thickness of the wall of 
the arterioles may be the seat of inflammatory thickening, in conse- 
quence of which the calibre of the vessels is narrowed.f There is, 
however, some reason to think that a similar affection of the vessels 
may occur apart from syphilis.J 
In the very rare chronic tubercular meningitis the inner surface of 
the dura mater is covered with a layer or layers of tubercles, in various 
stages of development, mingled with inflammatory products. The 
arachnoid may also contain degenerating tubercles, and the two 
membranes may be united together by the new formation. The 
condition occurs independently of bone disease.§ 
Symptoms.—The symptoms of chronic internal meningitis, like 
those of the acute form, are due to the irritation of the membranes, 
to the damage to the nerve-roots, and to that of the cord. But the 
absence of acuteness in the process involves, as we have seen, a dif- 
ference which produces a contrast, rather than a resemblance, in the 
manifestations of the two diseases ; the spasm which dominates the 
aspect of acute meningitis is almost entirely abseut in the chronic 
form. When this is eliminated, similar disturbances of function 
remain, but their relative subordination renders the similarity in the 
features of the two maladies unobtrusive. Still, the three pathological 
elements just mentioned occur in the chronic as well as in the acute 
form, and in different cases one or another of the corresponding 
sets of symptoms predominate. Hence the varieties, while possess- 
ing many characters in common, may differ considerably in their 
clinical aspect. In some cases, we can infer with accuracy the 
special seat of the disease, but in many others we cannot carry our 
diagnosis beyond the conclusion that chronic internal meningitis 
exists, and are unable to say, even with probability, which membrane 
is primarily affected. 
The common symptoms are these : Pain in the back, increased by 
movement, sometimes, however, amounting only to heavy dull dis- 
comfort, and accompanied by some stiffness of the back, and, when in 
the cervical region, by some retraction of the head. The pain is 
increased by pressure on the vertebral spines, and its increase by 
* Gilbert and Liou, ‘Arch. Gen.,’ 1889. 
f Schmaus, ‘ Deut. Arch. f. kl. Med.,’ 1889. 
X Hochhaus, ‘Thesis,’ Kiel, 1S89. 
§ Weiss, ‘ Wiener med. Wochenseh.,’ 1885. INTERNAL MENINGITIS. 
285 
movement may cause a fixation of mobile parts, as tbe neck, in some 
abnormal position. The pain is apparently due to the irritation of 
the meningeal nerves, and the rigidity is to be regarded as a reflex 
effect of this irritation. But these are not the paroxysms of spasm, 
so conspicuous and so distressing in the acute form. 
More obtrusive, in most cases, are the radiating or excentric pains 
due to tbe irritation of the nerve-roots, and referred to the region in 
which the nerves are distributed, back of the head, neck, arms, 
thorax, abdomen, loins, or legs, according to the position of the disease- 
These pains are often very severe, sharp, darting, burning, or rheu- 
matoid in character, paroxysmal in occurrence, and sometimes worse 
at night. They may be accompanied by a painful sense of constriction, 
and by various unpleasant sensations—numbness, tingling, formica- 
tion, in tbe same areas. Hypersesthesia may also exist, so that pain, 
sometimes thrilling in character, is produced by touehipg the skin, or 
by slight degrees of heat or cold, and a hot or cold sponge passed along 
the skin of the back may reveal the chief seat of the disease by the 
change of sensation at its level, as in the acute form. The liyperaes- 
thesia may be more marked to one form of sensation than to another. 
Cutaneous eruptions, such as result from other nerve-lesions, have also 
been observed in association with the pains. In the same regions, 
muscular twitching, tremor, or even spasm, may result from the irrita- 
tion of the motor root-fibres. These symptoms correspond in their 
level to the part of the membranes chiefly diseased. When the 
lumbar membranes are affected, the radiating pains are felt in the 
legs; but when the disease is higher up, the legs may merely feel 
heavy, and be the seat of slight abnormal sensations. 
After a time, weeks or months, the pains persisting or ceasing, 
certain paralytic symptoms manifest themselves in the regions in 
which the severe pains were felt, and are dependent on further damage 
to the nerve-roots. Sensation becomes lessened, or even lost, in 
certain areas, to touch, or pain, or both. The muscles in the same 
region become weak, and waste; usually with the reaction of degene- 
ration for a time, and ultimate loss of all irritability. The wasting 
often affects the muscles irregularly, from the unequal damage to the 
roots and the fibres of single roots : entire groups sometimes atrophy 
from the complete interruption of the roots of one or more segments. 
Beflex action in these parts is lost. In the trunk this loss of reflex 
action, with ansesthesia, may be the chief local symptom, and is of 
much diagnostic importance. As the disease progresses, the cord 
itself suffers, by compression, or by extension to it of the inflamma- 
tion. The parts below the seat of the disease then become paralysed, 
the legs are weak and the seat of dull heavy pain ; reflex action in 
them may be increased, while their muscular nutrition continues 
good, unless the lumbar membranes are diseased, or the myelitis 
descends the cord. Defect of co-ordination in the legs is not 
uncommon, and is probably due to the implication of the fibres from 286 
SPINAL MEMBRANES. 
the muscles in the posterior columns and cerebellar tracts. Power 
over the sphincters may be lost and bedsores form, but chiefly in 
cases in Avhich the disease is severe over the lumbar region or cauda 
equina. 
When the inflammation affects chiefly the pia mater and arachnoid 
(ichronic leptomeningitis) the symptoms of meningeal irritation are 
conspicuous,—vertebral pain and rigidity of the back, with cutaneous 
hypersesthesia, and the radiating pains may also be considerable. 
These symptoms are especially marked in cases of subchronic menin- 
gitis, such as are sometimes due to alcoholism. The local paralytic 
symptoms—anaesthesia and muscular wasting—may be absent in these 
cases, or may only come on in slight degree after the other symptoms 
have lasted for a considerable time. On the other hand, weakness 
and pains in the legs, from affection of the cord itself, may be 
early symptoms. 
When the inflammation begins in the dura mater (internal pachy- 
meningitis) the symptoms of spinal irritation, pain and stiffness of 
the back, although occasionally present, are much less prominent 
symptoms than are those which depend on the irritation of, and 
damage to, the nerve-roots. The radiating pains are very severe, and 
are often the earliest symptom. At a later stage the muscular weak- 
ness, followed or accompanied by wasting, chiefly attracts attention, 
and the wasting may be so great that the disease is mistaken for 
progressive muscular atrophy. This is especially the case when the 
lesion is in the cervical region, the “ cervical hypertrophic pachy- 
meningitis ” of Charcot and Joffroy. In this affection, pains in the 
back of the head, neck, shoulders, and arms, often accompanied with 
a painful sense of constriction, precede the muscular atrophy. The 
wasting may involve many muscles, but usually those supplied by 
the radial nerve are less affected than the others; the escape of the 
long extensors of the wrist and fingers, while the flexors of the wrist 
and fingers and the interossei atrophy, leads to a peculiar deformity; 
the unopposed muscles cause persistent over-extension of the wrist; 
the phalangeal joints are flexed and the metacarpo-phalangeal joints 
are extended, but from the position of the wrist they are not over- 
extended, and the hand thus differs from the claw-like hand (p. 30). 
With this muscular wasting in the arms there is paraplegic weakness, 
from the pressure on the cord. In rare cases the disease affects the 
membranes over the lumbar enlargement or cauda equina, and then 
the legs are the seat of the pains, paralysis, and atrophy already 
described, and the sphincters are early paralysed. 
If the pachymeningitis is confined to the dorsal region, the root- 
symptoms are limited to the trunk. In such a case anaesthesia over 
the region supplied by the dorsal nerves was associated with para- 
plegia from compression of the cord. In another, areas of anaesthesia, 
with severe pains, existed over the legs, trunk, neck, and back of the 
head, without any indication of damage to the cord itself. These 287 
INTERNAL MENINGITIS. 
■examples illustrate the great variations presented by different cases, 
owing to the different distribution of the disease. An important 
characteristic of this form is the fact that it involves the membranes 
equally around the cord, and so gives rise to bilateral symptoms., 
Chronic syphilitic meningitis may cause symptoms resembling those 
of any other variety of chronic inflammation, even the hypertrophic 
pachymeningitis being sometimes due to this cause. But its most 
frequent and special characteristic is the focal character of the sym- 
ptoms, and their tendency to be associated with those of partial and 
local damage to the spinal cord itself. This is in consequence of the 
tendency of local tissue-formation to be associated with the inflamma- 
tion. Hence, pains of irregular distribution on one side are usually 
soon followed by impairment of sensibility, and often by weakness in 
the corresponding leg. 
In hsemorrhagic pachymeningitis the symptoms are those of a slight 
chronic inflammation, without any distinctive features that can be 
referred to the haemorrhagic infiltration. 
Diagnosis.—The diseases with which chronic internal meningitis 
is liable to be confounded, are different according as the symptoms of 
irritation, of damage to the cord, or of compression of the nerve-roots, 
predominate. By far the most important diagnostic symptoms are 
those that depend on the damage to the nerve-roots—their early irrita- 
tion and later structural damage. 
The spinal pain and stiffness may be mistaken for simple rachialgia 
or “ spinal irritation,” but in this condition the whole spine is tender, 
several separate points are much more tender than the rest, and there 
are not the radiating pains or paralytic symptoms of meningitis. 
Pain in the back is related in greater degree to posture and exertion, 
and it has a tendency to pass from the neck to the occiput. The 
patients have usually suffered from neuralgia in other situations, 
which may alternate with that in the back. 
Peripheral pains, especially about' the trunk and legs and shoulders, 
are prominent symptoms in some cases of muscular rheumatism or 
rheumatic neuralgia. In these, however, there are not the pain and 
tenderness of the spinal column; and although there may be apparent 
increased sensitiveness in the region of the pains, it is of the deeper 
structures and not of the skin, while the relation of the pain to move- 
ment and muscular action is a conspicuous feature. 
Radicular neuritis is probably associated in many cases with some 
affection of the adjacent membranes, but meningeal symptoms are 
altogether subordinate; the symptoms are confined to the region 
supplied by the nerve-roots, and spinal pain is absent. 
The muscular wasting may be mistaken for atrophy due to degene- 
ration or subacute inflammation of the anterior cornua of the cord 
(progressive muscular atrophy, subacute polio-myelitis). The cer- 
vical hypertrophic pachymeningitis bears special resemblance to 
this disease, since the wasting in the arms is often associated with 288 
Sl’INAL MEMBRANES. 
paraplegic symptoms in the legs. The distinction is that the atrophy, 
in the meningeal form, is preceded by severe pains, and often accom- 
panied by areas of hyperaesthesia or anesthesia, and is random in 
distribution. In chronic affections of the anterior cornua both pains 
and anesthesia are usually absent, and the wasting often affects the 
muscles in a certain order, which will be descriled in the account of 
the disease. Thus, in a man who was supposed to have cornual 
disease on account of wasting of some muscles of both legs, irregu- 
larly distributed, a history of severe sharp pains, and the discovery 
of a patch of anaesthesia on one leg, the presence of a burning pain 
round one side of the trunk, and the irregular distribution of the 
wasting, led to a diagnosis of chronic meningitis damaging the nerve- 
roots ; there was a history of syphilis, and appropriate treatment 
completely removed the symptoms. The pains also constitute a 
distinction from another affection which presents somewhat similar 
symptoms—syringomyelia. Chronic disseminated myelitis may cause 
muscular wasting, but does not cause the pain in tbe back, or the 
rigidity of the spine, which occur in meningitis, and the paralysis 
from damage to the cord is the leading symptom. It must be remem- 
bered that the two conditions of meningitis and myelitis are often 
combined, and the fact has to be recognised in our diagnosis. 
Some authorities believe that the symptoms of “ ataxic paraplegia,” 
which result from combined lateral and posterior sclerosis, are 
often produced by the agency of chronic meningitis, invading the 
peripheral layers of the cord. It is not probable, Jiowever, that this 
mechanism is operative in the cases in which considerable paraplegia 
shows that the lateral pyramidal tracts are extensively involved. 
The diagnostic problem is considered in the chapter on this disease. 
When the meningitis is lumbar, the pains in the legs may resemble 
some of those that occur in locomotor ataxy, and knee-jerk may be 
lost in each disease ; but the loss in meningitis is associated with 
muscular weakness and wasting, there is not the degree of ataxy 
common in tabes, and true “ lightning pains ” are not met with in 
meningitis. The greatest resemblance to chronic meningitis is pre- 
sented by some cases of tabes in which the cord disease reaches a 
greater degree in the dorsal than in the lumbar region. There are 
then pains and anaesthesia in the trunk, and the atrophy in the legs 
may be little marked. In meningitis, if the membranes over the 
lumbar enlargement are normal, the knee-jerk is preserved and often 
increased, while it is lost in tabes. The anaesthesia and loss of the 
trunk reflexes are more general and uniform in tabes than in menin- 
gitis. 
Caries of the spinal bones produces many of its symptoms by the 
agency of chronic meningitis, which always results from it. Hence 
the diagnosis depends on the recognition of the presence of the 
disease of the bone, in addition to that of the membranes. 
Multiple neuritis, in the paralytic variety, presents nerve-symptoms INTERNAL MENINGITIS. 
289 
of the same character as those of chronic meningitis, but the special 
symmetry and peculiar distribution of the atrophic palsy, the promi- 
nence of limb-tenderness, and the absence of cord symptoms, pre- 
clude such similarity as can cause actual confusion between the two 
diseases. 
Prognosis.—The differences between the forms of chronic menin- 
gitis, and between the degrees of the same forms, are so vast as to 
render the prognosis of the disease a matter of individual consideration 
in every case, to be estimated independently, from the pathological 
characters. The severe degrees of the affection are attended with 
danger to life, and even the slighter forms may entail serious conse- 
quences, since many effects of the disease, especially the damage to the 
spinal cord itself, tend to increase by the myelitic tendency which is 
set up. The neuralgic pains, which result from the damage to the 
nerve-roots, are extremely obstinate. But in many cases the symptoms 
ultimately pass away—the irritation ceases and the compressed 
structures slowly regain their function. The prognosis is most 
favorable in the cases which result from injury and from syphilis. 
But in all cases, even those of syphilitic origin, in which there is 
reason to infer considerable formation of new tissue, the prognosis 
must be cautious, since the cicatricial contraction of this tissue may 
perpetuate the damage to coi’d and nerves which its pressure has 
produced. The prognosis is better, in other cases, in proportion to 
the general health of the patient, to the moderate degree of the 
mischief, and to the extent to which its causes are under control. 
Treatment.—Best is essential; in severe cases it should be 
absolute, and in every case movements which increase pain should be 
avoided. The pain is the expression of irritation, which tends to 
maintain the morbid process. Measures, previously ineffective, will 
often be followed by improvement if rest is added. Posture is also 
of great importance. The prone couch, impracticable in acute 
meningitis, can often be employed in chronic cases with advantage, 
to lessen mechanical congestion of the spine. Warm baths and 
diaphoretic baths have been recommended as useful, especially in 
subacute cases. Next in importance to rest and posture is counter- 
irritation. Bepeated sinapisms or stimulating liniments may be used 
if mild counter-irritation only is required, but in most cases greater 
good will result from more energetic means, blisters, the thermic 
hammer, or the actual cautery. The last is especially recommended 
by Joffroy for the hypertrophic pachymeningitis. It is probable that 
posture favours the beneficial influence of counter-irritation in a very 
important degree. 
Sedatives are usually needed to relieve the pain—morphia, chloral, 
Indian hemp, injections of morphia or cocaine, or sedative liniments 
of chloroform, belladonna, &c. In employing sedatives it must be 
remembered that they will usually be needed, in chronic cases, for 
many months, and after a time, by the artificial need they create, they 
YOL. I. 290 
SPINAL MEMBRANES. 
may apparently keep up the pain. It is therefore well, if possible, 
to alternate two or more sedatives, to make cocaine take the place of 
morphia as much as possible, and to lessen the dose from time to 
time, tentatively, and without the knowledge of the patient. 
Iodide of potassium and mercury are the agents that have most 
influence over the morbid process itself. Both are effective in syphi- 
litic cases, but in other forms of the disease mercury has far more 
influence than iodide; it may be rubbed in over the spine, as 
recommended in the acute form. The ointment and oleate may be 
rendered counter-irritant, if necessary, by the addition of cantharides 
ointment. In many cases, tonics, as iron, quinine, and cod-liver oil, are 
needed. The muscular wasting which results from damage to the 
nerve-roots requires treatment by galvanism, rubbing, and by passive 
movement, to prevent contractures. If haemorrhagic pachymeningitis 
is suspected, ergotine may be used in addition to the measures suited 
for the ordinary form. Treatment appears, however, to exert little 
influence upon it. 
Other measures are the same as have been described for the acute 
form. 
HAEMORRHAGE INTO THE SPINAL MEMBRANES; 
HH3MATORACHIS. 
Spinal haemorrhage may he outside the dura mater, between it and 
the bones (extra-meningeal), or within the dura mater (intra- 
meningeal). In the latter situation the extravasation may be sub- 
dural, between the dura mater and arachnoid, or it may be sub- 
arachnoid, between this and the pia mater. Haemorrhage outside the 
dura mater is more common than within it. 
Causes.—Meningeal haemorrhage may occur at all ages. It is met 
with in newly-born children, but in them is due to rupture of vessels 
during birth, and the blood often merely descends into the spinal 
membranes from those of the brain. Spontaneous haemorrhage is 
unknown in early childhood, but occurs at all other ages, and is more 
common in men than in women. Of the immediate causes, injury is the 
most frequent, fractures of the spinal column, blows or falls on the back 
which do not fracture the vertebrae, and even falls on the feet or 
buttocks. It is occasionally found after death from severe convul- 
sions, epilepsy, puerperal eclampsia (in which an altered state of 
the blood may assist), chorea, strychnine poisoning, and tetanus. In 
some instances no symptoms were observed during life which could be 
referred to the haemorrhage, and it is probable that the extravasation 
occurred only during the last moments of life. Hence it seems 
likely that muscular spasm, resulting from a meningeal haemorrhage, HAEMORRHAGE. 
291 
may sometimes have been looked on as primary and independent—• 
the cause of the haemorrhage when it was really the effect thereof. 
This seems certain in many cases of tetanoid spasm in newly-born 
children—in most cases, indeed, in which such spasm occurs almost 
immediately after birth and is associated with meningeal haemorrhage. 
Such cases should be separated from those to which the term tetanus 
neonatorum is applied. They are further considered in the account of 
haemorrhage into the cerebral membranes in vol. ii. Severe and pro- 
longed muscular exertion has been, in a few cases, the apparent cause 
of spontaneous haemorrhage. It also occurs in some diseases in 
which there is a haemorrhagic tendency, such as purpuric states, and 
the haemorrhagic forms of some acute specific diseases, smallpox, 
yellow fever, &c., and very rarely in typhoid fever, apart from any 
haemorrhage elsewhere. In most of these cases its occurrence has not 
been suspected until the post-mortem examination revealed it, and 
it probably occurs generally during the last moments of life. A rare 
cause is the bursting of an aortic aneurism into the spinal canal, 
after erosion of the bodies of the vertebrae, the blood being effused 
outside the dura mater. Haemorrhage within the dura mater has 
also resulted from the rupture of an aneurism of a vertebral artery. 
Blood may descend into the spinal membranes from the cranium, in 
cases in which a cerebral extravasation, especially about the pons, 
escapes into the meninges ; this may occur in adults as well as in the 
meningeal haemorrhage that is produced during birth. Lastly, in 
cases of intense meningeal inflammation, ecchymoses, and sometimes 
considerable extravasations, have been found on both sides of the 
dura mater or in the pia mater. 
Pathological Anatomy.—Extra-dural haemorrhage comes from the 
plexus of large veins which lie between the dura mater and the bone. 
It is usually not of large extent, and the blood collects chiefly on the 
posterior aspect, where, in the recumbent posture, gravitation favours 
accumulation, and the space between the membrane and the bone is 
greater than in front. But sometimes the extravasation is very 
extensive, covering a large part of the dura mater, and in such cases 
it may extend through the intervertebral foramina, along the nerves. 
Haemorrhage is more common in the cervical region than elsewhere, 
but may occur in any part. The blood is usually coagulated, wholly 
or partially. The dura mater is blood-stained, sometimes even 
through to the inner surface. The spinal cord may be compressed, 
but the amount of blood is not often sufficient for this. 
It is easy to fall into grave error regarding the presence of meningeal 
haemorrhage; when a body has been lying on the back, the veins 
outside the dura mater become distended with blood, and this escapes 
when their walls are divided in opening the spinal canal. Care must 
be taken to avoid the error, on the one hand, of regarding the blood 
thus escaping as an ante-mortem extravasation, and, on the other, of 
overlooking a haemorrhage which actually exists. In all cases of 292 
SI’INAL MEMBRANES. 
acute spinal disease, in which a post-mortem examination is to be 
made, the body should at first lie face downwards. 
Intra-meningeal haemorrhage.—An extravasation into the sac of the 
dui-a mater (subdural haemorrhage) may be small in quantity, or may 
fill the whole cavity. When small it may pass from one part to 
another. In subarachnoid haemorrhage, the blood comes usually from 
the vessels of the pia mater ; it may surround the cord for an inch 
or two, or may fill the whole subarachnoid cavity. Such extensive 
effusions are rare, except when the blood descends into the arachnoid 
from the cerebral membranes. Blood effused into the spinal arachnoid 
has been known to ascend as high as the pons, and even to break 
through the valve of Vieussens and get into the cerebral ventricles.* 
Simultaneous cerebral and spinal haemorrhages have been known to 
occur from a common and powerful cause, as, for instance, in a case 
of puerperal eclampsia (Charrier). 
In meningeal haemorrhage, cerebral as well as spinal, the spinal fluid 
is often blood-stained, and thus spinal haemorrhage may be thought 
to be more considerable than it really is. The spinal cord is often 
discoloured and compressed, and is especially damaged when the 
haemorrhage is beneath the arachnoid. In extensive extra-meningeal 
haemorrhage, the subarachnoid fluid may be driven away from the 
compressed part, and may distend the arachnoid beyond the area of 
compression, the limit of which is thus marked. In cases which have 
lasted more than a few days there are usually signs of meningitis, set 
up by the irritation of the blood. 
Symptoms.—As already slated, slight meningeal haemorrhage is 
sometimes found post mortem in death from convulsive diseases when 
no symptoms of it were observed during life, and in these cases it is 
probable that the extravasation occurs during the lethal convulsions* 
In the cases in which haemorrhage causes symptoms, these are, for the 
most part, those of meningeal irritation, and thus bear some resem- 
blance to the symptoms of meningitis. They differ in the suddenness 
and violence of their onset, to which exceptions are extremely rare., 
These symptoms are nearly the same whether the haemorrhage is out- 
side or inside the dura mater. 
The first indication of the lesion is usually sudden and violent pain in 
the back, corresponding in position to the seat of the haemorrhage, but 
generally felt along a considerable extent of the back, and often severe 
in the loins. This pain in the back is usually accompanied by pain 
along the course of the nerves passing through the membrane near 
the extravasation, darting or burning pains, often of great intensity ; 
they are paroxysmal in character, and between the pains there may 
be various abnormal sensations, tingling, &c., referred to the same 
parts, and accompanied by hypermsthesia. Muscular spasm usually 
coincides with the pain, and involves partly the vertebral muscles, 
* As in an apparently conclusive case reported by Leprestre, ‘Arch. Gen. de 
Med.,’ xxii, p. 331. HAEMORRHAGE. 
293 
causing rigidity of tlie spine or actual opisthotonos, partly the muscles 
supplied by the nerves in which the pain is felt, partly the muscles 
supplied from the cord below the seat of the haemorrhage. The con- 
vulsive movements are sometimes general. Intense pain in the back 
and general convulsion have been known to be the only symptoms. 
Occasionally there is persistent contraction of muscles, and there is 
usually spasmodic retention of urine. These symptoms of irritation 
are no doubt due in part to the irritation of the membranes (causing 
the vertebral pain and reflex spasm), and partly to the irritation of the 
nerve-roots, motor and sensory. Paralytic symptoms quickly follow— 
weakness and lessened sensitiveness in the limbs below the lesion. In 
some cases there is, at last, complete loss of motion and sensation in 
the lower limbs, but such absolute paralysis is not common. Loss of 
power at the onset of the symptoms usually indicates either simul- 
taneous haemorrhage into the cord or the effusion of a very large 
amount of blood. It occurs, for instance, when an aneurism bursts 
into the spinal canal. 
The symptoms necessarily differ in situation according to the seat of 
the disease. When haemorrhage is in the cervical region (a frequent 
seat), the pains are felt in the neck and arms, and the rigidity may 
cause absolute immobility of the neck, while dysphagia, interference 
with respiration, and dilatation of the pupils may be added to the 
other paralytic symptoms. When it is in the dorsal region, intense 
pain encircles the chest or abdomen. If in the lumbar region, the pain 
is felt in the legs, and there are early paraplegic symptoms, with loss 
of reflex action in the legs, and the paralytic incontinence of urine and 
faeces described on p. 225. 
As a rule, in spinal haemorrhage, the cerebral functions are un- 
affected ; the unfortunate patient is conscious of all his sufferings 
from first to last. Occasionally, however, consciousness is lost for a 
short time, apparently from shock, and delirium or coma may come on, 
either as an indirect effect of the spinal lesion on the brain, or in con- 
sequence of a sudden increase in the intra-cranial pressure, due to the 
displacement upwards of the cerebro-spinal fluid. But in most cases 
in which cerebral symptoms coexist with those of spinal haemorrhage, 
the former have been due to simultaneous intra-cranial disease ; this is 
the case when the blood found in the spinal canal comes from within 
the skull, as in most cases of meningeal haemorrhage in newly-born 
•children (see vol. ii). In very rare cases the symptoms of spinal 
haemorrhage have come on insidiously, without pain, as in a case in 
which extensive haemorrhage outside the dura mater in the cervical 
and upper dorsal region, in a girl of fourteen, caused only very 
gradual weakness in the arms, and difficulty of breathing, from 
which she died at the end of a fortnight.* Such a case illustrates 
the almost universal law that there is hardly anycharacteristic ” 
symptom of a disease that is not sometimes absent, and that the 
* R. Jackson, ‘ Lancet,’ 1869, p. 5. 294 
SPIRAL MEMBRANES. 
absence of such symptoms has incomparable less significance than their 
presence. 
The symptoms of meningeal haemorrhage, in acute cases, usually 
reach their height in two or three hours, but sometimes not for a few 
days. Death may occur when the effects are fully developed; or, after 
the symptoms have reached their height, they may decline, to be 
renewed, a day or two later, by secondary meningitis. This is accom- 
panied by some pyrexia, and may cause death ; but if moderate, the 
symptoms of inflammation last a week or ten days, and then, in 
favorable cases, permanent improvement commences. 
The period of the disease at which death is most common is a few 
hours after the onset of the symptoms. It may be due to exhaustion, 
in consequence of the violence of the pain and spasm, but is more 
often caused by the interference with respiration that results from the 
conjoined effect of the palsy and spasm. 
Diagnosis.—In cases in which definite symptoms are produced, 
the diagnosis rests on the combination of sudden local pain in the 
back, with the other evidence of irritation of the membranes, nerve- 
roots, and cord, above enumerated. When the haemorrhage is of 
traumatic origin, the fact that the symptoms rapidly followed an 
injury facilitates the diagnosis. In the extremely rare cases in which 
the symptoms come on insidiously, without pain, the diagnosis of the 
exact nature of the disease is scarcely possible. 
In haemorrhage into the substance of the cord, vertebral pain is 
much more frequently absent than in meningeal haemorrhage, and 
when it occurs is less intense and does not spread. The symptoms of 
injury to the cord itself are prominent from the commencement; there 
is sudden paralysis, it may be at first partial, and rapidly increasing; 
even if there is some spinal pain at the onset, the loss of power is 
soon recognised, not being concealed either by the severity of the 
pain or by spasm. In meningeal haemorrhage, severe pain and 
symptoms of irritation usually precede considerable paralysis. In 
cases which i-ecover, the paralytic symptoms are more persistent when 
the haemorrhage is into the substance of the cord. But haemorrhage 
into the cord often breaks through into the membranes, and the sym- 
ptoms of both lesions are then combined. 
Meningitis is distinguished by the more gradual onset of the 
symptoms and by the presence of fever from the first; the fact that 
inflammation results from haemorrhage must be kept in mind. In 
myelitis, pain is commonly absent, and the symptoms of irritation are 
insignificant. The diagnosis from tetanus depends on the absence of 
trismus, on the presence of severe spinal pains, and on the sudden 
onset. In newly-born children the diagnosis is supposed to be diffi- 
cult, but during the first few hours or days the tetanoid symptoms 
which sometimes occur are the l'esult of meningeal haemorrhage and 
injury to the motor cortex. 
One case of spinal haemorrhage has been recorded in which the HEMORRHAGE. 
295 
symptoms very closely simulated those of strychnine poisoning. 
Violent paroxysms of muscular spasm, with intense general pain, but 
without spinal pain, followed by death in two hours, were apparently 
due to an extensive haemorrhage into the sac of the dura mater.* 
Analysis revealed no strychnia in the stomach. In such a case the 
diagnosis would have to be guided as much by circumstantial evidence 
as by the symptoms, and even the post-mortem discovery of haemor- 
rhage could only be received as evidence of the cause of the convulsion 
if no other were found. 
Prognosis.—In all severe cases, death in a few hours is to be 
feared. The prognosis only becomes less grave when the symptoms 
have distinctly reached their height, although there is still some danger 
until the period of secondary inflammation is over. Paralytic sym- 
ptoms often persist for some time, but even these, in the end, may 
pass away. At the onset, the prognosis must be governed by the 
rapidity with which the symptoms develop and by the seat of the 
disease. Haemorrhage in the cervical region is especially serious, 
because the mechanism for breathing is directly involved. 
Treatment.—The first point to secure is absolute rest. Even 
passive movement should be avoided. Posture is also of most urgent 
importance. It should be on the face or side, and not on the bach, so 
that the spine may not be the lowest part. The prone position for a 
few hours adds greatly to the chances of less damage. Venesection 
has been employed in strong individuals, with the object of arresting 
haemorrhage by rapidly lowering the blood-pressure. Leeches or wet 
cupping to the spine, or leeches to the anus, have also been recom- 
mended in cases in which venesection is unadvisable. It is probable 
that the local abstraction of blood does more in this than in most 
internal haemorrhages, on account of the communication between the 
venous plexuses and the veins in the retro-vertebral tissues ; and it 
is probable that the wisest treatment at the onset would be scarifica- 
tion beside the spine, opposite the seat of pain, the blood being 
allowed to flow freely. This may be followed by the application of 
ice and by the administration of ergotine by the skin or mouth. 
Afterwards the bowels should be freely opened. Sedatives a re usually 
required to relieve the pain. The stage of meningitis must be treated 
on the principles laid down for the management of the acute form of 
that disease. The l-esidual palsy requires treatment by electricity, &c., 
in the same manner as the consequences of meningitis. 
In extra-meningeal haemorrhage it seems justifiable to remove 
blood that is compressing the cord, by opening the canal and perhaps 
even washing out the canal with an astringent and antiseptic solution. 
Even when the blood is within the dura mater, the operation seems to 
deserve consideration if life is threatened. 
* Dixon, ‘ Lancet,’ 1879, p. 333. 296 
SPINAL CORD. 
DISEASES OF THE SPINAL COED. 
ANAEMIA AND HYPEREMIA OF THE SPINAL CORD. 
The condition of the vessels of the spinal cord after death, their 
fulness or emptiness, affords no indication whatever of their state 
during life. Inferences as to the ante-mortem state, drawn from the 
post-mortem condition, are altogether erroneous, with the rare excep- 
tion of local change, in which the vascular condition of one part 
differs from the rest. Practically, such local variation occurs only as 
part of a local lesion, as, for instance, in the hypersemia that attends 
inflammation, and the anaemia that results from pressure. Hence 
the occurrence of variations in the state of the vessels of the cord, 
and the effects that such variations may produce, are matters of 
inference from symptoms observed during life—symptoms that are, 
in themselves, open to various interpretations. Where the ground is 
barren of facts, theory is always luxuriant. Anaemia or congestion of 
the cord affoi’ds a ready explanation of symptoms the cause of which 
is unknown, and it is scarcely surprising, therefore, that such an 
explanation has been often given. But the extent to which the 
conditions have been invoked transcends any measure of justification, 
and surprise cannot but be felt at the absolute confidence and pre- 
cision of detail with which these states have been assumed to exist, 
when there has been no tittle of definite evidence. Positive asser- 
tions always receive some credence, however unwarranted the asser- 
tions may be, and positions incapable of proof are sometimes also 
incapable of disproof. It would be a futile and useless task to 
attempt to refute in detail the various statements that have been 
made regarding the influence of anaemia and hypersemia of the spinal 
cord. It will be sufficient to point out briefly what may be reasonably 
surmised regarding these morbid states. 
Permanent diminution in the blood-supply to considerable areas of 
the spinal cord must be a result of the general narrowing of the 
arteries that has been met with in some cases of chronic meningitis; 
but it is then associated with sti’uctural changes in the organ, the effects 
of which obscure any symptoms that can be ascribed to the anaemia. 
Nothing is practically known of the special consequences of this 
condition. The same statement may be made of the arrest of the 
blood-supply to limited areas, although it may safely be asserted that 
loss of function of the part must be a necessary consequence. This 
has been also demonstrated by experiment. Suddenly produced, 
anaemia at once abolishes function and quickly causes necrosis of the 
Anemia of tiie Coed. AN2EMIA. 
297 
nerve-elements—some of which, however, break up less rapidly than 
others, and retain, for a longer time, the power of resuming function 
if the blood-supply is restored. It is possible that such local arrest 
of the circulation is the initial process in some organic lesions of the 
cord, but the fact has still to be demonstrated. The question of the 
occurrence of embolism is referred to in a separate section. 
Transient diminution in the blood-siipply may conceivably be the 
result of imperfect embolism, but has not been proved to have this 
origin. It is sometimes supposed to be due to arterial spasm, 
dependent on the vaso-motor nerves. This has been assumed as an 
explanation of certain passing symptoms occasionally complained of, 
loss of power in the legs, and sensory disturbance, tingling, “pins 
and needles,” &c\, in the legs and arms. It may possibly also be 
the cause of the tetanoid cramp and tingling in the hands with which 
patients sometimes wake up during the night. The theory is tenable, 
but it is also conceivable that such symptoms are due to transient 
functional states of the nerve-cells of the cord. A functional 
derangement of these cells must be the immediate cause of the 
symptoms, whether such derangement is primary or is produced by 
spasm of the vessels. The opinion that the “nocturnal tetany ” (as 
it may be called) has the latter origin is supported by the fact that 
the occurrence of the symptom may be prevented by a small dose of 
digitalis, taken at bedtime. 
The curious symptom known as “ intermitting lameness ” (which 
would be better termed “ paroxysmal lameness ”) is supposed to 
depend on temporary diminution of the blood-supply consequent on 
arterial degeneration, but it is not known whether the seat of this is 
the spinal cord or the brain. The character of the symptom suggests 
the former, but its associations the latter, and it is not known that 
the arteries of the cord are ever the seat of atheroma in the cases in 
which this condition causes the cerebral symptom commonly associated 
with it, “ dyslexia,” a peculiar intermitting difficulty in reading which 
will be described in vol. ii. The lameness consists in a sudden 
weakness and stiffness of one leg, accompanied with tingling and 
blunting of sensibility, and of pain on an attempt to use it. The 
symptoms are increased by an effort to continue walking, and pass 
away after a rest of ten minutes or so, usually returning, on renewed 
exertion, again and again. The difficulty only occurs during exertion. 
It is familiar to veterinary surgeons as occurring in horses. The 
dyslexia with which it may be associated is of grave significance, as the 
cerebral cause seems always to have a strongly progressive character. 
In general anaemia, such as occurs in chlorosis and pernicious 
ansemia, the nutrition and function of all organs suffer, and the spinal 
cord shares the general state. The readiness with which fatigue of 
the legs is induced in such conditions may be due to the spinal cord 
as well as to the muscles. The legs often ache, and are sometimes 
the seat of various disordered sensations. It is probable that these 298 
SPINAL COED. 
are the result of the impaired nutrition of the nerve-elements, in con- 
sequence of which their functions are readily deranged. In some 
patients graver symptoms occur,—weakness of the legs, sometimes of 
the arms also, which may increase slowly to complete pai'alysis. 
Sensation and the sphincters are usually unaffected. The nature of 
these cases is uncertain. It is probable that many are cases of what 
is called hysterical paraplegia. Others may be due to organic changes 
induced by the anaemia. The well-established fact that optic neuritis 
may result from chlorosis is interesting as proof of the intensity of 
changes in nerve-structures which anaemia may excite. The cases of 
chlorotic paraplegia are very rare, and need further study. 
In the quantitative anaemia that results from loss of blood, besides 
the symptoms just described, paraplegia sometimes comes on, under 
conditions which exclude the idea of hysteria. The source of the 
haemorrhage has most frequently been the stomach, kidneys, and 
uterus. The paralysis is usually motor only, but Leyden has observed 
accompanying hyperaesthesia. It may come on a few hours or 
days after the loss of blood, or only at the end of one or two weeks. 
Most cases recover. The pathological process which causes the para- 
lysis is not known. The loss of power is comparable to the loss of 
sight which occurs from the same cause, and in which there may be 
no visible morbid change, or inflammation may be found, sometimes 
succeeding the loss of sight, and therefore to be regarded as a result 
of the derangement of the nerve-elements, or of the influence to which 
this is due, rather than the cause of the amaurosis. 
The treatment of the symptoms due to general anaemia is of course 
essentially the improvement of the blood-state. Symptoms which can 
be ascribed, with probability, to vaso-motor spasm may be pi’evented 
by drugs that cause a more uniform arterial tone, such as digitalis or 
belladonna, coupled with nux vomica or strychnia, to render the effect 
permanent. 
Hyperemia of the Spinal Cord. 
The conditions of the return of venous blood from the cord probably 
shield it effectually from the mechanical congestion from which 
almost every other organ of the body suffers when the movement of 
blood through the thorax is hindered. The chief mechanical conges- 
tion to which the cord is liable is that which results from the influence 
of gravitation, and occurs when a person is lying on the back. The 
distension of the veins outside the dura mater, and also of those of 
the pia mater, which occurs when the heart has ceased to act, and the 
blood is free to obey the only mechanical force which then acts upon 
it, sufficiently proves the power of gravitation to congest the cord. 
But it is not probable that gravitation has anything like the same 
influence during life, counteracted, as it then is, by many other forces. MYELITIS. 
299 
Some persons with imperfectly nourished cords (easily fatigued, 
liable to tingling, &c., in the legs) suffer from aching in the legs or 
spine when they lie on the back. Since this ceases when the pos- 
ture is changed, it is probably due to the mechanical congestion of the 
cord or membranes. It is doubtful whether any other symptoms can 
be, with confidence, assigned to mechanical congestion. 
Of active congestion our definite knowledge may be summed up in 
the statement that it occurs in the early stage of inflammation. We 
know nothing of it as an independent condition. Nevertheless many 
pages might be filled by the enumeration of the various symptoms of 
congestion of the spinal cord,—in which the unrestricted play of 
“ scientific ” fancy has elaborated a symptomatology for the separate 
congestion of every part of the spinal cord. Probably the only case 
in which we are warranted in suspecting a primary active congestion 
of the cord or membranes, is that in which symptoms identical with 
those of commencing myelitis, and following a cause of myelitis, pass 
away in the course of a few days. These cases will be mentioned in 
the account of inflammation of the cord. 
An active congestion, which may be called secondary, seems to 
result from prolonged and violent action of the nerve-elements of the 
spinal cord. Thus local dilatation and distension of vessels, migration 
of leucocytes into the sheath and into the adjacent tissue, and even 
small extravasations, are found in some cases of hydrophobia, of 
tetanus, and of strychnine poisoning, and it is probable that a 
similar congestion attends all violent physiological activity, violent 
and continued muscular exertion, coitus, &c. Coitus several times 
repeated has been known to cause haemorrhage within the cord which 
must be preceded by an intense congestion. Yascular dilatation, 
with an increased blood-supply, is the physiological attendant of 
functional activity in all organs, and doubtless also in the cord, but 
it is morbid only when excessive. It is doubtful whether it causes 
symptoms unless it goes on, as it probably may, to actual inflammation. 
INFLAMMATION OF THE SPINAL CORD j 
MYELITIS. 
Inflammation of the spinal cord is a, common lesion in the acute, 
snbacnte, and chronic forms. It usually causes a considerable 
diminution of consistence, and hence the term “ softening of the spinal 
cord” has been used as a synonvm for it. But the term is not 
accurate, because inflammation does not always cause softening, and 
a diminution of consistence may occur without inflammation. 300 
SPINAL CORD. 
The spinal cord differs from most other structures in that its powei 
of recovering functional capacity after damage by inflammation is 
comparatively small. The symptoms persist for a long time, and are 
not unfrequently permanent. Hence the distinction between acute 
and chronic inflammation is to be drawn, not from the whole course 
of the disease, but from the mode of onset. It is this which indicates 
the character of the morbid pi’ocess. Acute myelitis is that form in 
which the symptoms indicating inflammation of the cord come on 
rapidly and reach a considerable height in a short time, in less than 
two weeks. When the onset occupies from two to six weeks the 
inflammation is regarded as subacute. When a still longer time 
elapses before the symptoms reach a considerable degree of intensity 
the myelitis is termed chronic. There is, of course, no sharp distinc- 
tion between these classes. The subacute and acute forms may be 
conveniently described together. Other varieties are based on the 
distribution of the disease. The grey matter may be affected only or 
chiefly, polio-myelitis (from ttoX.ios, grey), a form that has distinctive 
characters which make its separate description desirable. When 
the whole thickness of the cord is affected in a small vertical extent 
the myelitis is said to be transverse. This is one of the most common 
forms. When an extensive area of the cord is continuously inflamed the 
myelitis is said to be diffuse; when one small area is affected the 
inflammation is called focal; when there are many foci contiguous 
or distant the myelitis is said to be disseminated. Inflammation 
of the grey matter, around the central canal, extending into the 
intermediate grey substance and to a less extent into the cornua, has 
been termed central myelitis. A further important distinction is that 
between parenchymatous myelitis, an acute affection beginning in the 
nerve-elements, and the interstitial form, which begins either in all 
the elements or in the connecting tissue, and in which vascular dis- 
turbance takes a prominent part. The latter is the common form of 
myelitis, whether transverse or disseminated, but the former is of 
importance on account of the limited class of symptoms to which it 
gives rise and of its special causal relations. This distinction is 
already familiar in regard to multiple inflammation in the nerves. 
Acute Myelitis. 
Etiology.—Remote causes.—Little is known of tlie influence of 
hereditary predisposition, but myelitis is sometimes met with in 
members of families in which other evidence of a neuropathic 
tendency can be traced. Males suffer more frequently than females. 
It may occur at all ages, but the form which occurs in young children 
is usually confined to the anterior cornua; other forms of myelitis 
are most common between ten and forty years. 
Immediate causes.—Myelitis, acute and subacute, is readily pro- ACUTE MYELITIS. 
301 
duced "by injuries to the cord of all kinds,—lacerations, bruises, and 
punctured wounds. It also seems to follow simple concussion, but in 
many of these cases there have been minute foci of structural 
damage. The myelitis produced by concussion is often, however, far 
more extensive than the primary lesion, for the latter may cause few 
symptoms, and a few days later a complete transverse myelitis may 
develop. Hmmorrhage into the cord, especially of traumatic origin, 
may have a similar effect; it may be followed after a short interval 
by extensive myelitis. In cases in which an interval of more than a 
few days elapses, pain in the spine may show that a morbid process 
is going on by which the myelitis is produced. Thus, in one case of 
acute myelitis, two weeks after a fall, there was continuous pain 
during the interval, corresponding to the seat of the later inflamma- 
tion. Concussion also sets up the subacute form of myelitis, and 
this is especially common after railway accidents (see Traumatic 
Lesions). 
Allied to injury as a cause is violent action of the muscles attached 
to the spinal column, which has sometimes appeared to be the sole 
agent in producing an acute inflammation in the adjacent part of the 
spinal cord. The disease has been known to follow a single violent 
contraction of the dorsal muscles, as, for instance, a successful 
but violent effort to prevent a fall. It is possible that there is an 
actual injury to the cord in these cases, but more probably inflam- 
mation is set up in the fibrous tissues of the vertebral column or 
nerve-roots and spreads to the cord. It is also possible that 
compression of the vessels may be concerned in the mechanism. In 
several cases the disease has resulted from attempts to lift heavy 
weights. Thus a man, two days after such an attempt, became 
rapidly paraplegic, and ultimately died; softening of the cord was 
found at the level of the fifth and sixth cervical vertebrae. Slow 
compression (q. v.) is constantly attended by inflammation in the 
compressed part; the myelitis thus set up may have an independent 
course, acute or subacute, and may not be proportioned to the 
pressure. In cancer of the vertebral bones, for instance, very slight 
pressure may cause an acute inflammation; there is probably some- 
times an extension of inflammation to the cord from the external 
disease, but such extension is not necessary for the occurrence of the 
myelitis; the inner surface of the dura mater is ojften normal. Acute 
myelitis also results from internal meningitis, in which some degree 
of invasion of the cord is almost invariable. 
Another exciting cause is exposure to cold, especially when the 
body is heated, lying on damp grass or on snow, bathing in cold 
water, &c. This cause has been supposed to act by suppression of the 
functions of the skin, since myelitis has been produced by varnishing 
the skin of animals,* but it is unlikely that this is the sole mechanism. 
* Feinberg, ‘ Virchow’s Arcliiv/ Bd. lix. In Vulpiau’s laboratory similar experi- 
ments failed. 302 
SPINAL CORD. 
Exposure of the back to cold sometimes seems especially effective. 
Myelitis has been produced experimentally in rabbits by freezing the 
skin of the back with ether spray (Eeinberg). It is probable that 
cold usually acts by the mechanism of a morbid blood-state, such as 
that which causes rheumatic fever, but which certainly varies greatly 
in its precise character and pathogenetic power. It is also certain 
that local exposure frequently causes inflammation in organs corre- 
sponding to the part of the surface that is especially chilled, although 
this influence may be chiefly to determine the incidence of the effect 
of the blood-state. In myelitis from cold, local exposure can seldom 
be traced, and the common mechanism is probably that of a blood- 
state. It is instructive to compare the analogous facts regarding the 
causation of multiple neuritis. Over-exertion is another powerful 
cause, and is especially effective when combined with insufficient 
food, and exposure to cold. 
The sudden suppression of the menses and of other habitual 
discharges has been supposed to cause the disease. In most in- 
stances of the kind there has also been exposure to cold, to which the 
suppression and the myelitis may both have been due, and it is 
impossible to say how far the former has been concerned in the 
process. Thus, a girl sat on wet grass during menstruation, which 
was immediately arrested, and myelitis followed, a day or two later. 
It is conceivable that the sudden arrest of the discharge may lead to 
a morbid state of the blood, or modify that which a chill alone is 
capable of producing, and that the derangement of the uterine func- 
tions may have a direct influence on the cord and dispose it to suffer. 
It is noteworthy that, in the case referred to, the inflammation was 
in the part of the cord to which the pelvic organs are related, the 
lumbar region. 
Functional over-action of the cord may cause inflammation in the 
part that is thus over-exerted. It has been already mentioned that 
long-continued stimulation of the sensory nerves may cause myelitis 
at the spot related to the nerves stimulated. As we have just seen, 
active function everywhere involves vascular dilatation, which, if 
excessive, amounts to active congestion, and, when prolonged, is 
attended by the escape of leucocytes that renders the condition one 
of inflammation. However excited, such a process has a tendency 
to independence of course, and to proceed beyond the degree corre- 
sponding to its cause. It is especially local functional over-action 
lhat has a tendency to cause myelitis. Thus the affection seems to 
be sometimes produced by sexual excesses. Occasionally, however, 
general over-action of the cord, as in severe, long-continued exer- 
tion, has been followed by the disease. In one case, it was due to 
lying to rest on damp ground, after an unusually long walk on a 
hot day. 
Toxic blood-states constitute a well-marked class of causes, and 
their influence is rendered the more distinct by the analogous causa- 303 
ACUTE MYELITIS- 
tion of multiple neuritis. They may be acute conditions due to some 
organised virus, perhaps allied to those that produce the acute specific 
diseases. Inflammation of the cord occasionally comes on in the 
course of, or after, typhus, typhoid, and especially variola and 
measles, as well as acute rheumatism and severe puerperal diseases. 
The onset may be during the acute disease, at any period after it 
has existed for about a third of its duration, or it may occur during 
convalescence, or a month or more after the disease is over. Whether 
syphilis is a cause of acute myelitis is a question on which opinions 
differ. Attacks of acute myelitis are not uncommon in syphilitic 
subjects, and it seems on the whole probable that there is a causal 
relation to syphilis, although it remains to be ascertained whether 
the mechanism is by disease of the vessels, such as is found in the pia 
mater in some cases,* or whether it is by the agency of a blood-state. 
The myelitis that occurs in acute specific diseases is probably due to 
tho virus of the primary disease, or to a product of it, and the 
fact that the inflammation is commonly disseminated suggests that 
some specific organisms have a tendency to fix themselves in the 
spinal cord and set up inflammation. In diphtheritic paralysis 
the cells of the cord may present changes that amount to a paren- 
chymatous myelitis. The fact that chronic changes in the cord may 
be a late effect of syphilis (as in tabes) makes it the more easy to 
conceive that acute processes should sometimes occur in an earlier 
stage of the disease. 
In another class of diseases, a special influence of the virus appears 
to be associated with the results of functional over-action. This 
effect is especially seen in hydrophobia. In some cases of this disease, 
foci of a somewhat diffuse myelitis of slight degree are conspicuous 
on microscopical examination. Still more intense myelitic changes 
are sometimes met with in the chorea of the dog, although, in other 
instances, the cord is normal. 
Chronic blood-states and constitutional conditions may also cause 
acute myelitis. Alcoholism is an occasional cause, and frequently 
produces the subacute form. The most potent agent of this class 
is gout. This is known to be a frequent cause of inflammation in 
various structures,—of the nerves among the rest; and cases of acute 
and subacute myelitis are met with, especially of the disseminated 
and relapsing forms, for which no other cause can be discovered. 
In one such case the patient had but lately recovered from a 
severe and prolonged attack of gouty inflammation of several intra- 
ocular structures. Like other chronic general causes, gout probably 
often acts as a predisponent when the malady is excited by some 
other cause. 
Irritation and inflammation of peripheral organs, as the uterus, 
bladder, kidneys, intestine, &c., has been supposed to be an occasional 
# Sudden paraplegia occurred in a case in which there was diffuse arteritis, sup- 
posed to be syphilitic (Schmaus, * Arch, f. kl. Med./ 1889). 304 
SPINAL CORD. 
cause, but tliis influence is exceedingly doubtful, except in tbe rare 
cases in which inflammation of a nerve ascends to the cord. In a 
considerable number of cases we are able to discover no cause to which 
myelitis can be ascribed. Many of these are probably due to a blood- 
state which may have no other consequences or may also cause 
simultaneous inflammation elsewhere. 
Pathological Anatomy.—In recent acute inflammation of the 
cord, the pia mater, at the affected part, is usually red and vascular, 
and the cord itself may be slightly swollen. Its tissue is reddened and 
often marbled from distended vessels, and the distinction between 
white and grey matter is indistinct and lost. 
The diminution of consistence which occurs in acute inflammation 
may be so great that the affected part is diffluent, like cream, and 
flows out when the pia mater is divided. It does not follow that the 
consistence is lessened to this degree during life; post-mortem soft- 
ening occurs more readily at an inflamed part. When the vascular 
disturbance and extravasation are considerable, the condition is termed 
“red softening;” so much blood may be effused into the tissue that 
the part looks as if there had been an actual haemorrhage, and in 
some cases an extensive extravasation does actually exist; this form 
is termed “ haemorrhagic myelitis.” If the inflammation has existed 
fur some time, the effused blood is altered in tint, and the colour of the 
softened part may be rather chocolate than red. After a longer 
time the changes in the blood-pigrnent cause the colour to be lighter, 
“yellow softening.” In many cases the breaking up of the nerve- 
elements (partly, as just stated, post mortem) is out of all proportion 
to the extravasation of blood, so that the softening is “ white.” It is 
said that red and yellow softening may ultimately become white from 
the removal of the blood-pigment, but the evidence of this is inade- 
quate. The period at which these changes of colour are found varies 
according to the amount of extravasation at tbe onset. At a later 
period the yellow or white opaque aspect is changed to a grey 
translucent appearance, from the absorption of the fatty products of 
degeneration, and an increase in the connective tissue. If the 
myelitis is very limited in extent, cavities may be formed within the 
cord. 
The microscopical appearances in myelitis vary much according tc 
the duration and form of the inflammation. In the fresh state the 
most conspicuous objects are the products of degeneration of the 
fibres, granules and masses of myelin, and granule corpuscles, with, 
in older cases, the peculiar bodies termed “ corpora amylacea ” 
(Fig. 93, d). With these are numerous red blood-discs, leucocyte- 
like corpuscles, and, after the first week, distinct cells, round, oval, 
spindle-shaped, or angular, with nuclei which resemble leucocytes in 
size, and are readily mistaken for them. Fragments of axis-cylinders 
may also be seen, granular in aspect, and with irregular swellings 
(Fig. 93,a). ACUTE MYELITIS. 
305 
Tbe softened and even diffluent state of the tissue prevents us from 
learning much, by microscopical examination, of the condition of the 
parts in which the inflammation 
is intense and diffuse, because 
the breaking up of the tissue 
and separation of the fragments 
renders it impossible to obtain 
sections of the hardened organ. 
It is only where the inflamma- 
tion is less intense, or less uni- 
formly diffused, that a thorough 
examination can be made. The 
products of degeneration are 
best seen in the fresh state or in 
sections mounted in glycerine 
(Fig 93). The fragments and 
globules of myelin in part occupy 
the position of the nerve-fibres 
from which they have come, 
in part are aggregated into 
masses. 
In sections rendered trans- 
parent in the ordinary way, 
the fatty products of the de- 
struction of the nerve-elements 
are invisible, and the most con- 
spicuous alterations are the dila- 
tation of vessels, which is often 
very great, and the accumulation of leucocytes and other cell- 
elements in the tissue and especially about the vessels. In the white 
substance the larger vessels are conspicuous by their enlargement, 
and in the grey substance the dilated arteries and capillaries may 
occupy a considerable part of the tissue (Figs. 94, 95, a). The nuclei 
of the capillaries are large and numerous. The walls of the smaller 
arteries are encrusted with leucocytes in the early stage, and, later 
on, in both white and grey substance, are much thickened by cells, 
the nuclei of which are often elongated and more or less concen- 
tric to the lumen of the vessel (Fig. 98, d). Outside this thickened 
wall the perivascular sheath is enormously distended, at first by leuco- 
cytes, among which, afterwards, other cells are mingled, round, 
fusiform, angular, with leucocyte-like nuclei (Fig. 98). In transverse 
section this distended sheath may look, at first sight, like an enormously- 
thickened wall. Fed blood-corpuscles distend the vessels and are seen 
also in the adjacent tissue, sometimes uniformly scattered through it 
(Fig. 98, f), sometimes aggregated in small extravasations due to the 
rupture of minute vessels. The grey substance is densely set with 
round corpuscles, staining deeply, many of which are the nuclei of 
Fig. 93.—Myelitis. a, an irregularly 
swollen axis-cylinder. b, section of 
nerve-fibre with swollen axis-cylinder. 
c, section of white substance, with 
granule-masses and atrophied nerve- 
fibres. d, corpora amylacea. (From 
Leyden.) 
VOL. I. 306 
SP1NAL CCmD. 
small fusiform or angular cells (Figs. 95, A; 97. b) wuiie the inter- 
vening substance is much more granular than in nealth. The nerve- 
cells are much swollen and granular, often contain distinct globules, 
strongly refracting, and probably fatty. The cell-processes appear 
shrivelled or lost (Fig. 95, a). In slight cases the margins of the 
cells may be less sharply defined than in health, and the bodies then 
may contain large vacuoles, sometimes wholly within the cells, some- 
Fig. 94.—Subacut ; myelitis, lumbar region; both white and grey sub- 
stance uniformly affected. In the latter the numerous distended vessels 
appear as lines; here and there a larger one is visible. 
Fig. 95.—Portions of the section shown in the last figure, more highly magnified 
A, from the left ant. cornu ; distended capillaries with numerous nuclei ; larger 
vessels with slight distension of perivascular sheaths; numerous round and stellate 
cells; ganglion-cells, swollen, with shrivelled processes. C, from front of post, 
column; scattered nerve-fibres separated by amorphous material in which small 
cells can be seen, round and irregular, some distinct, others indistinct, vessels 
with thickened walls. B, from near the posterior surface, shows similar changes 
but with more open spaces from which nerve-fibres have perished. (From sections 
prepared by Dr. Money.) ACUTE MYELITIS. 
307 
times partly within and partly outside them in an adjacent albuminous- 
looking substance.* In some cases, however, especially those of 
disseminated interstitial myelitis of moderate degree, the nerve-cells 
appear little changed in hardened and cleared specimens, although a 
granular condition can usually be seen in the recent state. 
In the white substance, cleared sections show a great increase and 
alteration in the interstitial tissue. The change may be uniformly 
distributed, or greatest in the neighbourhood of the vessels (Fig. 98, 
c). The increase is due in part to an amorphous material, contain- 
ing nuclei here and there, some of which belong to cells such as 
have been described in the grey substance; and these may constitute 
extensive tracts between the spaces where nerve-fibres once existed 
(Fig. 98). In older cases the tissue may have a fibrous aspect in 
places. The large cells, with many processes called “ spider cells,” 
or “ cells of Deiters,” are 
often conspicuous objects 
(Fig. 96). The processes 
extend between the nerve- 
fibres. We have seen (p. 165) 
that their existence in the 
normal cord has been doubted, 
but in the inflamed cord, in 
which they are enlarged, 
their presence is distinct. 
The changes in the nerve- 
fibres vary much. They 
always sutler destructive 
changes, but the products of 
their degeneration, above 
described, are scarcely to be 
seen in cleared specimens. 
The slightest change in the myelin appears to consist in an alteration 
in its chemical nature, in consequence of which it stains more readily 
than in health. Fibres are thus changed adjacent to any increase 
in the interstitial tissue, and they contrast with the unstained healthy 
fibres in the vicinity (Fig. 97, c). With or without this change in 
the myelin, there is an irregular swelling of the axis-cylinders, such 
as is seen on examination in the fresh state. If the fibres are divided 
transversely at the places where the axis-cylinder is swollen, this 
appears much larger than normal (Fig. 93, b). Examples of this 
will be found in most of the figures. These intense degenerative 
changes cause the breaking up of the myelin, and may involve the 
destruction of the fibre, the space occupied by it being left empty. 
Fig. 96.—Subacute disseminated myelitis ; 
part of the posterior column. Nerve-fibres 
separated by granular material and products 
of degeneration, and by numerous large 
spider cells. The myelitis in this case was 
attended by optic neuritis. (From a sec- 
tion lent by Dr. Dresclifeld.) 
* The significance of this vacuolation has been much discussed. It is probable 
that the vacuoles form after death, perhaps during the process of hardening, but 
that they do not form unless the cells have been altered by disease. They have thus 
some pathological significance. 308 
SPINAL CORD. 
In other cases, however, the axis-cylinder persists and remains sur- 
rounded by a narrow zone of myelin. Often a large number of such 
shrunken fibres may be found in a part which at first sight appeared 
devoid of fibres. This shrinking of the fibres occurs not only as the 
result of pressure on them by the connective-tissue elements, but also- 
where there is little interstitial change and no compression. 
Fid. 97.—Acute transverse myelitis, fatal in three weeks. Carmine 
preparations. A, section through most diseased part, at first lumbar 
segment. Foci of inflammation scattered through the whole area of this 
cord, most abundant in the posterior columns (the apparent enlargement 
of which is probably due to the direction of the section). Dilatation of 
the central canal. B, from the anterior cornu at A, b, a distended 
vessel; the tissue crammed with lymphoid and other cells,among which 
run normal nerve-fibres. C, from the posterior column, A,c. The areas 
staining deeply are seen to consist of thickened trabeculae, lymphoid cell-, 
amorphous tissue, and also of nerve-fibres, the white substance of which 
stains with carmine while that of the neighbouring healthy fibres does 
not.* 
* I am indebted to Dr. Dreschfeld for the section from which these drawings are 
**ade. The patient was a girl aged twenty-three; paralysis, motor and sensory, 
was complete at the end of two days j the application by her mother of hot bottles 
to the feet caused such extensive sloughing ulcers that amputation of one leg was 
deemed necessary three weeks after the onset, and the patient died the next day. ACUTE MYELITIS. 
309 
The relative amount of change in the nerve-elements and in the 
interstitial tissue varies very much. In some cases the interstitial 
changes are evidently primary, and the fibres at first present little 
change in slight cases, but afterwards are altered secondarily, being 
narrowed, and even destroyed, as they are surrounded and enclosed 
by the products of the inflammation. In other places, or even other 
parts of the same section, there is but little increase in the neuroglia, 
although the fibres have suffered extensively; empty spaces are limited 
by septa but little thicker than normal, although with more nuclei, 
and often with numerous granules, the nature of which is uncertain. 
Occasionally there is a more diffuse change in the white substance ; 
the neuroglial tissue is increased by small cells and amorphous 
material in such a manner that all appearance of septa and spaces is 
lost; a few nerve-fibres are included in it, and the spider cells are 
very conspicuous objects, their processes apparently representing the 
septa that exist in the normal condition (Fig. 96). 
The distribution of these changes is very variable. The whole 
thickness of the cord is uniformly affected in pressure myelitis (see 
“Compression of the Spinal Cord”). In transverse myelitis the 
changes may be so intense in all the structures at the affected level 
that the cord is diffluent, and, as already stated, only separated pro- 
ducts of degeneration and inflammation, and blood-corpuscles are to 
be seen. In slighter cases the alteration is seldom distributed uni- 
formly, and in either a single section, or a series of sections taken 
near together, each part may present variations in the damage, which 
may, however, be such that no part escapes in all (see Fig. 98). In 
meningo-myelitis the periphery of the cord is always most affected, 
and in old cases the thickened pia mater may send tracts of dense 
tissue into the interior of the cord, from which branching processes 
of tissue may pass on all sides. The condition is similar to that met 
with in chronic myelitis. A similar extension is often conspicuous 
in cases in which there is no special inflammation of the membranes, 
and the interstitial changes often extend from the septa that normally 
pass into the cord and from the walls of the vessels, the course of 
which may thus be marked out when the vessels cannot be seen. 
Hence the white columns may be broken up by lines of tissue passing 
from the surface of the cord towards the grey substance. 
In disseminated myelitis, the foci of inflammation may exist 
through a wide extent of the cord and appear on the surface as red- 
dish-grey areas, closely resembling those of disseminated sclerosis, 
but less sharply outlined. Under the microscope, in the early stage, 
smaller foci stud the grey and white substance irregularly, some- 
times extending into larger tracts. They may be most abundant in 
the grey or the white substance. At first the vascular changes are 
the more conspicuous, but afterwards the evidence of destruction of 
nerve-elements and the inflammatory products, exudative and cellular, 
described above, characterise these foci, while ultimately a condition 310 
SPINAL COLD. 
Fig. 98. ACUTE MYELITIS. 
311 
of irregular focal sclerosis remains. In central myelitis there is a 
great increase in the nuclei about the central canal, with vascular 
changes in the commissure adjacent, but there may also be evidence 
of slight widely-diffused myelitis. It is necessary to remember that 
the nuclei around the central tissue vary much in number, and that 
it is easy to mistake a normal for a diseased condition. 
Little is known of the morbid appearances in the parenchymatous 
forms, except that in a variety of anterior polio-myelitis, and in 
diphtheritic and other toxic paralyses, the nerve-cells present granular 
changes, and the interstitial grey substance may be but slightly 
affected. 
The nerve-roots coming from a much inflamed part are usually 
damaged, and may present histological changes similar to those 
within the cord, distension of vessels, increase of nuclei and of con- 
nective tissue about the vessels, breaking up of the myelin, swelling of 
the axis-cylinders. Degenerative and neuritic changes may descend 
the motor nerves, although rarely to the same degree as in polio- 
myelitis, except in the cases in which there is extensive inflammation 
in the lumbar or cervical enlargement. 
From the foci of inflammation, ascending and descending degenera- 
tions pass along the tracts of long fibres that have been already 
described, downwards in the pyramidal tracts, upwards in the poste- 
rior median columns, the direct cerebellar tracts, and the antero- 
lateral ascending tract. In cases of transverse myelitis, moreover, 
changes that are definitely inflammatory in nature may be traced 
in certain tracts for a short distance above or below the chief 
lesion; they may accompany the secondary degeneration, or may be 
found extending along a tract that degenerates in the opposite 
direction. Thus distinct inflammation may pass, for a short distance, 
up the pyramidal tracts, so that, an inch or two above the upper limit 
of the general inflammatory changes, an ascending inflammation of 
these tracts may be combined with an ascending degeneration of the 
tracts that always present secondary ascending degeneration. 
If the patient survives, the new interstitial tissue slowly undergoes 
Fio. 98.—Acute transverse myelitis; from a case fatal in a month. A, B, C, 
neighbouring sections from the inflamed part, in the mid-dorsal region, to show 
the varying distribution of the inflammation. (Stained with aniline blue black.) 
Distended vessels are all suri-ounded by thick zones of clear tissue, in places 
divided obliquely, while outside this, ramifying tracts of darker tissue extend into 
the white substance. In D, from the front of the posterior column, the changes 
are shown, more highly magnified. The zone around the vessels is seen to consist 
of the perivascular sheath distended by cellular elements, round, oval, fusiform, 
angular. The white substance is crammed with similar cells, and hardly any 
trace of nerve-fibres or of normal structure can be perceived. In E, from a less 
affected part of the lateral column, stained with carmine, the alveoli remain, 
although the tissue between them is thickened, and in many places studded with 
refracting granules and larger nuclei. In many spaces nerve-fibres are seen 
much smaller than normal in consequence of the wasting of the white substance. 
F represents a similar condition, with fewer nerve-fibres, and extensive infiltration 
of the alveoli with blood-corpuscles. (From sections prepared by Dr. Money, For 
the specimen I am indebted to Dr. Hadden.) 312 
SPINAL COED 
changes which give it a fibroid aspect, although for some time 
cell-forms may preponderate in it. We know very little of the nature 
of the process that occurs in the cases which slowly recover, and 
subserves restoration of function. The fact that a long period of total 
palsy may be succeeded by the slow return of considerable power, 
shows that even greatly damaged fibres may regain functional 
capacity. It is easy to conceive that the fibres which are only so far 
changed, that the axis-cylinders are swollen and the myelin stains 
readily, may speedily recover. We can also understand that the 
fibres in which a very narrow layer of myelin remains around the 
axis-cylinder, may also regain the power of conducting. We must 
presume that in these fibres there is no interruption of the axis- 
cylinders, but there are cases in which we can scarcely believe that 
the axis-cylinders retain their continuity, although conducting capacity 
is ultimately restored. An absolute motor palsy of twelve months’ 
duration must depend ou changes that involve an absolute inter- 
ruption of the fibres, and yet in such a case some return of power 
may occur. Is this effected by a growth of new fibres such as occurs 
in nerves? In the lower animals such a growth of fibres has been 
proved to occur; in man it has not yet been demonstrated, but it is 
difficult to conceive any other explanation of the clinical facts. The 
very interesting appearance presented by the section of a cord shown 
in Figs. 99, b, and 100 suggests strongly a process of regeneration. The 
cord was crushed in the mid-dorsal region by a fracture of the spine, 
and motor and sensory paralysis remained absolute, up to the level of 
the lesion, till the patient’s death, six months later. At the seventh 
cervical (Fig. 99, a) the cord presents only the usual ascending 
degenerations, but at the eighth cervical (Fig. 99, b) opaque tracts 
extend through the grey and Avhite matter, and adjacent to these 
there is everywhere an extensive destruction of nerve-fibres. In 
these tracts within the lateral columns a large number of very minute 
nerve-fibres can be seen, each consisting of a fine axis-cyliuder sur- 
rounded by myelin (Fig. 100, c). The fibres are smaller than any 
met with in the normal cord. The appearance is as if there had 
been an irregular ascending myelitis, which had extended up the 
cord as high as between the seventh and eighth cervical segments, 
and from the lower extremity of the normal fibres there had occurred 
a growth of new fibres such as effects the regeneration of nerves.* 
We seem to have here an actual process of renewal of fibres that had 
been destroyed by such inflammation as has caused the empty spaces 
in the vicinity. If this is a correct interpretation of the appearances, 
they constitute proof that, even in the human cord, it is possible to 
have a new formation of destroyed fibres. That pyramidal fibres may 
be renewed after they have been degenerated in consequence of pres- 
sure, there is abundant clinical evidence, since complete paralysis with 
* For these sections I am indebted to Dr. F. G. Penrose. Unfortunately I have 
been unable to obtain any other sections of this part of the cord. ACUTE MYELITIS. 
313 
Fig. 99.—Ascending myelitis from fracture of spine completely destroying the cord 
in the mid-dorsal region. A, from the seventh cervical, presents only ascending 
degenerations in post. med. col., direct cerebel. areas, and ant.-lat. ascending tract. 
B, from the eighth cervical, presents also numerous areas of finely granular aspect 
under a low magnifying power, the finer structure of which is shown in Fig. 100. 
Fig. 100.—From the outer part of the front of the lateral column in B, Fig. 99. a is 
the antero-lateral ascending tract, the fibres completely degenerated, except a few, 
probably of other nature and belonging to b, a narrow zone, nearly healthy, of the 
antero-lateral ground fibres, c represents the outer part of one of the finely 
granular tracts. Under the higher magnifying power these tracts are seen to con- 
sist of very minute nerve-fibres with a granular material between them in which 
few cell-forms can be distinguished. Adjacent to these tracts there has apparently 
been extensive destruction of the fibres, large spaces being occupied by products 
of degeneration and appearing empty in the cleared section. 
an intense spastic state of the limbs may be recovered from perfectly, 
even though it has lasted for many months. Such an event is 
common in cases of pressure-myelitis (q. v.), and a remarkable 314 
SPINAL CORD. 
instance will be mentioned in the account of tumours of the cord. 
But in such cases, although it is not likely that the axis-cylinders of 
the fibres have preserved their integrity, the neuroglial space, which 
represents the nerve-skeatk, has probably remained intact, aud the 
re-growth of a fibre within it is a far simpler thing than a new forma- 
tion of fibres in an area in which all the morphological framework 
has perished. 
Symptoms.—The symptoms of myelitis vary much according to its 
degree and form. The most common variety, which may be regarded 
as the typical form, is acute transverse myelitis, and to this especially 
the following description applies. The conspicuous symptoms are 
those which depend on the interference with the functions of the cord, 
and these, in most cases, are also the first indications of the disease. 
They are sometimes preceded, and more often accompanied, by general 
symptoms, such as attend inflammation of other internal organs— 
malaise, shivering, headache, depression, loss of appetite, pyrexia,— 
symptoms which may attend any form of acute myelitis, or may be 
altogether absent. When due to cold and commencing some days 
after exposure, general rheumatic pains may occur in the interval. 
The spinal symptoms, if not prominent at first, quickly become so. 
The most obtrusive is the motor weakness, but this may be preceded, 
for a few hours or days, by sensory symptoms in the limbs— 
“ numbness,” tingling, or burning sensations. Occasionally there 
are rheumatoid pains at the onset, sometimes referred chiefly to 
the joints. Pain may be felt in the back, as well as in the limbs, 
but the vertebral pain is seldom prominent, and soon ceases. 
Occasionally spasmodic twitchings in the limbs or painful cramps 
attend the onset. In rare cases there is a general convulsion. This 
is most frequent in children, and then may be sometimes the expres- 
sion of the general disturbance of the system. But convulsion 
occasionally attends the onset of acute myelitis in adults, even when 
there is no cerebral complication. Three instances of this have come 
under my own observation. 
The motor paralysis usually comes on rapidly, and reaches a con- 
siderable degree in the course of a few hours. A patient after such 
sensations as have been described, or without any warning, finds that 
his legs feel heavy ; after walking for a few hours he is obliged to sit 
down and rest. When he tries to walk again his legs feel “ as if made 
of lead.” He lies down for an hour, and then finds that he cannot 
stand, and in a few hours more is unable to raise his legs, although 
perhaps he can still move the feet or toes ; next day, even this power 
may be lost. Occasionally the mode of onset is still more rapid, and 
occupies only a few minutes. The legs are found suddenly to be 
heavy and tingling, the sufferer sits down on a chair for a quarter of 
an hour, and then finds that he cannot stand. Such rapid onset 
resembles that of spinal haemorrhage, and it is probable that in most 
of these cases there is haemorrhage in addition to inflammation— ACUTE MYELITIS. 
315 
“ haemorrhagic myelitis.” Such cases are, however, sufficiently rare 
not to interfere with the diagnostic rule that a sudden onset means a 
vascular lesion,* and that the characteristic onset of myelitis is rapid 
but not sudden. Now and then the onset is in the night, during 
sleep; a patient goes to bed well, and wakes up in the morning with 
complete paraplegia. On the other hand, the onset of the paralysis 
may occupy several days, or even a week ; when longer than this, 
from ten to forty days, the myelitis is to be regarded as subacute. 
Occasionally the onset is by a series of sudden attacks of weakness at 
intervals of a few hours or days, or even weeks. In the latter case 
there may be some recovery from one attack before the next comes on. 
Frequently, there is gradual partial loss of power for a few days, and 
then complete paralysis comes on rapidly; the first symptoms may 
be slight, and their nature only recognised when the disease has 
developed. 
Wheu the paralysis has reached its height, and has ceased to 
increase, it is usually complete; sometimes it is incomplete, the limbs 
can be moved, but with little power, or the patient may be able to 
contract certain muscles but not to move the parts to which they are 
attached, perhaps only to move the toes. The distribution of the 
paralysis depends on the position and extent of the disease. In the 
majority of cases, the legs and lower part of the trunk only are affected, 
because the dorsal region of the cord is the most frequent seat of 
myelitis. If it is incomplete in the legs, the flexor muscles usually 
suffer more than the extensors, although this may not be apparent as 
the patient lies in bed, because the leverage at the knee renders neces- 
sary considerable power to extend the joint against gravitation. When 
the disease is in the cervical region the arms as well as the legs are 
involved, and the arms are sometimes paralysed before the legs. If 
the lesion is extensive in the cervical region, the damage to the grey 
matter and root-fibres causes atrophic palsy in the arms, while the 
legs are the seat of simple and ultimately spastic paralysis. In such 
cases, the intercostals are paralysed and breathing is carried on by the 
diaphragm. Myelitis above this level, if complete, abolishes all 
respiratory power, and necessarily causes death with great rapidity; 
but occasionally, in partial inflammation, the diaphragm may escape, 
or the intercostals retain some power and life be preserved. In such 
rare cases the arms as well as the legs may be the seat of simple 
palsy, and the neck muscles may become atrophied. This was seen 
in one patient, in whom the sterno-mastoids and the upper part of 
each trapezius were wasted, while the arms as well as the legs 
presented an increase of myotatic irritability. In such cases dis- 
seminated inflammation may spread into the medulla, the pharynx 
and the tongue may be affected, vomiting may occur, and the heart’s 
action be interfered with. The range of motor symptoms, when the 
* Indeed, it is possible that these cases constitute no exception to the rule, the 
myelitis being set up by vascular obstruction. 316 
SPINAL COED. 
disease is at different heights, is indicated in the table of functions 
(p. 210). 
Sensation is frequently impaired as well as motion. At the onset, 
indeed, it is involved in some degree in all cases of general transverse 
myelitis. In severe cases it is absolutely lost up to the level of the 
lesion. The upper limit of loss is often oblique, being higher in front 
than behind. In slighter cases the loss may be partial, and only 
certain forms of sensation may be impaired, either in consequence of 
the position of the disease, when touch or pain may be lost alone, or 
of its slight degree, when touch is generally impaired and painful 
sensibility preserved. Occasionally there is general hypersesthesia in 
the limbs at the onset. At the level of the lesion, there is usually a 
zone of hypersesthesia, corresponding to the distribution of the nerves 
that pass through the upper part of the affected regiou, i. e. through 
the lowest, merely irritated, portion of the cord above the disease. 
The hypersesthesia may readily be detected by passing a hot sponge 
down the spine; the sense of warmth changes, at the hyperaesthetic 
zone, into one of pain. Corresponding to this zone of hyperaesthesia 
there is often a sense of painful constriction, a “ girdle pain,” which 
may persist for a long time, even after the loss of sensibility below 
the lesion has passed away. Occasionally it only comes on some time 
after the onset, probably from cicatricial compression and irritation of 
the root-fibres. Its position varies with that of the disease. It is 
most commonly felt between the umbilicus and ensiform cartilage, 
sometimes around the lower part of the abdomen, about the anus, or 
in the legs. It is of much practical importance because it is evidence 
of the existence of organic disease, and also of the upper limit of the 
lesion. It is sometimes a very early symptom. Any initial pain in 
the limbs usually ceases when sensation becomes abolished. When 
pain persists in the legs, it is often less when these are flexed. 
The state of reflex action varies, and depends on the position of the 
disease, in accordance with the laws already stated (p. 220). An 
acute lesion in any part of the cord may cause an initial, inhibitory 
loss of reflex action in the parts below, but if the lesion is above the 
lumbar enlargement, reflex action returns in the course of a few 
hours. Frequently there is no initial depression. Subsequently the 
reflex action becomes excessive, that from the skin rapidly, that from 
the muscles more slowly. Ultimately each attains a high degree of 
exaltation. If the disease involves the lumbar enlargement all forms 
of reflex action are lost.* When in the cervical regiou, it maybe lost 
in the arms, excessive in the legs. In dorsal myelitis the trunk- 
reflexes are often impaired, and may give important information as to 
the seat of the disease. The abdominal reflexes should be examined 
at various levels, and the greater impairment of these on one side 
than on the other may reveal clearly the unequal distribution of the 
lesion and its vertical extent. 
* See, however, the facts stated on p. 229. ACUTE MYELITIS. 
317 
The muscles of the legs are sometimes at first flabby and toneless 
during the stage of initial depression of reflex action, doubtless from 
the same influence. This condition soon passes off if the lesion is 
above the lumbar enlargement, and as reflex action returns, the 
muscles regain their tone. If, however, the myelitis involves the 
lumbar enlargement in considerable degree, the muscles of the legs 
remain flaccid, and lose all influence on the posture of the limbs. 
The feet fall into an extended position, so that the instep is in a line 
with the tibia (Fig. 101). The muscles also waste rapidly, and often 
Pia. 101—Posture of feet in myelitis of lumbar enlargement with rapid 
wasting of muscles. 
j>resent the reaction of degeneration. The wasting in these cases is 
often extreme. In many cases of myelitis above the lumbar enlarge- 
ment there is a slighter and slower wasting of the muscles, without 
loss of reflex action and generally with excess of the muscle-reflexes 
the ultimate amount of wasting may be considerable, but it is never 
so great as when the lumbar grey matter is diseased. There is never 
the reaction of degeneration, but only a slight change in irritability, 
similar to each current; first an increase, which, after some weeks or 
months, gives place to a slight diminution. 
The sphincters are usually affected from the first, except in very 
slight cases, and they often afford the earliest indication of the com- 
mencing lesion. There is usually first retention of urine, which not 
rarely exists for several hours, or even for a day or two, before other 
symptoms are added to it. There is afterwards incontinence, over- 
flow or reflex (see p. 225), when the disease is above the lumbar 
region ; if the lumbar centre is diseased there is persistent incon- 
tinence from the first without retention. In the former case there is 
involuntary action, in the latter inaction, of the sphincter ani, and in 
both cases incontinence of fseces. This may be inconspicuous in the 
early period, on account of constipation, due to intestinal paralysis. 
In cases of partial myelitis, as of the anterior cornua, the sphincters 
are often unaffected. The urine is frequently alkaline in reaction, 
and the change sometimes comes on so rapidly that it is evidently 
the result of an alteration in the secretion. In all cases of retention, 
decomposition in the bladder increases the alkalinity. Cystitis often 
follows, so that the urine contains pus. 
The temperature of the paralysed limbs is usually at first raised one 318 
SPINAL CORD. 
or two degrees above that of the mouth, but it afterwards falls, and 
remains a degree or so lower than that elsewhere. The skin is often 
dry, sometimes covered with sweat. Its nutrition often suffers, and 
bedsores result. In some cases they are due to long-continued pres- 
sure and neglect, but they may occur early and intensely when the 
disease affects the lumbar enlargement or irritation extends down to 
it from above. The least pressure on the skin may then cause a 
bulla containing sanious liquid, and sloughing occurs with readiness, 
especially over the sacrum. Now and then there is effusion into the 
knee-joints. Occasionally the tendency to sloughing of the skin is so 
intense that the lesions appear to be spontaneous. 
Such trophic disturbances sometimes occur in the cellular tissue of 
the lower part of the body, especially in the neighbourhood of the 
bladder and rectum. A remarkable example of such disturbance 
was presented by the case from which Figs. 94 and 95 are taken. 
Symptoms of subacute myelitis were followed by those of cellulitis in 
the lower part of the abdomen, on account of which the patient was 
admitted into "University College Hospital under the care of my col- 
league, Mr. Marcus Beck. Subcutaneous emphysema developed about 
the groins, and suppuration occurred near the rectum. In consequence 
of this inflammation the patient died, the cord symptoms having slowly 
increased ; after death no lesion of the intestine or local cause of the 
cellulitis could be discovered. It is probable that the derangement of 
the trophic influence of the cord facilitates the occurrence of cystitis 
from retention of urine, and intensifies its effect on the kidneys. 
Ulceration of the bladder, which sometimes occurs with remarkable 
rapidity, may be thus produced, or a small abscess may form in the 
wall of the bladder, and thus an opening may be formed into the 
peritoneal cavity and fatal peritonitis may be induced. A vesico- 
vaginal fistula may be developed in the same way. Ulceration of the 
urethra, and consequent extravasation of urine, have been observed 
under similar conditions.* In another case the inflammation of the 
bladder was intense, and suppurative cellulitis occurred outside the 
organ and set up a fatal peritonitis ; the kidneys were the seat of 
very acute suppurative inflammation.f These effects of cystitis may 
probably always be prevented. 
When the disease is in the cervical region the pupil may be affected. 
In rare cases of myelitis, optic neuritis has been observed, without 
any intra-cranial complication to cause it.J It is probably not the 
result of the inflammation of the spinal cord, but is an associated and 
similar lesion, the i-esult of the cause of the myelitis, which, in such 
cases, is probably a blood-state. It is noteworthy that most of the 
* S. West, ‘St. Barth. Hosp. Rep.,’ vol. x. 
f Sharkey and Lawford, ‘ Trans. Oplith. Soc.,’ 1883. 
X Optic neuritis was present in the case of disseminated myelitis under the care of 
Dr. Dreschfeld from which Fig. 96 is taken, and also in that of Sharkey and Lawford 
just mentioned. See ‘Medical Ophthalmoscopy,’ 3rd ed., p. 189. 319 
ACUTE MYELITIS. 
cases thus accompanied have been instances of disseminated myelitis, 
a form that suggests a cause acting widely on the nervous system. 
In one case*' the optic neuritis reached its height some weeks before 
the occurrence of the first spinal symptoms, and in the cord were two 
separate and distant foci of inflammation; in another, the neuritis was 
found a fortnight before the onset of disseminated myelitis.f 
In cases of rapid development the degree attained by the symptoms 
at their onset may not be exceeded. In some cases a slower increase 
or extension ensues in the course of a few days. The myelitis, begin- 
ning below, may ascend the cord, and the arms and respiratory mus- 
cles may gradually become involved. The upward extension may be 
steadily progressive, or it may occur in successive separate attacks. 
In the latter case, it seldom extends above the dorsal region. Or 
inflammation, beginning in the dorsal region, may slowly descend into 
the lumbar enlargement. The extension may be by the grey matter, 
especially of the anterior cornua, or by the posterior region. In 
each case the extension downwards is indicated by loss of the reflex 
action present in the earlier stage: in the one there is rapid muscular 
wasting with loss of faradic irritability ; in the other the muscles 
retain their nutrition and irritability, but sensation, if before present, 
becomes lost. 
The constitutional symptoms, which have been mentioned as attend- 
ing the onset, vary greatly in their severity and course. They are, as 
a rule, less in the simple transverse myelitis than in the disseminated 
form. In most cases they reach their height on the second or third 
day after the onset of severe symptoms. Thus in one case the tempe- 
rature was normal on the first day of indisposition, when the patient 
complained only of slight headache and slight numbness of the legs. 
During the next three days these gradually became completely para- 
lysed, and the temperature was successively 102°, 103°, and 104'5°, 
and then gradually fell to normal at the end of a week. In another 
case, in which the toxsemic state was part of that of measles, the tem- 
perature rose from 100° to 103'8° on the first day of the symptoms of 
myelitis, and on the next day to 104 2°, but fell (partly from antipyrin) 
on the third day, on which death occurred, to 100'2°.J In less acute 
cases, in which foci of inflammation develop progressively with 
spreading palsy, during one or two weeks, moderate irregular pyrexia, 
99° to 101°, may go on as long as the disease is increasing, and may be 
renewed at any subsequent relapse. The temperature is also raised 
by any complications, and especially by cystitis. On the other hand, 
in simple cases, with a single focus of inflammation, the initial eleva- 
tion may be trifling, and after the first day or two the temperature 
remains normal. 
If the patient survives, the course of the symptoms varies according 
• Sharkey and Lawford, op. cit. 
f Achard and Guinon,' Arch, de Med. Exp./ 1889. 
J Barlow, ‘ Med.-Chir. Trans./ 1887, p. 76. 320 
SPINAL CORD. 
to the intensity of the lesion. The paralysis, motor and sensory, may 
remain complete. More frequently sensation is recovered after a few 
weeks or months, while motor power continues absent for a much 
longer period. The excessive reflex action may lead to the gradual 
development of spasm in the legs. This is especially related to the 
increase of the muscle-reflex action which follows the secondary de- 
scending degeneration of the pyramidal fibres. Ultimately the condi- 
tion is that termed “ spastic paraplegia,” and described in detail in 
another section. The occurrence of this spasm is not incompatible 
with the recovery of some voluntary power. The muscles in these cases 
are often well nourished, and may even increase in size; the spasm 
constitutes a powerful stimulus to their growth. Spasm may, however, 
coexist with the slow moderate wasting described above (p. 223), but 
is rarely intense in these cases. 
In some cases, flexor spasm, after a time, takes the place of the 
extensor spasm, at first in transient attacks but at last permanently, 
and becomes fixed by contracture and shortening of the flexor 
muscles. It may be so great that the knees are against the abdo- 
men and the heels against the nates. This substitution of flexor for 
extensor spasm occurs chiefly in cases in which the paralysis is 
absolute, and the organic disease of the cord so considerable and of 
suck duration as to make recovery impossible. It is therefore a very 
grave sign. 
Death may occur early in the disease from respiratory paralysis, or 
from the extension of disseminated myelitis into the medulla oblon- 
gata ; subsequently it may be due to various effects of the trophic 
disturbance, acute or chronic, and to blood-states induced by bed- 
sores or by kidney disease resulting from cystitis, &c., mechanisms 
that have been already mentioned in the account of the symptoms. 
Improvement, when it occurs, is usually slow, but continues for a 
long time, and recovery may be complete in cases of moderate 
severity. When there is much damage to the cord, however, 
recovery is often impei’fect, and some weakness remains, accom- 
panied either by spasm or by wasting. It is rare for there to be no 
improvement, but occasionally the palsy remains absolute, although 
life is prolonged for years. In some cases improvement occurs, slight 
or considerable, and is followed by a relapse, which leaves the patient 
worse than the first attack; and this may occur again and again, each 
relapse being the expression of a fresh extension of the inflammation 
in the cord. This relapsing course is met with especially in the 
disseminated form, and in the subjects of gout, either acquired or 
inherited. Other cases, again, present what may be termed a re- 
current course, improvement, and perhaps a considerable degree of 
recovery, continuing for months, when a fresh attack occurs. On 
the other hand, in many cases, especially of simple transverse 
myelitis, when improvement is established it goes on, and there is no 
tendency to recurrence. ACUTE MYELITIS. 
321 
Varieties.—The different pathological forms of myelitis are attended 
by some differences in the symptoms. Those of transverse myelitis 
have been described as the most common and typical manifestations 
of the disease. Focal myelitis, in which there is a single spot of 
inflammation, not extending across the cord, may occur in various parts 
of the cord, but, on account of the slight degree of severity of the 
symptoms, little is known of them except when the focus of inflam- 
mation is of some size or is situated in one anterior cornu (as a 
variety of polio-myelitis), because such cases are rarely fatal. It is, 
however, probable that this variety is not uncommon. Cases are 
occasionally met with in which symptoms of very limited range come 
on acutely, and may reasonably be ascribed to such a lesion. They 
may be one-sided, and various in character, often being limited to a 
single limb. 
A much more frequent focal form is disseminated myelitis, in which 
there are several foci of inflammation in the same or different parts 
of the cord. The onset of this form is often subacute, and constitu- 
tional symptoms are frequently absent. The most important special 
symptoms are those which indicate interference with the central func- 
tions of the cor-d in more than one locality, but the combinations 
produced are very variable. In many cases, the several foci of in- 
flammation develop successively, not simultaneously, and then we have 
a corresponding succession of symptoms. Thus a myelitis in the 
cervical region, causing atrophy of some groups of muscles in one arm 
and paralysis of the corresponding leg, may be followed by paralysis 
of the other leg with such loss of reflex action in it as shows a 
separate focus of inflammation in the lumbar enlargement, and this 
again by the development of a girdle pain corresponding to the 
middle of the dorsal region, from a fresh area of inflammation in 
that situation. When numerous foci of myelitis occur in the dorsal 
region, as is not uncommon in syphilitic cases and after injury, the 
symptoms may closely resemble those of a transverse myelitis, because 
by one or another of these foci each of the elements of the cord is 
interrupted. The only distinction may be the extensive impairment 
of the trunk-reflexes, or the detection of loss of irritability in the 
corresponding muscles. 
In the rare form of diffuse central myelitis there is usually rapid 
loss of power, of sensation, and of reflex action, considerable elevation 
of temperature, speedy trophic disturbance, and often death at the 
end of two or three days. Rarely, sensation and reflex action have 
been lowered and not lost. On the other hand, the loss of sensation 
is said to be sometimes absolute, when motor palsy is incomplete. 
The symptoms have begun in arms and legs simultaneously, or in 
either of these, and have accordingly spread upwards or downwards. 
Practically nothing is yet known of any slight non-fatal forms of this 
variety. Haemorrhagic myelitis is scarcely a special form, since any 
acute inflammation of the cord may be attended by a sudden extrava- 
VOL. I. 322 
SPINAL CORD. 
sation of blood. Its manifestation is tbe sudden onset of severe 
symptoms after slighter disturbance such as indicates a commenciug 
myelitis. 
Parenchymatous myelitis is known only in a few forms, and we have 
much yet to learn regarding it. In diphtheritic paralysis there is an 
acute degenerative change in the nerve-elements, especially in the 
nerve-cells, which must be regarded as essentially a lesion of this 
form. In some cases of polio-myelitis the motor nerve-cells suffer 
primarily, and the interstitial tissue is not affected except in the 
severer cases of this form. In all inflammations, whether parenchy- 
matous or interstitial in nature, all the tissues of an organ tend to 
be involved if the process is acute. Other symptoms that are of im- 
portance, as suggesting this variety, are those of acute ataxy, clearly 
dependent on an affection of the cord, occasionally met with. Thus 
a married woman, who was certainly the subject of syphilis, and 
had presented secondary symptoms a year previously, found one 
day that she could not walk so well as usual, and the next morning 
could not stand, on account of extreme inco-ordination in the legs. 
When she tried to use them, the resemblance to the extreme degree 
of locomo’or ataxy was perfect. The knee-jerk was normal on the 
right side, almost lost on the left. The left leg was thought to be a 
little weak, but in a day or two its power was good. For the first 
few days there was great hyperaesthesia of the lower part of the 
trunk and legs, but at the end of a week this was reduced to a band 
at the level of the lower half of the abdomen, where even a touch 
occasioned pain; subsequently a girdle pain developed in this region. 
Her condition lasted unchanged for two months, and then, iodide and 
belladonna being given, slowly improved, but it was not until four 
months after the onset that she could walk a little, and then only in 
a highly ataxic manner. Her recovery was ultimately perfect. 
In another group of cases, of which I have seen several instances, 
inco-ordination comeson acutely in one arm, and may be accompanied 
by complete muscular anaesthesia, so that the power of estimating 
weights is absolutely lost, a poker and feather seeming alike, although 
cutaneous sensibility is perfect. The condition has reached its height 
in the course of a few hours, remained complete for weeks, and slowly 
passed away, in the cases I have seen. The precise nature is uncertain, 
but provisionally it seems best to class them together as cases of acute 
myelitic ataxy. Their dependence on an organic spinal lesion seems 
certain, and the onset of this is incompatible with any other than an 
inflammatory process. It is possible that some of these cases are due 
to a focus of ordinary inflammation, so situated as to affect structures 
of a common function, while others may be parenchymatous. 
Pathology.—Very little is known of the pathology of acute 
myelitis, that is, of the actual mechanism by which it is produced, 
of the nature of the causes to which it is due, and of the relation 
of the morbid process to its causes. The spinal cord differs from ACUTE MYELITIS. 
323 
most organs in its great liability to primary inflammation, in wliicb 
it presents a remarkable contrast to the brain. The liability is not 
equally distributed in the cord, but is least in the parts nearer the 
brain, less in the cervical than the lumbar enlargement, and less in 
these than in the dorsal region, so far as the most common form is 
concerned. The special liability of the dorsal region to transverse 
myelitis may be associated with the readiness with which this part 
undergoes post-mortem softening, but we are ignorant of the condi- 
tions by which this liability is determined. The disseminated form 
has less tendency to be localised in any special part. A question of 
considerable interest is whether acute inflammation of the cord 
always begins as such, or whether, in any case or form, it is set up 
by vascular obstruction, such as thrombosis in a minute vessel. It 
is conceivable that such an initial lesion may ultimately disappear 
in the intense inflammation it excites. Myelitis may be readily 
produced by the arrest of the blood-supply even for a short time, as 
numerous experimenters have shown, but their researches throw little 
light on the disease as it occurs in man ; the effect is to produce first 
necrotic breaking up of the nerve-elements, and long after this the 
vascular lesions of ordinary interstitial myelitis. The processes are 
essentially different. But the experiments show that the lumbar 
enlargement is thus damaged with special readiness, and this suggests 
that the proclivity to disease of this part is due to its inherent sus- 
ceptibility. 
At present the questions of chief interest are the extent to which 
the disease is due to a morbid blood-state, the probable nature of such 
a cause, and the mechanism by which it acts. The chief facts that 
throw light on the subject have been mentioned already, the most 
important being the occurrence of myelitis in the acute specific 
diseases (in which we must ascribe it to the organised virus of the 
primary malady), and the evidence of an influence acting throughout 
the system, afforded by the wide extent of the disseminated form 
and its occasional association with disease elsewhere, such as optic 
neuritis. It is to this form that our knowledge chiefly relates. Of 
the pathology of simple transverse myelitis we have only the fact 
that it is often due to cold, which brings it into closer analogy with 
the simple inflammations of other organs. 
The knowledge that has been gained of the influence of toxic 
blood-states on the peripheral nerves gives us the help of analogy 
in conceiving that myelitis may often have the same origin. But a 
difference exists in the fact that the multiple neuritis so produced 
is commonly parenchymatous, while the myelitis is conspicuously 
interstitial. Of the pathology of parenchymatous myelitis we know 
almost nothing. The question of causation will be again alluded to 
in considering the special inflammation of the grey matter. 
The chief relation of the symptoms to the lesion has been con- 
sidered in the general account of the symptoms of spinal cord disease, 324 
SPINAL CORD. 
and those relating to the destructive and regenerating processes have- 
been mentioned in the section on pathological anatomy. We may, 
however, further note that the vascular changes, which take so large 
a share in the process of interstitial inflammation, as seen, for 
instance, in the disseminated form, must extend the process. The 
escape of leucocytes into the sheaths tends to interfere with the 
lumen of the vessel and the flow through it, while their accumula- 
tion in the tissue must entail local destruction of the nerve-elements. 
If the cause of the myelitis is a persistent influence, such as the 
poison of a progressing specific disease, or the agent, whatever it 
be, that is effective in gout, it is easy to understand that the local in- 
fluence of the lesion itself will co-operate with that of its cause, and 
induce the progressive tendency that is a characteristic of this form. 
Diagnosis.—Myelitis is recognised by the rapid onset of symptoms 
indicating structural disease of the cord. Among these the failure of 
power is the most significant, although the subjective sensations that 
accompany it are often more obtrusive at the onset, and prevent 
mistake as to the meaning of the weakness. When they are absent 
the eufeeblement may be mistaken for mere prostration in cases in 
which some general illness coincides, and it is probable that slight 
myelitis sometimes occurs during an acute specific disease and alto- 
gether escapes detection. But among the early symptoms no one is 
more important, for its definite significance, than retention of urine; 
and its importance is increased by the fact that it may precede all 
symptoms in the legs and give a warning, the heed of which might 
sometimes enable lasting palsy to be prevented or life itself preserved. 
The diagnosis may be aided by the presence of such general sym- 
ptoms as attend the occurrence of inflammation in other organs, but 
the absence of these is of little negative significance, while the 
presence of constitutional disturbance is as likely to mislead, as it is to 
suggest a local affection. The position of the myelitis must be 
inferred from the considerations already described. Its upper limit 
is indicated by the upper limit of the paralysis; that of sensation is 
most readily defined, and usually corresponds to that of motion. But 
the upper limit uo more shows the extent of the disease below it, than 
the surface of water does its depth. The extent downwards must 
be gauged by the impairment of the functions of the cord as a 
central organ (reflex action and muscular excitability) in the parts 
paralysed, while the degree to which the various structures of the 
cord are damaged must be inferred from the character and degree 
of the symptoms in the affected parts. In ascertaining the state of 
the lower dorsal region the trunk and cremasteric reflexes are espe- 
cially important. 
Thus if called to a patient who has rapidly become paraplegic, the 
practitioner should first note the degree of motor aud sensory para- 
lysis of the legs (indicating whether the lesion is total or partial),, 
and how high up the trunk the symptoms extend. He should then ACUTE MYELITIS. 
325 
test the reflex action in the affected limbs and trunk, and ascertain 
the state of myotatic irritability in the limbs. These indicate the 
condition of the reflex arcs in the lower portion of the cord. Further 
information on this point is afforded by the state of muscular nutri- 
tion, and especially by the evidence of the state of nutrition of the 
nerve-fibres which is revealed by faradism. If reflex action is per- 
fect and the muscles have preserved their tone, this examination is a 
matter rather of scientific interest than of practical importance. It is 
useless to apply this test until five or seven days after the onset, 
because four or five days, and often eight or ten, elapse before the 
degenerative changes occur in the nerve-fibres. The examination may 
then be made without any risk, provided a very gentle current is 
employed, just sufficient to cause a contraction in the corresponding 
muscles of a healthy limb, and the current need not be applied to 
each spot for more than a second. The isolated faradic shock may 
be employed with advantage on account of the absence of the strong 
sensory stimulation that is caused by the current (see “ Atrophic Para- 
lysis”). If no change is found, the examination may be repeated at 
the end of ten days from the onset. If no muscles, at the end of that 
time, present any considerable diminution of contractility, it shows 
that no considerable nutritive change is taking place in the nerves, 
and that the grey matter from which the nerves proceed is not 
inflamed. On the other hand, if certain muscles present a diminu- 
tion of irritability, others being normal, there is a focal lesion in the 
corresponding grey matter. If all the muscles of both legs present 
such a failure there is inflammation of the lumbar grey matter, 
and if sensation is also lost, a total lumbar myelitis. So, if there is 
cervical myelitis with paralysis of all four limbs, the condition of 
irritability of the arm muscles shows whether the disease involves, or 
is above, the grey matter in the lower half of the cervical enlarge- 
ment. If there is impairment of irritability, its extent in the two 
arms will afford an indication as to whether the myelitis is total, or 
whether it affects chiefly certain spots. The distinction from simple 
polio-myelitis depends on the fact that the symptoms are not purely 
motor. It is only when the myelitis is cervical or lumbar that the 
diagnosis is a matter of difficulty; in these cases the arms and legs 
are the seat of atrophic paralysis in ordinary myelitis, because the 
grey matter is involved. There is, indeed, polio-myelitis in such cases, 
but there is also more, and the impairment of sensation, together with 
the simple palsy of the legs when the disease is in the cervical region, 
shows the involvement of other parts than the anterior cornua,—which 
is the essential distinction. The most equivocal condition is that 
which exists when simple but severe polio-myelitis in the cervical 
region spreads to the white columns immediately contiguous, and 
causes weakness of the legs. But it never causes complete loss of 
power, even for a short time, and the legs soon recover, whereas in 
ordinary cervical myelitis the loss of power in the legs is often com- 326 
SPINAL CORD. 
plete and prolonged, and is accompanied by impairment of sensation, 
not met with in polio-myelitis. 
The distinction of the other varieties of myelitis rests on the 
special features already described. That of the disseminated form 
rests on the irregular distribution of the symptoms and the evidence 
of damage extending through a considerable vertical extent of the 
cord, but in some parts incomplete in degree. An inflammation 
which continues to extend after the first two or three days is certainly 
disseminated, and most subacute cases are of this variety, and so are 
those that are secondary to blood-states. The distinction is impor- 
tant, because this form is far more grave than any other, and more 
likely to cause death. It is doubtful whether central myelitis can be 
diagnosed during life; there is usually a slighter degree of myelitis 
in the other elements which causes symptoms resembling the ordinary 
form. There is, however, one exception to the rule that a spreading 
myelitis is disseminated; the diffuse transverse form that is secon- 
dary to some other morbid processes, either to compression from 
without, or to haemorrhage within the cord, often undergoes sub- 
sequent extension. Acute myelitis in syphilitic subjects, even if due 
to syphilis, presents no distinguishing features, nor is its course influ- 
enced by antisyphilitic treatment. But the latter fact is true of 
all acute syphilitic inflammations—the tissue destroyed by the process 
cannot be restored by the removal of the cause. In rare cases, how- 
ever, an acute parenchymatous myelitis in a syphilitic subject is 
suggested by the limited impairment of a certain function. In such 
cases, and in others in which the symptoms point to a toxic blood- 
state acting on the nerve-elements without destruction of tissue, the 
effect of treatment seems to confirm the diagnosis. 
If transverse myelitis has been diagnosed, the question should 
always be asked, Is it primary, or secondary to some other process, 
of which the most common is compression of the cord ? We have 
seen that myelitis may result, even in acute form, from external 
pressure, which may be that of a growth or of disease of the bone. 
The indications are, first, the fact that root-pains at the level of the 
disease preceded the myelitis for at least some weeks ; and secondly, 
the direct evidence of a disease, as caries or cancer of the spine, 
to which the inflammation may be secondary. The spinal column 
should be carefully examined in all cases, not merely once, but again 
and again. When the myelitis is developed there may be no signs of 
bone disease, and yet these may appear in the course of a few weeks 
or months. Myelitis in a cancerous patient should always suggest a 
secondary growth in the spine. A woman, shortly after the removal 
of a cancer from the breast, became paraplegic; no evidence of bone 
disease could at first be found, but in a few weeks the vertebral 
column became distinctly enlarged from secondary cancer. This 
element in diagnosis has become of great importance from the 
certainty that some simple external growths can be removed. 327 
The diagnosis from other lesions of the cord is chiefly by the mode 
of onset. In haemorrhage the symptoms develop in a few minutes, and 
it is chiefly in the cases of haemorrhagic myelitis that any diagnostic 
difficulty presents itself. The sudden paralysis is then commonly 
preceded by slight sensory symptoms, tingling, &c., and sometimes by 
fever. If these are absent in cases of actually sudden onset, primary 
myelitis is far less likely than haemorrhage. The acute spinal pain 
that is common in haemorrhage is absent in myelitis. If an onset 
indicating haemorrhage is followed by a gradual extension of the sym- 
ptoms during the next twelve or twenty-four hours, myelitis secondary 
to haemorrhage may be inferred. 
When acute myelitis ascends the cord, so that the legs, muscles of 
the trunk, and the arms are successively paralysed, its course resem- 
bles that of acute ascending paralysis, or “Landry’s paralysis,” in 
which no lesion of the cord is found after death. The most important 
distinction is that in ascending myelitis sensation is affected, and 
if the patient survives, there is a strong tendency to trophic disturb- 
ance in the skin, while many muscles waste and present loss of faradic 
irritability. Iu acute ascending paralysis, on the other hand, sensa- 
tion is little impaired; some parts maybe spared by the ascending 
palsy; bedsores do not form; and, if the case is not fatal, there is no 
change in the electric irritability of the muscles. 
In meningitis the symptoms of irritation, severe pains, muscular 
rigidity, &c., are prominent, while they are absent in simple myelitis. 
But in many cases the two conditions co-exist, and which disease is 
predominant can only be decided by the order and degree of the 
development of the symptoms. In meningeal haemorrhage there is 
severe pain in the back and acute irritation of the nerve-roots. 
The distinction from multiple neuritis has been considered in the 
account of that disease. It chiefly arises in the cases of polio-myelitis, 
presently to be considered, but a difficulty may exist when a paren- 
chymatous myelitis affects the structures on which co-ordination 
depends and produces the condition of myelitic ataxy. Such cases 
tire distinguished from those of neuritic pseudo-tabes by the fact 
that some other structures are involved, so that symptoms are 
present that are only met with in diseases of the spinal cord. A very 
acute onset, so that the symptoms reach a high degree in a few hours, 
is also evidence of the myelitic origin. The case mentioned on p 322 
affords an illustration of these distinctions. 
Myelitis is far from rare in patients of the age and sex in which 
h steria especially prevails, and many cases are mistaken for hysterical 
paraplegia—sometimes because symptoms of hysteria concur, often 
merely because the patient is a girl and her legs well nourished. The 
converse error is very rare. The mistake occurs especially in cases of 
transverse dorsal myelitis, in which there is no wasting of the muscles 
of the legs. The gradual development of considerable excess of 
myotatie irritability is a symptom of great diagnostic value, and 
ACUTE MYELITIS. 328 
when this increases to characteristic extensor spasm there should he 
no room for doubt. If one leg is lifted from the bed, and the other 
moves with it owing to the rigid extensor spasm, organic disease is 
certain; hysterical contracture never fixes the legs to the pelvis so as 
to permit this effect. In hysterical paraplegia there may be reten- 
tion of ui’ine, but there is not incontinence. Among other conclusive 
symptoms of organic disease, a girdle pain, and incontinence of faeces, 
are of especial value. Trophic changes in the skin sometimes decide, 
even alone, the nature of the case. 
Prognosis.—The primary danger to life in myelitis depends upon 
the risk of respiratory palsy, and hence on the region of the cord in 
which the disease is situated. A disposition to spread is always of 
grave significance, and so also are indications of a serious blood- 
change, which is likely to increase the damage it has caused. On 
this account the prognosis is worse in disseminated than in simple 
transverse myelitis, and it is longer before confidence can be felt that 
arrest will endure. The risk is great whenever the cervical region is 
diseased, so that the intercostal muscles are paralysed, and in propor- 
tion to the nearness of the lesion to the origin of the phrenic nerve, 
on which life then depends. Hence a careful examination of the 
respiratory movements should be the first concern. Any indications 
that foci of inflammation have developed in the medulla oblongata 
are of extremely grave significance. Another danger is from acute 
trophic disturbances, and on this account the prognosis must be 
guarded whenever the lumbar enlargement is diseased, or is threatened 
by the extension of the inflammation. Hence bedsores, if forming 
early, within the first month, are an unfavorable indication; at a later 
period they have less influence on the prognosis. The occurrence of 
cystitis, and especially of any indication of secondary kidney disease, 
increases very much the gravity of the case. 
The prospect of recovery of power chiefly arises ivheii the onset is 
over, and the disease has become stationary. It depends (1) on the 
intensity of the disease, as shown especially by the loss of sensation 
as well as of motion, and (2) on its vertical extent as indicated by the 
impairment of the central functions of the cord; (3) on the early 
occurrence of symptoms of improvement. The longer loss of sensa- 
tion continues, the less is likely to be the degree of ultimate recovery. 
(4) It is influenced to some extent by the cause of the myelitis, being 
better if this is due to a removable cause, such as pressure, than if 
spontaneous. (5) It is better when the disease is confined to the 
dorsal region than when rapid atrophy, &c., of the muscles show that 
the lumbar grey matter is involved. The longer motor palsy remains 
absolute, the less perfect will be the ultimate recovery. If some 
power returns within a fortnight, the amount that will be regained 
will probably be great; but even complete loss of poAver for six mont hs 
does not preclude the ultimate return of the ability to walk, and I 
have even known this result after complete paralysis for a year from 
SPINAL CORD. ACUTE MYELITIS. 
329 
transverse myelitis. The development of increased myotatic irrita- 
bility shows that improvement will not speedily occur, but even 
rigidity and the state of “ spastic paraplegia ” does not lessen materi- 
ally the prospect of some recovery in a case in which the loss of power 
remains complete for a month or more. Indeed, the spasm often 
enables the patient to stand with a slighter degree of voluntary power 
than would suffice if the limbs were supple. 
The fact of preceding syphilis must be allowed very little influence 
on the prognosis in a case of simple acute myelitis, but greatly 
improves the prognosis if there are indications that the inflammation 
is secondary to a more chronic process outside the cord. 
Treatment.—If a case comes under observation at the earliest 
period, when only slight sensory disturbance and slight weakness of 
the legs indicate the commencing process, the question arises whether 
any treatment can avert the further development of the inflammation. 
If the symptoms are clearly due to exposure to cold, a hot bath, 
followed by free diaphoresis, should be employed, and followed by 
eounter-irritation and the other measures now described. If consider- 
able paralysis shoAvs that the process of inflammation is fully 
developed, little can be expected from these measures, and it is 
better not to subject the patient to treatment that is incompatible 
with perfect rest. This, in all cases, is of paramount importance. 
Both functional excitation of the cord and movement of the spinal 
column should be avoided. The remarks regarding posture made in 
the account of the treatment of inflammation of the membranes 
apply also to that of the cord itself; it is most undesirable that the 
spine should be the lowest part of the body, and it is rather less 
difficult to keep the patient off the back in myelitis than in menin- 
gitis. A plank back-rest in the bed will be found a great assistance 
in securing comfortable rest on the side. If there is any reason to 
suspect haemorrhage, or if there are indications of rapid extension of 
the inflammation, the prone position should be adopted, and even in 
myelitis it is Avell to adopt it at times as a change from the lateral 
posture. 
The removal of blood from the skin of the back over the affected 
region, by leeches or wet cupping, is an old measure, Avhich finds some 
theoretical justification in the fact that the blood from the structures 
behind the spine passes into the same veins as the blood from the 
spinal cord itself. Hence this measure may conceivably have some 
influence on the circulation in the cord. If the patient’s strength is 
not such as to render the abstraction of blood desirable, dry cupping 
may be employed, or the vessels of the skin may be dilated by hot 
fomentations, or a mustard plaster, or hot water bags. By stimulating 
the cutaneous nerves, these agents may also influence, in a reflex 
manner, the vessels of the cord. The application of cold to the spine, 
as by a spinal ice-bag, has also been recommended. Contrary as these 
therapeutic agents seem, it is probable that each moderates local 330 
SPINAL CORD. 
inflammation in the same manner, by causing first contraction and then 
dilatation of the vessels of the inflamed part, and so lessening the 
tendency to stasis of the blood, on which some effects of inflammation 
depend. Unless there is reason to suspect haemorrhage, the application 
of warmth is the safer and probably, judging from experience, 
the more effectual. At the very onset of inflammation mild counter- 
irritation is unquestionably useful, and even a blister may be 
employed; but when the process has reached a considerable degree, 
it is very doubtful whether counter-irritation has much influence 
until the acute stage is over. 
In other respects the treatment of acute inflammation of the cord 
must be guided rather by the nature of the process than by the 
character of the organ in which it occurs, and fact that it is an 
acute local inflammation should be kept in view. A nutritious but 
unstimulating diet, aperients, and diuretics, are desirable in-all cases. 
If there is constipation a free purgative may be given. Whenever 
there is evidence of a morbid blood-state, it is important that this 
should, if possible, be improved, but we have still to learn how most 
toxsemic states can be neutralised. Nitrous ether may be given as a 
diuretic with some tincture of digitalis, which tends to render the 
circulation uniform and to lessen stasis by its influence on the small 
arteries. The reason for diuresis is that probably no local inflamma- 
tion occurs that, is not associated with a morbid state of the blood 
which may be to some extent relieved by the action of the kidneys. 
If any special drug is given, it may be combined with those above 
named. It is as difficult to ascertain the influence of the drugs which 
are supposed to exert a special influence on myelitis, as it is in the 
case of other local inflammations, which have no predetermined 
degree, and tend to subside when they have reached their height. 
Ergot was recommended by Brown-Sequard, chiefly on theoretical 
grounds, and has been extensively employed. In rare cases it has 
seemed to do good. In cases of haemorrhagic myelitis it may reason- 
ably be given with greater confidence, or ergotin (3 to 5 gr.) may be 
injected beneath the skin. Belladonna has also been recommended, 
but the evidence that it influences the morbid process is not strong. 
Mercury has been largely employed, given by the mouth and by 
inunction. The influence of mercury on the inflammation of internal 
organs does not seem so great as upon that of the fibrous tissues and 
of the structures that invest organs. Certainly in myelitis its effect 
is less distinct than it is in many cases of meningitis. Iodide of 
potassium seems to be no more efficacious than mercury. In cases of 
transverse myelitis occurring in syphilitic subjects the treatment for 
syphilis seems to have but little influence on the morbid process. It 
is true that such treatment is rarely adopted at the very onset of 
acute myelitis, but after the disease has developed energetic treatment 
does not seem to modify its subsequent course. This is true also of 
the subacute disseminated myelitis that occurs in the subjects of ACUTE MYELITIS. 
331 
syphilis, and might he expected to be more amenable. I have known 
this form, concurring with syphilitic disease of the cerebral arteries, 
to develop and run its course to a fatal termination in spite of con- 
tinuous antisyphilitic treatment, to which the arteritis yielded. 
In the general management of a case of myelitis, two points are of 
extreme importance. One is to avoid, by extreme cleanliness and 
care, the exciting causes of bedsores. The skin should be most care- 
fully watched, and any indication of deleterious pressure met by a 
change of position or an alteration of the mode of supporting the part. 
Cotton wool is very useful for this purpose. If there is a marked 
tendency to trophic changes the patient should be placed on a water- 
bed. When there is incontinence of urine, the difficulty of avoiding 
irritation of the skin is greatly increased. For males, a bed urinal is 
sometimes useful, but often it causes irritation and even sloughing of 
the prepuce, and then does more harm than good. A quantity of 
boracic or salicylic absorbent cotton wool, changed as often as it 
becomes saturated, is one of the best means of meeting this difficulty. 
It must be remembered that the prevention of bedsores is the preven- 
tion of one common cause of death. Should offensive sores form, a 
quantity of picked oakum, placed outside the immediate dressing, is a 
cheap and most effective means of preserving the air of the room 
from the fcetor of the sores, and is also a useful substitute for absorb- 
ent cotton wool, in the case of the poor, to absorb the urine or receive 
faeces that are passed unconsciously. Such material is also useful for 
relieving pressure when a water-bed cannot be obtained. The second 
point in management is the treatment of retention of urine. If there 
is either simple retention or overflow incontinence, the bladder must 
be regularly emptied by the catheter, great care being exercised to 
prevent the introduction of contaminating germs. The importance of 
daily examining the abdomen to see that retention has not occurred, 
cannot be exaggerated. If the bladder is left full and the urine 
allowed to dribble away, inflammation is sure to be set up, and 
probably also pyelo-nephritis. If cystitis occurs, antiseptic washes 
must be used to lessen, as far as possible, the decomposition of the 
urine. Under this influence the cystitis usually lessens, and one grave 
danger to life is obviated. 
When the disease of the cord has become stationary, the patient 
may be allowed to move, and a more tonic treatment may be adopted. 
Iron, quinine, or arsenic may be given. Strychnia must be given only 
in very small doses if there is any excess of reflex action. Occasional 
counter-irritation may be employed, repeated frequently if any im- 
provement seems to result. The limbs may be rubbed, and any 
muscular wasting treated with electricity. It is not desirable to use 
electricity as a therapeutic agent while the cord disease is in an acutely 
active stage. There is no evidence that the application of electricity 
to the spinal column has any influence on the process of recovery of 
the cord. Its chief value is to maintain, as far as possible, the 332 
SPINAL CORD. 
nutrition of any muscles of which the nerves have undergone de- 
generation. In cases of dorsal myelitis, in which the legs are well 
nourished, and the reflex action is excessive, it is better not to 
apply any form of electricity. The unavoidable stimulation of the 
sensory nerves tends to increase the reflex over-action. Careful atten- 
tion should, in all cases, be paid to the position of the limbs during 
the stage of helplessness, so as to avoid as far as possible the develop- 
ment of contractions. Por the condition of active spasm, which often 
develops after severe myelitis, not much can be done; such special 
treatment as can be adopted is described in the chapters on Primary 
Spastic Paraplegia. 
Abscess of the Spihal Coed. 
Simple inflammation of the spinal cord scarcely ever goes on to 
the formation of pus, although leucocytes may accumulate at certaiu 
points of the grey matter so densely as to constitute microscopic 
collections of pus, and in very rare cases of this kind such minute 
abscesses have been sufficiently large to be visible to the naked eye. 
Pus only forms in the substance of the cord in considerable quantity 
in cases of purulent meningitis. In most instances the purulent 
meningitis has been of septic origin, rarely traumatic. In the former 
case, suppuration within the brain may coincide with that in the 
spinal cord, and in the latter it may be very extensive and occur at 
more than one spot. The symptoms are those of an acute irritative 
myelitis, but they are often lost in those of the purulent meningitis 
which precedes the disease of the cord itself. Their special feature is 
their association with a cause of septic suppuration, as well as with a 
high temperature and other symptoms of a septic blood-state. 
A good example of the disease is a case recorded by Nothnagel. 
A patient suffering from cough and most offensive expectoration was 
suddenly seized with severe pains on both sides of the abdomen, 
attended by a sense of constriction and quickly followed by paralysis 
of the bladder and of the legs, with loss of sensation and of reflex 
action. An abscess of the cord was diagnosed. After death there 
was extensive purulent spinal meningitis, and the dorsal and lumbar 
cord contained au extensive collection of gangrenous offensive pus, 
which seemed to occupy the central part of the cord, from the cervical 
enlargement downwards. Some abscesses were found also in the 
white substance of the brain. In another case described by Ullmann* 
two extensive foci of suppuration existed in the cord, one cervical, the 
other lumbar; the former had caused extensive destruction of tissue, 
and the pus had escaped into the subdural space. The affection 
was supposed to be secondary to gonorrhoea. 
* ‘ Zeitsclir. f. kl. Med.,’ xvi, 18S9. CHRONIC MYELITIS. 
333 
Embolism op the Spinal Cord. 
The occurrence of embolism in the spinal cord has not yet been 
proved, but a few cases have been met with which suggest the 
possibility that the process has been the exciting cause of an acute 
myelitis. In a young man with mitral regurgitation, considerable 
weakness of the right leg came on suddenly—in a moment—with 
transient spasm. The onset indicated a sudden lesion in the cord, 
which might well have been the embolic obstruction of a small vessel. 
In a case recorded by Weiss, a boy aged sixteen, with chronic mitral 
disease, was suddenly seized with complete paraplegia, followed by 
bedsores, &c. He died four months after the onset, and the lumbar 
enlargement was found completely softened, with old coagula in the 
arteries. There was embolism of the kidneys and spleen, and the 
cortex of each cerebral hemisphere presented small foci of softening. 
Such cases justify a suspicion that embolism may be the cause of a 
sudden lesion of the cord in a patient in whom a source of embolism 
exists, and the process has occurred in other organs. 
Chronic Myelitis. 
The spinal cord may be the seat of chronic inflammation, which 
develops slowly, as such, in the course of a few or many months ; and 
the condition may also occur as the sequel to acute myelitis, which 
instead of subsiding, may persist, manifesting from time to time signs 
of activity. It is often difficult to say whether such a condition 
should be regarded as an acute myelitis that has not subsided or a 
chronic inflammation beginning acutely. In many instances, indeed, 
it is probable that the disease is most accuracely regarded as a 
combined form in which the causes of both are operative, and a 
subsiding acute inflammation is arrested and maintained by the 
influences that would be capable of inducing a primary chronic 
myelitis. Such progressive tendency is especially conspicuous in the 
disseminated form, in which the foci of inflammation may remain and 
fresh ones may develop from time to time in a chronic or subacute 
manner. 
The lesions of chronic myelitis resemble those of acute myelitis in seat 
and distribution, and intermediate cases connect them by analogous 
subacute forms. They differ from acute inflammation both in the 
longer time occupied in their development, and in the absence of the 
considerable vascular disturbance which forms part of the acute 
process. Such chronic myelitis may be focal, disseminated, or diffuse. 
In the former case it may involve the whole thickness of the cord at a 
certain level, chronic transverse myelitis, or only part of it, sometimes 
one half, occasionally for a considerable vertical extent. The chronic 334 
SPINAL COLD. 
disseminated myelitis may resemble the corresponding subacute form 
in distribution, many points of inflammation being scattered through 
a small region, or through a large part of the cord, and its symptoms 
may become diffuse by the union of the effects of the disease. 
The term “ chronic myelitis ” has, however, been used in a much 
wider sense, and has even been applied by some to all local processes 
attended by an increase of interstitial tissue, whether this is primary 
or is merely secondary to a degeneration of the nerve-elements. Thus 
the degeneration of the nerve-cells in progressive muscular atrophy 
has been regarded and described by many as a chronic myelitis of the 
grey substance, notwithstanding the fact that there is usually a 
degeneration of the whole motor path, in both segments, from the 
cortex of the brain, through the pyramidal tracts and motor nerves, 
and that the anterior cornua merely constitute, as it were, a focus in 
which the effects of the processes are especially conspicuous. Such 
a morbid process is evidently quite different in nature from a focus of 
ordinary inflammation, in which the primary change is interstitial 
and random in range and effects, and presents no limitation to func- 
tion in the incidence of the consequences on the nerve-structures. 
Whenever this latter feature can be traced, the malady must be 
regarded as a “ system disease,” i. e. as a disease affecting a system of 
nerve-structures that have a common function. If “ system diseases ” 
are forms of inflammation, they are “ parenchymatous inflammations 
and those that are chronic in course from beginning to end are more 
commonly termed “ degenerations,” and are so classed and described 
in these pages. Only then the chronic interstitial processes of random 
position and influence are here considered. 
Etiology.—The causal relations of chronic myelitis, even as thus 
limited in conception, are very various. An inherited neuropathic 
tendency can sometimes be traced, but far more rarely than if the 
cases are included in which the nerve-elements suffer primarily. The 
disease is most common in early and middle adult life, but it occurs 
occasionally in old age; it is met with in both sexes, and is perhaps 
more prevalent in females in the first half of middle life and in males 
in the second—an important fact, because so many of the cases in 
young adult women are thought to be hysterical in nature. 
Various conditions which lessen constitutional strength predispose 
to the disease. Definite causes often cannot be traced, although 
many of the exciting causes of acute myelitis seem capable of giving 
rise to the chronic form, when acting for a considerable time, or 
frequently repeated, or in specially predisposed persons. Thus while a 
single intense exposure to cold may produce acute myelitis, frequent 
habitual exposure may cause the chronic form. * Injury is a frequent 
cause, and seems to act in more than oneway. Chronic inflammation 
may develop in the vicinity of a damaged spot, when the traumatic 
lesion may have been too slight to cause pronounced symptoms, or 
may have caused slight effects which are subsequently lost in the CHRONIC MYELITIS. 
335 
more severe and extensive consequences of the myelitis. In other 
cases the effects of the lesion may be too slight in degree to be at first 
perceptible, but (either by a slow influence on the processes of 
nutrition, or by extensive minute interstitial lesions that induce 
secondary traumatic inflammation) the symptoms of extensive damage 
to the cord slowly follow an injury that has no immediate effect on 
function. These cases will be further considered in a subsequent 
chapter. Repeated over-exertion has also seemed effective in some 
cases. Sexual excess has been thought to be a cause, but on less 
clear evidence. 
Chronic myelitis may be secondary to other local morbid processes, 
especially to adjacent inflammation, which, when it also causes com- 
pression, invariably gives rise to chronic myelitis; the inflammation 
that results from pressure on the cord may be either chronic or 
acute. 
Another series of causes consists of constitutional states capable of 
giving rise to local inflammations. Chronic alcoholism is, perhaps, 
the most influential and important of these. Chronic myelitis due 
to it is usually associated with chronic meningitis, and most intense at 
the periphery, beneath the inflamed membranes ; but it thence extends 
into the substance of the cord, and sometimes tracts of irregular 
extent and position are involved, without connection with the 
membranes. This cause is one of especial importance, because it 
often co-operates with others, and determines effects that may seem 
to be independent. Its effect is met with, for example, in many 
cases of chronic myelitis that are excited by injury and seem to be due 
solely to the excitant, although the results of this would have been 
trifling and transient but for the tendency induced by the preceding 
and often profound effect of chronic alcoholism on the tissues. It 
also complicates many cases of multiple neuritis due to the same 
cause, in which the effects of the peripheral lesion obscure to a large 
extent those of the central mischief, by causing symptoms that 
prevent the recognition of the latter, since its consequences are lost, 
as it were, in those of the damage to the nerves. 
The gouty diathesis is another cause of chronic myelitis. We are 
only beginning to realise how often it acts on many organs and tissues, 
and how frequently inflammation is thus induced. It is certain that 
this is a common cause of inflammation in the substance of organs 
and in mucous membranes, and chronic, as well as acute myelitis, is 
among its effects. Many cases are due to this influence, and it is 
instructive to note that, like chronic alcoholism, it is also a cause of 
inflammation of the peripheral nerves. The disseminated and 
progressive forms of chronic myelitis are especially due to it, and the 
analogy should be noted which these present to the irregular forms 
of perineuritis, of which this state is also a common cause. It is 
probable that many cases of chronic myelitis in young adults, at 
present mysterious in origin, and in the obstinately progressive 336 
SPINAL CORD. 
character they sometimes manifest, will be found to be due to the 
influence of inherited gout, which is certainly capable of causing 
analogous inflammation elsewhere in the nervous system, as, for 
instance, in the optic nerves. 
Another cause of chronic myelitis is constitutional syphilis. The 
forms that are apparently due to this are of two types. (1) A diffuse 
interstitial inflammation, most intense at the periphery, with much 
new formation of tissue and thickening of the walls of the vessels, 
both processes extending into the cord from the pia mater, in which a 
similar damage exists. This form may be subchronic in course, and 
presents some histological correspondence to known syphilitic pro- 
cesses. (2) A focal very chronic indurating myelitis, such as shown in 
Fig. 102, which has no distinctively syphilitic feature, may occur in 
very late stages of the constitutional disease. In neither form does 
the influence of treatment afford evidence of the relation to syphilis. 
In the second, sclerotic variety, it does not appear that treatment has 
any power to modify the morbid process, and in the first it is evident 
that any cicatricial process that could be induced would only maintain 
the damage to the nerve-elements, which would suffer further from the 
maintained or renewed compression under the prolonged contraction 
of the enclosing tissue. Yet the occurrence of these forms in the 
subjects of syphilis, the absence of other causes, and the circumstances 
that the negative facts are not without analogies, make this causation 
on the whole the probable one. 
Pathological Anatomy.—The morbid appearances vary much in 
the different forms. In most cases the disease is revealed to the 
naked eye by a change in the aspect of the affected part, in which the 
white substance is grey in tint, and the grey matter darker than 
normal, while both are reduced in size in cases of long duration, so 
that the whole cord may be lessened at the affected part, and its 
shape changed when the disease does not involve its entire thickness. 
But in recent cases, the alteration in tint may be the most conspicuous 
change, and may be visible on the surface, even through the pia 
mater; this may be thickened at the spot if the disease reaches the 
surface. The consistence of the affected area may be lessened or 
increased. Barely, in recent cases, there is a slight increase in the 
size of the affected part. In some recorded cases in which a great 
increase in size has been described, it is probable that an infiltrating 
glioma was mistaken for chronic inflammation. When there is one 
considerable focus of disease there may be other slighter foci in the 
neighbourhood. In what is called the “diffuse” form, the diseased 
areas are scattered through a considerable extent of the cord; they 
may blend into a lesion that is truly diffuse, or may remain, in point 
of fact, disseminated, but be so placed that their effects blend in 
what may be termed a diffuse influence. Thus it maybe found, post 
mortem, that there are numerous foci of disease when nothing in the 
character of the symptoms prepared us for a disseminated lesion. CHRONIC MYELITIS. 
337 
It is probable, indeed, that tbis is tbe rule in tbe chronic form, and 
an actually diffuse extensive inflammation is much more rare than is 
suggested by the symptoms of the disease. In the secondary form, 
the inflammation is usually confined to the neighbourhood of the 
morbid process which causes it. That which is secondary to menin- 
gitis is most intense in the peripheral part of the cord, but sometimes 
extends deeply, especially when the cause of the meningitis is one, 
such as alcoholism, capable also of giving rise to myelitis. In this 
Fig. 102, 
Fig. 103. 
Fig. 102.—Chronic myelitis. (After Charcot and Gombault.) B, section at 
the level of the third dorsal, shows both the posterior columns and whole 
of left half inflamed, except the inner part of the anterior column. The 
affected part was grey and uniform in aspect, vascular, and firmer than 
normal. Pia mater and arachnoid thickened. A, section from cervical 
enlargement, showing secondary degeneration in the post.-med. columns. 
Similar foci existed in the pons, &c.* 
Fig. 103.—Chronic sclerotic myelitis. (After Troisier.) A, posterior view 
of the affected part, lower dorsal region. The diseased areas were grey 
in aspect and are indicated by shading. B, middle ot lesion, showing 
extensive damage ; C, 2.) cm. higher up, slighter damage; D, cervical region 
ascending degeneration, post.-med. cols., and a spot of disease in lateral 
column (probably part of the ascending ant.-lat. tract, secondarily dege- 
nerated. E, lower part of lesion. (See next figure.)f 
# The patient had had syphilis twenty-one years before. The spinal symptoms 
slowly developed during fifteen months, and consisted in paralysis with hyper- 
costhe.-ia on the left side, with loss of sensibility without paralysis in the right, and 
a band of anaesthesia to pain around the thorax at the level of the lesion, but the 
mental dulness of the patient prevented accurate observation during the last few 
months of her life. (Charcot and Gombault, ‘Arch, de Phys.,’ 1873, vol. vi, 
p. 143.) 
f The patient was a woman forty years of age. The symptoms slowly developed 
during the three years before death, and consisted of weakness with rigidity in the 
left leg, and impairment of sensibility in the right, first of the temperature-sense 
and afterwards of touch. (No observations were made on sensibility for the last 
fi teen months of the patient’s life, during which the lesion was slowly progressing.) 
(Troisier, ‘Arch, de Physiologic,’ 1873, vol. v, p. 716, Case 2.) 
VOL. I. 338 
SPINAL CORD. 
condition almost the whole thickness of the cord may be involved (cf. 
a and b, Fig. 105). Now and then, when there is no primary menin- 
gitis, the superficial layers of the cord are chiefly damaged, a form that 
has been termed chronic annular myelitis or annular sclerosis, because 
the affection extends like a ring around the cord. This form of lesion 
is, however, as we have seen, sometimes merely an ascending degene- 
ration of fibres that lie near the surface, and degenerate above the 
primary lesion. 
In chronic myelitis, according to the limited use of the term 
already explained, the microscope shows that the inflammation is 
primarily interstitial. The affected areas always stain deeply with 
carmine in consequence of the great increase in their connective-tissue 
elements, and may be occupied by a dense fibrous reticulum, in which 
few nerve-elements can be discovered, as in Fig. 104. In less affected 
Fig. 104.—Chronic sclerotic myelitis, same case as Fisr. 103; section near B, 
reversed. Almost the whole left half of the cord (right in the figure) is 
changed into a dense mass of shrunken connective tissue, and the right half 
is being invaded in many parts by the same process. The upper small figure 
is from the posterior column, showing a thickened vessel surrounded by nucleated 
tissue, among which lie nerve-fibre*, many of them much smaller than normal, 
and some with swollen axis-cylinders. The lower small figure is from the right 
anterior column (left in figure); the pia mater is thickened and contains many 
nuclear elements; from it thick trabecnl® extend into the white substance and 
enclose spaces, from many of which the nerve-fibres have perished.* 
parts of the white columns there is an irregular increase of the 
interstitial tissue, partly fibrillated, partly amorphous, or studded with 
nuclei (Fig. 104, upper small figure), while in other parts it may contain 
many nucleated cells, oval, fusiform, or stellate. The large stellate 
* From a section by Prof. Picrret, kindly lent me by Dr. Dreschfeld. CHRONIC MYELITIS. 
339 
‘‘spider cells” are sometimes very conspicuous, and interstitial 
fibrous tracts may be traced to their ramifications. 
The nerve-fibres waste before the interstitial process, or undergo 
destructive changes from the beginning. They may at first present 
the change by which their myelin stains more deeply than normal; 
afterwards they become narrowed, and the axis-cylinder is often 
irregularly enlarged. Ultimately many or all the fibres disappear 
FlO. 105.—Chronic meningo-myelitis, due to alcoholi-m. Syringo-myelia, 
congenital, with central gliomatosis. A, lowest part of cervical enlarge- 
ment; pia mater thickened, and from it tracts of tissue extend into the 
cord. The greater part of the section is the seat of a diffuse myelitis, 
in which the nerve-fibres could be seen with difficulty, and were sepa- 
rated by inflammatory products. The grey matter was also affected, 
and the nerve-cells much changed. The clear spaces in the right ant. 
cornu appeared occupied by products of degeneration. Central canal 
greatly dilated and surrounded by new growth, which in B (lumbar sec- 
tion) has obliterated the canal and thus caused its dilatation above. In 
this section the myelitis is chiefly peripheral, and the grey matter has, 
for the most part, escaped. 
from tlie affected area. Here and there the destruction of fibres may 
be out of proportion to the increase in the interstitial tissue, so that 
thickened and often granular trabeculae enclose empty spaces. This 340 
SPINAL CO HD. 
is seen in the lower small illustration in Fig. 104 ; it is apparently the 
result of the participation of the nerve-fibres in the inflammatory 
process during a more general stage, in which all the elements of the 
tissue were involved. In the recent state, products of degeneration, 
granule corpuscles, &c., may be found abundantly in the altered 
regions. The walls of the vessels are thickened, and by this 
thickening the cavities of the arteries maybe ultimately lessened;: 
those of smaller size may even be closed. Not only is the 
wall of the arteries thickened, but around them the increase of inter- 
stitial tissue is often greater than elsewhere, so that the appearance is 
as if it had spread thence into the adjacent structures. Undue signi- 
ficance has been attached to this condition, especially in old patients 
with arterial degeneration ; it has been regarded as evidence that 
arterial disease sets up the myelitis, but it is a common appearance in 
all forms of chronic myelitis, and also in the later stages of acute 
inflammation. It is probably due to the greater activity of the process 
in the immediate vicinity of the vessels, and to the share taken by 
escaped leucocytes in the formation of new interstitial tissue. The 
peripheral arteries, moreover, occupy tracts of neuroglial and fibrous 
tissue proceeding from the pia mater, and the increase of interstitial 
tissue is connected with these; some of it is, on this account, found 
in the vicinity of the arteries. 
In the grey substance there is a similar increase of connective- 
tissue elements, so that the altered part takes a deeper stain with 
carmine than the normal grey substance, and has a denser structure, 
from the greater amount of supporting tissue. The nerve-elements 
become atrophied; the ganglion-cells, at first swollen and rounder, 
afterwards shrink, until ultimately they may be reduced to small 
angular bodies, and they even may disappear. The nuclear corpuscles 
about the central canal are often increased in quantity, and the canal 
obliterated, but this condition is so common in otherwise normal cords, 
that no importance can be attached to it. A considerable increase of 
tissue about the central canal, closing it below and causing it to be 
dilated above (Fig. 105, “ syriugo-myelia ”), has been ascribed to 
chronic inflammation around the canal, but the abnormal tissue is 
probably always of gliomatous nature, consisting of a development 
of tissue that is in congenital excess, owing to an arrest of develop- 
ment. 
The pia mater is greatly thickened over the inflamed parts, as 
already stated, and in some cases the affection of the membrane is 
general, and that of the cord most intense beneath it—a condition 
termed “chronic meningo-myelitis.” It is this form that is shown in 
Fig. 105. The tracts of new tissue that pass into the cord are dense 
and wide. As already mentioned, this change may be accompanied 
by a deeper and sometimes a more diffuse inflammation, as in a, Fig. 
105, in which the affection of the cord is greater and that of the mem- 
branes less than in b. The chronic myelitis that occurs in syphilitic CHRONIC MYELTTIS. 
341 
subjects may present no specific characters. In some cases, however, 
the cell-formation has been abundant, and has been associated with a 
tendency to fatty degeneration in the older portions of the lesion and 
with a similar degenerating hyperplastic inflammation of the pia 
mater. The condition is, however, clearly one of chronic inflamma- 
tion, and not of a syphilitic growth.* Nevertheless an actual growth 
does sometimes coexist with a focus of syphilitic myelitis; it is pro- 
bable that in such cases the growth is usually the primary change. 
This may be distinguished by the indications of compression and 
displacement of the adjacent elements of the cord, a condition which 
shows that there is an actual new formation. 
The more recent the inflammation, the larger is the proportion of 
cells and nuclei in the interstitial tissue; the longer it has existed, 
the greater is the amount of fibrillation it presents. The very chronic 
indurating forms are sometimes called “ sclerotic myelitis,” or “focal 
sclerosis of the cord.” From the various areas of inflammation 
secondary degenerations proceed, ascending or descending, and these 
may complicate the aspect of the disease—a fact which has not always 
been sufficiently considered in interpreting the morbid appearances. 
Symptoms.—The symptoms of chronic myelitis vary much according 
to the character of the morbid process. For the most part they cor- 
respond in character to those that are produced by acute inflamma- 
tion, differing, however, in their mode of onset. It is therefore not 
necessary to repeat them in detail. Different cases may manifest 
almost every symptom that can be produced by disease of the spinal 
•cord. There may be various motor and sensory paralyses, contrac- 
tures, and even muscular atrophy, but their common feature is their 
gradual, and often successive development. In the most common form, 
focal myelitis of the dorsal region, partial or transverse, the symptoms 
are paraplegic. They differ but little whether there is a single area 
of disease or several foci near together implicate adjacent structures. 
Motor power is usually impaired far more than sensibility. Subjec- 
tive sensations are often prominent and early symptoms, whether 
there is anaesthesia or not,—tingling, “ pins and needles ” in the legs, 
a sensation as if fur or wool covered the skin, sometimes with dull pain 
in the legs and back, especially after exertion, and commonly also with 
a well-marked girdle-pain at the level of the chief lesion. Some loss 
of sensibility, partial in kind or in seat, will often be found if care- 
fully searched for, but there is not often absolute loss of sensation 
except in the rare cases of intense local sclerotic myelitis, by which 
conduction may be arrested as completely as by a growth. The 
onset of the motor weakness is gradual; many months may pass 
before the power of walking is considerably impaired. As the legs 
get weak, excess of reflex action is developed (unless the reflex struc- 
tures are damaged). The knee-jerk is increased; foot-clonus occurs 
# See Moxon, * Guy’s Hosp. Reports,' 1871, and Charcot and Gomhault, ‘Arch, de 
Physiologic,’ 1873. 342 
SPINAL CORD. 
when the legs are in certain positions; and a tendency to spasm 
gradually develops, and increases to the condition typical of “ spastic 
paraplegia.” The sphincters frequently share the impairment of 
voluntary power. Co-ordination of movement is sometimes affected, 
usually as general unsteadiness, and defect of equilibrium, rather 
than as pure ataxy. 
The symptoms may come on simultaneously in the two legs, or one 
may be affected before the other, and occasionally the paralysis 
reaches a high degree in one leg while the other still possesses fair 
strength. When one half of the cord is affected almost alone (as in 
the lesion shown in Fig. 105), there may even be a crossed paralysis 
of motion and sensation. 
Chronic polio-myelitis is often regarded as a distinct variety, but 
much confusion has arisen from the fact. If chronic myelitis 
develops in the cervical and lumbar enlargement, muscular wasting 
is usually added to the other symptoms. Similar atrophy occurs also 
in the widely diffused form of chronic myelitis, in Avhich almost all 
parts of the cord suffer, and it may, indeed, be the most conspicuous 
symptom. It is always irregular in distribution in these cases, and it 
may be combined with other symptoms, palsy and anaesthesia, also 
irregular in extent and seat. The muscular wasting varies in the 
rapidity of the development, according to the character of the inflam- 
mation, and there are corresponding variations in the relations to it of 
the loss of power in the muscles and also in the electrical reactions 
they present. In very chronic cases there is a slow failure of electrica 1 
irritability to both currents ; in others of more rapid course the voltaic 
irritability persists longer than the faradic irritability, and there 
may be a distinct degenerative reaction. The symptoms may com- 
mence in the arms or in the legs, but they ultimately become general 
in most cases, and, according to the place of their commencement, 
may seem to have an ascending or descending course. Occasionally 
the disease begins in the dorsal region, and after a time, perhaps 
years, it spreads to the enlargements, and the muscular wasting is 
added. 
The course of chronic myelitis is usually slow and progressive. The 
symptoms often increase so gradually as only to attain a considerable 
degree at the end of two or three years. At any stage the progress 
of the disease may cease. The chronic course may be varied by 
occasional more rapid increase of the symptoms, due to subacute or 
even acute processes in the diseased parts. Every degree of chronicitv 
is met with, and subchronic cases, in which the symptoms develop in 
the course of a few months, effect a gradation to the acute and sub- 
acute forms of myelitis. The duration of the disease varies from six 
months to ten years or more. Thus in one case the symptoms 
slowly increased during about seven years, and then became stationary, 
and the patient died twenty-three years after the onset. 
Diagnosis.—The diagnosis of chronic myelitis rests on the slowdeve- CIIRONiC MYELITIS. 
343 
lopment of symptoms indicating a random process in the spinal cord, 
i. e. a process which damages irregularly structures of various functions, 
and thus cannot he looked on as a “system-disease.” The maladies 
from which it has to be distinguished differ according to the seat and 
character of the inflammation. Dorsal transverse or focal myelitis 
maybe confounded with compression of the cord, with a tumour in it, 
and with primary lateral sclerosis. The distinction from pressure 
rests on the absence of a cause of compression, such as bone disease, 
—especially the absence of the signs of a morbid process outside the 
cord, preceding those of damage to the cord itself, e. g. the pains 
that indicate irritation of nerve-roots. A tumour within the spinal 
cord also causes, in most cases, more irritation of the root-fibres than 
does chronic myelitis. If myelitis involves one half of the cord 
much more than the other, the symptoms may closely resemble those 
of an intra-medullary growth. But a tumour never causes much 
damage to one half of the cord without interfering considerably with 
the functions of the other half, and the symptoms in chronic myelitis 
may be strictly unilateral. The distinction from primary spastic 
paraplegia, the so-called “ primary lateral sclerosis,” is often one of 
some difficulty. The motor state of the legs may be identical in the two 
diseases ; in each there is the same extensor spasm, and in each there 
is a slow, gradual, and apparently simultaneous onset of the weakness 
and spasm. The distinction is that in primary spastic paraplegia the 
symptoms are purely motor; there is no indication that the lesion 
extends beyond the motor structures. In chronic myelitis, on the 
other hand, there is such indication, either by the impairment of 
sensation, or by the presence of a girdle pain. This distinction is 
sufficient in the majority of eases. 
The form that involves the grey matter has to be distinguished 
chiefly from pachymeningitis and degenerative muscular atrophy. 
In pachymeningitis, the muscular wasting may be similar, but 
anseshesia is usually much more considerable in range and in degree, 
and there is more pain in the limbs. If there are similar symptoms 
in both arms and legs, myelitis is far more probable than pachy- 
meningitis, since the chronic inflammation of the membranes is less 
extensive than that of the cord. From progressive muscular atrophy, 
the chief difference is in the random distribution of the wasting, the 
absence of symmetry, and the indications of irregular damage to other 
structures in the cord, as the occurrence of pain and of loss of 
sensation. But it must be remembered that, by some authorities, 
most cases of chronic spinal muscular atrophy are regarded as due to 
chronic myelitis. 
For the distinction from other less common diseases, the reader 
must be referred to the description of them. Like all other organic 
diseases, cases without wasting of the muscles, occurring in females, 
are often regarded as “hysterical paraplegia;” the distinction rests 
on the points already described. It is, however, one of the diseases 344 
SPINAL COED. 
in which the least excusable errors in diagnosis occur, and in which 
their effects are often t be most disastrous. 
Prognosis.—Chronic myelitis is a very grave disease, on account of 
the intractability of the morbid process, its frequently progressive 
tendency, and the persistence of damage which is slowly produced. 
But cases vary widely, especially in the two former features, and it is 
a disease in which general prognostic rules can scarcely be formulated. 
The observed tendency of an individual case is alone a trustworthy 
guide. Arrest of the disease is often obtained, but actual recovery 
is rare. The prognosis is little affected by the seat or extent of the 
process, except that the implication of the grey matter of the enlarge- 
ments is generally an unfavorable indication. The severity of the 
lesion, as shown by the degree of the symptoms, is significant chiefly 
in cases of long duration, and is subordinate to the course and mode 
of onset. If it can be arrested, the prospect of improvement is 
better the slower has been the development of the disease, and the 
shorter the time the symptoms have lasted. In general, moreover, 
the prospect is better, the fewer the foci of inflammation, in males 
than in females, and in cases of uniform than of recurrent or 
relapsing course. Preceding syphilis does not materially modify the 
prognosis ; hence the great importance of the diagnosis from syphilitic 
growth, in which suitable treatment has a most certain effect. The 
ultimate danger to life is least in focal myelitis in the dorsal region ; 
it is greatest in the disseminated form, especially in the less chronic 
cases with a tendency to sloughing of the shin, and in the more 
chronic forms with muscular wasting. The indications drawn from 
the invasion of the respiratory muscles, and from the presence of any 
of the complications that so often terminate life, are the same as in 
other diseases of the cord. 
Treatment.—The first and most important measure is the improve- 
ment of the general health, by rest, change of air, and tonics. All 
causes of physical and mental depression must, as far as possible, be 
removed. Over-exertion, and even fatigue, should be avoided, and 
the patient should be kept, as far as possible, from exposure to cold. 
Absolute rest for a short time is often useful at the outset of the 
treatment, especially when there has been a somewhat rapid develop- 
ment of symptoms. In cases of purely chronic course, absolute rest 
should not be maintained for more than a few weeks, or the patient 
may find it hard to regain his former muscular power. Counter- 
irritation at the situation of the disease is often useful, and most so in 
cases in which there is spinal pain or tenderness. Repeated sinapisms 
or blisters may be employed, but a mild form of the actual cautery is 
on the whole the most useful. A superficial burn or even slight vesica- 
tion is sufficient on each side of the spine opposite the affected part. 
It should be repeated as soon as the skin has healed, and if linear 
cauterisation is adopted the fresh line can be made beside the old one. 
A hot douche to the back, at a temperature of 103° or 104° F., applied COMPRESSION. 
345 
daily, has been strongly recommended by Brown-Scquard. Warm 
brine baths, and various thermal mineral waters, have been also said 
to do good. A sea voyage is often of service, combining as it does 
the maximum of fresh air with the minimum necessity for exertion. 
Drugs, unfortunately, often fail to influence the morbid process, but 
nevertheless they are occasionally useful, so as distinctly to j ustify their 
cai’eful trial in most cases ; and it is important to remember that those 
that are useless in one stage or period of the disease may yet be of 
unquestionable service at another stage. Tonics, as quinine andiron, 
should be given if indicated. Most of the measures recommended, 
and precautions advised, in the treatment of acute myelitis are 
needed in the chronic form, and it is therefore superfluous to repeat 
them. Those drugs that most deserve a trial are arsenic, small 
doses of mercury (such as gr. of the red iodide), and iodide of 
iron. Energetic mercurial treatment rarely does good, even when the 
patient has had syphilis, and sometimes it does harm. Iodide of 
potassium seems to have little influence on the disease. Nitrate 
of silver, ergot, and phosphorus have been recommended. Strychnia 
is chiefly useful in cases in which there is muscular wasting, but is of 
far less value than in the degenerative muscular atrophy. The 
treatment of other symptoms is that suitable in primary spastic 
paraplegia or progressive muscular atrophy, and described in the 
account of those diseases. 
COMPRESSION OF THE SPINAL CORD. 
Compression of the spinal cord is a common consequence of various 
morbid processes. Inflammation is almost always excited by the 
pressure, and interference with function occurs, partly from the 
pressure and partly from the resulting myelitis. The symptoms pro- 
duced have, in different cases, many characters in common, although 
they vary according to the mechanism of the compression and the 
acuteness of the inflammation. It is only when there are indications 
that an acute myelitis has damaged the nerve-elements that we are 
justified in regarding the interference with function as an effect of 
the inflammation. 
Causes.—The morbid processes that may compress the cord are 
those that involve an encroachment on, or occupy part of, the vertebral 
canal. The chief are the following:—Disease of the bones of the 
spinal column, especially caries; growths in the spine; aneurism 
eroding the bones and then compressing the cord ; growths in the 
membranes ; thickening of the dura mater. These processes have 
usually only a small vertical extent, and the pressure they exert rarely 
extends over more than a few inches. 346 
SPINAL COED. 
Pathological Anatomy. — Tlie cord 
usually presents evidence of the compres- 
sion it has endured in considerable nar- 
rowing at the spot, where it may be in- 
dented and flattened, or cylindrical. Some- 
times the reduction in size is extreme; for 
an inch or so the cord may he reduced to 
one third of its normal diameter, and it 
has even been found no thicker than a 
crow-quill. An example of flattening is 
shown in Fig. 106. On the other hand, 
there is sometimes very little narrowing 
to be discerned. At tlie compressed part 
the cord is usually grey in tint; its consist- 
ence is lessened in early cases, and in- 
creased in those of long duration. The 
change in colour and consistence is due 
to the inflammation of the substance of the 
cord which always results from pressure, 
and may often be traced for some distance 
above and below the compressed part. 
When there is much compression there is 
always much inflammation, but considerable 
myelitis may occur when the amount of com- 
pression is slight. The inflammation may 
be chronic and slow, developing in propor- 
tion to the pressure, or it may be subacute 
or acute, even when the pressure is 
gradual. The signs of inflammation are 
very distinct on microscopical examina- 
tion, and resemble those in other forms of 
myelitis. There is a general increase in 
the interstitial tissue ; in this, at first, 
Fig-. 106.—Compression of the spinal cord and pres- 
sure-myelitis, in a case of caries of the spine. D, 
mid-dorsal region, near the chief point of greatest 
compression; the cord is narrowed from before 
backwards, and is uniformly damaged by inflam- 
mation, so that the grey substance can scarcely be 
distinguished. C, inches higher up, show's a 
slighter degree of myelitis, still extending through 
the whole thickness of the cord. B, first dorsal; the myelitis is much slighter 
and the chief disease is in the posterior columns, in which ascending degeneration 
occupies the post.-median columns and exiends outwards into the post.-external 
columns. E, 1$ inches below' the point of greatest pressure; inflammation still 
extending through all the elements of the cord. F, 2 inches lower down, show's 
only descending degeneration in the pyramidal tracts, anterior and lateral, and 
also the “comma-shaped” descending degeneration in the anterior part of the 
post.-exterual column. In G, at the lowest part of the dorsal region, the comma- 
shaped degeneration has ceased, and only that of the pyramidal tracts remains. 
(From preparations by Dr. F. G. Penrose.) COMPRESSION. 
347 
various cell-forms may be found, but it ultimately presents the 
appearance of a dense reticulum. The nerve-elements undergo de- 
generation, and abundant masses of myelin, granule corpuscles, and 
corpora amylacea ai’e visible in the fresh state or in glycerine pre- 
parations of the hardened cord (Fig. 107, c). Many nerve-fibres 
persist, however, with a narrowed sheath of myelin, and it is probable 
that these regain the power of conducting, in spite of the persistence 
of considerable, and even dense sclerosis in the part. In extreme 
cases all the fibres seem to be destroyed at the point of chief compres- 
Fie. 107.—Pressure-myelitis; portions of the section D in Fig. 106 more 
highly magnified. A, from the grev matter, numerous angular and 
fusiform cells; vessels with walls thickened by a growth of cells, nar- 
rowing the cavity, which in some is obliterated. B, from the white 
columns; thickening of the interstitial tissue, nerve-fibres in part 
destroyed, in part narrowed ; a vessel with thickened walls. C, glycerine 
preparation from white substance; abundant products of degeneration of 
the nerve-fibres, in part aggregated into granule-masses. D, section of 
a nerve-root passing by compressed area ; increase of interstitial tissue, 
many nerve-fibres narrowred, some with swollen axis-cylinders. 
sion, but there is never an actual division of the cord itself. The grey 
matter can scarcely he distinguished from the white, even with the 
microscope, and the ganglion-cells become shrunken and atrophied. 
The walls of the small vessels are often thickened by spindle-cells, 
disposed more or less concentrically to the cavity, which is encroached 
upon and may be obliterated (Fig. 107, A, b), a process that must add 
to the degree of damage to the cord. The signs of inflammation 
gradually lessen above and below the compressed part, but often 348 
SPINAL CORD. 
extend for some inches in each direction. Beyond its limits the usual 
ascending and descending degenerations may be traced (Fig. 106;. 
The nerve-roots passing by the seat of compression suffer from the 
pressure, and from interstitial inflammation excited in them. They 
are usually grey in tint and ultimately waste, and may even be 
reduced to fibrous threads. The microscope shows increase of the 
interstitial tissue, wasting of many nerve-fibres (Fig. 107, n), and 
enlargement of some axis-cylinders. 
Symptoms.—The effects vary much according to the degree of pres- 
sure, its rapidity, its direction, the amount and character of the inflam- 
mation produced, the amount of damage to the nerve-roots, and the 
position of the disease. The symptoms in most cases enable the 
fact of slow compression to be inferred, even when there is no indica- 
tion of the cause. They are of two classes: (1) interference with 
the function of the nerve-roots at the level of the morbid process; 
(2) interference with the functions of the cord itself. The cord 
symptoms consist chiefly in impaired conduction, manifested in the 
parts below the lesion. The central functions of the cord (reflex 
action, &c.) at the level of the lesion are abolished by the pressure, but 
the symptoms of this abolition are often lost in those of the damage 
to the nerve-roots. 
Of the rout symptoms the most constant is pain, extending along 
the course of the nerve-fibres, and through the area of their distribu- 
tion. The seat of these pains depends on the position of the disease ; 
they may be felt in the arms, around the thorax or abdomen, or in the 
legs. They are usually sharp pains, resembling neuralgia in character, 
sometimes accompanied by tender points. Occasionally, when felt in 
the limbs, they are referred especially to the joints. The pain may be 
intermitting or constant. It may exist alone, for a long time, in a dis- 
ease that increases slowly, and sometimes may be the only symptom, 
although some compression of the cord occurs. "With it there is usually 
hypersesthesia of the skin, often intense. After a time anaesthesia 
develops in irregular areas, in spite of the persistence of the pain,— 
the condition termed “ anaesthesia dolorosa.” Irritation of the motor 
nerve-roots may cause painful contracture of the muscles, but this is, 
on the whole, rare, and the chief motor symptoms are due to the 
interruption of the fibres—muscular weakness, gradual in onset, and 
accompanied by wasting. The rapidity of the atrophy varies much, and 
with it the electrical reaction. When slow, there may be merely a pro- 
gressive diminution in irritability to faradism and voltaism ; when 
rapid, there is often the degenerative reaction, and sometimes the 
“ mixed form,” from the partial damage to the fibres that supply a 
muscle. 
These local root symptoms are usually the first, and to them are 
added, after a time, the indications of interference with the function 
of the cord itself. There is weakness in the parts supplied from the 
cord below the lesion. The loss of power is usually gradual, but COMPRESSION. 
349 
sometimes comes on rapidly, even in the course of a few hours, when 
an acute myelitis is set up by the compression. With the weak- 
ness there is a marked and early increase in the superficial reflex 
action, more constantly conspicuous than in most other diseases of 
the cord, and therefore of some diagnostic importance. The myotatic 
irritability is also increased, a foot-clonus being almost always present. 
Pains in the legs may occur, even -when the disease is above the lumbar 
enlargement, usually dull and aching. There is often formication and 
tingling. There may be no impairment of sensibility in the parts 
below the lesion, even when there is complete motor palsy ; in many 
cases, however, there is some sensory loss, complete only when the 
spinal lesion is very severe. Conduction of painful impressions may 
be delayed, sometimes for thirty or even forty seconds. When the 
pressure is lateral, one leg may be first and most affected, but the 
other side is usually soon involved, since neither the mechanical effect 
nor the inflammation remains limited to one side of the cord. The 
sphincters are often affected. The tendency to the formation of bed- 
sores is rarely great, unless the lumbar enlargement is compressed or 
myelitis descends into it. 
The course of the symptoms varies according to that of their cause. 
When an acute myelitis has been set up, improvement may occur for 
a time even if the cause of pressure is slowly progressive. This is true 
also of root symptoms when they are rapidly developed. If the com- 
pression ceases to increase, the cord may recover its conducting 
function, although it remains narrowed. Sensation is often regained 
in the legs when motion remains absent, but both motion and sensation 
may be regained although the narrowing of the cord persists. It has 
even been found no larger than a goose-quill at the compressed spot, 
although the paraplegia had passed away. In such a case many 
narrowed nerve-fibres are found in the section of the compressed por- 
tion, and it is probable that many axis-cylinders persist, with an 
envelope of mvelin so narrow as to be recognised with difficulty, but 
which suffices for their conducting function. Under slow pressure the 
axis-cylinders may not suffer interruption, although the myelin dis- 
appears. Regeneration of axis-cylinders, as in the peripheral nerves, 
is also possible. In some cases, especially when a considerable 
myelitis has been set up, the motor path may recover, but the posterior 
columns remain affected, so that power returns, but without co-ordi- 
nation,—“ secondary ataxy ” resulting. 
The Diagnosis of slow compression rests on the root and cord 
symptoms already described, and especially on their coincidence 
with a cause of compression. Of the former, the sensory sym- 
ptoms are the most characteristic. In many cases other indications 
of the compressing disease assist the diagnosis. These vary in 
character ; the most frequent is considerable local tenderness of the 
spine. If root symptoms are absent, the diagnosis is much more diffi- 
cult, unless the morbid process manifests itself externally. If there 350 
SPINAL COfiD. 
is a suspicion of compression in a case of slow paraplegia, an early and 
considerable excess of superficial reflex action gives additional weight 
to the suspicion. Even without any other symptoms to indicate com- 
pression, this is suggested by symptoms which begin on one side and 
gradually spread to the other. 
The chief disease from which compression of the spinal cord has to 
be distinguished is a subacute or subclironic transverse myelitis. 
Besides the indications of a cause of compression already mentioned, 
the chief distinction depends on the presence of symptoms indicating 
irritation of the nerve-roots, and especially on the fact that these sym- 
ptoms precede those of the lesion of the spinal cord itself. Although 
a very chronic myelitis is occasionally attended by much irritation of 
the nerve-roots, the symptoms of this succeed, instead of preceding, 
the damage to the cord, and the course of chronic myelitis is often 
much slower than is that of most forms of slow compression. The 
distinction from a growth within the spinal cord rests chiefly on the 
early occurrence of impairment of the central and conducting func- 
tions of the cord, and also on the partial distribution, and often slower 
course, of the The effects of an intra-medullary growth vary 
widely in different cases, and if there is an early irritation of root-fibres, 
the distinction may have to depend on the presence or absence of the 
signs of an external compressing process. 
The diagnosis of the cause of compression is often much more 
difficult than that of its occurrence. The facts that the patient is in 
the first half of life, and that he inherits a tubercular tendency, suggest 
caries. Slightness of root symptoms is also in favour of caries or a 
tumour within the spinal cord; the presence of these symptoms does not, 
however, render caries less likely, unless the pain is extremely severe 
and is greatly increased by movement,—characters that should always 
suggest a growth in the bones of the spine. Boot symptoms extending 
over a considerable vertical area suggest pachymeningitis. Additional 
details of the differential diagnosis will be found in the account of the 
several compressing diseases. 
Prognosis and Treatment.—The prognosis depends on the cause, 
and the amenability of this to treatment. As a general rule, however, 
the more rapidly the cord symptoms develop, the more chance there 
is of improvement, because the greater share does inflammation take 
in their production. The treatment is that of the cause of the com- 
pression and that of myelitis. ACUTE ATfiOPniO PAIiALYSIS, 
351 
ANTERIOR POLIO-MYELITIS; ATROPHIC SPINAL 
PARALYSIS. 
In certain diseases of the spinal cord, wasting of the muscles is a 
prominent symptom. In these the lesion involves, exclusively or in 
part, the anterior grey cornua, and the muscular atrophy depends on the 
■destruction of the nerve-cells, from which the motor nerve-fibres pro- 
ceed, and on the consequent degeneration of the fibres. The muscular 
wasting does not depend on the nature of the lesion ; it occurs equally 
whether the nei've-cells are destroyed by haemorrhage, by inflamma- 
tion, acute or chronic, by slow degeneration, or by pressure. But the 
rapidity with which the destruction occurs influences the character of 
the symptom. Time is required for the change in the nutrition of 
the muscles; one or two weeks elapse, even in the most acute cases, 
before wasting is distinct. The nerve-cells also form part of the 
voluntary motor path, and their disease at once interrupts this ; hence, 
in acute cases, paralysis is rapidly developed, and the atrophy succeeds 
it after an interval. In chronic lesions, on the other hand, the changes 
in the cells and muscles progress so slowly that the weakness and 
wasting appear to come on together. The wasting may even seem to 
precede the weakness, but a careful examination will show that power 
is defective as soon as there is distinct atrophy. It is customary to 
separate the two groups by terming those in which the palsy precedes 
wasting, “ atrophic spinal paralysis;” and those in which wasting is 
apparently simultaneous with weakness, “ spinal muscular atrophy.” 
The atrophic paralyses are due to an acute or subacute process in 
the anterior cornua. The lesion is probably, in most cases, inflamma- 
tory in character, a cornual myelitis, or “polio-myelitis” (Kussmaul). 
In some cases, which differ chiefly in the suddenness of the onset, 
it is probable that the lesion is haemorrhage and not inflammation. 
The chronic atrophies are due to a slow degeneration of the cells and 
fibres. Between the two forms, however, we meet with others of inter- 
mediate course, subacute or subchronic, due to processes of correspond- 
ing character,—usually inflammation, interstitial or parenchymatous. 
Acute Atrophic Paralysis; Acute Anterior Polio-myelitis. 
Infantile Paralysis ; Essential Paralysis of Children. 
Acute atrophic paralysis is a disease in which voluntary power is 
lost in the course of a few hours or days, and in which some of the 
paralysed muscles undergo rapid wasting while others recover. The 
onset of the palsy is often preceded or accompanied by indications of 
general disturbance. The muscles which waste usually remain weak, 
and contraction of their opponents leads to permanent distortion of 352 
SPINAL CORD. 
the pai*alysed limbs. Although it is usually a form of acute myelitis, 
its characters and course are sufficiently special to mahe its separate 
consideration desirable. The disease is the most common form of 
paralysis in young children, and has hence received the name of 
“ infantile paralysis.” Before anything was known of the lesion on 
which it depends, it received (from Rilliet and Barthez) the unmean- 
ing designation of the “ essential paralysis of children,” a term that is 
falling into merited disuse. The spinal lesion was first demonstrated 
by Prevost (1865), and soon afterwards by Lockhart Clarke and by 
Charcot and Jofi'roy. Its constancy has been abundantly proved by 
numerous observations during the last twenty years. The occurrence of 
similar symptoms in adults was noted by Yogt (1858) and Duchenne 
(1864). 
Etiology.—The disease occurs at all ages, but is ten times as 
frequent in the first decade as in all the rest of life. It is, 
moreover, especially a disease of later infancy. Of the cases in 
early life, three fifths occur in tlm first three years of life, nearly 
one fifth in each year. The numbers in each successive year 
(of -116 cases of which I have notes) were—in the first 21, the 
second 21, third 25, fourth 9, fifth 17, sixth 4, seventh 2, eighth 
6, ninth 4. Of the cases that begin during the first year, nearly all 
begin in the second six months; the earliest of the series occurred at 
four months, but one at the twelfth day is described by Duchenne. 
The friends often date the disease from birth, but there is no real 
evidence of its intra-uterine development. After childhood it is 
most frequent between ten and twenty, and very rare over forty. 
Many supposed subacute cases in adults have been examples of 
multiple neuritis. In childhood the two sexes suffer equally (males 
59, females 57), but after ten the malady is practically confined to the 
male sex. The influence of heredity is small, but a family tendency 
to suffer may now and then be traced ; two and even three brothers 
or sisters have been affected (Seeligmuller, &c.). One of my own 
patients had a sister, and another two cousins, affected with the same 
disease. The inherited tendency may be indirect; of a patient in 
whom the disease came on in adult life, two brothers had suffered from 
hemiplegia, and an uncle from paraplegia. 
The disease presents a remarkable relation to season, occurring far 
more frequently in summer than in winter. Sinkler, who first called 
attention to the fact, found that in Philadelphia four fifths of the 
cases commenced in the five hot months, May to September. In this 
country the relation is equally apparent; three quarters of the cases 
occur during the hottest third of the year, June to September. The 
distribution of 71 cases was as follows : One occurred in each of the 
first five months ; in June, 11 ; July, 13 ; Aug., 13 ; Sept., 15 ; Oct., 6 ; 
Nov., 2; Dec., 5. In many cases, the weather was very hot at the 
time; in some, however, the disease came on in cooler weather after 
a hot period. It would, therefore, seem that the heat generally acts ACUTE ATROPIIIO PARALYSIS. 
353 
as a remote cause, and is only occasionally concerned directly 
in the exciting mechanism. Tlie fact is the more important because 
cold has long been regarded as the most potent exciting cause. That 
exposure to cold is an occasional cause is certain, although the number 
of cases in which it can be traced is not large; and it is usually a 
general and not a local exposure, and has not often been immediately 
preceded by exposure to heat. Exceptions are chiefly met with in 
adults. Thus one patient, aged sixteen, when perspiring from a long 
ride after the hounds on a hot day in September, lay down on a sofa 
beneath an open window from which a draught blew on his back. 
Two days afterwards the first symptoms commenced. I have twice 
known the disease to be due to sitting on damp grass. Two or three 
days is the interval which usually elapses between the exposure to 
cold and the onset of the symptoms, but great variations are met 
with, and the constitutional disturbance may commence within twenty- 
four hours of the exposure. 
Over-exertion in walking seems occasionally to aid in exciting 
the disease ; in some cases the child has walked far more than 
was proper the day before the onset, and in others habitual over- 
exertion has been permitted. A traumatic influence, such as a fall, 
occasionally precedes the onset in such a way as to make its influence 
probable. Thus, in one severe case, a boy eight years old was thrown 
over the head of a donkey, and the onset occurred five days afterwards. 
In most cases the fall has produced no immediate symptoms, and has 
perhaps acted generally rather than locally. Thus a girl of four fell 
off a chair, striking her head, and was stunned for a moment; two 
days later she was sick and feverish; the temperature (101°) con- 
tinued raised till the sixth day, when general loss of power was found, 
and the residual state was atrophic palsy of both legs and the right 
deltoid. The cases following falls and over-exertion present the same 
relation to season as do the rest. 
There is no proof of any relation between the disease and the 
process of dentition. The period of dentition coincides with the 
rapid functional development of the nervous system which succeeds 
its structural development in the first few months of life. Moreover, 
this period is often one of deterioration of health, in consequence of 
changes of diet and other causes. The disease occurs before and 
after the period of teething, and it exhibits no increase in frequency 
at the period of the second dentition. 
Many children are perfectly well at the time when the disease 
occurs. A few are in conspicuously defective health. Thus in one 
case the child had been rendered feeble by long-continued diarrhoea. 
I have only once seen the disease in the subject of inherited syphilis. 
It has been thought to be occasionally secondary to acute febrile 
diseases, but the frequency of the relation has been unquestionably 
overrated ; in some supposed cases in adults there has been multiple 
neuritis only, and in children initial general disturbance is constantly 
VOL. I. 354 
SPINAL CORD. 
mistaken for an independent general disease, and the opinion is often 
maintained after the discovery of the paralysis, which is then sup- 
posed to he of secondary origin. Thus in one case initial pyrexia, 
headache, and vomiting were supposed to indicate scarlet fever. 
Paralysis of all four limbs came on, with difficulty in swallowing, and 
the latter was supposed to render certain the diagnosis of scarlet 
fever, although there was no sore throat or rash. In older children 
and adults the disease is often thought to be secondary to rheumatic 
fever, in consequence of the rheumatoid character of the pains. The 
error is the more likely to occur if the symptoms follow exposure to 
cold. It is conceivable that catarrhal affections may be produced by 
the exposure to cold that induces the disease; but of the 116 cases 
referred to above, not one was related to any acute specific disease, 
or to rheumatic fever. Chronic alcoholism has been thought to be 
a cause in adults, but it is probable that most cases supposed to be 
due to this influence have been instances of multiple neuritis. 
Symptoms.—The general characters of the symptoms have been 
already mentioned—an acute onset, often with constitutional disturb- 
ance ; paralysis, at first wide-spread, afterwards passing away, except 
from a region in which the muscles rapidly atrophy, and in which, 
although partial recovery may occur, more or less weakness and wasting 
persist. 
The general disturbance, which is apparently due to a morbid 
blood-state, may be severe or slight. In most cases there is pyrexia, 
with its usual accompaniments, headache, prostration, loss of appe- 
tite, restlessness. Yomiting is very common, and often causes the 
illness to be mistaken for stomach disturbance. Occasionally there 
is also diarrhoea. In children, vomiting is very common, and gene- 
rally causes the illness to be mistaken for simple stomach disturb- 
ance. These symptoms of general disturbance usually last for a 
few days, sometimes for only a few hours, and they are occasionally, 
but not often, absent. The palsy develops in most cases in the course 
of this disturbance. A common history is for a child to seem ill 
and feverish, to be put to bed, and the next morning to be found to 
have lost power. In other cases the febrile disturbance lasts for 
several days before the paralysis comes on. But the relation of the 
general disturbance to the onset of the paralysis presents great 
variations, which appear (from a comparison of cases) to be indepen- 
dent of any variations in, or special features of, the spinal symptoms. 
The constitutional symptoms occasionally succeed the onset. Thus 
a child, well one day, was found next morning to have both legs 
paralysed and was feverish and sick; the general disturbance con- 
tinued for a week. The elevation of temperature is usually moderate 
in degree ; an example of its character, in what may be regarded as 
a fairly typical case, is that of a child whose temperature on the 
second day of illness was 101‘2°; on the third, 101°; the fourth (on 
which the palsy developed), 100°; the fifth, 99 5°; the sixth, 98°. 355 
ACUTE ATROPHIC PARALYSIS. 
It is usually, as in tliis case, highest at the commencement, and 
sometimes reaches 103°, 104°, or even in rare cases 105°. The 
constitutional symptoms are present in most of the cases in which a 
fall appears to excite the disease, and are of the usual character; they 
are as marked in the cases that appear to be spontaneous as in those 
that follow exposure to cold. 
Convulsions occasionally attend the onset, chiefly in young children. 
In some instances, moreover, the initial symptoms are those of severe 
cerebral disturbance. Thus one child had repeated general convul- 
sions during 30 hours, and afterwards was in a state of deep coma for 
36 hours, the temperature at the onset being 105°. This was 
succeeded by slighter pyrexia and prostration for three weeks, and it 
was only at the end of that time that general loss of power was 
found to have come on. The arms recovered, but atrophic palsy per- 
sisted in the legs. In another case, a child of seven months became 
ill, febrile (102 8°) and comatose with pin-point pupils ; it remained 
in that state for four or five days, and then gradually recovered, but 
with general powerlessness, rigidity of the legs, and tenderness of 
legs and back. The rigidity and pain passed away, but the right 
deltoid and, to a less degree, the biceps and triceps and the whole of 
the right leg remained paralysed, and presented characteristic 
atrophy. In adults there is sometimes marked somnolence before the 
onset, and occasionally slight cerebral symptoms, such as diplopia, 
giddiness, or (very seldom) delirium. A medical student found, one 
day, that he saw double; on the next day he felt giddy, and became 
feverish (102°) ; he slept for forty-eight hours, and on the fourth 
day found his right arm was weak ; atrophy of the deltoid, &c., 
followed. The cerebral symptoms always pass away together 
with the indications of general disturbance, and hence are probably 
due to the blood-state. In rare cases, the onset is accompanied by 
symptoms of slight transient spinal meningitis, which must be 
regarded as a coincident effect of the cause, since there is no evidence 
in these cases that the myelitis reaches the surface of the cord, and 
the membranes may be apparently affected early. Thus a child, 
after being feverish and vomiting for two days, became universally 
rigid, so that strychnine poisoning was thought of. The rigidity 
passed away two days later, when the right arm and leg were found 
to be paralysed. Another child presented all the symptoms of spinal 
meningitis a week after the onset of paralysis of the arm, and as they 
passed off the leg also was found affected. When the general illness 
is severe, the paralysis is often not discovered for some time, especially 
in a child ; the immobility of paralysis is often mistaken for the inertia 
of prostration. 
In older children and adults, another common initial symptom is 
the pain already mentioned, sometimes referred to the muscles, some- 
times to the limbs generally, occasionally to the course of the nerves. 
It is often absent, but may be very severe and accompanied by extreme 356 
SPINAL COED. 
tenderness of tlie limbs. In such cases the pain may be supposed t(r 
be in the joints, because it is produced by moving them, when it is 
really in the nerves, which are mechanically disturbed by the move- 
ment of the joints. In these cases there is neuritis, which may come 
on at the same time as the palsy, although independent of it. Pain 
may be felt also in the back. In character it is dull and aching. It 
may be severe, especially when there are symptoms of spinal meningitis. 
Instead of being initial, the pain may succeed the onset of paralysis,, 
and it occasionally continues for several weeks, especially when seated 
in the nerve-trunks. In cases of paralysis of the thighs there is some- 
times persistent pain on movement at one hip or groin, the cause- 
of which is not clear. Tingling or formication in the limbs may 
be described by older patients. 
The paralysis is almost always rapidly developed. It varies much 
in its initial range. Only part of a limb may be affected, or there 
may be universal loss of power ; but in the majority of cases the para- 
lysis is intermediate between these extremes. Two or three limbs are 
affected—both arms, both legs, or the legs and one arm. When all 
four limbs are paralysed the neck-muscles also may be weak, and even 
swallowing may be impaired. The other muscles supplied by the 
cranial nerves escape, as a rule, and the sphincters are unaffected. 
Occasionally there is incontinence of urine, chiefly in severe cases, and 
it may then last a long time. For instance, a child aged two and a 
half years woke up one morning with headache, fever, and weakness 
of the legs, which rapidly increased to complete paralysis. Four days 
later the arms also became weak, and in a day or two more the urine 
esciiped involuntarily. The arms began to recover in six weeks, and 
were well in six months ; both legs wasted and remained permanently 
paralysed ; the incontinence of urine lasted for a year. In another 
case, with incontinence for a few weeks, the residual palsy was in the 
lower legs. As in these instances, the symptom is met with chiefly 
when the lumbar region is diseased. 
The paralysis may commence in one limb and quickly spread, 
reaching its maximum extent in a few hours to a few days, but 
very often the actual onset is so rapid or so escapes careful observa- 
tion in consequence of the general illness that all the parts first 
affected are found to be paralysed when it is discovered. Occasion- 
ally the onset is in two distinct stages, separated by a few days ; now 
and then the loss of power develops slowly in the course of one or 
even two weeks, in cases that must be regarded as “ subacute,” but 
do not differ in other respects from the ordinary form. Examples of 
the common onset have been already given ; as another may be men- 
tioned the case of a boy, aged a year and four months, who one day 
seemed ill, was sick, and was put to bed. The next day he could scarcely 
stand alone ; on the following day he could neither move the legs nor 
sit up in bed. In about ten days the left leg began to improve, but 
there was enduring paralysis and wasting of the whole of the right, AOITE ATROPI3IO PARALYSIS. 
357 
and of the lower part of the left, leg. In another case, a child seemed 
ill, and was kept in bed for five days; on the third day it was noticed 
that the left arm was not moved so much as the right, and by the 
fifth day the arm was quite powerless ; at the end of a fortnight 
improvement commenced. In the adult, the mode of onset presents 
nearly the same characters. A lady, twenty-five years of age, sat 
down for some time on wet grass. Two days later general rheumatic 
pains came on, very severe in the legs on the following day, and the 
legs were distinctly weak. In the course of the next forty-eight 
hours the arms also became feeble, and at the end of a week she could 
scarcely move her arms, and her legs were absolutely paralysed. In 
a fortnight improvement commenced, first in the arms and then in 
the feet; but the hip- and thigh-muscles remained paralysed and 
rapidly wasted. 
Cases are sometimes seen similar m other respects to those now 
under consideration, but in which the paralysis comes on suddenly, 
•and without general disturbance. Thus a child, aged two, was 
walking along, when he suddenly could not stand, and fell down 
on his knees; both legs were powerless. Slow improvement fol- 
lowed in the left leg, and wasting in the right. The suddenness 
of the onset makes it probable that the lesion is kcemorrhage, and 
not simple inflammation. Spinal haemorrhage is known to occuT 
in early childhood. Hence, while we must class these with the othe 
acute spinal atrophies, we are not justified in regarding them as cases 
of polio-myelitis, since we do not know whether the haemorrhage is 
secondary to commencing inflammation or is primary. It is probable 
however, that even a primary extravasation into the grey matter is 
due to the same causes that give rise to inflammation, because the two 
sets of cases occur under the same general conditions of onset, and 
hence they cannot be separated. Moreover, constitutional disturb- 
ance is more often absent in cases of actually sudden onset than in 
others, alihougli it is sometimes considerable. Thus a child had beer 
ill for two weeks, when, being able to walk about, it suddenly fell to 
the ground; the left leg was found powerless, and the right weak. 
It is probable that a sudden onset is more frequent than is suggested 
by the facts that can be ascertained, since the palsy often comes 
on during the night or during rest; for instance, in one case a 
•child sat on a chair for an hour, when the left leg was found 
powerless. 
In some cases of sudden onset the initial palsy is universal, and in 
such cases as the following it is probable that a limited hemorrhage 
in the cervical region causes rapid pressure on all the adjacent 
structures, which afterwards recover from the effects of the pressure. 
A girl, aged seventeen, suddenly felt tingling in the left hand. In 
a few minutes the whole arm was powerless, and then the right arm 
became paralysed. She had a strange sensation at the back of the 
neck, and went upstairs ; as she was going up, her legs became weak, 358 
SPINAL CORD. 
first tlie left and then tlie right. In less than half an hour from the 
time of the first symptom, there was absolute universal paralysis, with 
difficulty in breathing and in swallowing. Improvement (in the 
opposite order to the onset) commenced the same evening and was 
complete in about six weeks, with the exception of the muscles of the 
left forearm and hand, which rapidly wasted and were permanently 
paralysed and atrophied. Another girl, while walking across a road, 
suddenly felt a “ sort of shock” as if someone had given her a knock 
between the shoulders. She became giddy, and instantly felt tingling 
in both arms, especially in the right, which became weak before she 
had got to the other side of the road. Ultimately the arms recovered, 
but permanent paralysis and wasting of the intrinsic muscles of each 
hand were left. 
The initial loss of power is as a rule far more extensive and severe 
than the permanent affection; in a small number of cases the 
two correspond. But the extent of the early palsy, that of the 
enduring atrophy, and the relation between the two, vary extremely, 
so that no general or even common laws can be discovered. Indeed, 
in all features of the disease variability prevails to such an extent 
as to baffle attempts to describe them in general terms, and a better 
conception of the malady can be gained from such illustrative instances 
as are here given, than from general descriptions. One general fact 
is unfortunately true of almost all cases, namely, that the palsy 
scarcely ever passes away entirely, and that where wasting occurs, 
wasting remains. 
After the paralysis has reached its height and ceased to increase or 
spread, whether the point is attained suddenly or rapidly or slowly, 
it remains stationary for a time, which varies from a few days to six 
weeks, and then lessens. The improvement occurs first in the parts 
last affected, and gradually spreads until, usually at the end of 
from one to three months, all parts have recovered except those which 
are to be permanently affected. In these the muscles are toneless and 
flaccid from the first, and in two or three weeks there is distinct wast- 
ing, which rapidly increases, until the shape of the limb is changed, 
and, in extreme cases, scarcely any of the volume of the muscle can 
ultimately be detected. In fat children the appearance of the limb 
may be less altered, and it seems that, in some of these, an interstitial 
growth of fat makes up for the diminution of muscular tissue. In 
older children and adults the muscles are often tender to the touch 
during the process of wasting. 
When the atrophy is distinct the muscles no longer contract to 
faradism, and, if the motor nerves are tested, they also will be found 
to have lost irritability. The change depends on degeneration of 
the nerves, and the muscles usually present the “ degenerative 
reaction ” in its characteristic form. The loss of faradic irritability is 
distinct, in severe cases, as early as the end of the first week, and even 
by the fifth or sixth day. In a patient, for instance, who is universally, ACUTE ATROPHIC PARALYSIS. 
359 
and apparently uniformly, paralysed, one or more groups of muscles 
may be found to have lost irritability, and in these we know that there 
will be lasting paralysis and wasting, while the other parts will recover. 
In a severe case, in which the muscles most affected atrophy completely, 
the loss of faradic irritability maybe permanent. The voltaic irrita- 
bility remains, increased in degree, for two, three, four, or six months, 
then slowly falls, as the muscular fibres themselves degenerate, and 
ultimately, at the end of one or two years, it disappears. It may, 
however, persist for a long time, if the fibres are stimulated by elec- 
tricity,—even for three or four years, although the paralysis remains 
absolute. In rare cases, electrical irritability quickly disappears, even 
to the voltaic current, from the destructive degeneration of the 
muscular fibres. More commonly, after six or twelve months, some 
faradic irritability returns. It may be slight, due to the recovery of 
a few fibres, insufficient in number to restore any bulk or power, but 
the new fibres which recover do so perfectly, so that the irritability 
becomes normal in degree, although the contraction which can be thus 
produced is very slight in amount. In other cases considerable 
recovery occurs, so that some power and volume are regained, 
although the muscles remain below the normal size. In the muscles 
which are weak but do not waste there is no degenerative reaction, 
although there may be slight diminution of excitability to each 
current. 
The paralysis, as a rule, is motor only. Sensation is impaired only 
in extremely rare cases (about 1 in 50), in which inflammation in the 
lumbar region is so intense as temporarily to impair all the conduct- 
ing functions of the cord. Thus, in a girl aged five, in whom the 
permanent state was a symmetrical atrophy of all the muscles 
below the knees, with a slighter affection of the thigh-muscles and 
flexors of the hips, the initial general loss of power in the legs was 
accompanied, for a few days, by complete loss of sensation below the 
knees. In the similar but more severe case of a boy, aged four, in 
whom the lasting palsy was general throughout both legs, the anaes- 
thesia continued for two months. When sensation is lost there is 
always incontinence of urine. 
Reflex action is necessarily lost in the parts related to the affected 
muscles. That from the skin is at first lost where there is weakness, 
but it returns with or soon after the recovery of power in the less 
affected parts. Where there is persistent paralysis it remains absent. 
The myotatic irritability is lost in the same or even gi-eater degree. 
For instance, no knee-jerk can be obtained if the extensors of the 
knee are affected even in slight degree. The loss depends on the 
interruption of the muscle-reflex centre by the disease in the grey 
matter. In rare cases of severe cervical polio-myelitis, the inflam- 
mation spreads beyond the grey matter to the lateral white columns; 
there is wasting of the arms, but paralysis without wasting in the 
legs, and in the latter the myotatic irritability may be increased 360 
SPINAL CORD. 
above the normal, so that the foot-clonus may be obtained. In the 
course of a few months, however, the condition of the legs becomes 
normal. 
A common effect of the disease is to retard the growth of the bones 
in the affected limb, so that this gradually becomes shorter than its 
fellow, and the difference in size increases with the amount of general 
growth. Hence, it is greater, the younger the patient at the onset of 
the disease. If one part of a limb is more affected than another, the 
corresponding bone suffers most in growth. The effect is sometimes 
considerable, when the atrophy is slight. Seeligmiiller has described 
the opposite effect—an actual elongation of the bones, attributed 
to the fact that the growing epiphyses suffer traction instead of the 
normal compression. 
Those joints that depend for their support on tendons which pass 
over them become lax when the muscles are paralysed, and the 
articular surfaces may be no longer kept together. Thus when the 
deltoid is wasted, the head of the humerus may fall out of the glenoid 
cavity. The head of the femur may fall from its proper position in 
the acetabulum, and actual luxation may occur when the paralysis of 
the muscles is unequal, and the less affected unopposed muscles 
undergo the secondary contracture immediately to be described. 
That of the abductors and rotators may cause infra-pubic dislocation, 
and that of the adductors iliac dislocation.* 
During the chronic stage of the disease there is great tendency to 
the occurrence of permanent shortening of muscles, with consequent 
displacement of the parts to which they are attached. Grave de- 
formities are thus produced. It occurs only when the several muscles 
acting on a joint are unequally paralysed; the less affected muscles 
are no longer subject to the normal extension by their opponents, and 
hence gradually become contracted, and the contraction is fixed by 
tissue changes in them, so that they cannot be passively extended. 
It may occur in muscles which are unaffected, and it is uncertain how 
far it is favoured by a slight degree of paralysis. Posture also aids 
the production of these muscular contractions, and so also in the case 
of the foot does the relative shortening of the limb. 
Bedsores are almost unknown, even in the acute stage of the disease. 
A slight local elevation of temperature in the most affected parts has 
been observed in the early stage, but subsequently the affected limb 
is colder than the other. This is due, in part at least, to the want 
of the aid to the circulation which is, in health, supplied by the 
muscular action. 
The persistent paralysis may occupy the whole or part of one or 
more limbs. The legs suffer three times as frequently a,s the arms; 
the respective percentage being 21 and 68. It is less frequent for both 
legs or for one arm to suffer, and still rarer combinations are those of 
both legs and one arm, of both arms, of the arm on one side and the 
* See Karewski, * Arcliiv f. klin. Chir.,’ Bd. xxxvii ACUTE ATROPHIC) PARALYSIS. 
361 
leg on the other, while the rarest of all is the affection of leg and arm 
on the same side. The limbs on the left side of the body are more 
often permanently affected than those on the right; the difference is 
greater in the leg than in the arm. The left leg is paralysed alone 
twice as often as the right. 
When the paralysis of a limb is incomplete, the part involved varies 
much in different cases, and as different parts of two or more limbs 
may be affected, the combinations of palsy which result are extremely 
varied. The grouping of adjacent muscles is sometimes distinctly that 
of functional association ; often it is random ; but the most frequent 
condition is to have an irregular affection of the muscles that are 
associated in the centre. While the grouping is that of function, 
some of the muscles are only slightly affected, and others suffer with 
them that are not functionally associated. In the legs, the paralysis, 
in very severe and fortunately very rare cases, may be absolute, 
involving all the muscles of both limbs. Usually it is partial, and 
then the muscles below the knee suffer more often than those above 
the knee. The calf-muscles 
are affected less frequently 
or in less degree than the 
muscles in front of the tibia 
or the peronei. Hence talipes 
equinus is a common defor- 
mity, and its occurrence is 
FlO. 108.— Old atrophic spinal paralysis. 
Talipes valgus in the right leg from p ira- 
lysis of the anterior tibial; t. varus in the 
left, from paralysis of the peronei. 
FlO. 109.—Atrophic spinal para- 
lysis, affecting chiefly the calf- 
muscles, with resulting contrac- 
tion of the flexors of the foot, 
causing talipes calcaneus. 
aided by the shortening of the limb, in consequence of which the 
foot has to be extended to bring the ball to the ground. Either 362 
SPINAL CORD. 
the tibialis anticus or the peronei may be more affected, with the 
resalt, in the former case, of talipes valgus, in the latter of talipes 
varus. In the case shown in Fig. 108 the peronei have suffered most 
in the left leg and least in the right, producing an unsymmetrical but 
corresponding distortion of the feet. This affords an illustration of 
another fact, namely, that when there is 
a partial affection of both legs the para- 
lysis may be unsymmetrical in the two. 
Much less commonly the calf-muscles 
suffer more than the others, and there 
results talipes calcaneus, as in the cases 
shown in Fig. 109, and the intrinsic 
muscles of the foot often suffer with 
those of the leg. In the thigh, the ex- 
tensors of the knee are affected more 
frequently than the flexors, and hence 
flexor contraction is very common, and 
may even cause subluxation of the joint. 
The flexors of the hip often suffer, 
generally with the extensors of the knee. 
Less commonly the glutei are involved, 
but never alone. 
In the arm, almost all the muscles are 
sometimes affected, as in the case shown 
in Fig 110, but all are seldom entirely 
paralysed. The intrinsic muscles of the 
hand often suffer: either the thenar 
muscles or the interossei may be most 
damaged. An instance of such para- 
lysis of the interossei is shown in 
Fig. 111. The forearm muscles are 
frequently affected, but the supinators 
may escape when the other muscles are 
involved. The deltoid suffers more fre- 
quently than any other single muscle of 
the arm. It may be paralysed alone or in 
association with other muscles; occasionally the deltoid, supra- and 
* 
FiG. 110.—Atrophic spinal para- 
lysis, infantile form. Wasting 
of all the muscles of the left 
arm from the deltoid down- 
wards, and of the right ser- 
ratus magnus. 
FiG. 111.—Atrophic spinal paralysis (adult form) affecting the interossei 
and thenar muscles, and also the deltoid. ACUTE ATROPHIC PARALYSIS. 
363 
infra-spinatus, biceps, and supinators are all involved in the “ upper 
arm type ” of palsy of Erb* (seep. 91). But other muscles than 
these may be associated with the deltoid. The irregularity of the 
grouping is shown by the fact that the triceps is often affected with 
these muscles. In the case shown in Pig. Ill the deltoid and intrinsic 
muscles of the hand were wasted, and no other muscles. The serratus 
magnus is occasionally affected, as in Fig. 110 ; in this case, although 
the left arm had suffered severely, as the figure shows, on the right 
side only the serratus was involved. With the serratus, the upper 
part of the pectoralis major is sometimes associated in paralysis 
(as it is in normal function, see p. 30), the lower part being unaffected ; 
it was so in this patient. The middle part of the trapezius and other 
scapular muscles are occasionally involved. The neck-muscles rarely 
suffer, but the diaphragm is occasionally paralysed. Although the 
intercostals and other truuk-muscles are so often weakened in the 
early stage, considerable permanent atrophy is very rare. Curvature 
of the spine is sometimes produced in consequence of the patient 
being allowed to sit up while the muscles are weak. It may be a 
lateral or an antero-posterior curve, according as the weakness is 
on one or both sides. I have met with considerable depression of 
the lower part of the wall of the thorax on the left side from para- 
lysis of the intercostal muscles at the spot, perhaps combined with 
hindered growth of the ribs. The muscles supplied by cranial nerves 
are scarcely ever affected. I have once seen complete paialysis of 
one side of the face, associated with wasting in the limbs, in an other- 
wise characteristic case, and an instance of affection of the face and 
tongue has been recorded by Pasteur.f 
The Course of the disease has been already sketched. There are (1) 
an initial stage of paralysis, rapidly increasing, often accompanied with 
fever; the duration of this stage is from a few hours to a week or 
even more ; (2) a stationary period, which lasts for a week to a month ; 
(3) a stage of “ l’egression,” during which the palsy passes away, 
except from certain parts in which wasting occurs; this regressive 
period usually occupies from one to six months; (4) a chronic stage, 
during which the atrophy continues; slight improvement may occur, 
but contractures and deformities are developed. The duration of this 
stage is indefinite, because, wherever muscular tissue remains and 
some voluntary pjower returns, this slowly improves, by increased 
development of the muscle under the influence of use, and this 
continues in slight degree for years. This gain is often, however, 
more than counterbalanced by the interference with growth, and by 
the occurrence-of deformities. Even in the slightest cases complete 
recovery is extremely rare, and the limb remains smaller than its 
fellow. On the other hand, death from the disease is equally 
uncommon, and occurs chiefly in the early stage. It is not improbable 
* See a paper by Dr. Beevor, ‘ Med.-Chir. Trans.,’ 1885. 
f * Lancet,’ 1887, ii. 364 
SPINAL CORD. 
that some children die from the initial disturbance before its nature 
is recognised. Now and then death occurs at the end of the first 
week or ten days, from universal paralysis or from some such severe 
cerebral disturbance as existed in the cases mentioned above, or as 
followed the spinal lesion in a case in which paralysis in the arms 
came on upon the third day of the initial fever and reached its height 
on the fifth day, faradic irritability being lost by the seventh in 
many muscles of the left arm ; a little rigidity of the neck then 
occurred, and on the tenth day the patient began to vomit, complained 
of increased headache, and had hallucinations ; on the eleventh day he 
became comatose and died. Bronchial catarrh is an occasional cause 
of death, when the respiratory muscles are weak. 
Relapses are very rare, and occur chiefly in the form of a separate 
later extension of the disease. Second attacks are almost unknown ; 
one instance only was met with in the series of 116 cases. 
Sequelae, beyond those mentioned as part of the symptoms of the 
disease, are also very rare. As a rule the general and nervous health 
of the patients, and the duration of life, are uninfluenced by the local 
palsy. In a few cases, ho /ever, some other chronic affection of the 
spinal cord has come on when the subjects of infantile paralysis have 
reached adult life. Progressive muscular atrophy has been several 
times observed to start from the paralysed limb, and sometimes to be 
apparently excited by a fracture of the bone.* Acute and subacute 
polio-myelitis in adult life has also been observed, and I have twice 
seen the symptoms of lateral sclerosis, without atrophy, slowly 
developed, in one case at seventeen, in the other at twenty-eight. In 
the spinal cord of the subject of old infantile paralysis there seems 
thus to persist a disposition, slight though it be, to fresh disease, and 
the cases of lateral sclerosis mentioned show that the liability to 
disease is not limited, as has been thought, to the grey matter f The 
altered structure of the bones has been known to facilitate this fracture; 
in one case the bones in the affected limb were broken on three sepa- 
rate occasions (Dutil). 
Pathology.—For a long time, infantile paralysis was believed to be 
a peripheral affection, having its seat in the muscles. But improved 
methods of examining the nerve-centres have shown that changes in 
the spinal cord invariably exist, and have the characters of an acute 
inflammation of the grey substance of the anterior horns. The 
correspondences, between the infantile and adult forms, make it certain 
that the latter are, in most instances, of the same nature. Subacute 
atrophic paralysis in adults has been found, however, to depend on 
disease of the nerves in some forms that were thought to be spinal, 
but the acute disease is certainly identical with the infantile form. 
Observations on the changes in the spinal cord in the early stage 
are few. A case recorded by Dr. D. Drummond, in all probability 
* Raymond, ‘ Prog. Med.,’ 1880 : Dutil, * Gaz. Med. de Paris,’ 1881. 
f Compare Ballet and Dutil, * Revue de Medeeine,’ January, 1884, p. IS. ACUTE ATPOPHIO PA11ALYSIS. 
365 
one of thin disease, is by far the earliest on record, and is indeed the 
earliest possible * A child, five years old, died alter a few hours' 
acute illness. The spinal cord, in the region of the fourth and fifth 
cervical nerves, presented undue redness of the anterior grey matter. 
The vessels running from the surface to the cornu were distended 
with blood. The microscope showed distension of capillaries and 
minute extravasations in the 
grey substance, swelling of 
the neuroglial elements and 
of the ganglion-cells, which 
were granular with indistinct 
processes. Another important 
early observation is that of 
Dr. Charlewood Turner,f six 
weeks after the onset (Fig. 
112). In this and other 
somewhat later cases, acute 
changes have been found in 
the anterior cornua, more 
advanced than in Drum- 
mond’s case. They are often 
widely spread in slight de- 
gree, and attain considerable 
intensity in one or more foci, 
usually in the cervical or 
lumbar enlargements or both. 
At these spots the anterior 
horn is softened ; sometimes 
there is haemorrhagic infiltra- 
tion, sometimes an actual 
cavity (Fig. 112, A, b). The 
microscope shows extrava- 
sated blood, often massed 
along the vessels (Fig. 112, 
c),and scattered through the 
grey matter with other cells 
such as are met with in mye- 
litis. There are also granule 
corpuscles and other products 
of degeneration of the nerve- 
elements. These elements, 
and especially the motor 
nerve-cells, have almost entirely disappeared. 'Where the change is 
slighter in degree there is a leucocytal infiltration, a few granule 
corpuscles are seen, while the nerve-cells may be structurally intact, 
but swollen, and granular. The morbid appearances may be con- 
Flo. 112.—Acute anterior polio.myelitis in a 
child years old, six weeks after the onset. 
(After Charlewood Turner.) a. Section 
through the lowest part of the lumbar en- 
largement, showing a cavity visible to the 
naked eye, on the left side. b. Lett ante- 
rior half of the cord under a low magnify- 
ing power, showing destruction of almost 
the whole anterior cornu, c. Portion of 
anterior cornu in the upper part of the 
lumbar enlargement. Numerous corpuscles 
lie in the granular protoplasm and reticulum 
of fine fibres. A small artery is encrusted 
with several layers of corpuscles and nuclei. 
* Brain,’ April, 1885. 
t * Path. Trans./ vol. xxv, p. 203. 366 
SPINAL CORD. 
fined to the anterior cornua, or may extend in slighter degree into 
the adjacent lateral column, in which the nerve-fibres near the grey- 
matter may undergo destructive degeneration, and other signs of 
inflammation may be seen. The posterior columns are always un- 
affected. In very severe cases there may be signs of slight local 
meningitis corresponding in position to the region chiefly affected. 
This region corresponds to the origin of the nerves supplying the 
muscles in which there is most wasting, and the anterior nerve-roots 
which arise from this part present the signs of acute degeneration. 
Such changes indicate a general or interstitial inflammation of the 
grey matter. But some observations have revealed only alterations 
in the motor nerve-cells, which have presented granular degeneration, 
the basis-substance between them being quite unaffected.* This 
suggests that there is a form of polio-myelitis in which the changes 
are essentially parenchymatous and not interstitial. 
At a later pei*iod, years after the onset, the appearances presented 
accord with those described as commonly found in the early stage, 
allowance being made for the difference in time. The anterior cornu 
at one or more places is shrunken (Fig. 113), and in part stains 
FiO. 113.—Atrophic spinal (infantile) paralysis. A. First lumbar ; the left anterior 
cornu is sma ler than the right, and its ganglion-cells have disappeared with the 
exception of the inner group, b. Fourth lumbar; the whole left half of the cord 
is smaller than the other, in consequence of the diminution in size of the ant. 
horn. Of the ganglion-cells only a fewr remain, belonging to the antero-lateral 
group. Similar changes existed throughout the lumbar enlargement.f 
deeply with carmine, in consequence of its nervous structures being 
replaced by connective tissue, in part less deeply in consequence of 
“granular disintegration” of the substance. The motor nerve-cells 
are absent, partially or entirely. Sometimes a few shrivelled cells 
remain, sometimes one or more groups may be unaffected: or one or 
two nerve-cells of normal appearance may alone remain (see Fig. 113). 
Small foci of disease may be seen in the unaffected part of the 
* Rissler, ‘Nord. Med. Ark./ xx. 
f For these sections I am indebted to Dr. H. Humphreys, of St. Leonards. The 
paralysis came on at one and a half years of age, twc years before death, and involved 
most of the muscles of the left leg, those of the calf in greatest degree, so that 
talipes calcaneus had developed. ACUTE ATROPHIC PARALYSIS. 
367 
grey matter, and in these the motor cells may be smaller than 
normal; the intervening plexus may have perished. When one horn 
is much damaged, the other may merely present fewer nerve-cells than 
normal, with perhaps a little condensation of the interstitial tissue. 
The antero-lateral column is usually lessened in size, and may 
present slight sclerotic changes, especially in a zone contiguous to the 
grey substance, whence thickened septa may radiate into the white 
column. This is evidently due to the extension of an intense inflam- 
mation of the grey substance to the adjacent part of the white column. 
Sometimes a slighter sclerosis can be traced through the lateral 
column ; this is seen chiefly in cases of long duration, and is probably 
secondary. With extreme damage to both cornua there may be 
ultimately great wasting of the white columns on each side.* In 
consequence of these alterations, the affected half of the cord is 
conspicuously smaller than the other, even to the naked eye, and the 
difference is greatest where the damage to the grey matter is most 
intense. The anterior nerve-roots at the most affected part are 
small and grey, and the degeneration of the motor fibres may be 
traced down the nerve-trunks. Often a few fibres present a normal 
appearance although the rest have perished; those that remain may be 
for the sympathetic system. 
The muscular fibres, in early cases, have been found narrower than 
normal, and in a state of granular degeneration, with an increase in 
the nuclei of the sheath and of the interstitial tissue. G-ranules and 
pigment-masses accumulate between the sarcolemma sheaths. In 
extreme cases the degeneration proceeds to complete disappearance of 
the fibres, the place of which is occupied by fibrous tracts, developed 
partly from the sarcolemma sheaths and partly from the interstitial 
connective tissue. It is common to find, here and there, a fibre 
presenting normal appearances. Sometimes fat accumulates in the 
interstitial tissue, so that the reduction in the bulk of the muscle 
may be less than that of the fibres. In slighter cases, in which 
partial recovery takes place, some of the fibres probably regain their 
normal appearance, even though they have undergone slight granular 
degeneration. Usually, however, many fibres perish ; those which 
recover are smaller than normal, and the original volume of the 
muscle is rarely regained. Although there may be a permanent increase 
in the interstitial tissue, this undergoes contraction and comes to 
occupy but a small bulk. Muscular fibres are often seen that are 
larger than normal, and this is not (as has been thought) a transient 
condition, for it has been observed seventy and forty-five years after 
the onset.f It is perhaps sometimes a true hypertrophy.! 
* See ‘ British Med. Journal/ 1887, p. 187. 
f Joffroy and Achard, ‘Arch, de Med. Exp./ 1889: Deierine and Huet, ‘Arch, 
de Phys./ 1888. 
J Dejerine. It is said to have been met with in muscles totally paralysed; but 
it is doubtful whether “ total palsy ” of a muscle excludes voluntary contraction of 
some fibres in it. 368 
SPINAL CORD. 
The bones have been found, not only shorter than normal, but also 
smaller, with their angles rounded, the compact substance more 
uniform, and the Haversian canals smaller (Joffroy and Achard). 
The brain has been almost always found normal. In one case with 
extensive paralysis, of long duration, some atrophy was found in the 
motor region of the cortex (Sanders). It is probable that some 
acute changes would be found in cases that die with the cerebral sym- 
ptoms already described. 
No observations have as yet been made on the acute primary poly- 
neuritis that seems occasionally to coincide with the inflammation of 
the cord. It is probable that, in the cases in which the nerves are 
tender in the middle of their course, the sheath will be found inflamed, 
and only the motor fibres will present such signs of secondary degene- 
ration as always result from the lesion of the cord. 
Pathology. —Both the character of the lesion and its mode of 
onset suggest that it is inflammatory in the majority of cases. In rare 
instances, as already stated, the almost instantaneous onset makes it 
probable that the lesion is different in character, is vascular in its 
nature, probably haemorrhage. These cases have, moreover, the 
features of a primary haemorrhage, not of haemorrhagic myelitis. 
Signs of inflammation do not precede the sudden onset. Thus these 
cases, while they belong to the clinical group of acute atrophic 
paralyses, cannot be placed in the pathological category of polio- 
myelitis. They usually differ from the inflammatory cases in another 
respect, that the lesion is confined to one spot in the cord, whereas in 
the cases that are certainly myelitic it is frequent for several parts 
of the cord to be damaged. 
The symptoms are well explained by the pathological facts that 
have been ascertained, extended by the simple inferences that are 
indicated by the symptoms. The lesion interrupts the motor path, 
causing immediate palsy, which results from damage to the cells and 
nerve-plexus of the grey matter, whether slight or severe. The 
recovery of the slightly damaged structures restores the voluntary 
path, and even if the fibres from the cells degeuerate, they seem to 
regain normal nutrition by regeneration when the cells recover. But 
when the motor cells are destroyed the fibres from these degene- 
rate permanently. As the damage is usually far wider than the 
destruction, the initial palsy is more extensive than the persistent 
atrophy, aud the extent of such is purely a matter of this relative 
area of trifling and severe degree of lesion. Nerve-cells that are 
destroyed are never renewed, and hence the permanence of the muscular 
wasting that depends on such destruction. When a few nerve-cells 
escape destruction, a few nerve-fibres recover and a little muscle-tissue 
remains, too slight, it may be, to be of use. The occasional interference 
with the conducting tracts in the white columus is explained by the 
obvious extension of the inflammation, which, when very intense, may 
even spread through all the structures of the cord, as in the cases in ACUTE ATROPHIC PARALYSIS. 
369 
which sensation, as well as motion, is lost. But such cases, which are 
most rare, differ from true transverse myelitis in the rapidity with 
which the damage restricts itself to its special seat, and the functions 
of the white columns are restored. The fact that these are diseased 
in only a secondary and trifling manner is emphasized by the fact 
that, even in these cases, there are never the acute bedsores that 
would surely ensue in a case of true transverse or total myelitis of 
corresponding seat. 
The observations mentioned on p. 366 suggest that there are two 
varieties of the inflammation of the grey matter, such as we have 
recognised in myelitis generally; a parenchymatous inflammation 
consisting in a primary change in the nerve-cells, and an interstitial 
or general inflammation, as in the common forms of myelitis, 
involving the nerve-cells only as one of many structures equally 
damaged by a process that has no special relation to the nerve- 
elements. The distinction is important, because we should expect to 
find, in the former cases, a wider slight initial affection than in the 
others, and finally a more definite relation to function in the parts 
diseased. 
The true pathology of the malady, its relation to its causes, is still 
obscure. The one salient fact that we can discern, though scarcely 
define, is the evidence of a blood-state afforded by the general 
symptoms. That these symptoms are not the consequence of the local 
inflammation is shown by their disparity in degree and difference in 
time. It is probable, therefore, that the spinal lesion is not the cause of 
the constitutional disturbance, but is rather an effect of the cause of 
the latter. It seems impossible otherwise to understand the extreme 
variation in the two forms of disturbance. But we have no evidence 
as to the nature of the blood-state, and there are no other effects, 
commonly associated with the myelitis, to indicate the general patho- 
logical tendency of its cause. The closest analogy is with some 
forms of multiple neuritis, and this, as we have seen, may co-exist with 
the spinal lesion, as a consequence, at any rate, of exposure to cold. 
The variations, alike in the general symptoms, and in the inflam- 
mation of the cord, and especially the indications that the latter may 
be either parenchymatous or interstitial, suggest that the causal state 
also varies considerably in different cases. We have no indication of 
the way in which the remarkable relation to season is produced, 
whether by predisposing the individual or favouring the development 
of some toxic agent. We must, however, recognise as an essential 
element the predisposing influence of age, which we may associate 
with the facts that the structural development of the nervous system 
is complete, but the function of the nerve-elements must lack the 
stability that comes only from continued use, and that the period is one 
of the first serious demand on the functional energy of the grey matter 
of the cord. We may remember also the vascular activity that all 
function entails, and the readiness with which the vaso-motor system 
VOL. I. 370 
SPINAL CORD. 
of children is disturbed. Such a glimpse of the pathological relations 
of the disease is all that we can at present obtain. 
Diagnosis.—This rarelv presents any difficulty except in the early 
stage. When the initial paralysis is passing away, and the wasting is 
distinct, the nature of the case is sufficiently evident, and is cor- 
roborated by the electrical reactions, by the loss of reflex action, and 
by the absence of any impairment of sensibility. At the onset, 
however, the symptoms may readily be misinterpreted. The most 
common error is to attach too much importance to vomiting, and 
to regard the attack as simply gastric. General disturbance is 
naturally ascribed to some general cause until nervous symptoms 
manifest themselves. Even then there is risk of error. On the one 
hand, as we have seen, a diagnosis of a general disease is not always 
relinquished when paralysis appears, but the latter is regarded as 
secondary. On the other hand, especially in young children, the 
existence of paralysis is often overlooked at first, and it is supposed 
that the child does not move because it is prostrate. This error will 
not be made if it is remembered that mere prostration never causes 
total immobility, and a fortiori it does not produce local immobility. 
When the pyrexia ceases, and the loss of power persists and increases, 
the existence of paralysis is always unmistakable. The initial general 
disturbance must then be regarded as part of the disease unless there 
is the clearest evidence of its independent nature. 
In adults, the danger of mistaking paralysis for prostration is con- 
siderably less, but, on the other hand, the general symptoms are as 
likely to be misinterpreted as in the case of children. The rheuma- 
toid pains, which are so common, are usually regarded as evidence of 
acute rheumatism, especially when the affection follows exposure to 
cold. Whenever rheumatoid pains are not localised in the joints, 
and especially when they are spontaneous, and not influenced by move- 
ment, the possibility of their spinal (or nerve) origin should be remem- 
bered, and other indications of spinal mischief, such as local loss of 
power, tingling or formication, should be carefully watched for and 
receive due weight. 
Of other spinal cord diseases, all chronic lesions are distinguished 
at once by the onset. From other acute diseases, moreover, the dis- 
tinction is only difficult in the early stage. As soon as the initial 
palsy begius to lessen, and the muscles in one part lose fai'adic irrita- 
bility and begin to waste, the nature of the case admits of no doubt. 
The diagnosis may be thus made with certainty after the end of the 
first week by the electrical reaction. If we find loss of faradic irrita- 
bility, it is certain that the characteristic alteration in voltaic irrita- 
bility will follow. The isolated induced shocks should be used, instead 
of the induced “ current,” because any harmful stimulation of the 
sensory nerves is thereby avoided. 
Acute transverse myelitis is only simulated when the inflammation 
of the grey matter is bilateral and so intense as to extend to the ACUTE ATROPHIC PARALYSIS. 
371 
white columns, but the age of the patient generally suggests correctly 
the nature of the disease. The myelitis of childhood is polio-myelitis. 
The pseudo-transverse variety—polio-myelitis, transverse through its 
intensity—is seated in one of the enlargements ; the true transverse 
form usually occurs in the dorsal region. Real difficulty is confined to 
adults, in whom there is extensive cervical or lumbar myelitis involving 
the grey matter. In young adults, polio-myelitis is more likely ; this 
is indicated also by what is best described as a regressive onset in 
contrast to one that is progressive. In the former, a wide extent is 
quickly reached and the symptoms then tend to lessen; in the latter, 
the morbid process is a longer time reaching its height: in the former, 
the symptoms clearly show that the most severe affection is of the 
anterior grey matter ; in the latter, severe anaesthesia or trophic dis- 
turbance may point to an equally intense lesion of the other parts of 
the cord. If attention is paid to the character and significance of the 
symptoms, the difficulties will soon vanish ; and the cases that present 
them are really few. Most perplexities will, indeed, be prevented by 
the recollection of the fact just mentioned, that primary myelitis in 
children is always polio-myelitis. The separation of subacute from 
acute myelitis of the grey substance is, to a large extent, arbitrary. 
The symptoms are similar, but the onset is less rapid and occupies 
more than a week. The distinction of diphtheritic paralysis and of 
multiple neuritis is from the subacute rather than the acute spinal 
-atrophies, and is considered in the next section. 
The diagnosis from paralysis of cerebral origin is usually easy. In 
cerebral palsy there is never loss of faradic irritability or extreme 
muscular wasting, or loss of the muscle-reflex action. In the spinal 
affection there is no trace of the mobile spasm that is common in 
infantile hemiplegia. Any cerebral symptoms which may attend the 
-onset of polio-myelitis are subordinate in significance to the state of 
the muscles, as evidence of the permanent lesion. Convulsions at the 
onset of infantile spinal paralysis are general; those that result from 
a cerebral lesion are usually unilateral or commence locally. 
The exceedingly slow onset of pseudo-hypertrophic paralysis, 
developing gradually, as it does, with the child’s growth, ought to 
render its confusion with polio-myelitis impossible. A reasonable 
doubt can only arise in a slight case in which the onset was unnoticed 
or forgotten. I have once known slight atrophic palsy of the exten- 
sors of the knee to induce the habit of putting the hand on the knee 
in rising from the gi’ound—an action often thought to be peculiar to 
the pseudo-hypertrophic disease, but acquired when weakness of the 
extensors occurs in early childhood from any cause. If this is not 
known, it may puzzle the observer. 
Diseases outside the nervous system which have been mistaken for 
infantile paralysis are chiefly those in which local pain interferes with 
the movement of the limbs, and the child is young. I have known, 
for instance, the mistake to be made in the case of hip-joint disease^ 372 
SPINAL CORD. 
necrosis of the femur, and the affection termed “ scorbutic rickets,” iu 
which there is enlargement of the shafts of the long bones, extreme 
pain on movement, and spongy gums. In all these cases, a careful 
examination will show that movement is interfered with only by the 
pain ; there is no actual paralysis, and there is no interference with 
reflex action. The preservation of the knee-jerk is often of great 
significance; it at once excludes atrophic palsy in any case in which 
the extensors of the knee are weak. 
The points above described will always enable the diagnosis to be 
made. It is impracticable to enumerate the distinctions from every 
disease with which confusion is possible, for experience shows that 
there is no form of palsy with which a common disease, such as this, 
is not at some time confounded. 
Prognosis.—The danger to life is probably greatest when there is 
severe constitutional disturbance, and is in consequence of this, often 
before the development of the characteristic paralytic symptoms. In 
the stage of paralysis, there is peril only when the chief disease is in 
the cervical region, and respiration is interfered with ; but this danger 
is small unless an attack of bronchial catarrh is intensified by the 
palsy. Definite cerebral symptoms involve danger proportioned to 
their character and degree, but it is generally less in reality than in 
appearance. In the vast majority of cases the disease involves no 
immediate danger to life. But children are left with little power of 
resistance to other morbid influences, and occasionally succumb to 
some other illness, as an acute specific disease, or an attack of 
bronchitis, a few weeks or months after the onset of the paralysis. 
As soon as the paralysis has become stationary, i. e. has not 
increased for twenty-four hours, the danger of further extension is 
small. But the question at once arises, and is anxiously asked,— 
What will be the permanent condition ? Will there be lasting 
paralysis? An answer cannot be given until the end of the first 
week or ten days, and then only by means of an electrical examina- 
tion. Whatever muscles, at the end of that time, have lost faradic 
irritability, will certainly waste, will remain for a long time paralysed, 
and will probably be permanently affected in some degree, slight or 
severe. On the other hand, if there is no loss of irritability at the end 
of ten days, but it is apparent at the end of a fortnight or three 
weeks, the wasting will be slighter in degree, and some ulti- 
mate recovery may be anticipated even in the most affected part. 
Where there is no loss of irritability, the paralysis will pass away in 
the course of a few weeks, or at most of a few months. Where 
faradic irritability is lost early and completely, the wasting will be 
rapid and great, and it is unlikely that there will be much recovery 
of power or nutrition, although some use may be regained. The 
return of faradic irritability that has been lost is a favorable indica- 
tion ; it signifies nerve-regeneration, and will be followed by an 
increase in voluntary power. Without an electrical examination it is ACUTE ATROPHIC PARALYSIS. 
373 
necessary to wait longer before a prognosis can be given, until 
distinct wasting on tbe one band, and improvement on the other, 
indicate the regions in which the paralysis will persist and in which 
it will pass away. Even then the prognosis must be much less 
definite. 
In the chronic stage, the prospect of ultimate recovery depends on the 
rate at which wasting developed, on the electrical reaction, and on the 
duration of the case. Where there is no sign of returning power at the 
end of three months, very little recovery will occur; the nerve-cells 
are destroyed and their renewal is impossible. The preservation of 
voltaic irritability (of the muscular fibres) is so far satisfactory that 
it shows there has been no destructive degeneration of the muscles ; 
and if voluntary power is increasing, it indicates favorable condi- 
tions for its exertion, but it does not lessen the grave significance of 
persistent palsy and the absence of faradic irritability that indicates 
persistent nerve-degeneration. Oh the other hand, if, at the end of 
one or two months, some faradic irritability can be still detected, 
although low in degree (i. e. elicited only by a strong current), 
improvement is probable, and may be considerable in the course of a 
few months. It is necessary, in the case of children, to remember, 
and to warn the friends, that the growth of the most affected limb will 
be hindered, and that this, in the case of the leg, may render the 
effect of the paralysis more obtrusive by its interference with the 
gait. Otherwise they are distressed by what seems to them an 
increase in the disease, but is really compatible with continued 
improvement. 
Treatment.—The treatment of the acute stage of the disease is 
essentially the same as that of myelitis, already described, and the 
rules and principles already stated need not be here repeated. In the 
initial stage it should be that of tbe general state, guided by any 
special causal indications that may be detected; such as free sweat- 
ing, followed by salicylate of soda or salicin, in a case distinctly due 
to exposure to cold. We may hope that future observations will 
afford us some indications regarding the means of counteracting 
other blood-states that apparently exist at the onset, and are con- 
cerned in the production of the lesion. At present we are without 
this help, and can only treat the initial stage as we should any other 
local inflammation, directing our treatment to the symptoms that 
may be present, and the conditions that apparently underlie them. 
The child should be kept at perfect rest, on the side, and warmth 
applied over the affected part of the cord by poultices or fomenta- 
tions. The marked relief these give when there is spinal pain, make 
it probable that they exert a beneficial influence in all cases. 
In such a disease—in which there is a natural tendency for the 
morbid process to cease to spread, and then to lessen in extent—the 
difficulty of ascertaining the effect of treatment on the lesion of the 
spinal cord is very great. Full doses of belladonna or ergot have 374 
SPINAL COED. 
been credited with the control and arrest of the morbid process, 
but onlj ou the evidence of a coincidence in isolated cases, the value 
of which is small in a disease so irregular in its course. Either may 
apparently be employed, however, without fear of harm. 
When the acute onset is over and the spinal lesion has become 
stationary the careful management of the early stage must be 
continued for a time, because a relapse or recurrence, however rare, 
is not entirely unknown. Such care is especially needed in cases in 
which the constitutional disturbance has been prolonged, or has 
continued after the onset of the spinal symptoms, or the latter have 
come on in distinct stages. Under these' circumstances, perfect 
rest should be maintained for one or two weeks more. The same 
prolonged care is needed when there is persistent tenderness in the 
limbs or any indications of an independent neuritis. Where wasting 
is taking place, some tenderness of the nerves and of the muscles 
must be expected to accompany the process, and this, being purely 
secondary in nature, does not call for special treatment. 
When the acute stage is over, and the condition of the patient is 
stationary or improving, tonics are generally both useful and needed, 
especially iron and quinine. Strychnia may be given in all cases, but 
it should be commenced only two to four weeks after the disease has 
become stationary. Although clear proof of its utility is not forth- 
coming, and cannot indeed be expected in a disease in which merely 
damaged nerve-elements always tend to recover, the drug has a certain 
influence on the nutrition of the structures that are specially affected, 
and it is reasonable to suppose that it promotes their recovery, and 
is capable of rendering this more perfect. But an agent that has so 
powerful an influence on function (and therefore on nutrition) is 
likely to do harm, rather than good, until normal conditions are being 
restored. If function cannot respond properly to a stimulus, it is not 
likely that nutrition can be influenced aright, or that its derangement 
can be other than increased. Hence, the more severe the lesion the 
longer time should elapse before strychnia is commenced, and the 
smaller the dose that should at first be given. It is probably never 
either necessary or desirable to give it by hypodermic injection in this 
disease. 
The disease frequently occurs at the age at which any illness causes 
the hindrance to general development that constitutes the condition 
known as rickets, and this fact should be remembered in treatment. 
In the case of children who are still in the period of the first denti- 
tion, it is, therefoi’e, wise to anticipate the danger by giving, during 
convalescence, those agents that have most influence in counteracting 
the tendency, especially cod-liver oil and iron ; the lacto-phosphate of 
lime and iron is especially useful. 
The use of electricity is an important part of the treatment, although 
for reasons very different from those that first led to its use, and it is 
desirable that they should be clearly comprehended to secure its ACUTE ATROPHIO PARALYSIS. 
375 
benefit and prevent its harmful or useless employment. There is no 
evidence that it can or does influence the process of recovery of the 
damaged elements in either the spinal cord or the nerves. Moreover, 
as long as the nutrition of these is actively disordered, its stimulating 
influence is likely to increase the derangement rather than promote 
the restoration of a normal state. The reasons for its use depend on 
the fact that the disease entails nerve-degeneration, and are essen- 
tially the same as those that justify and determine its employment in 
other nerve-lesions, and have been already explained. The muscular 
fibres whose nerves are degenerated suffer changes in nutrition, 
and ultimately perish, if no nerve-regeneration occurs. While the 
influence normally exerted by and through the nerve-fibres is in 
abeyance, the muscles are destitute of this influence, and without any 
functional stimulation. If they are excited, from time to time, by 
electricity, their sensitiveness to stimulation is distinctly increased, 
and this not only to electricity but to the voluntary stimulus. This is 
clearly shown by cases that have been untreated ; the muscles may 
not respond at all to the first application, but when they have been 
galvanised two or three times a distinct contraction may be obtained, 
and, within a week, some voluntary power may return. Wherever 
cell and fibre have perished, nothing that electricity effects can 
be of service; but where there has been damage, not destruction, 
and the fibres slowly recover, but regain their influence on nutrition, 
and their capacity for conveying impulses, only after some months, 
the failure of muscular nutrition may be disproportionately great, and 
may even render useless some regained nerve-power. This result 
electricity is probably able to prevent. It does not, as far as we 
can perceive, prevent or even lessen the visible wasting of the 
muscles; it is powerless to counteract the effects of a destructive 
lesion, but it does seem to hasten recovery from the effects of 
partial damage and to lessen the ultimate degree of this. It does so 
solely by its influence on the muscular tissue, and only voltaic elec- 
tricity can stimulate this tissue when the nerve-fibres are degenerated. 
The mode of application should be the same as for nerve-lesions. 
The muscle is only stimulated when the circuit is interrupted, as by 
repeatedly stroking the muscles with one terminal (a sponge, or con- 
ductor covered with water-holding material, well wetted with salt and 
water), which should be lifted from the skin between each stroke. 
The other terminal is kept still; it may be placed on the upper part 
of the muscle, where its nerve enters it. By some, this terminal is 
placed on the spine, over the affected region (and then a larger flat 
terminal is employed), under the impression that the electricity may 
influence the morbid process in the spinal cord; but there is no 
evidence even that the spinal cord is reached by electricity so applied. 
When applied to the muscles, the strokes may be made with the 
negative terminal, since each pole will influence the tissue, and the 
normally greater irritability to the negative often persists. The appli- 376 
SPINAL COED. 
cation can be made perfectly well by an intelligent nurse, since tlie 
diffusion of the voltaic current is so great that it is sure to reach the 
affected muscles. Each time the sponge is placed on the skin, the 
affected muscles should be seen to move or swell up in slight contrac- 
tion, and it is desirable to use as many cells of the battery as will 
produce this result. Sometimes this cannot be done without causing 
so much pain as to distress the child, but in many instances the 
distress is really due to a needlessly strong and painful current 
having at some time been used, and an amount of alarm produced 
that the child never gets over. It is on this account that it is so im- 
portant to make a test examination with great care, and to employ the 
faradic shock rather than the current. Emotional disturbance may 
generally be avoided by commencing wiih a very weak current. It is 
better, indeed, to commence with no current at all, applying the 
sponges in the way directed, so that the child may be famiiar with 
them, and cease to fear them. Then two or three cells may be used 
and the strength gradually increased day by day. In this way a 
current strong enough to cause contraction will often be tolei'ated. 
If, however, in spite of these precautions, this strength cannot be 
employed without distressing and disturbing the child, the attempt 
to obtain muscular contraction should not be persevered in, but only 
such a current employed as does not disturb the child. An influence on 
nutrition, if slighter, is still exerted, and if the application is con- 
tinued for a longer time it is probable that equal good is done. The 
electrical treatment may be commenced at the end of the third or 
fourth week after the onset. It should not be used earlier, lest it 
excite increased disturbance in the spinal cord. The application 
need only be made to those muscles in which faradic irritability is 
lowered or lost. Other muscles will either recover perfectly without 
its aid, or (as in the case of paralysis of the legs from implication of 
the lateral columns in the cervical region) will be uninfluenced by 
electricity. 
Another measure which should be employed is systematic rubbing 
of the limbs. This stimulates the circulation, which is always defec- 
tive, as the blue, cold surface shows. It no doubt also increases the 
movement of the fluids in the tissues outside the vessels, and so 
p>robably increases the interchange of material, and promotes nutri- 
tion. The muscles should be daily rubbed and gently kneaded, 
upward rubbing being especially useful. No liniment is required ; the 
uncovered hand answers best. Cod-liver oil is sometimes rubbed on ; 
some of it is probably rubbed in, without good or harm. Great care 
should be taken, at all times, to keep the affected limbs as warm as 
possible. 
In all cases in which the trunk-muscles are weak, even in slight 
degree, bronchial catarrh must be guarded against with great care. 
In such cases the muscles of respiration are weakened, and although 
normal breathing may not be impaired, the diminution in strength ACUTE ATROPHIC PARALYSIS. 
377 
may render an acute bronchial catarrh rapidly fatal, and this even 
months after the onset of the paralysis. 
When some voluntary power is regained, the systematic use of the 
muscles is of great service, and should be carefully attended to. 
Systematic planned movements may generally be adopted, and an 
improvement of muscular nutrition and power may be secured much 
earlier than if the limbs are left to the chance influence of such move- 
ments as a child spontaneously adopts. Most of the good that is 
done by “ movement cures ” may be obtained by such simple mus- 
cular exercises as can be readily arranged with the help of a little 
consideration on the part of the doctor, and can be efficiently carried 
on at home, given the necessary perseverance on the part of those 
who have charge of the patient, and which, unfortunately, is less 
often forthcoming. Such movements need to be specially arranged 
to meet the exigencies of each case, so as to call into action those 
muscles that are weak but not powerless, or that may supplement 
the muscles that are paralysed. 
A very important element in the management of the chronic stage 
is the prevention and treatment of the muscular contractions, and of 
the deformities to which these give rise. The contractions cannot be 
entirely hindered, but they may often be prevented reaching a high 
degree by careful attention to the position of the limbs, and by 
watching for and treating the earliest indication of shortening of the 
muscles. It is needless to discuss in detail the varied influence of 
posture in these cases ; careful and frequent examination of the patient 
will show whether any deviation from normal relations is being deve- 
loped, and its counteraction is chiefly a matter of common sense and 
a, little practical ingenuity. Of especial importance, however, are the 
prevention of the curvatures of the spine which are caused by allowing 
the patient to sit up before the back-muscles have regained the neces- 
sary power, and the prevention of the shortening of the flexors of the 
hip and knee-joints that occurs when the patient is allowed to lie in 
bed with the legs drawn up. More difficult of prevention is the con- 
traction of the calf-muscles, often aggravated in consequence of the 
lessened growth of the limb. Something may be done during the 
process of rubbing, for the prevention of deformities. While the con- 
tracted muscles are rubbed upwards, they should be extended gently 
but finally. Thus, if the calf-muscles are shoi'tened, the foot should be 
steadily pressed upwards while the calf is rubbed. A slipper with 
elastic straps to a knee-band, may be worn at night, often with great 
benefit. For developed deformities, due to great shortening of the 
muscles, surgical treatment by splints or tenotomy is usually necessary, 
nnd is often important because it enables the patient to use the limb 
in ways that would be impossible without it. 
For this and other reasons, mechanical appliances are of unques- 
tionable value. Counteracting deformities, and supplementing weak 
muscles, they often enable a child to walk, who could not do so 378 
SPINAL CORD. 
without their aid, and power is often increased to a remarkable extent 
in indirect ways. In ail these cases, however, the instruments require 
frequent attention and alteration to adapt them to the changes due to- 
growth, and patience is required in the management of these cases 
through their long and tedious course. 
Two facts deserve a final emphasis. At the end of six months all 
possible l’ecovery is nearly completed, and certainly at the end of a 
year the lesion has become a cicatrix, and further improvement will be 
merely by the slow growth of the muscle that has recovered, under 
the stimulus of use. Secondly, this process of slow improvement as 
the result of use will go on for years,—will go on whatever treatment 
is adopted, and whether special measures are employed or not. The 
therapeutic specialist who carries on his treatment month after month 
will claim it as his achievement, but it would occur equally without 
his aid. From its nature, however, as already stated, it may pro- 
bably be always augmented by some contrivance to increase the in- 
fluences that are really improving the power of the muscles. 
Subacute and Chronic Atrophic Spinal Paralysis 
(subacute and chronic polio-myelitis). 
Under this designation cases have been described of a miscellaneous 
character, in which paralysis, followed by muscular atrophy, comeson 
less rapidly than in the acute form, its development occupying from 
ten to thirty days, in the cases which are termed “ subacute,” and 
from one to six months or even more, in those which are called 
“ chronic.” Many cases included under this name differ much in 
their characters, and are sometimes described as “ chronic 
but among the cases placed, even until lately, in this group, are forms 
of multiple neuritis. Most subacute atrophic palsies are due to nerve 
disease; almost all, indeed, which present symmetrical palsy. 
The cases of spinal atrophic paralysis, in which the onset is not 
acute, mav be placed in three classes. 
(1) Cases of subacute polio-myelitis which differ from the acute 
form, already described, only in their less rapid development. They 
present the same initial general disturbance and wide 
and the same recovery, except in a limited region in which muscular 
wasting occurs. They are thus distinguished from polyueuritis, and 
also by the irregular distribution of the symptoms. Mostof the sufferers 
have been adults. Little is known of the exciting causes of this form 
further than that it certainly sometimes follows exposure to cold,, 
and is probably sometimes the result of a toxaemic influence. The 
symptoms and general history of these cases present no important 
difference from the acute form. 
(2) Cases are met with that differ from the type just described in 
the fact that their course is progressive. The onset is subacute or sub- 
chronic, occupying from a fortnight to several months, but instead of CHRONIC ATROPHIC PARALYSIS. 
379 
arrest followed by improvement, the more or less rapid onset is fol- 
lowed by slower gradual increase, until at last wide-spread chrome 
muscular atrophy is developed. Many of these are really cases of 
progressive muscular atrophy with a subacute onset. For example, I 
have more than once known a case of this disease, ultimately typical, 
to begin by a subacute atrophic paralysis of the extensors of the 
wrists. These cases will be considered in the account of that disease. 
Others present differences from that malady and symptoms of more 
irregular character, which show that the lesions are distributed through 
various structures in the cord, and these must be regarded as cases of 
chronic myelitis involving the anterior cornua. This form also is 
chiefly confined to adults. It occasionally results from cold, and 
sometimes from injury, as a fall on the back. Intemperance and 
venereal excesses are also said to cause it. The wide-spread muscular 
atrophy which sometimes results from lead-poisoning is probably of 
this nature. The muscles at first present the degenerative reaction, 
or normal faradic irritability with increase to voltaism ; sometimes, 
however, there is a loss to both faradism and voltaism. The sphiucters 
usually escape. In many cases, the affection exhibits a persistently 
progressive character; muscular atrophy slowly increases and extends, 
until the case ultimately resembles one of progressive muscular 
atrophy, and the patient dies at the end of one or two years from 
exhaustion, or from interference with the respiratory movements. 
In other cases, the atrophy, after slowly progressing for many 
months, becomes stationary, and considerable improvement may 
ultimately take place. This course is seen especially in traumatic 
cases. Few observations on the pathological anatomy of the affection 
have been made. Cornil and Lepine found, in one case, at the end 
of four years, softening of the lower part of the spinal cord, chiefly 
in the anterior cornua, disappearance of the ganglion-cells, increase 
of the connective tissue, and sclerosis of the white substance around 
the anterior horns. 
The diagnosis from the first form rests on the slow onset and pro- 
gressive course of the disease. Although the degenerative electrical 
reaction may be found, it is frequently absent, and this is another 
distinction from the acute variety. On the other hand, the fact that 
paralysis precedes wasting is a distinction from progressive muscular 
atrophy. In the most chronic form, however, this distinction fails, 
and cases are met with which present a gradation between the two 
diseases. 
The prognosis is grave except in traumatic cases, but is influenced 
by the observed rate of progress, and the presence or absence of any 
indications of arrest. When the result of injury, considerable im- 
provement is not uncommon, and it is remarkable how great a degree 
of paralysis and atrophy may, in these cases, ultimately pass away 
almost completely. The treatment of the disease must be influenced 
by the rapidity of its onset. In the subacute stage and form it should 380 
SPJNAL COfiD. 
be conducted on the same principles as that of acute cornual myelitis. 
Iu the chronic form the treatment must be the same as for progressive 
muscular atrophy. 
(3) Many subacute and chronic cases, which have been described 
as atrophic spinal paralysis, are peripheral, not central in their nature, 
and are cases of multiple neuritis, the symptoms and diagnostic 
indications of which have been already described. The history of the 
subacute spinal disease has been largely written from cases of multiple 
neuritis. In the statements just made, this fact has been kept in 
view. While multiple neuritis may simulate closely chronic polio- 
myelitis, it is certain that the converse is also true, and the central 
affection has been sometimes thought to be peripheral. The facts at 
present available suggest that the central aud peripheral structures of 
•common function possess common susceptibilities to the action of 
morbid influences, and there is still danger that the two classes may 
be confused. The most important criterion is the greater irregularity 
in distribution of the central disease,—the more perfect symmetry of 
the peripheral affection. The presence of tenderness of the nerve- 
trunks, and of the structures to which the nerves are distributed, is of 
more value, when it exists, than is the suggestion afforded by its 
absence that the disease is central, because, in the periphery, only 
fibres of one function may suffer; we may then have none of the sym- 
ptoms that we commonly associate with neuritis, and look for as proof 
of its existence. In purely motor neuritis there may be no tender- 
ness or pain. But such an affection is either unilateral or perfectly 
symmetrical. Imperfect symmetry indicates an affection of the 
cord. 
ACUTE ASCENDING PAEALYSIS. 
Ascending paralysis, which commences in the legs and ascends to 
the muscles of the trunk, the arms, muscles of the neck, the diaphragm 
and the pharynx, is a feature of several diseases—meningeal haemor- 
rhage, ascending myelitis, &c.; but it occurs also in cases in which the 
spinal cord, after death, appears healthy to both naked eye and 
microscopical examination. Such cases have, however, certain charac- 
teristic features which make it desirable to distinguish the condition 
from other diseases, and the affection has, therefore, been provisionally 
termed “ acute ascending paralysis" in the absence of any evidence of 
its nature. It was first described by Landry in 1859, and hence is 
often called Landry's paralysis. Acute ascending paralysis is a most 
formidable malady, most cases pi'oving fatal in a few days. Its 
nature is mysterious, but recent discoveries regarding multiple ACUTE ASCENDING PARALYSIS. 
381 
neuritis have disclosed instructive analogies between the two affec- 
tions. These have, indeed, led some observers to the opinion that this 
ascending paralysis, without organic central lesion, is an affection of 
the nerves. As we shall see, it is not probable that this opinion is 
correct, although it is possible that the nerves, as well as the centres, 
are sometimes affected. 
Causes.—The etiology of the disease resembles, in general, that of 
acute multiple neuritis more nearly than that of any other affection. 
The disease affects males more frequently than females. It occurs 
chiefly between twenty and forty years of age, but has been observed, 
in rare cases, in older and younger persons, and even in children. 
Some sufferers have been the subjects of alcoholism. Severe exposure 
to cold has been the apparent cause in many instances. In other casea 
the disease has occurred under conditions such as cause toxsemic 
states, or after the occurrence of some known blood-disease. Thus 
it has occurred during convalescence from some general disease, 
smallpox, diphtheria, typhoid fever. It has also followed febrile 
diseases of obscure nature. In these cases, it should be noted, the 
disease has followed at an interval of a week or a few weeks. It 
also sometimes succeeds some traumatic process, such as a wound, 
and here also after an interval, and usually when the wound was 
apparently healed. I have known it thus to follow an attack of pelvic 
cellulitis. In these respects it closely resembles polyneuritis. The 
disease has been repeatedly observed in the subjects of syphilis, and 
has apparently been arrested by the treatment for this disease.* The 
circumstance that when some malady or wound preceded the disease, 
the former was often of a trivial character, prevents surprise at the fact 
that, in many cases, no influence could be traced to which the disease 
could be ascribed. 
Symptoms.—Premonitory symptoms have been noted in some cases 
-—general malaise, pains in the head and back, tingling in the extremi- 
ties—for a few days or a week before the onset. The first definite 
symptom is usually weakness of the legs, often commencing in one 
and spreading to the other. The weakness increases rapidly, so that 
the power of standing is lost, sometimes in a few hours, sometimes at 
the end of two or three days; it goes on to complete paralysis, with 
relaxation of the muscles. As the legs become motionless, the muscles 
of the trunk become weak, first of the pelvis, loins, and abdomen, 
then of the thorax. The weakness next invades the arms ; either the 
upper arm muscles or those of the forearm and hand may be first 
attacked, and one arm is often weakened before the other. The 
paralysis of the arms may become absolute, like that of the legs, or 
some power of movement may remain. The diaphragm and neck 
* Much weight should not be placed on this fact as proof of causal relationship, 
because (apart from the fallacy of independent cessation) it is probable that the 
treatment that is effective against the virus of syphilis is also effective against 
other blood-states that depend on agents of similar nature. 382 
SPINAL CORD. 
muscles then suffer, and difficulty of swallowing comes on, sometimes 
with paralysis of the muscles of the palate, and often speech becomes 
difficult, nasal, and indistinct. The inability to swallow may become 
so great that the patient has to be fed through a tube, and the para- 
lysis may involve the muscles of articulation to such an extent that 
utterance may be altogether unintelligible. There is often dyspnoea 
from the weakness of the muscles of respiration, or from interference 
with the respiratory centre in the medulla, and the cardiac centime may 
also be involved. The affection of the bulbar nerves is determined by 
functional relations; thus the lips may be paralysed with other 
muscles of articulation when the upper part of the face is unaffected. 
In rare cases the eve-muscles are paralysed in some degree, usually 
only as loss of accommodation, inequality or dilatation of the pupils, 
impaired reaction to light, or slight strabismus. 
The tingling and analogous subjective sensory disturbance has been 
followed, in some cases, by hvpersesthesia of the skin and tenderness 
of the muscles, but it is probable that, in such cases, there has been 
multiple neuritis. There may be some blunting of sensibility in the 
extremities, but there is not definite loss of sensation in the typical 
disease. A firm touch can usually be pei’ceived anywhere; percep- 
tion of painful impressions and of heat or cold is sometimes delayed. 
At first, reflex action is lost in the affected limbs, both cutaneous 
reflex action aud myotatic irritability. In cases rapidly fatal the 
loss has continued till death. In cases that have recovered, reflex 
action has returned, but recorded cases have presented considerable 
differences in this respect, and, as there is some doubt as to the 
nature of many non-fatal cases, there is some uncertainty as to this 
point. In some the myotatic irritability has soon returned, and has 
oven become excessive. In the majority it has remained absent, and 
not until all paralytic symptoms have disappeared has the knee-jerk 
returned. 
In spite of the early flaccidity of the muscles, if life is prolonged 
they present neither wasting nor change in electrical irritability. A 
trifling reduction in size may occur, but there is no muscular atrophy 
such as occurs in polio-myelitis, and even after several weeks the most 
careful examination fails to reveal any abnormal electrical reaction— 
a very important feature of the disease. The sphincters, moreover, 
escape in the vast majority of cases, but not in all; there is no ten- 
dency to the occurrence of bedsores. The cerebral functions are not 
usually involved, and the state of the patient who, with unimpaired 
intellect, cannot express himself either by speech or gesture, is painful 
in the extreme. In exceptional cases, however, there is mental dulness 
or slight delirium, as if from the influence of a blood-state on the 
brain. In girls, this may take the form of hysterical manifestations, 
and by these the nature of the disease may be masked. 
As a rule there is no elevation of temperature, even during the rapid 
•development, of the symptoms, but in one or two cases, which were not ACUTE ASCENDING PARALYSIS. 
383 
fatal, "brief pyrexia attended the onset, and in a few others moderate 
febrile disturbance (2° or 3°) occurred at a late period. Profuse 
sweating has been occasionally noted. Enlargement of the spleen 
{first noted by Westphal), such as occurs in other acute diseases, is 
very frequent. 
Thus the chief feature of the disease is an almost purely motor 
paralysis, progressive in character, with relaxation of the muscles 
-during the acute stage of the disease. It usually has an ascending 
course, but irregular cases are met with in which the order of invasion 
is varied. Thus the arms are occasionally involved before the legs, 
the diaphragm before the intercostals ; the bulbar symptoms have 
been known to precede the others, and I have seen them reach a high 
degree with a fatal involvement of the cardiac centre, before the upper 
muscles of respiration were affected or the hands quite powerless. 
Analogous cases have been recorded by others, ihe special features 
-and course being those characteristic of the disease. In some cases, 
however, of irregular course, changes have been found in the electric 
irritability of the muscles; it is probable that, in such cases, the peri- 
pheral nerves are affected, although we cannot, on this account, at 
present separate these from the typical cases of the disorder—a point 
that will be explained in connection with its pathology. 
The disease varies considerably in the rate of its progress. It may 
run its course and end fatally in forty-eight hours. Death usually 
results from either respiratory or cardiac paralysis—the latter in the 
•cases of irregular course. A large proportion of the fatal cases last 
less than a week. On the other hand, the disease may only attain its 
height at the end of two, three, or even four weeks. In some cases, 
apparently of the same character, the paralysis of the limbs has not 
been complete. There may be a rapid extension of the paralysis to a 
certain point, and it may then cease to spread, and the limbs last and 
least affected may slowly regain power. A patient may lie for days 
in a condition of universal palsy, save for a little respiratory power, 
and then improvement begin. As a rule, the order of recovery of the 
muscles is the opposite to that of their invasion. In favorable cases 
the recovery of power is usually slow; two or three months often 
elapse before the weakness entirely disappears. Occasionally there 
has been a more rapid improvement, and the patient has been well in 
a few weeks. 
Pathology.—As a rule the most careful and skilled examina- 
tion has failed to discover any morbid appearance in the spinal cord, 
nerves, or muscles. Minute haemorrhages, met with occasionally, have 
probably occurred during the last moments of life. In a few cases, 
apparently similar to the others, slight scattered indications of 
inflammation have been found in the grey matter of the cord, with 
drgenerative changes in the ganglion-cells (Immermann) ; but, as a 
rule, the central nervous system shows no trace of lesion. Of late 
.more attention has been paid to the peripheral nerves, and slight 384 
SPINAL CORD. 
indications of acute changes, both parenchymatous and interstitial,* 
have been found in them, although in some cases they have been appa- 
rently normal. In addition to the enlargement of the spleen observed 
during life and found also after death, the mesenteric glands have 
been found swollen, and also the closed follicles of the intestines. 
Organisms were found in the glands by Baumgarten, but most 
observers have searched for them without success in all cases of 
typical character. 
These negative facts, taken in conjunction with the conditions under 
which the disease occurs, and with the course of the malady, have 
suggested the idea of a toxic influence acting on the nerve-centres; 
and this idea receives support from the discovery that acute swelling 
of the spleen is common, and of the lymphatic glands not rare— 
lesions that indicate a morbid blood-state. The limitation by func- 
tion of many toxmmic palsies, e.g. that of accommodation, affords 
confirmation of this view, since the isolated acute paralysis of a func- 
tional centre, not anatomically separate from others, is known only as 
a consequence of a toxic influence. Further confirmation is afforded 
by the fact that cases of acute multiple neuritis, certainly due to a 
toxaemia, may run a similar course, and that indications of such com- 
mencing neuritis may actually be found in this disease. But this 
does not exclude a central process. It has, indeed, been conjectured 
that the nerves are always the structures impaired, but this view is 
rendered unlikely by the common absence of altered excitability of 
the muscles, since the motor nerves seem never to escape invariably 
in peripheral neuritis of any variety, however common their freedom 
from affection in the type. At the same time this does not exclude the 
periphery: the nerves may suffer also in some cases, and there may, 
indeed, be gradations to the cases of acute multiple neuritis of ascend- 
ing course described at p. 128. If we ask on what nerve-structures 
this toxic influence is usually exerted, we meet with the difficulty that 
while it is clearly upon some part of the motor path, the integrity of 
the muscles shows that the interruption is not in their nerves or 
nerve-cells, and their relaxation, with the prolonged impairment of 
myotatic irritability, suggests that the structures interfered with are 
not far from the motor centres. Curara abolishes the function of the 
termination of the lower segment of the motor path, i. e. of the nerve- 
endings in the muscles. It may be that, in this disease, some toxic 
influence impairs in an analogous manner the function of the ter- 
mination of the upper segment, paralyses the ramification in which, 
as we have seen (p. 175), the pyramidal fibres must end in the grey 
matter, and by which they are connected with the lower segment. It 
has been already pointed out (p. 218) that the nutritional stability of 
the termination is probably lower than that of any other part of each 
segment, since it is the part furthest from the nerve cell from which 
the fibre proceeds, and on which its nutrition depends. The greater 
* Eisenlohr, ‘ Deut. med. Wochenschr.,’ 1890, No. 38. ACUTE ASCENDING PARALYSIS. 
385 
length of the fibres for the lumbar region may render their termination 
more susceptible than that of the fibres for the arm, and hence the 
ascending course of the paralysis. It is, moreover, readily conceivable 
that the effect extends in slight degree to other structures in the grey 
matter—those, for instance, which intervene between the sensory and 
motor cells ; aud thus the loss of reflex action and myotatic irritability 
is explained, as well as the muscular relaxation, since, as we have seen, 
muscular tone must be ascribed to a reflex process. The structures 
affected may vary somewhat in different cases, and thus the state of 
reflex action may vary. The facts of diphtheritic paralysis also show 
that the effects of such a toxic influence may be revealed, in varying 
degree, by visible changes having the characters of inflammation, and 
we can thus understand that indications of such inflammation in the 
grey matter may be occasionally met with. The bulbar symptoms 
come under the same explanation. The motor path through the 
nuclei of the medulla has the same pathological relations as that 
which passes through the grey matter of the spinal cord. The separate 
affection of nerve-structures, distinct from others only in function, is 
common in the phenomena of toxic actions. There are no facts to show 
the nature of the blood-state, except those that suggest its alliance 
with the influences that act on the peripheral nerves ; multiple neuritis 
should be studied in connection with this disease. These facts suggest 
that the virus is a product of the preceding growth of organisms, at 
least in some cases ; and if so, it is natural that the organisms them- 
selves should not be found. 
Diagnosis.—The disease is recognised by the rapid development of 
paralysis, usually ascending, with relaxation of the muscles, aud with 
loss of reflex action, without considerable pain or loss of sensation, 
and if the patient survives, without wasting of the muscles or change 
in electrical irritability. The latter characteristic distinguishes the 
disease from acute atrophic paralysis, while the absence of pain in the 
back and of spasm is a distinction from meningeal haemorrhage. The 
diagnosis from general ascending myelitis has been already con- 
sidered ; it rests especially on the involvement of all the functions of the 
cord in inflammation. The distinction from multiple neuritis has been 
mentioned in the account of that disease (p. 140), but, it may be, is not 
always absolute* since tue nerves probably suffer, as well as the cord, 
in some cases of ascending paralysis. The distinction from poly- 
neuritis, founded on the course of the ascending form, is subject, 
moreover, to the reservation that while ascension to the arm through 
the trunk is a feature of the central disease, this is not excluded by a 
more irregular course, and the character of the individual symptoms 
must be taken into consideration (see also p. 383). 
Prognosis.—The affection is one of extreme gravity. The danger 
to life is in proportion to the interference with respiration aud with 
the functions of the medulla oblongata, especially with the cardiac 
centre, and also to the rapidity with which the palsy comes on. But 
VOL. I. 386 
SPINAL CORD. 
the cases which develop with comparative slowness are not devoid of 
danger. Even when the symptoms only reach their height at the end 
of three or four weeks, death may occur in the same way as in the 
more rapid cases. On the other hand, recovery has been known 
although the patient has lost all power of motion at the eud of the 
second day. The danger is great as long as the symptoms are in- 
creasing, and only when distinct improvement can be recognised is it 
justifiable to anticipate recovery. The earlier the bulbar symptoms 
appear, the more serious is their significance. Mental symptoms also 
increase the gravity of the prognosis, as they usually indicate a severe 
blood-change, the effects of which on the nervous system are likely to 
reach a high degree. 
Treatment.—During the early stage of an attack of acute ascend- 
ing paralysis, in the absence of other indications, the treatment should 
be that suitable for myelitis, since, at the onset, the diagnosis between 
the two diseases can never be certain. A warm bath, or still better, 
a vapour bath, should be given if the symptoms followed exposure to 
cold. It should be followed by counter-irritation over the spine by a 
long, narrow mustard plaster. More energetic counter-irritation, even 
the actual cautery, has been recommended. The body should be 
kept in as perfect rest as possible. In a very few cases have drugs 
appeared to exert any influence on the course of the disease, and the 
malady is so rare that experience accumulates slowly. Salicylate of 
soda seems to deserve a trial in cases that follow exposure to cold. 
Ergotin has been given, and one case in which it was used deserves 
special mention. The patient was a man aged fifty-seven, who, a 
week after exposure to cold and wet, complained of a feeling of weight 
and weakness in the legs; the temperature rose to 103°; the loss of 
power gradually became complete in the legs and spread to the arms, 
without loss of sensation. At the end of the second day there was 
■difficulty in swallowing, in articulation, and in breathing, and death 
seemed near. Ergotin was given every hour, and during the night 
the patient took twenty grains. In the morning the bulbar symptoms 
were better, the arms stronger, and there was a trace of motor power 
in the legs. The patient rapidly improved, and at the end of a week 
was well. If swallowing becomes difficult, care must be taken to 
administer a sufficient amount of nourishment, either- by the rectum 
or by the nasal tube. Several cases have been recorded in persons 
who had had syphilis, in whom arrest of the disease followed the 
administration of iodide of mercury. The chief lesson of modern 
researches is certainly that we must look for the means of effective 
treatment to the neutralisation of the toxic influence on which the 
malady apparently depends. At present, however, nothing has been 
ascertained regarding antidotal agents available in the acutely active 
stage of these toxsemic states. It is, however, probable that mercury 
is capable of doing this in some cases, and that when the causation 
is obscure, and the disease develops slowly enough to permit mercurial DIVERS* PARALYSIS. 
387 
treatment, it is wise to adopt this irrespective of the fact of preceding 
syphilis. In cases that follow traumatic lesions, especially if there 
have been any indications of septicaemia, full doses of perchloride 
of iron offer, I believe, the best means of destroying the activity 
of the blood-state. Urgent symptoms require the same treatment 
as iu myelitis. 
PARALYSIS FROM LESSENED ATMOSPHERIC PRES- 
SURE; DIVERS’ PARALYSIS. 
Divers, and especially those who work in caissons, at such, a 
depth "beneath water that they are exposed to considerable pressure, 
may become paralysed soon after their return to the surface.* 
Apoplectic attacks and hemiplegia also sometimes occur, but paralysis 
of the legs is by far the most common effect, and it is, therefore, clear 
that the spinal cord suffers in greater degree than any other part of the 
nervous system. Miners have been said to suffer also, but this is 
doubtful, because a pressure equal to at least an additional atmosphere 
seems necessary for the production of the symptoms. Most of the 
subjects of the disease have worked at a depth of from forty to 
ninety feet below the surface of water, and under a pressure of two 
to four atmospheres. In the extensive works involved in laying the 
foundations of bridges, in which many men have been employed, a 
•considerable proportion of the workers have suffered in some measure ; 
but severe degrees of affection are rare, because the conditions under 
which they occur can be avoided. They only occur in those who have 
been exposed for more than a certain time, which is the shorter the 
greater the pressure. At a depth of ninety feet beneath the surface, 
immunity from severe symptoms (and commonly from all symptoms) 
is obtained by reducing the periods of work to an hour. The danger 
is greater in those who have had several previous periods of work on 
the same day, and especially if slight symptoms have been experienced 
after one of these. It is also greater in those unaccustomed to the 
conditions. I have met with one case of hemiplegia in a diver after 
only half an hour’s work in a well at ninety-six feet, but the man had 
been down twice before with only intervals of rest of half an hour, 
and the attack passed off in the course of an hour. In another case 
paraplegia occurred after working for an hour under only fifty feet of 
* See, on this subject, Babington and Cuthbert, * Dubl. Quart. Journ.,* 1863* 
p. 312 (cases at Londonderry) ; Eads, * Med. Times and Gaz.,’ 1871, p. 291 (cases 
at St. Louis); Leyden, ‘ Arch. f. Psychiatric,’ ix, Heft 2; and Moxon, ‘ Lancet,* 
1881, ii, 529. 388 
SPINAL COED. 
water, but the man bad worked on tbe preceding day at a depth of 
one hundred and twenty feet below the surface. It is evident, therefore, 
that the power of resisting the dangerous influence varies, and that 
predisposition to suffer may be caused by the conditions which also 
induce an attack. 
It is not during exposure to the abnormal conditions, but on 
returning to the normal atmospheric pressure, that the symptoms 
come on; often immediately, and always within half an hour or at 
most an hour of the return to the surface. The onset is usually 
preceded by other symptoms, and especially by pains in tbe ears and 
in the joints. The latter is very common, and occurs after a much 
slighter degree of exposure than is needed to produce paralysis. 
They are felt chiefly in the larger joints, and may continue for days 
and even longer. Very rarely there is also swelling of the joints. 
It is important to note the conditions under which the symptoms 
come on. Not only do those who are unused to such work seem 
especially liable to suffer, but there are also considerable individual 
variations in the degree of liability. 
Paraplegia or hemiplegia may occur, but the former is far more 
common. The onset of the paralysis is sudden. The legs feel heavy 
and are found to be weak, and in a few minutes the patient is unable 
to move them. Sensation is often lost as well as motion, and in all 
severe cases the sphincters are affected. The arms are seldom 
involved. In slight cases the loss of power is incomplete, and one 
leg may be more affected than the other. The impairment of sensa- 
tion is often imperfect or irregular. If the paralysis is incomplete 
the power may return in the course of a few days, but in severe cases 
the palsy usually lasts for xveeks or even months, and it may be 
permanent. Death may occur at the end of a week or more, in the 
same way and from the same causes as in acute myelitis. When the 
paralysis is hemiplegic it is generally moderate in severity and 
transient, passing off in a few hours or days. It may be even still 
more brief, as in the case referred to above, in which a diver, after 
half an hour’s work ninety-six feet below the surface, suddenly felt 
tingling across his loins, and that his right arm and leg were almost 
powerless; in half an hour he had recovered sufficiently to walk home. 
If cerebral symptoms are more intense, they are generally very severe, 
with sudden loss of consciousness, continuing as deep coma, irregular 
breathing, and indications of cardiac paralysis. Such cases usually 
end in death in the course of a few hours. 
Pathology.—The most probable explanation of these cases ascribes 
them to the escape from the blood of gases, with which it has become 
charged during the exposure to the high pressure. It is certain that 
a great excess of gas must he dissolved in the blood during the expo- 
sure, and that the amount, at least of oxygen and of carbonic acid, 
contained in the blood when the person emerges from the caisson must 
be vastly greater than normal. It must, moreover, be greater the DIVERS* PARALYSIS. 
389 
longer has been the exposure, since the absorption of tbe excess will 
be a gradual process, talcing place through the lungs in respiration, 
but it will be more rapid as the pressure is greater. These conditions 
agree with observed facts. After returning to the normal atmospheric 
pressure, tbe excess of gas probably passes off gradually by tbe lungs 
in most instances; but if extreme, gas may escape from tbe blood 
within tbe body. The occurrence of this has been proved experiment* 
ally (Hoppe-Seyler and P. Bert). G-as, so escaping, is no doubt 
quickly reabsorbed, but must exert a pressure capable of arresting the 
function of the structures of the nervous system. If abundant, it 
may conceivably rupture these. Further, the special effect on the 
nerve-centres may be connected with the position of these within 
cavities that are practically closed. These conditions, coupled with 
the extremely circuitous course of the blood from the cord, may 
explain the incidence of tbe effects on the nervous system. 
The few ascertained facts harmonise with this pathology. Such 
escape of gas has been proved to result from diminution of tbe 
atmospheric pressure.* In many cases no visible lesions have been 
found, and it is obvious that gas, widely effused, may exert dangerous 
pressure, and yet may be speedily removed, so that no indication may 
remain of the cause that has completely arrested function. 
It was once thought that the symptoms were due to local haemor- 
rhages, but extravasations are seldom met with, even in tbe results of 
•experiment, and it is certain that they take but a trifling part in the 
production of symptoms. Tbe only positive pathological observation 
agrees with the opinions above stated. Leydenf found (in a case of 
characteristic paraplegia) small irregular fissures in the inid-dorsal 
region, chiefly within tbe posterior and hinder parts of tbe lateral 
column. Tbe fissures were filled with round-cells, but contained no 
red blood-corpuscles, and from their well-defined edges they were cer- 
tainly not produced by tbe infiltration of tbe cells found within them. 
The only explanation that is satisfactory, or in any harmony with 
their features, is that they were produced by tbe sudden escape of gas, 
and were afterwards occupied by the round-cells. Tbe physical 
firmness of the cord is far less in tbe dorsal region than in the en- 
largements; and p>robably, as Leyden suggests, this is tbe reason why 
the dorsal region suffers structural damage from tbe escape of gas 
more than other parts. It is evident, however, that such escape may 
■occur, in the brain, for instance, even to a fatal degree, and leave no 
traces unless it occurs so rapidly as to cause laceration of tbe tissue. 
The absence of haemorrhage of the ordinary character may be further 
•explained by tbe fact that the effused air will resist the effusion of 
blood. Some other anomalous features, such as the transient cha- 
racter of the symptoms in some cases, are also explained by the peculiar 
nature of the lesion, which may exert a wide-spread and considerable 
* Hoppe-Seyler, ‘Muller’s Archiv,’ 1887; P. Bert, ‘ Coiuptes Rend.,’ 1871-2. 
f * Arch. f. Psych.,’ ix, Heft 2. 390 
SPINAL C011D. 
influence, and in a short time may have vanished by the reabsorption 
of the compressing air. Haemorrhage must be regarded as an acci- 
dental consequence, and even tbe production of such fissures as were 
found by Leyden may not be a necessary part of the lesion, even in 
grave cases. The mechanical effects of the gas may be considerable, 
and arrest the function of the nerve-elements, without the passage of 
the gas outside the capillary vessels. 
Tbe fact that the spinal cord suffers more than other organs may 
be partly due to the plexuses through which the blood can return only 
slowly to the lungs, where its relief from the surcharge of gas is effected. 
The same considerations apply to the brain. In both organs the 
escape of air is more instantly disastrous than elsewhere, and, indeed, 
may not only occur, but act in a peculiar way, on account of tbe posi- 
tion of the organs within chambers that are, to a large degree, closed. 
The conditions are too complex to permit us to follow them in detail,, 
or analyse fully the mechanisms that determine the effect on tbe 
nerve-centres. The escape of the excess of gas in the lungs can only 
take place gradually, as successive quantities of the surcharged blood 
pass through tbe capillaries of the air-cells. If, in consequence of the 
slowness of the circulation in tbe cord, any escape of air occurs in its 
capillaries, the effect of this will be still further to hinder tbe local 
circulation, and to favour the further escape of gas. In this way we 
are able to discern something of the mechanism which determines the 
special affection of the spinal cord. The less the external support the 
less will be tbe resistance to the escape of gas, and the incidence of 
the lesion on the posterior part of the cord may be in part at least 
determined by the adoption of the recumbent posture when the first 
symptoms are perceived. 
At the onset, when the first symptoms are experienced, it is probable 
that a return to a greater degree of pressure might arrest the develop- 
ment of the mischief. It is certain that, in all cases of exposure to a 
high degree of pressure, the transition to the normal pressure should 
be made gradually. When developed symptoms indicate that a 
definite lesion of the cord has occurred, tbe further treatment must 
be conducted on the same principles as in acute myelitis—the morbid 
process that has, in fact, been set up. 
IliEMOKRHAGE INTO THE SPINAL COED; 
HiEMATO-MYELIA. 
Primary haemorrhage into the spinal cord, sufficient to cause sym- 
ptoms, is a very rare disease, and it is even more rare than is suggested 
by the cases now and then recorded as such. We have already seen 
that haemorrhage may accompany myelitis ; a considerable extravasa- H2EM0RKBAGE. 
391 
tion may occur when the inflammation is only commencing, during the 
state of congestion, and while the symptoms are slight. Such cases 
are easily mistaken for primary haemorrhage. The risk of error is not 
always removed by pathological examination. Inflammation results 
from haemorrhage, and when indications of myelitis are found about 
a clot, it may be impossible to sav whether these are primary or 
secondary. It is probable that many cases of secondary myelitic 
haemorrhage have been regarded and described as primary, and it is 
possible that a few cases of primary haemorrhage have been regarded 
as secondary. One writer, Hayem,* goes so far as to deny the occur- 
rence of primary non-traumatic haemorrhage ; but such an exclusive 
view is unwarranted. It is certain, however, that the history of 
primary haemorrhage has been largely written from uncertain data, 
and will need extensive revision when a sufficient number of exact 
observations have accumulated. 
Etiology.—The rarity of haemorrhage into the cord is especially 
great in comparison with the frequency of haemorrhage into the brain. 
The difference probably depends on the tortuous and long course of 
the arterial path to the cord, whereby the vessels are preserved from 
the high pressure which is the chief cause of the degeneration, dilata- 
tion, and rupture of the cerebral arteries. Miliary aneurisms are not 
found within the spinal cord. Haemorrhage is far more common in 
males than in females. It may occur at any age, and has been met 
with in young children, even so early as seven months,f while some of 
the subjects have been in advanced life; but it is most common 
between twenty and forty, i. e. during the first half of adult life. 
Many cases occur in young adults apart from injury or obvious 
exciting cause, and apart also from initial myelitis, which accounts, 
however, for some of the cases. It has been met with as a conse- 
quence of a haemorrhagic tendency, as in a case in which it succeeded 
severe epistaxis, to which the patient, a young man of twenty-four, 
was liable. X 
Of immediate causes, injury is the most frequent, especially falls 
which involve a severe concussion of the spine; the spinal column may 
or may not be injured at the same time. Over-exertion and exposure 
to cold have in rare cases preceded the onset. Chronic alcoholism and 
sexual excess have been thought to predispose. In one case within 
my knowledge, an extensive haemorrhage into the grey substance at 
the top of the lumbar enlargement resulted from coitus four times 
repeated, the symptoms commencing suddenly during the fourth act. 
Minute extravasations are often found after death from diseases which 
* * Des Hemorrhagies intra-racliidiennes/ Paris, 1872. 
f Clifford Allbufct, ‘ Lancet/ 1870, vol. ii, p. 84. Numerous haemorrhages were- 
observed in the grey matter of the lumbar and cervical enlargements (probably 
polio-myelitic, but occurring the day after a fall) in a child of four by Chaffey 
(‘ Path. Trans./ 1885). 
J Sinclair, * Lancet/ 1885, ii, p. 1043. 392 
SPINAL COED. 
interfere with respiration and cause venous congestion, and tbev are 
especially frequent in maladies which, at the same time, cause func- 
tional excitement of the cord, as tetanus and all severe convulsions. 
They cause no symptoms, and are probably produced during the last 
moments of life. They have been termed “ accessory.” The diseases 
of the cord that lead to secondary haemorrhage are chiefly inflamma- 
tion, tumours, and cavities in the cord. The last-named condition is 
especially important. It is probable that haemorrhage occurs more 
readily in spinal cords that contain a congenital cavity or fissure, due 
to an arrest of development, and surrounded by embryonal neuroglial 
tissue. Hence this condition will be found in disproportionate fre- 
quency in cases of haemorrhage. 
Pathological Anatomy—The minute extravasations just men- 
tioned, as met with after asphyxial and convulsive diseases, are found 
in both the grey and white substance, but especially in the former. 
They are usually microscopic, or visible to the naked eye as minute 
red points, distinguishable from distended vessels only by their 
slighter resistance to a stream of water. The extravasation may 
occupy the perivascular sheath, or the cavity in which the vessel lies, 
or extend between the nerve-elements. The larger non-traumatic 
haemorrhages, which cause symptoms, always begin in the grey 
substance, and are often confined to it, extending into the white 
columns only when large in size. The vessels of the grey substance 
are more numerous than those of the white, have less external support, 
and probably undergo more considerable changes in state. The 
effusion forms a cavity in the coi’d, sometimes rounded, sometimes 
irregular, in transverse section, and half an inch or more in vertical 
extent. The cord is enlarged at the seat of the haemorrhage, and 
this may be visible externally as a dark swelling the size of a nut or 
a bean. Very rarely the haemorrhage tears the layer of cord which 
limits it, and blood, usually only in small quantity, escapes into the 
membranes. The tissue adjacent to the clot is usually broken down, 
stained, and softened, and inflammatory changes may be recognised 
in it with the microscope, just as in the neighbourhood of haemor- 
rhages into the brain. As in the latter, the effused blood slowly 
undergoes changes in tint, becoming first rusty and then yellow, and 
ultimately a cyst may remain. Several extravasations may coexist, 
usually in the same part of the cord. In contrast to this focal 
haemorrhage there may be an infiltration of the grey matter with 
punctiform extravasations, which may appear, until closely examined, 
to be a single haemorrhage. The tissue between these small extra- 
vasations is broken down. It is probable that this form is always 
secondary to myelitis, as in the case mentioned in the foot-note on 
p. 391. In such secondary cases a careful microscopical examination 
usually reveals indications of inflammation much more extensive than 
the area affected by the haemorrhage. A growth into which haemor- 
rhage occurs is usually a glioma, unaffected parts of which will be 393 
HAEMORRHAGE. 
found in the neighbourhood of the extravasation. The cavities in the 
■cord into which blood may escape are sometimes of considerable 
vertical extent. I have known a fissure in the posterior column to be 
filled with blood thi’ough almost the whole length of the cord. This 
condition thus favours both the occurrence and the extension of 
haemorrhage. 
Symptoms.—Slight symptoms, “ prodromata,” have been observed 
in some cases, chiefly in the form of trifling sensory disturbance, 
tingling, &c., in the limbs afterwards paralysed. They have existed 
for a few hours or days, or even for two or three weeks before the 
onset. It is probable, however, that these have been cases of secon- 
dary myelitic haemorrhage, and that there are no premonitory 
symptoms in primary extravasations. The actual onset is always 
sudden; the symptoms attain a considerable degree in the course of 
a few minutes, but they sometimes increase during one or two hours, 
when the haemorrhage is from a small vessel and slowly increases in 
size—probably augmented by the rupture of other vessels which are 
torn in the tissue lacerated by the blood. Occasionally there has 
been transient loss of consciousness without any cerebral lesion, pro- 
bably from the upward influence of the shock. Rarely the onset has 
been by a series of sudden augmentations of the symptoms. Some- 
times the symptoms come on during sleep. The suddenness of the 
onset is the characteristic of the disease. 
The symptoms which thus develop vary according to the seat and 
extent of the extravasation. In the majority of cases there is para- 
plegia, complete motor and sensory paralysis up to the level of the 
lesion, with loss of power over the sphincters. Pain commonly but 
not invariably accompanies the sudden palsy; it may be felt in the 
spine or in the sacrum, round the trunk, at the front of the thorax, 
or at the epigastrium, sometimes seeming to pass thence through the 
trunk to the spine, or it may be felt in the legs. If in the spine it 
is local, and does not extend through a considerable length of the 
spine, as in meningeal haemorrhage, and there is not the initial spasm 
and rigidity which characterise the latter disease. This pain may 
precede the palsy, even for half an hour or an hour; it begins suddenly, 
and is no doubt due to the first slight extravasation, which afterwards 
increases (when some resistance yields), and effects the compression 
that produces the paralysis. Thus a girl aged fifteen was seized 
with sudden sharp pain, referred to the sternum at the mammary 
level, and to the corresponding region of the spine; this continued 
for half an hour, when the legs suddenly became powerless and insen- 
sitive. It is highly probable that, when there is such initial medial 
or bilateral pain, the haemorrhage occurs in the central region of the 
grey matter, perhaps from one of the commissural or anastomotic 
arteries (see p. 188), and that the pain is due to the irritation of the 
fibres of the posterior commissure, in which the paths for pain cross 
the middle line. The spinal column may be tender opposite the 394 
SPINAL CORD. 
affected spot. Usually tlie paralysed muscles are relaxed. Some- 
times they are the seat of early clonic contractions, or these may 
come on a few days after the onset. When the haemorrhage is in the 
cervical region all the limbs are powerless ; one arm is often affected 
before the other. The state of reflex action varies according to the 
seat of the disease; if it is at first abolished it quickly returns in the 
legs (unless the haemorrhage is in the lumbar enlargement), and it 
soon becomes excessive unless destroyed by secondary myelitis—a 
not unfrequent consequence. In one case there was a remarkable 
initial increase of myotatic irritability a few hours after the onset, 
probably irritative, and quickly giving place to loss.* Yaso-motor 
and trophic changes in the skin are common and often intense; there 
is often vascular dilatation; bedsores readily form, and cystitis may 
result. Frequently the secretion of sweat is increased for a tune. 
The temperature is normal at the onset, but it generally rises in the 
course of a few days from secondary inflammation in the cord. 
The palsy developed at the onset usually continues for a week or 
ten days, although the pain may lessen. The symptoms do not always 
increase during the stage of inflammation, perhaps because this only 
involves the structures which are already impaired by pressure; but if 
the patient has been brought near to death by the primary haemor- 
rhage, the secondary inflammation may end life. Occasionally, more- 
over, symptoms of an ascending or descending myelitis may come on, 
and the former may cause death by its interference with the muscles 
of respiration. This extension is greatest probably in cases of 
myelitic haemorrhage, in which the extravasation is merely an incident 
in the course of a commencing inflammation, but it seems also to occur 
in cases of primary haemorrhage. The slow extension upwards of the 
symptoms, during the first week, may be very distinct; and the occur- 
rence of descending inflammation may be shown by the loss of reflex 
action and by the failure of electric irritability in the muscles, sometimes 
only in those supplied from the upper part of the lumbar enlargement. 
The symptoms pass into a chronic stage, improvement being usually 
slow. Some lasting loss of power remains in most cases, and there is 
often some permanent muscular wasting on account of the frequency 
with which the haemorrhage is in the cervical or lumbar grey matter. 
Occasionally there is rapid recovery up to a certain point; a haemor- 
rhage of small size may abolish conduction in the white columns by 
the suddenness with which it compresses them, and the effects of the 
pressure may quickly pass away, while those remain that are due to 
the destruction of the grey matter. 
Diagnosis.—The diagnosis rests on the actually sudden onset of 
the symptoms, and on the occurrence of pain, in a limited region, as 
part of these. The former is evidence of a vascular lesion (rupture 
or closure), and the latter shows an acute irritation of the nerve- 
elements, such as may be produced by their laceration, but not by 
Sinclair, loc. cit. H2EA10RRHAGE. 
395 
mere deprivation of blood. It must be remembered, however, that 
we cannot assume that symptoms which come on during the night’s 
sleep are of sudden onset. Neglect of this consideration sometimes 
causes a mistake in diagnosis. The mode of onset is a sufficient 
distinction from all other organic diseases, except haemorrhagic 
myelitis and meningeal haemorrhage. The former (really a variety 
of haemorrhage) is distinguished by the existence of slight symptoms 
before the sudden attack. We are not justified in regarding as 
primary haemorrhage any case in which premonitory symptoms existed 
for more than a few minutes, unless such symptoms were so pro- 
nounced and sudden in onset that they might have been due to a 
definite extravasation, afterwards increasing. Initial fever (within 
the first six hours) always makes myelitis probable, provided there 
is no other cause for it. The distinction from meningeal haemorrhage 
has been mentioned in the account of the symptoms, and in the 
description of that disease. 
Prognosis.—In all cases in which the symptoms are considerable in 
degree or wide in range, the danger to life is great, and remains great 
until they begin to subside. The prognosis is better when the disease 
is in the dorsal region than when it is in the enlargements, for the 
same causes as influence the prognosis in myelitis. It is better when 
sensation returns in the course of a few days, but if the enlargements 
are affected other sources of danger remain considerable. Early 
trophic changes also render the prognosis worse, for they show an inten- 
sity of degree that may involve grave danger. After the onset is over, 
the forecast must be guided by the general principles that determine 
the prognosis in acute myelitis. 
Treatment.—The treatment of haemorrhage into the substance of 
the cord is the same as that of haemorrhage into the membranes 
(p. 295). The measures requisite are few, simple, and all-important. 
Absolute rest and the prone position are to be secured before anything 
else is thought of. Ice should be applied to the spine over the seat of 
the haemorrhage. The bowels should be opened freely, and full doses 
of ergot or ergotin may be given : 5ss of the liquid extract or five 
grains of ergotin may be given by the mouth, or three grains of ergotin 
may be injected under the skin, and the dose may be repeated two or 
three times, at intervals of two hours. A few large doses are probably 
more effectual than smaller doses continued for a longer time, since 
the haemorrhage probably does not go on for long. The after- 
treatment must be that for myelitis. The disease is one of those in 
which most of t’ e good that can be done by treatment—and in few 
diseases is the opportunity more urgent—rests with those in whose 
hands the patient is immediately after the onset. 396 
SPINAL COliD. 
DEGENERATIONS OF THE SPINAL CORD. 
A large and important class of diseases of the spinal cord consists of 
those in which there is a slow degeneration of the nerve-elements, with 
an overgrowth of connective tissue, and in which structures are affected 
that have a common function, while others that have a different 
function escape even when they are adjacent to the elements that are 
diseased. Affecting thus functional “ systems,” they are termed 
“ system diseases.” This term has been used in several senses, more 
or less special (even based on the developmental relations of the 
structures), and hence the question whether a given malady is a 
“ system disease ” or not, is one to which various answers have been 
given. The term is here used in its widest and simplest sense, as 
meaning an affection of the structures that have a function either the 
same, or so far allied that they work together as parts of one system, 
distinguishable as such from other sets of structures. A “ system 
disease” may involve all the structures of the system, or only some or 
one of them; its chief distinction is from a random disease that 
involves structures irrespective of function—merely, for instance, 
because they are contiguous, or supplied by the same artery. 
In “ system diseases,” the primary change is, as a rule, in the 
nerve-elements, and the overgrowth of interstitial tissue is secondary. 
The process is analogous to that which occurs iu the secondary 
degeneration of nerve-fibres, in which the first change is certainly in 
the nerve-elements, the destruction of which is followed by an over- 
growth of nuclei and supporting tissue, amounting ultimately to 
-a “ sclerosis,” as it is termed. The process is by some regarded as a 
chronic parenchymatous inflammation, an inflammation beginning in 
the proper functional elements of the organ, but it seems undesirable 
thus to widen and loosen our conception of inflammation ; so far as 
the process is concerned the question is one of name rather than of 
nature. 
Another question of much greater interest is the relation of the two 
elements in the process, the wasting and the growth, the atrophy of the 
nerve-tissue, the hypertrophy of the connective tissue. The failure of 
nutrition in the one causes an increased energy of nutrition in the 
other. We have seen this relation in the nerve-fibres. The degene- 
ration of a fibre is attended by an active growth of its nuclei and 
protoplasm. The nutrition of the two elements, the neural and the 
adventitial, is evidently connected in the closest manner, but in inverse 
course. It is important to recognise the fact that the process of 
growth of the connective-tissue e’ements is an active manifestation of 
nutritional energy, which, when once excited, may be to some extent 
independent of its cause. It may, when very active, pass bevond its 
proportional limits, and be greater than corresponds to the nerve LOCOMOTOR ATAXY. 
397 
atrophy that causes it; invading adjacent structures as if an independ- 
ent process. It may, when very rapid, have some of the characters 
of an interstitial inflammation, and even an acute inflammation. 
Such excess is quite unusual; as a rule the secondary process is sub- 
ordinate and proportioned to the primary change. 
These degenerative diseases fall into certain types so far as the spinal 
cord is concerned, but they are subject to some variety of combina- 
tion even there, and to great diversity of association with degenerative 
changes elsewhere. The affection of the cord is of either the sensory 
or the motor elements, or both. The type of the former is tabes ; of 
the latter, either spastic paraplegia or muscular atrophy, according as 
the lower segment at the motor path is affected or free. Other com- 
binations of affection will be better understood when the diseases are 
described. 
The degenerative diseases are not numerous, but they are of great 
importance. They are degeneration of the anterior cornua and anterior 
root-fibres, causing muscular atrophy; degeneration of the posterior 
columns and posterior root-fibres, causing locomotor ataxy; and 
degeneration of the pyramidal tracts, causing spastic paraplegia, a 
disease the exact pathological position of which is not quite certain. 
These degenerations may be variously combined, and some combina- 
tions need separate description. 
LOCOMOTOR ATAXY; TABES DORSALIS. 
The malady thus named is the most common chronic disease of the 
spinal cord. It consists in a degeneration in the posterior columns of 
the spinal cord, or the peripheral sensory nerves, or both, and is mani- 
fested, when considerable, by inco-ordination of movement, peculiar 
pains, defective sensibility, and loss of the myotaticirritability (muscle- 
reflex action), of which the knee-jerk is the most convenient manifes- 
tation. When slight in degree, the symptoms may be limited to the 
pains and the loss of the knee-jerk. The name “ locomotor ataxy” 
was given to the disease by Duchenne ; “ tabes dorsalis,” or “ wasting 
of the back,” is a term applied by Hippocrates to certain symptoms 
supposed to be due to venereal excess, and long ago limited in Germany 
to symptoms believed to depend on atrophy of the spinal cord. It 
then included all chronic paraplegias, but was further restricted to 
this disease by Romberg. It has lately obtained wider use on account 
of the discovery that inco-ordination may be absent when the disease 
is slight in degree. 
The symptoms vary much in different cases. Besides the varieties 398 
SPINAL CORD. 
thus produced, there are two allied affections that ought not to be 
classed with it. Oae is the so-called “ hereditary ataxy.” The other 
is that in which both weakness and inco-ordination co-exist from the 
first; “ataxic paraplegia” it may be called. Each differs from other 
varieties with sufficient constancy to merit separate consideration. 
These varieties are not included in the following account. 
History.—The inco-ordination of movement and other symptoms 
of the disease were frequently noted, during the first third of this 
century, in cases of disease of the spinal cord, but such cases were not 
distinguished from those with actual loss of power. The inco-ordina- 
tion was found to be associated with disease of the posterior columns 
by Stanley.* The first really exact account of the disease was pub- 
lished in 1847 by Todd,f who distinguished the cases with inco-ordina- 
tion and without weakness, from simple paraplegia, and, apparently 
not aware of Stanley’s observation, he inferred (from the character 
of the symptoms and his theory that the posterior columns contain 
fibres connecting segments of the cord at different levels) that the 
posterior columns would be found diseased ; and he verified this 
inference by finding in two cases disease of these columns. The credit 
of the discovery of the disease belongs, if to anyone, unquestionably 
to Todd, and few diseases can with greater truth be said to have been 
‘‘discovered.” Four years later (in 1851) Romberg described the 
disease and the lesion in the posterior columns, but he failed to exclude 
loss of power from the symptoms. Russell Reynolds, in 1855, gave 
an accurate description of the symptoms, and, in attributing the 
ataxy to muscular anaesthesia, was the first to give what we must now 
regard as the true explanation of the chief symptom.J A. series of 
cases was described by Gull in 1856 aud 1857. Tiirck first observed 
with the microscope the wasting of the fibres in the posterior 
columns. Duchenne in 1858-9 published an independent and very 
able analysis of the symptoms of the disease, and gave it the name 
“ locomotor ataxy.” He obtained for it (with the help of Trousseau’s 
“ Lectures ”) the recognition that previous descriptions had failed to 
secure, and achieved such a degree of success that the malady is 
called in France, Duclienne’s disease. H any name is attached to it, 
that of Todd alone can be right. 
Causes.—The disease is much more frequent, in this country at 
least, in urban than rural populations. Inherited influence is to he 
traced only in a small proportion of the cases, perhaps in not more 
than 10 per cent. It is usually a general neurotic heredity, manifested 
by such diseases as insanity, epilepsy, and other degenerative diseases 
* ‘Med. Gazette,’ Feb., 1840, and ‘Med.-Chir. Trans.,’ vol. xxiii. 
f * Cyclopaedia of Anatomy and Physiology,’ vol. iii, p. 721. 
t Reynolds,‘Diagnosis of Diseases of the Brain, &c.,’ 1855, “Anaesthesia Muscu- 
laris.” Certain words are worth quotingIt appears most probable that the 
centripetal tract of fibres is affected, and that the locality of lesion is very 
variable” (p. 165). LOCOMOTOR ATAXT. 
399 
of the nervou3 system. Instances of this are—father epileptic; 
father insane; two sisters insane. Direct inheritance of the disease 
is extremely rare (the special hereditary form being always excluded). 
A boy with distinct symptoms and optic nerve atrophy was the son of 
a man who presented characteristic indications of the early stage of 
tabes (Remak). But in most instances of this character the inherit- 
ance is effected by means of syphilis. 
Males suffer far more frequently than females, the proportion being 
about ten to one, and this implies some proclivity inherent in the male 
sex. A like preponderance of males obtains in a disease that has some 
alliances with tabes—general paralysis of the insane. The middle 
period of adult life is that in which locomotor ataxy usually commences. 
No less than half the cases begin between thirty and forty, one 
quarter between forty and fifty, and rather less than a quarter 
between twenty and thirty. It rarely begins after fifty, but I have 
once known it to develop at sixty-six. Under twenty it is still more 
rare, but cases are met with as early as ten, and even in quite young 
children, the subjects of the cause next described. 
Among the individual causes, one overshadows all the rest—the 
influence of syphilis. A very large proportion of the sufferers have 
had, at some previous time, constitutional syphilis, either distinct 
secondary symptoms or an indurated sore. The proportion is almost 
as large in the upper and middle classes as in the lower. Of fifty con- 
secutive cases of the disease in men, seen in private consulting practice, 
no less than twenty-nine, or 58 per cent., gave a history of a chancre 
known to be hard, or of secondary symptoms; and eight others had 
had a venereal sore of unknown nature. In the lower classes the 
proportion is higher, aud has been estimated at 80 per cent., or even 
more. The ascertainable facts are certainly below the real facts, as I 
have pointed out elsewhere.* When a deduction is made for possible 
accidental coincidence, there remains at least one half of the cases in 
which numerical coincidence must depend on causal relationship. It 
is probable, indeed, that, taking all cases, a causal proportion of three 
quarters would be nearer the truth. In women also antecedent syphilis 
can often be traced, although rather less frequently than in men. At 
the same time the facts are even more difficult to ascertain, since in 
married women syphilis so often runs a latent course. But in the 
cases of tabes that succeed syphilis the lesion is not syphilitic in histo- 
logical character; it is as degenerative as in the cases in which syphilis 
can be excluded, and it is not influenced by the treatment for syphilis. 
Hence it must be regarded as a degenerative sequel of syphilis rather 
than as a true syphilitic disease. It is probably the influence of syphilis 
that determines the greater incidence on the urban than on the rural 
population, and the preponderance of cases in middle life. Inherited 
syphilis is also capable of causing the disease, and is to be traced 
in all cases in children. After the acquired disease the interval 
‘Lettsomian Lectures/ 1889. 400 
SPINAL CORD. 
between primary syphilis and the first symptoms of tabes varies from 
one to twenty years. It is, however, rarely less than three years, and 
in most cases it is between six and twelve years. In rare cases the 
first symptoms occur during the active stage of syphilis.* 
It is certain, however, that syphilis is not the only cause of the 
disease. In a few cases, less than 10 per cent, of the whole, it can be 
excluded with confidence. The causes operative in these can be 
traced also in some of the patients who present a history of syphilis, 
and in such cases the causation of the malady is probably complex. 
One of these causes, which can sometimes be clearly traced, is in- 
jury, such as involves concussion of the spine. The immediate results 
of the injury, whether slight or grave, transient or lasting,are followed 
by the symptoms of the degenerative malady. In one case a man fell 
from a height on to the deck of a ship ; transient paraplegia resulted, 
but six weeks after the accident the man presented extreme ataxy, with 
good power, and no knee-jerk (Arnold). I have known the symptoms 
to develop gradually a few months after a fall from a horse. Exposure 
to cold and wet has occasionally preceded the onset so directly that 
it must be regarded as a cause. In other cases the disease has 
succeeded excessive fatigue and over-exertion, and also certain acute 
diseases, especially (it is said) acute rheumatism and typhoid fever; 
it follows diphtheria in rare cases, but the ataxic form of diphtheritic 
paralysis, passing away, is far more common than true tabes. (See 
also section on Pathology.) Alcoholic excess has been noted in 
some instances, and the influence of this cause is intelligible since it is 
known to cause sometimes such a form of puerperal neuritis as 
occurs in tabes. Indeed, it is strange that this cause cannot be 
traced more frequently. Sexual excess has been supposed, by some, 
to be a cause; but its influence can rarely be detected, and its signi- 
* Although an occasional relation to syphilis had been noted by several preceding- 
observers, Fournier was the first (in 1876) to assert the wide extent of this relation. 
Ilis statements were received with doubt (because syphilitic patients constituted his 
field for observation), but they were confirmed from the neurological side by myself 
(‘ British Med. Journal,’ Match 1,1879) and Erb (‘ Arch. f. klin. Med.,’ July, 1879); 
while abundant corroboration has been since afforded. Many who at first doubted 
have been convinced by fresh observations. Facts collected without reference to 
the point at issue have proved useless, and freshly collected facts have thrown a 
new lij.ht on the subject. The proportion of cases with previous syphilis neces- 
sarily varies according to the absolute frequency of syphilis, because the number 
due to other causes will be the same. Syphilis is rare among Hebrews, and hence a 
smaller ratio of Jewish tabetics have had syphilis. The difference in the character 
of the lesion from that of changes known to be syphilitic was urged as an objection 
by many writers, but such considerations are theoretical, and must yield to facts; 
instead of denying that this or that lesion can be produced by a given cause, we may 
have to widen our view of the operation of that cause. Other degenerations of the 
nervous system seem also to have a relation to syphilis, as I pointed out some years 
ago (‘ Lancet,’ Jan. 15, 1381). As will be shown in the section on Pathology, 
recent discoveries lessen very much the difficulty of comprehending the rela- 
tionship. 401 
LOCOMOTOR ATAXY. 
ficance is uncertain, since sexual excitement is undoubtedly some- 
times an earlv symptom of the disease. 
Secondary Tabes.—Symptoms of locomotor ataxy sometimes succeed 
other diseases of the spinal cord, and such sequence is especially 
common in syphilitic subjects. Myelitis and syphilitic gummata 
may be thus succeeded by tabes. An officer in India, who had 
had syphilis, having suffered for a day or two from pains in the back, 
took a bath in snow water, and in a few days his legs were absolutely 
powerless. He gradually recovered power, but could not co-ordinato 
the movement: as power returned, lightning pains came on, and a 
year afterwards he presented the typical condition of locomotor ataxy. 
Again, a man, twelve years after syphilis, had a severe fall, followed 
by gradual loss of power, so that at the end of three weeks he could 
scarcely stand. The legs remained weak for a month, and then im- 
proved, but ataxy came on ; three months later, power was good, inco- 
ordination extreme. A similar succession may occasionally be observed 
in those who have not had syphilis. In many cases, however, the 
ultimate condition is one of combined weakness and ataxy. 
Symptoms.—A typical case of developed tabes presents certain 
motor, sensory, and reflex symptoms. There is inco-ordination of 
movement of the legs, sometimes of the arms also, without loss of 
power or muscular wasting. There are pains in the affected parts, 
especially sharp momentary “lightning” pains; there is some loss of 
sensation; there is often loss or diminution of reflex action from the 
skin, and almost always entire loss of the myotatic irritability that is 
revealed by the so-called “ tendon-reflexes,” and especially by the knee- 
jerk ; there may be retention or incontinence of urine, constipation, 
and often loss of sexual power. Of this group of symptoms, two 
usually precede the others—the pains, and the loss of the knee-jerk. 
These may exist alone, even for years, before inco-ordination comes on. 
Thus the symptoms are far wider in range than the name “ ataxy ” 
suggests ; and while inco-ordination, if it exists, is the most obtrusive 
objective symptom, it may never be developed. Hence physicians 
have extensively fallen back on the older term “ tabes dorsalis.” 
But recent expansion of our knowledge, especially the discovery of the 
extent to which the symptoms may depend on disease of the peri- 
pheral nerves, shows that even the qualifying “ dorsalis ” narrows the 
name unduly, and “ peripheral neuro-tabes ” has been added to the 
terminology of the disease. 
Besides the symptoms above enumerated, others are occasionally 
present. Of these the most important are atrophy of the optic nerve 
(and occasionally of other cranial nerves) ; trophic changes in the skin, 
the bones, and the joints ; peculiar paroxysmal visceral disturbances 
and occasionally motor paralyses and muscular wasting supervene. 
The combinations of symptoms present in different cases vary much. 
It will be convenient to consider first the individual symptoms in 
their various degrees, and then their grouping and sequence. 
VOL. I. 402 
SPINAL CORD. 
Motor Symptoms.—Tlie characteristic inco-ordinntion of movement 
develops gradually. It is usually increased (as Romberg pointed out) 
by closure of the eyes, and at first may only exist when the guiding 
influence of vision is thus withdrawn. Before it causes ataxy of 
movement, it may render difficult the maintenance of equilibrium when 
the base of support is narrowed by the feet being placed close together, 
toes and heels ; if then the eyes are closed, the patient sways, and 
tends to fall. In health slight unsteadiness is thus produced, varying 
in degree in different persons, but never amounting to even a sugges- 
tion of a fall. The effect of closure of the eyes is greatest when 
sensation in the soles of the feet is defective, but does not depend on 
this defect; it may be marked when sensation on the soles of the feet 
is perfect. The early defect in co-ordination may be discovered by 
the patient when he walks in the dark, or backwards, or, not un- 
commonly, when he shuts his eyes in the process of washing the face. 
In a further degree of in co-ordination there is inability to stand with 
the feet together, even when the eyes are open, and the patient is only 
steady when the feet are wide apart. If the feet are bare, the diffi- 
culty is greater, because muscular action has to replace the rigid base 
of the boot. The irregular contraction of the muscles is shown by the 
conspicuous movement of the tendons on the back of the feet. The 
patient may oscillate from toes to heels before he comes to rest. As 
the defect progresses, uncertainty is felt in walking even with full 
visual guidance, especially on uneven ground, or on a very smooth 
surface. A slight visible alteration in gait is then appreciable, the 
feet are not placed on the ground quite as in health, or there is distinct 
difficulty in maintaining equilibrium when the patient turns quickly, 
and he has to put a foot down suddenly to keep from falling. As the 
inco-ordination increases, the change in gait becomes greater, but 
varies much in its precise characters, according to the muscles that 
are most affected. Often the feet are raised too high, thrown for- 
wards too far, brought down too suddenly, and the whole sole comes 
in contact with the ground at once. There may be a tendency for one 
foot to be brought in front of the other, or moved too far outwards. 
Often the foot becomes inverted when it touches the ground. Efforts 
to correct error in movement have themselves to be corrected. In 
other cases the defect in maintaining equilibrium is greater than the 
actual disorder of movement of the legs, and the patient sways about in 
the manner of one who has cerebellar disease; this probably depends 
on a preponderant affection of the muscles of the hip-joint. 
As the defect progresses, the patient is only able to walk by steady- 
ing himself with a stick, or by taking hold of the arm of another person 
or of adjacent objects. At first a very slight degree of this help is 
sufficient; guidance rather than support is needed. Afterwards, 
however, considerable support is necessary, and ultimately the patieut 
may be unable to stand even with help. When he attempts to rise, 
the legs move hurriedly forwards and backwards, and if the upright LOCOMOTOR ATAXY. 
403 
posture is at last achieved, the legs slip forward, and only strong 
support saves the patient from a fall. The ataxy is manifest also in 
other movements of the legs. If the patient, when lying, tries to 
touch an object with his foot, the leg is moved irregularly, goes beyond 
the place, and then is brought too far back, and only at last does it 
come in contact with the object, often with unintended force. This 
inco-ordination, like that in standing, is much greater if the eyes are 
closed. 
The arms may present similar inco-ordination, although they often 
escape, even when the affection of the legs is extreme; very rarely 
the arms suffer before the legs. The commencing defect is revealed 
by delicate movements, such as writing. When slight, it may be 
conspicuous if the patient tries, with closed eyes, to touch some object, 
such as his own nose, or, having abducted his arms, tries to bring the 
forefingers together. As it increases, all movements become irregular; 
it is impossible for the patient to button his coat, or to pick up a 
small object from the table ; the fingers twist about in the attempt. 
The grasp is not sustained; first one finger is felt to relax and then 
•another. If the patient attempts to hold out his hand in a fixed 
posture, it is seen that the same irregularity obtains; instead of a uni- 
form balanced contraction the muse—j contract and relax involun- 
tarily, and slow unintended movements of the fingers result, some- 
times closely resembling those of athetosis. The same spontaneous 
movements may also be observed in the legs. They cease at once 
when the muscular effort is relinquished. Occasionally the muscles 
of the trunk present inco-ordination. Thus one patient could sit 
steadily on a chair when his eyes were open, but if he closed them would 
at once fall off. The movements of the head, face, tongue, and eyes, 
escape the characteristic derangement. 
Even with extreme inco-ordination, the power of the muscles may be 
unimpaired. Occasionally some group of muscles, as the flexors of the 
ankle, become weak for a little time and then strong again, just as may 
the eyeball muscles, as we shall presently see. In some cases motor 
power in the limbs remains unimpaired to the end ; more often, when 
the ataxy has become great, some muscular weakness supervenes, with 
or without wasting of the weak muscles. There is a distinct group of 
cases in which weakness and ataxy come on together, but these are 
considered separately (“ Ataxic Paraplegia ”). 
Sensory symptoms are prominent in most cases,—subjective sensa- 
tions, especially of pain, and loss of sensibility. Spontaneous pains 
are present in some degree in nine tenths of the cases of tabes. The 
most frequent and characteristic are the sudden and lancinating pains 
called “ lightning pains.” They occur chiefly in the legs, but may be 
felt in the trunk, arms, and even in the head. They are usually 
paroxysmal and apt to come on at night; attacks of such pains last 
for some hours or for a day or two, varying in seat, but often felt in 
the same part throughout an attack, or through many attacks. 404 
SPINAL CORD. 
Sometimes tliey are felt in a limited area of the shin; at others they 
seem more deeply seated; sometimes they dart down the limb. They 
may correspond to a nerve-trunk (esj>ecially the sciatic), but more 
frequently have no relation to the nerves. They may be felt near but 
not in joints. Although the pains are usually acute and “ stabbing,’* 
they are sometimes of different character. Thus in one patient the 
sensation was as if both legs were for a moment on fire. When 
referred to the skin, this often becomes tender after the pains have 
been felt for a time, and even the contact of the bedclothes cannot be 
borne. When pains continue at one spot for some days, vascular or 
trophic changes may occur there,—ecch vmoses have been observed, and 
I have known the grow tli of the hair to be changed where pains had 
been felt in the scalp ; each hair bent and broke short off, over an 
area the size of half-a-crown; after the pains ceased, the growth of 
the hair became normal. A sharp pain may be accompanied by a 
sudden reflex spasmodic movement of the legs, or by inhibitory 
weakness. Thus, in one case, a sudden pain would often make the 
patient fall on his knees. The pains may be so severe as to prevent 
sleep for several days. 
Other kinds of severe pain, less brief than the lightning pains, occur 
in some cases, and are described by various epithets, as “ burning,” 
“tearing,” “gnawing.” Burning pain in the toes distressed one 
patient. Much more common, and occurring writh other pains, are 
slighter dull pains like those of rheumatism, for which they are often 
mistaken, an error that is facilitated by the circumstance that any of 
the pains of tabes may be influenced by weather, being especially 
increased by damp cold. Such dull pains sometimes precede the 
sharp pains even for years. A painful sense of constriction is also 
common, and may be felt around the trunk or in the legs, groins, &c.; 
it is often referred to a considerable area—the patient may feel as if 
the whole trunk were tightly enveloped in a cuirass of brass. Darting 
pains also may be felt in the trunk and not in the legs. Such a sense 
of constriction is sometimes referred to the legs. In the arms and 
hands the paius are usually slight in degree, and seldom cause real 
distress. Visceral pains may also occur, usually paroxysmal, and 
referred to the stomach, bladder, rectum, &c. 
Pains are not only the most common, they ai*e often the earliest 
indication of the disease, and may be the only subjective symptoms 
in slight and stationary cases. They bear no proportion to the other 
symptoms, and are sometimes trifling—occasionally altogether absent. 
They seem sometimes to occur alone ; I have seen several patients 
who suffered lightning pains, characteristic in features, course, and 
general associations, both with and without the pupil symptoms 
common in tabes. Such isolated pains may be followed by 
ataxy. 
Sensations other than pain are also common. They are various in 
character, described as “tingling,” “pins and needles,” “creeping,” LOCOMOTOR ATAXY. 
405 
and very often as if the skin, especially of the soles, were covered by 
some soft substance. Sensations of cold or of heat are also common ; 
the feet may feel as if the legs were always in cold water ; a sensation 
of cold about the testicles is occasionally complained of. Similar 
cutaneous sensations are also common in the bands. Increased sensi- 
tiveness to pain may also exist, especially on the soles of the feet, and 
often accompanies lessened sensibility to touch. 
A diminution of sensibility is also present in most cases of the 
developed disease. It may involve all forms of sensibility, but seldom 
equally; some forms may be impaired and others normal. Either 
pain or touch may be affected alone; for instance, a prick may cause 
no sensation of pain, although the least touch of the finger is every- 
where perceived. A firm touch (i. e. slight pressure) may be felt 
when a slight touch is unperceived. When a touch is felt, the 
power of localising it may be impaired. Temperature sensations are 
rarely affected without other forms of sensibility, but they may be im- 
paired with pain when tactile sensibility is normal. On the other 
hand, there may be extensive loss to pain without any defect of the 
temperature sense. A prick may then cause only a sensation of heat, 
and extreme degrees of heat or cold cause pain less readily than 
normal. The temperature loss may be partial—either cold or heat 
may be unperceived while the other is recognised. When touch is 
slightly impaired, there may be an inability to discriminate differences 
in the degree of pressure on the skin. 
Accompanying the diminution or increase of sensitiveness there are 
sometimes curious changes in the sensation produced. One of these 
is a delay in the perception of pain, which may amount to several 
seconds. The greatest delay I have met with amounted to seven 
seconds, but one of fifteen seconds has been described (Eulenberg). 
The contact of a point may be felt at once, the pain only after a 
considerable interval. Often there is an after-pain, lasting sometimes 
for a quarter or half a minute or longer, and the maximum sensation 
may not be attained until some seconds after the pain is fh*st felt. 
Thus, in a case in which there was a delay of seven seconds, the 
maximum sensation was only felt twenty-five seconds after the prick 
(Obersteiner). Often there is a second or third maximum, a sort of 
rhythmical recurrence of sensation, quick or deliberate. A delay 
greater than normal may also attend the sensation of heat. The 
localising power is sometimes strangely perverted. A touch or prick 
-on one leg may be referred to the other, sometimes with singular uni- 
formity in position (allocheiria, p. 9). A prick in one spot may be felt 
in many places (polysesthesia) on the same, or on both legs. The 
reaction of the sensory nerves to electricity may be changed in the 
same way as that of the motor nerves when they are degenerated; 
instead of the earliest sensation, on closure of the circuit, occurring at 
the kathode, it occurs at the anode (Mendelssohn). 
Impairment of sensation is most frequent, and usually greatest, 406 
SPINAL CORD. 
in the lower part of the legs and feet. It may even be limited 
to the soles, and usually then ceases at the outer sharp edge of the 
foot, but extends for an inch or so up the inner side. Touch or 
pain may be lost on the sole only, and even, strange to say, the 
form of sensibility that is lost on the sole may alone persist in the legs. 
Although the sole is usually most affected, sensation may be perfect 
on the sole when lost elsewhere. One leg is often more affected than 
the other. The loss may extend to the trunk, and over part or the 
whole of it. In the arms it is usually greatest on the hands; often 
commences on the palmar aspect of the fingers, and may be limited to 
this aspect of the hands, just as it is to the soles of the feet. Sensa- 
tion may be lost on the trunk and not on the limbs—an important 
fact, because the anaesthesia may then readily be overlooked. On the 
head loss of sensation is rare and partial. 
The loss of sensibility is not confined to the skin, but affects the 
deeper tissues also in many cases. The contraction of the muscles 
on electrical stimulation may be unfelt, and the muscles may be less 
sensitive than normal to pressure or forcible extension. It is only 
from intelligent patients that this can be distinctly ascertained. 
Sometimes, however, the muscles may be quite insensitive when cuta- 
neous sensibility is little or not at all impaired. It is probable that 
the sensibility of the joints, fibrous tissues, and tendons is also 
involved. The position of the limbs in passive as well as in active 
movements may not be perceived. In slight cases this sense of pos- 
ture may not be lost, but in severe cases it may be so absolutely 
abolished that the patient has always to look to see where his legs are. 
The anaesthesia may extend to the viscera when the trunk is involved. 
In consequence of the loss of sensation, grave injuries to the limbs, 
such as burns, may be unperceived, and visceral disease may be 
unattended with the customary pain. Pleurisy, for instance, may be 
absolutely painless. 
But impairment of sensation is not invariable. There may be no 
loss even in patients who present considerable inco-ordination, and in 
those who suffer severe pains, as well as in those who have had none. 
But it is very rare to have no sensory defect when inco-ordination is 
considerable. 
Reflex action from the skin is usually impaired in proportion to the 
loss of cutaneous sensibility, and especially to the loss of tactile sensi- 
bility. It may be normal when pain is unfelt. The plantar reflex 
is most frequently impaired, and the progress upwards of the disease 
may be attended by a progressive loss of the gluteal, cremasteric, and 
abdominal reflexes. On account of the variations met with in health, 
it is uncertain whether reflex action is ever lessened when there is no 
impairment of sensation. On the other hand, in the early stage of 
the disease, there is sometimes a considerable and even extreme excess 
of all cutaneous reflex action. 
Loss of sexual power is an exceedingly common and often an early LOCOMOTOE ATAXY. 
407 
symptom of tlie disease, and may precede any impairment of sensory 
or reflex functions. On the other hand, exceptions are met with in 
which sexual power persists to a late period of the disease, even until 
after the patient has lost the ability to walk alone. 
If the condition of cutaneous reflex action is somewhat inconstant, 
this is not the case with the reflex process on which the myotatic 
irritability depends. A loss of the knee-jerk, as Westphal first 
pointed out, is one of the earliest and most constant symptoms of 
tabes. With it disappear also all other indications of this irritability. 
In cases with great excess of cutaneous reflex action the knee-jerk is 
lost as in other cases, and the contrast between the two forms of reflex 
action is very striking. It is exceedingly rare for the knee-jerk to be 
obtained in any case of true tabes, but an early case is sometimes 
met with in which it is not lost, although diminished, and commonly 
unequal on the two sides. In one or two cases I have found it slight 
on one side and lost on the other, when distinct ataxy was present, 
and have observed its subsequent disappearance. In one case, in which 
the jerk was lost in one leg only, lightning pains were confined to 
this leg. The loss often precedes for many years the development of 
inco-ordination. 
Eye Symptoms.—The functions of the internal muscles of the eye 
are often affected in tabes. In more than five sixths of the cases* the 
reflex action of the iris to light is lost; rarely the action remains perfect 
throughout. In most cases of reflex loss, the contraction on accommo- 
dation is preserved, as first noted by Argyll-Robertson. Often also (as 
Erb has shown) the dilatation that occurs on painful stimulation of 
the skin of the neck, &c., can no longer be produced. Sometimes 
the ciliary muscle is also paralysed, causing loss of accommodation. 
Very rarely there is loss of accommodation and of the associated con- 
traction of the iris, without loss of the light-reflex. When reflex con- 
traction is not lost, it may not be maintained; the pupil again 
enlarges; an actual inverted reaction to light and darkness has been 
observed.f The pupils are often very small (“ spinal inyosis ”), 
especially when there is loss of the reflex dilatation from the skin, a 
loss which seems to be accompanied by atony of the radiating fibres 
supplied by the sympathetic. The pupils are not always small; they 
may be of a medium size or still larger, and then I have usually 
found that the skin-reflex can be obtained, although the light- 
reflex cannot. They are often not perfectly circular, and are f requently 
unequal. Both eyes are usually affected in the same manner; occa- 
sionally the reflex action is lost in one and only lessened in the other ; 
indeed, almost every possible condition is occasionally met with. On 
the other hand, the intra-ocular muscles may be unaffected even in 
advanced cases. According to Berger, the ocular tension is often 
lessened. 
* Berger says 97 per cent, 
f L’Abunde, * La Psychiatria,’ 1SS9, vii, p. 283. 408 
SPINAL CORD. 
Paralysis of tlie external ocular muscles is also common in tabes, 
and occurs in several forms: (1) Transient weakness, lasting a few 
days or weeks and then passing away. (2) Permanent paralysis, 
complete or incomplete, of a single nerve or part of a nerve. Either 
form may occur at any stage, but the first is most common in the 
early, and the second in the later stages of the disease. The transient 
palsy renders diplopia a common sym- 
ptom in the early period ; any muscle 
may be affected, but the external 
rectus is that which most frequently 
suffers. The persistent palsy may 
affect one or more muscles; often 
the levator is involved, causing what 
has been termed “ tabetic ptosis ” 
(Fig. 114). Sometimes the whole 
third nerve is paralysed. (3) There 
may be a combined palsy, suggesting 
a central origin, as, for instance, loss 
of the movement of convergence asso- 
ciated with loss of accommodation, 
although the internal recti act in 
the movement towards one side. (4) 
Many or all the muscles of both 
eyes may gradually become paralysed, 
“ progressive ophthalmoplegia,” in- 
ternal or external—a condition that 
is more fully described in the account 
of ocular palsies in vol. ii. 
Atrophy of the optic nerve is 
the most serious ocular complica- 
tion of tabes. Its frequency is difficult to ascertain, but is certainly 
less than is often supposed; it does not occur in more than one case in 
ten. Atrophy is generally an early symptom, usually commencing 
before inco-ordination is developed, and in a large number of cases ataxy 
does not supervene ; there seems a tendency for the spinal malady to 
become stationary when the optic nerve suffers. The disc becomes 
pale, and its substance shrinks, so that recession begins at its edge 
instead of at the central “cup,” as may readily be perceived by the 
course of the vessels. The failure of sight usually commences with a 
peripheral limitation of the field and loss of colour vision, but sometimes 
central acuity fails early. When this remains good, the peripheral loss 
may reach a considerable degree before it is suspected by the patient. 
The visible pallor of the optic disc is not always proportioned to the 
failure of sight; the change in tint depends on wasting of the capil- 
laries, and this does not always correspond to the wasting of the nerve- 
fibres. The ultimate tint is grey, or a whitish grey, especially as seen by 
Fig. 114.—Double tabetic ptosis* 
* From a Salpetri&re photograph, for which I am indebted to M. Charcot. LOCOMOTOR ATAXY. 
409 
the direct method. When the disc was very vascular before the 
atrophy, the grey tint is generally deepest. The vessels are but little 
uarrowed. Occasionally there are slight signs of congestion in the 
early stage, and then some tissue of gelatinous aspect may develop in 
the disc, and the vessels may appear somewhat compressed.* 
The course of the atrophy is usually slowly progressive, and, in most 
cases, it ends in total or almost total blindness. It may, however, 
cease to progress, and even undergo slight improvement. The onset 
is not always gradual; sometimes sight fails considerably in the 
course of a few days, without ophthalmoscopic changes to account for 
it. I have met with one such case in which double temporal hemianopia 
indicated disease at the optic chiasma. In such cases the secondary 
interstitial process probably assumes inflammatory intensity (see 
p. 396). The atrophy is often more advanced in one eye than iu the 
ether, and very rarely one eye only suffers. Flashes of light are 
occasionally experienced in the course of the atrophy, comparable to 
the lightning pains in the limbs, but they are not common. 
Deafness, having the characters of nerve-deafness, is met with in 
some cases, sudden or gradual in onset, transient or lasting. The 
persistent deafness has been attributed to an atrophy of the auditory 
nerve, analogous to that of the optic nerve, but certainly in many 
cases without sufficient reason.f Only when there is a progressive'limi- 
tation of the range of hearing, analogous to the peripheral limitation 
of the field of vision, are we justified in assuming nerve atrophy. I 
have seen two cases of this kind. In each there was also optic nerve 
atrophy, and the other symptoms of tabes were distinct.J Attacks of 
vertigo are frequent in the cases attended by deafness, and seem to 
depend on the disturbance of the labyrinth or auditory nerve, and to 
be thus connected only indirectly with the primary disease. Anosmia 
occasionally occurs, and is probably not infrequent. It is apparently 
due to an atrophy of the olfactory nerve similar to that of the optic. 
The functions of the other cranial nerves are not often affected. 
Pains may be felt in the region of the fifth nerve, and there is occa- 
sionally loss of sensation in some part of the area supplied by it, on 
one side or both. Unilateral atrophy of the tongue has been sometimes 
noted. In the larynx, besides the spasm to be presently described, 
* Further details will be found iu * Medical Ophthalmoscopy.’ 
f It is very difficult to distinguish an affection of the nerve from one of the 
labyrinth independent of the nerve. Even in a case of bilateral deafness coming 
on in the course of tabes, in which the patient could hear only a loud voice, and 
deep notes better than high ones, in which atrophy had been diagnosed, Lucae found 
calcareous masses in each of the labyrinths, and the auditory nerves were qui.e 
normal. 
J In one, only notes between E2 and D could be heard. In the other the patient, 
when first examined, was absolutely deaf to notes above E2 and below Gj. A few 
months later, the restriction had confined the range of hearing to the octave in the 
treble clef, between E2 and E1, even Eb1 being inaudible. Thus the loss occurred 
chiefly from below upwards. Ultimately no note could be heard. 410 
SPINAL COED. 
paralysis of the vocal cords has been met with in rare cases, both as 
an isolated symptom and also after attacks of spasm have occurred 
for a long time. Both posterior crico-arytsenoids have been paralysed 
(Oppenheim), and in one case paralysis of one posticus occurred very 
early in the disease (Remak). 
Sphincters.—The functions of the bladder are frequently deranged ; 
there may be either sluggish micturition or a tendency to incontinence, 
and very the bladder is not perfectly emptied. These symptoms 
frequently occur early in the disease, and it may be indeed only for 
them that the patient seeks medical advice. The retention may become 
absolute, or there may be overflow incontinence; there is rarely para- 
lytic incontinence. The imperfect contraction, even when slight, may 
have serious effects. The residual urine tends to decompose, and 
gradually induces over-distension; cystitis is apt to occur, and 
secondary renal disease may develop insidiously, and is a not uncommon 
cause of death when the difficulty in micturition has been insignificant. 
The sphincter ani is often also weak, so that a loose stool can be 
retained with difficulty ; but its paralysis rarely reaches a high degree. 
Constipation is extremely common. 
Vaso-motor and trophic disturbances constitute an important group 
of symptoms, and may reach a considerable degree without a coinci- 
FlO. 115.—Perforating ulcer of the foot in tabes. (From a Salpetriero 
photograph.) 
dent increase in tlie other symptoms. Local sweating has been noted,, 
confined, for instance, to the palms and soles, or to one side of the 
head. The ecchymoses and altered growth of hair, in connection with 
attacks of pain, have been already mentioned. Pigment may disappear 
from the skin and hair in isolated spots. Herpes of the skin is not 
uncommon, and usually occurs in association with attacks of pain. 
The epidermis of the sole becomes thickened; blisters readily form 
beneath it and may lead to indolent ulcers. The curious affection 
known as “ perforating ulcer of the foot ” has been found to be almost 
confined to cases of tabes. Troublesome ulceration of the toes, espe- 
cially about the nails, is also occasionally met with, and may necessi- LOCOMOTOR ATAXY. 
411 
tate amputation. The growth of the nails of the feet, and sometimes 
of those of the hands, may be changed ; they may be thickened and 
the surface furrowed or irregular. The nails may even fall off and be 
slowly renewed. The teeth sometimes decay quickly, and may drop 
out. One patient who had previously lost many of his nails, found 
that all the teeth of the upper jaw fell out in the course of three days, 
without any pain or decay. Wasting of the muscles occurs only as a 
complication in the later stage of the disease. 
Changes in the nutrition of the joints and bones have attracted 
much notice since attention was directed to them by the careful 
investigations of Charcot, whose name is sometimes connected with the 
condition. They are not very common, but are sufficiently frequent 
and well marked to place their relation to the disease beyond doubt. 
The bones may become brittle, and may break readily, in so-called 
“ spontaneous ” fractures. The process of union is attended with the 
formation of a large amount of callus. Sometimes there is also ossi- 
fication or calcification of the structures adjacent to injured bones, 
and even of the fibrous tissues independent of the joints, such as the 
intermuscular and subcutaneous tissues. This may be rapidly in- 
flamed, and extremely quick swelling may occur, followed by indura- 
tion. A s the inflammation subsides, there is a remarkable tendency for 
ossification to occur even in the newly-formed inflammatory tissue 
beneath the skin. Such subcutaneous changes occur most frequently 
in the foot or thigh, especially near joints, but sometimes in the 
deeper fibrous tissues between the muscles. In the joints, the 
changes consist of erosion of the cartilage, wasting of the heads of the 
bones, and ossification of the ligaments ; sometimes irregular bony 
growths form, and occasionally the head or shaft of a long bone 
may undergo an extraoi'dinary increase in size by the development of 
new osseous tissue on the surface. The joint changes may thus 
assume an atrophic or hypertrophic character, and the movement 
may be either too free or too limited. Wasting of the head of the femur 
often renders dislocation of the hip easy. A remarkable instance of 
these osseous changes has been recorded by Charcot; a tabetic woman 
suffered successively, in the course of a few years, dislocation of both 
hips, fractures of the left femur, of both bones of each forearm, and 
dislocation of one shoulder; after death old fractures were found in 
both scapulae and the left clavicle. With such changes, and often 
when they are slight in degree, there may be great effusion within the 
joints and oedema outside them. The larger joints are those most 
commonly diseased—knee, hip, ankle, elbow,—but the small joints of 
the fingers have been known to suffer (Westphal). The relative fre- 
quency with which the chief joints are affected is approximately 
indicated by the following percentage :*■—knee, 45 ; hip, 20 ; shoulder, 
11; tarsus, 8 ; elbow, 5 ; ankle, 4. They often occur during the 
* Obtained by combining the collections of cases of Weizsauker (Bruns* ‘Beitr. 
z. kl. Cliir.,’ 1887) and Hotter (* Arch. f. kl. Chir.,’ Bd. xxxvi). 412 
pre-ataxic stage. The lesions are sometimes excited by injury, and 
the extraordinary changes that may follow traumatic influences, or 
occur alone, afford a conclusive indication that abnormal trophic in- 
fluences are at work. Fig 116 represents the arm of a man who fell 
SPINAL CORD. 
Fig. 116.—Locomotor ataxy, painless swelling of elbow-joint after a 
fall on it. One condyle of the humerus and olecranon were found, 
after death, to have been broken off. Several separate pieces of 
new bone had formed in the capsule of the distended joint. 
and struck his elbow, fracturing the olecranon and condyle. This was 
followed by extreme painless swelling, and bony masses could bo felt, 
gradually increasing in size. After death the fractures of the bones 
were found, and masses of new bone had formed in the capsule of 
the joints. The arthropathic changes occur also, however, without 
injury, and are probably due to disease of the nerves, which not only 
has a direct trophic influence, but also renders the structures 
insensitive to the injurious effects 
of prolonged tension or pressure 
(Rotter). When inco-ordination has 
developed, the variations in the mus- 
cular contractions involve varying 
strain on the ligaments, especially in 
the case of joints, as the knee, that 
depend for part of their support on 
Fig-. 118.—Tabetic foot (from a photo- 
graph by Mr. Marriott, B.Sc.), 
FiG. 117.—Locomotor ataxy; retro- 
flexion of knee-joints. LOCOMOTOR ATAXY. 
413 
the muscular tendons that pass by them. The knee-joint may thus 
become so lax that when the patient stands, the joint may become 
retroflexed, as in Fig. 117. Changes in the tarsal bones and articula- 
tions may cause the foot to become flat, with a projection inwards or 
backwards of the tarso-metatarsal articulations, and of the (often 
enlarged) tarsal bones. The condition has been called the “ tabetic 
club-foot,” by Charcot and Fere.* 
Visceral symptoms of peculiar character occur in many cases of 
tabes.f They consist almost entirely of paroxysmal disturbance of 
function, usually attended with great pain, and have been termed, 
by the French, crises, with qualifying adjectives according to the 
seat of the symptom. There is a tendency to over-elaborate this 
terminology. The most frequeut seat of such disturbance is the 
stomach, and these attacks are called gastric crises. They consist of 
paroxysms of severe gastric pain, felt in the epigastrium and often 
passing through to the back. The pain is accompanied by vomiting, 
with or without nausea. The vomiting is often incessant, and is first 
of food, then of clear liquid, which may be very abundant; ultimately 
bile is vomited, and sometimes blood, which may be altered in colour ; 
it has been ascribed to simultaneous vaso-motor disturbance in the 
mucous membrane. Retardation or irregularity of the action of the 
heart has sometimes attended such an attack, and, rarely, pyrexia has 
been noted. I have known frequent hiccough to accompany the 
vomiting. Such an attack lasts for some hours or days, and then 
subsides, to recur in a few weeks. During the intervals the functions 
of the stomach may be performed in a perfectly normal manner. 
Although pain and vomiting usually occur together, some patients 
have attacks of pain without vomiting, and in others there is vomiting 
without pain. Rarely there is nausea alone. A temperate man, in 
the early stage of tabes, suffered during three years from frequeut 
attacks in which, for several days, he had intense nausea each 
morning, passing away in the afternoon, and succeeded, in the evening, 
by an inordinate craving for food. He never vomited unless he made 
himself do so, in the vain hope of thus obtaining relief. After two 
years, attacks of laryngeal spasm were added to the nausea. 
The chief intestinal disturbance is constipation, but paroxysmal 
diarrhoea has been supposed to be of vaso-motor origin, and connected 
With the disease (Pierret). Paroxysms of rectal pain (rectal crises) 
may occur, and may be accompanied by distressing tenesmus, some- 
times by a sensation as if there were a foreign body in the rectum. 
* The trophic changes in hone and joint have been regarded by some as simple 
chronic osteo-arthritis, without causal relation to the nerve disease in their subjects, 
but the evidence is altogether opposed to this view. The arguments that can be 
adduced in support of it will be found in some of the speeches delivered at a dis- 
cussion at the Clinical Society, Nov. and Dec., 1885. 
t The occurrence of attacks of vomiting, sometimes early in the disease, was 
pointed out by Topinard, but thought by him to be a mere complication. (Topinard, 
‘ De l’ataxie locomotrice,’ Paris, 1864, p. 273.) 414 
SPINAL COffD. 
In rare cases, paroxysms of pain have precisely the character of attacks 
of renal colic (nephralgic crises), or are felt in the neck of the bladder 
or along the urethra or at the meatus (vesical or urethral crises). 
These may be attended by an intense desire to micturate, although the 
bladder may he empty and only a few drops of urine may be expelled. 
In one patient such pain was repeated several times an hour, and each 
attack lasted for several days. Blood may be passed after an 
attack. 
Laryngeal crises are, perhaps, after those of the stomach, the 
most common. They vary much in character. The most common 
form is a true laryngeal spasm, with noisy inspiration and expiration, 
cough, and often considerable dyspnoea. The paroxysms may resemble 
those of whooping-cough or of laryngismus stridulus. Pressure on 
the superior laryngeal nerve at its entrance into the larynx, or on the 
trachea, or the introduction of a sound, will sometimes induce an 
attack. The spasm may last for a quarter of an hour or for some 
hours, but rarely continues so long as the gastric crises. In one re- 
corded case the spasm spread to the pharynx, makiug swallowing 
impossible ; a violent attack extended to the muscles of respiration, 
and the patient died asphyxiated. Death from these attacks is, 
however, extremely rare. Paroxysms of rough cough have been 
termed “ bronchial crisesin one case such attacks ceased when the 
patient began to suffer from gastric crises. These crises are often 
early symptoms, and they may continue for many years. I have seen 
& patient, still in the first stage, who gave a histor’y of gastric crises 
during the preceding eighteen years. 
Comparable to these paroxysmal visceral disturbances, although 
very different in character and more alarming in aspect, are cerebral 
symptoms ; hut these are, fortunately, very rare. They resemble the 
attacks that are common in general paralysis of the insane, and con- 
sist of transient apoplectiform seizures, of transient hemiplegia, or of 
convulsions, general or one-sided. They may occur early in the course 
of the disease. The alarm they occasion is not without foundation, 
since death has been known to occur during an attack of apoplectic 
aspect. Occasionally an actual lesion occurs (probably thrombotic 
softening), causing persistent hemiplegia. Paroxysms of vertigo 
sometimes seem to be of similar nature, but they more often depend 
on derangement of the auditory nerve or labyrinth. 
Course and Termination.—It is convenient to divide the course of 
the disease into three stages:—(1) In which there is no alteration in 
gait, the common indications of the malady being the loss of the 
knee-jerk and the pains, often associated with loss of the light-reflex 
of the iris, and unsteadiness on standing with the feet together and 
eyes shut. (2) That in which there is distinct affection of gait, slight 
or considerable, but in which the patient is still able to walk, alone or 
with the aid of one or two sticks. (3) In which walking is possible 
only with the aid of another person, or it is impossible for the patient LOCOMOTOR ATAXY. 
415 
to wait or to stand. The first stage is not always present; inco-ordi- 
nation may be developed simultaneously with the loss of the knee- 
jerk, as one of the earliest symptoms. 
The course of the symptoms is extremely variable. The inco-ordi- 
nation usually supervenes gradually in the course of months, but it 
sometimes develops very rapidly. I have known it to become extreme 
in the course of a fortnight from its onset, after the first stage had 
■existed for a considerable time. The epithet “ progressive,” given to 
the malady by Duchenne, expresses a characteristic of a large propor- 
tion of the cases in which ataxy is developed, and he knew no other 
■cases of the disease. The inco-ordination, once developed, often 
increases, slowly or rapidly, until it reaches a moderate or a consider- 
able degree, and the sensory loss shoAvs a like tendency. The pains 
seldom correspond to the other symptoms in degree or course. They 
are often very severe in the early period of the disease, and may either 
lessen or continue unchanged as the loss of sensation develops. Their 
persistence, even in severe degree, does not show progress in the disease; 
once set up, they may persist for years without any increase in the 
•other symptoms, and seem in this to be analogous to neuralgia, being 
■evidence only of functional activity in the altered nerves. 
The power of recognising the first stage of the disease, which we 
■owe to Westphal’s discovery of the loss of the knee-jerk, has enlarged, 
and in enlarging has to some extent modified, our conception of the 
general tendency of the disease. It is exceedingly common for the 
first stage to remain stationary for a long time, for ten, twenty, and 
■even, in one case, for twenty-five years, if the duration of the light- 
ning pains may be accepted as proof of its existence. When all cases 
are taken together, and if the patients are subjected to careful treat- 
ment, I think that the disease shows a progressive tendency in less 
than one half of the cases. 
The other symptoms also do not always progress pari passu. Sen- 
sibility may fail although inco-ordination does not inci’ease. Con- 
versely, the ataxy may become greater although sensation remains the 
same, and even when it shows a distinct improvement. To this we 
shall return in considering the pathology of the disease. Thus a patient 
had slight ataxy, loss to pain on thighs, legs, and trunk, and no loss 
to touch or temperature. At the end of a year and a half pain was 
perceived on the thighs, and sensibility to touch, and temperature were 
still normal, although the ataxy had increased. So marked, indeed, is 
the contrast between the course of different symptoms in some cases 
that it suggests a certain alternative tendency. We have seen that if 
optic nerve atrophy develops, the spinal symptoms often remain 
stationary, and this is also true of visceral crises ; I have known gastric 
crises to cease when inco-ordination came on. In one patient all the 
symptoms of tabes passed away, optic nerve atrophy ceased to advanc e, 
and even the knee-jerk returned, when the patient became insane. 
The rate of increase, when this occurs, varies much. Sometimes it 416 
SPINAL CORD. 
is so slow that the ataxy is considerable only at the end of several 
years. On the other hand, it may be so rapid that in a few months 
the patient is scarcely able to walk. More commonly the course is 
variable; periods in which the disease is almost stationary alternate 
with others in which the symptoms increase rapidly. The exacerba- 
tions may seem spontaneous, or may be distinctly excited by some 
prejudicial influence—a chill, a fall, or some excess, alcoholic or 
sexual. They are sometimes very acute; a marked change may occur 
in the course of a few days, or even in a few hours. Thus I have 
known a patient to pass, in the course of twenty-four hours, from a 
condition in which he could walk fairly well to one in which he could 
scarcely stand. Muscular power may lessen in such a sudden exacer- 
bation, or the increase may be confined to the special symptom of the 
disease—the ataxy. But all such cases need re-investigation in the 
light of the facts that have been ascertained regarding the participa- 
tion of the peripheral nerves in the process. An acute exacerbation 
may be “parenchymatous” in nature, seated in the elements either 
of the spinal cord or peripheral nerves. The great difficulty of the 
problem is due to the fact that there may be a myelitic or neuritic 
complication, or merely an acute process in the nerve-elements in 
which the chronic disease was in progress, and similar in nature. 
It may be extremely difficult to determine which of these is the 
cause of the rapid increase in the symptoms. The conditions thus 
developed may pass away again, leaving the patient on a little 
lower level than before, or they may persist without any considerable 
recovei'y. 
There is nothing in the nature of the disease, in most cases, to 
produce death. The only direct effect of the malady, which has ended 
life, is laryngeal spasm or paralysis. Even the gastric symptoms, 
prostrating as they are, are never fatal. Patients who have reached 
the third stage have lived, bedridden, for twenty years. Death 
often results from intercurrent maladies, some of which are more 
dangerous to these sufferers than to others because they may develop 
painlessly, and attain a serious degree before their existence is sus- 
pected. But many patients die from indirect results of the disease. 
Kidney complications are the most common; they often develop 
insidiously, and only manifest themselves when life is in peril, as, for 
instance, by acute febrile symptoms, the exact nature of which may be 
unsuspected until the urine is examined. I have knowii a patient, 
still in the first stage, die thus after a few days’ illness. Bedsores 
and pyaemia occasionally cause death, although far less frequently 
than in most other diseases of the spinal cord. 
Complications.—Occurring, as most cases do, in syphilitic subjects, 
tabes is sometimes complicated by true syphilitic lesions of the brain 
or coi'd, generally the later lesions, such as gummata, or sudden palsy 
from the disease of a cerebral vessel. 
Acute or subacute myelitis may occur during the course of the LOCOMOTOR ATAXY. 
417 
disease with characteristic symptoms. Such a complication must not 
be confounded with the simple acute exacerbation in the special 
symptoms, which sometimes occurs with remarkable rapidity. 
Other system diseases of the cord may develop as complications of 
tabes. The lateral columns may be diseased with the dorsal posterior 
columns, giving rise to “ataxic paraplegia,” but this is a distinct 
affection, and will be so described. Weakness may, however, bo 
present from the first, or may supervene slowly, in the course of 
tabes, without muscular atrophy, and with a persistence of the special 
symptoms of the disease, from extension of the morbid process to the 
lateral columns. Another occasional complication is muscular atrophy, 
both the local atrophy already mentioned (and especially frequent in 
the tongue) and general atrophy, such as is met with in the pure 
spinal form. Thus a gentleman, who had had hemiplegia from 
syphilitic vascular disease, developed the first stage of tabes—pains, 
loss of knee-jerk, loss of the iris-reflex, and slight unsteadiness. He 
had two courses of mercurial treatment at Aix-la-Chapelle, and at the 
end of the second, atrophy began in the muscles of the hands, and 
spread during two years until almost all the muscles of the arms, 
shoulders, and back became extremely wasted. Local muscular 
wasting (according to the researches of Dejerine*) is usually the 
result of degeneration of the peripheral nerves; it is generally 
symmetrical. The extensive wasting, as in the case just men- 
tioned, is probably due, as a rule, to degeneration in the anterior 
cornua. 
In rare cases the legs present the symptoms of tabes, while in the 
arms there is the jerky inco-ordination of disseminated sclerosis, 
and the co-existence of the two lesions has been demonstrated. 
Another very important and frequent complication of tabes is 
general paralysis of the insane. The two diseases have many 
alliances. It is probable that syphilis predisposes to general para- 
lysis, as well as to tabes. Reflex iridoplegia is common in both diseases. 
The two maladies are often combined, and the symptoms of one or the 
other may preponderate. Thus many general paralytics present sym- 
ptoms of tabes, and its characteristic lesion is found after death. On 
the other hand, cases of tabes may present slight symptoms of general 
paralysis, perhaps only slight optimism and mental weakness, which 
may remain subordinate, or may increase to a pronounced and pre- 
ponderant degree. It may be difficult to say in which category a case 
should be placed. It is sometimes said that the disease may com- 
mence as ataxy, and may change to general paralysis, but a more 
correct expression of the facts is the co-existence of the two affections, 
and the dominance of the symptoms of one or the other. 
Of complications of tabes outside the nervous system, besides 
the indirect consequences of the malady, valvular heart disease is the 
most important, and usually develops without any of the usual ante- 
* Dejerine, * Revue de Med.,’ 1889. 
VOL. I 418 
SPINAL CORD 
cedents, and at an age at which 
degeneration is unlikely. It is not 
improbable that the coincidence is 
really one of cause, the valvular dis- 
ease being the result of a syphilitic 
process. Other complications are so 
rare as only to deserve notice when a 
causal connection can be traced or 
reasonably suspected. Coincident 
glycosuria has been ascribed to an 
affection of the medulla oblongata 
(or may be produced through the cer- 
vical spinal cord), but it is extremely 
rare. 
Pathological Anatomy.—In most 
cases the spinal cord presents changes 
visible to the naked eve. The poste- 
rior columns have a grey translucent 
appearance, which is due to the loss of 
the nerve-fibres and to au increase of 
tho* connective tissue (“ grey degene- 
ration ”). The whole of the posterior 
columns may be thus changed, or only 
parts of them, the distribution of the 
visible alteration being that of the 
histological changes revealed by the 
microscope and presently to be de- 
scribed. In the hardened cord the 
difference of tint in the diseased areas 
is even more distinct than it is in the 
fresh organ. The posterior columns 
are also smaller than normal, because 
the bulk of the connective tissue is 
less than that of the normal fibres: 
hence the shape of the cord is slightly 
changed. 
Fig. 119.—Locomotor ataxy involving the 
legs only. Sclerosis of the whole posterior 
columns in the lumbar region, gradually 
becoming limited, in the lower dorsal re- 
gion, to the root-zone and posterior median 
column. The latter only is affected in the 
upper half of the cord (ascending degenera- 
tion). There is also conspicuous degeneration 
in the antero-lateral ascending tract. This 
is rather greater on the left side, while the 
post.-median degeneration is greater on the 
right, in harmony with the fact that the 
latter consists ol fibies which do not decus- 
sate. LOCOMOTOR ATAXY. 
419 
In a section of the cord stained with carmine or similar reagent, 
and examined under the microscope, the affected areas are conspicuous 
by the deep staining of the connective tissue. The position of the 
excess of this tissue, of the “ sclerosis,” as it is termed, indicates the 
place in which the nerve-fibres have degenerated. In the most 
frequent condition, in which the legs only are affected, the sclerosis 
occupies the whole of the columns in the lumbar region (Fig. 119), but 
it is often slight in the anterior parts of the postero-external columns, 
which may even be free from sclerosis; also in the middle of these 
columns many more nerve-fibres may be seen than elsewhere. The 
sclerosis is most dense in the part adjacent to the posterior cornu, 
through which the posterior root-fibres run, and near the surface of the 
cord (Pig. 119, D 12). Above the lumbar enlargement the affection of 
the postero-external columns gradually ceases, but the degeneration is 
intense in the postero-median columns, and has the distribution of an 
ascending degeneration, as it in fact is, receding from the commissure 
in the upper cervical region. (Compare Fig. 119 with Pig. 74, p. 177.) 
In other cases the external band of sclerosis, adjacent to the cornu, 
continues separate through the dorsal cord and even through the 
cervical enlargement (Pig. 120) ; the median degeneration then extends 
FicJ. 120.—Tabes with ataxy of the arms as well as the legs. Section 
of cord in cervical region, showing sclerosis of the post.-med. column 
and root-zone of post.-ext. col. Degeneration of left ant. cornu. 
up to the commissure throughout the cervical region, just as does the 
secondary degeneration that results from a cervical lesion (see Fig. 76, 
p. 178). But in the cervical enlargement, the unaffected area in the 
anterior part of the postero-external column is usually much larger 
than in the lumbar enlargement. 
In rare cases, of severe and long duration, the posterior columns are 
occupied by connective tissue in their whole extent from one end of the 
cord to the other. A few fibres of the posterior roots and a few 
vertical fibres near the commissure may alone be recognisable. An 
instance of such almost complete sclerosis is shown in Fig. 121. 
On the other hand, in slight cases, in which the disease is still in the 
first, or in the commencement of the second stage, the sclerosis is 
moderate in degree, even in the regions of the cord most affected. 420 
SPINAL COBD. 
The separation of the sclerosed areas in the postero-external and tbe 
postero-median columns may be 
distinct throughout the cord, 
except in tbe lumbar enlarge- 
ment, where the median degene- 
ration expands into the external 
column. Tbe sclerosis of the 
postero-external column is then 
usually limited to tbe root-zone,, 
and varies in width, according 
to that of the area through 
which tbe root-fibres pass. In 
the dorsal region there is usu- 
ally a narrow band of sclerosis 
close to tbe posterior cornu ; in 
the lumbar region it reaches 
almost to the median septum. 
In some instances, however, a 
very slight degree of sclerosis 
extends from the most affected 
tracts through the rest of the 
columns, and is generally great- 
est in their posterior half. This 
condition existed in the very in- 
structive case shown in Fig. 122. 
The intensification of this dif- 
fuse sclerosis in tbe root-zone 
and median columns is very dis- 
tinct, although the affection of 
tbe latter is unusually slight. 
There is, moreover, in the dorsal 
region, sclerosis of another part 
of the postero-external column 
-—the comma-shaped tract of 
short fibres, which degenerates 
downwards for a few inches 
below a transverse lesion of the 
cord (see p. 1S1 and Figs. 76 
and 106, f). It is most distinct 
in 122 at d 8, but can be traced 
up to tbe cervical region, where 
its form is changed. 
The tract of fine fibres of the 
posterior root, discovered by 
Lissauer, is generally diseased.* 
* It was first described by Lissauer 
connection with its disease in tabes ; 
Fig. 121.—Locomotor ataxy: extreme in- 
co-ordination and anaesthesia in both 
arms and legs; the posterior columns 
are sclerosed throughout the cord in 
their entire extent. A, upper cervical, 
B. C, I), dorsal, E, lumbar regions. In 
D there is also some degeneration of the 
intermediate grey substance. LOCOMOTOE ATAXY- 
421 
The antero-lateral columns may 
be perfectly normal, even when the 
disease of the posterior columns 
is great. Often, however, in old 
cases, there is a slight general 
increase of the connective tissue 
throughout the cord. Sometimes 
there is distinct sclerosis of other 
definite tracts, e. g. of the ascend- 
ing antero-lateral tract (as in Fig. 
119), or of the direct cerebellar 
tract. In rare cases there is a 
distinct degeneration of the pyra- 
midal tracts. The -whole periphery 
of the antero-lateral column is 
thus occasionally the seat of scle- 
rosis, the connective tissue ex- 
tending in from the pia mater, 
which is usually also thickened; 
it is probable that this condition 
may be solely the result of the 
Fig. 122.—Loco, ataxy; sclerosis oe 
posterior columns.—In L 1 the pos- 
terior portion of both post. med. col. 
and post.-ext. col. is densely sclerosed, 
but in front only the post.-med. col. At 
D 10 the sclerosis is also general, but is 
dense only in the root-zone of the post.- 
ext. col. At D 8 and D 4 the change 
is slight, except in three areas, the root- 
zone, the middle part of the post.-med. 
col., and the comma-shaped tract in the 
front of the post.-ext. col. At D 1 the 
comma-shaped tract is narrow, and in 
C 7 it merges in a band of sclerosis, 
which bounds the anterior part of the 
post.-med. col. There is a little diffuse 
sclerosis through the rest of the column, 
and in the first dorsal there is some 
degeneration of the anterior cornua.— 
Symptoms of the first stage had existed 
for four years (lightning pains, slight 
analgesia, loss of knee-jerk and iris re- 
flex, gastric crises, optic nerve atrophy). 
A few weeks before death, the legs 
gradually became paralysed, and the 
arms ataxie ; retention of urine caused 
acute kidney mischief, which was the 
immediate cause of death. No lesion 
was found after death to explain the 
subacute paralysis, but the peripheral 
nerves were not examined, their dis- 
ease being then unknown. 
see * Neur. Cent./ 1885 p. 245 ; also ib., 
188fi, p. 419. 422 
SPINAL CORD. 
primary degeneration of the nerve-fibres even when it closely simulates 
the aspect of meningitic invasion. 
In slight cases it is difficult to distinguish any changes in the grey 
matter of the cord, although it is probable that there is some atrophy 
of the nerve-cells and fibres in the posterior horn in many cases. 
Various structural changes can be discerned in more advanced cases 
(as Lockhart Clarke first showed), and the posterior commissure 
may be reduced in size. The posterior vesicular column also shows 
distinct degeneration in many cases. Some atrophy of the plexus 
of fine fibres contained in this column is said to be almost invariable 
(Lissauer), but frequently the cells and vertical fibres waste, and 
sometimes only a few shrunken cells, scattered through a trans- 
lucent nucleated tissue, may remain. The atrophy of the cells is 
said to be especially associated with sclerosis of the direct cerebellar 
tract; also (but on slighter evidence) with that of large fibres in 
the pyramidal tract, which do not degenerate downwards. When 
the cells are unaffected, although the intervening substance is dis- 
eased, the cerebellar tract may be normal, and the fibres passing 
to it from the front of the vesicular tract may be unaffected. The 
degeneration of the grey matter often extends into the intermediate 
region between the cornua (Fig. 121, b) ; the intermediate lateral 
tract of cells may be atrophied, and occasionally even the anterior 
cornu and its cells suffer in a similar way (Figs. 120, 122, d 1). 
As we have seen, this change may be the cause of muscular atrophy, 
although in other instances the muscular wasting depends on altera- 
tions in the motor nerves. 
The sclerosis varies considerably in its histological characters. In 
slight cases, there is merely a moderate thickening of the trabeculae 
and their branches. The larger tracts are more fibrous than normal, 
and more nuclei are seen than in health. Everywhere the new growth 
of connective tissue proceeds chiefly from the pre-existing tracts, 
vessel-walls, &c. When the change is considerable, the trabeculae are 
very broad, and areas seem to consist wholly of connective tissue, 
fibrillated and nucleated. In old cases there is sometimes little 
appearance of fibrillation in the most affected region; cells and 
thickened vessels lie in a granular or homogeneous tissue. From the 
parts most changed, the nerve-fibres have wholly disappeared; in other 
parts, however, close examination reveals many fibres narrower than 
normal, and many stained points that may possibly be axis-cylinders. 
The walls of the vessels are usually increased in thickness, sometimes 
to a very considerable degree. The coat next the endothelium may be 
thickened and contain many nuclei, but the chief increase, in most 
cases, is in the outer coat and adventitia, whence the tracts of tissue 
pass off into the adjacent region. The pia mater is sometimes 
thickened over the posterior columns; the vessels in it may then be 
similarly changed. The alteration in the membrane may extend over 
the neighbouring part of the lateral column, and even around the LOCOMOTOR ATAXY. 
423 
cord (Fig. 123), and, as already stated, septa passing from it into the 
cord may be thickened in the circumferential zone. This peripheral 
sclerosis is probably the result of three distinct processes, the relative 
share taken by each varying in different cases : (a) a primary degene- 
ration of the peripheral ascending tracts; (b) a process of chronic 
Fig. 123.—Tahes. Chronic meningitis. Cervical region. Sclerosis of 
post.-median columns and slight diffuse sclerosis of the cord, least in 
ant. cols., dense in the right lateral column. Thickened pia mater, 
and damage to subjacent superficial layer of the cord. 
interstitial myelitis, spreading from the pia mater, which is the seat 
of an inflammatory tissue formation; this may cause (c) a secondary 
ascending degeneration in the fibres affected in the first process. 
It is important to recognise this complexity of mechanism. 
In cases of rapid course, products of degeneration, masses of myelin 
and granule-corpuscles, may be found in the affected parts, when these 
are examined by appropriate methods. 
In rare cases other lesions are found in the cord, corresponding 
to the complications already described. The lateral columns may be 
sclerosed apart from any thickening of the membranes. Diffuse 
mvelitis may be met with, and, occasionally, characteristic insular 
sclerosis has been found in the cervical region. 
The posterior nerve-roots may appear normal in slight cases ; it 
must be remembered that only a considerable degree of alteration can 
be detected even by the microscope. Often their disease is con- 
spicuous ; when the cord is much affected they are invariably affected, 
and may be atrophied, grey, and thin, to the naked eye, while the 
microscope shows wasting of the nerve-fibres and slight increase of 
connective tissue. The changes extend to the ganglia, where they cease. 
These structures are almost always normal, and the mixed nerve imme- 
diately beyond them is usually free from degeneration. The anterior 
nerve-roots are altogether normal, except in the rare cases in which the 
anterior cornua have suffered, and then some of their fibres may be 
degenerated, and the atrophied fibres may be traced also in the mixed 
nerve-trunk beyond the junction of the roots. 
The peripheral spinal nerves have been found degenerated and in 424 
SPINAL COED. 
various degrees of atrophy in a large number of cases of tabes.* Tbe 
change consists in a wasting of the nerve-fibres, beginning in the 
white substance, which may be reduced to a very narrow layer. 
Ultimately the axis-cylinders perish ; they are said to present irre- 
gular swellings when the sheath begins to waste.f There may be a 
slight increase in the interstitial tissue and nuclei, but the change (om- 
mences in the nerve-fibres themselves. The degeneration is greatest 
in the terminal nerve-filaments, and lessens in degree as the nerves 
are examined higher up, gradually ceasing in the larger trunks, and 
before the plexuses or corresponding main divisions are reached, the 
fibres are almost always healthy. The sensory fibres seem to be 
exclusively affected. The lesion has hitherto been found chiefly in 
the sensory nerves that supply the skin and 
joints, but that the sensory nerves of muscle 
undergo a similar change has been ascer- 
tained by Dcjcrine. It is probable that 
these afferent muscle nerves are invariably 
diseased, especially the fibres concerned 
in conducting the impressions that guide 
co-ordination, spinal and cerebellar,—on the 
former of which the knee-jerk depends, ac- 
cording to the theory maintained by the 
writer. The detection of this degeneration, 
among the unchanged motor fibres of the 
nerves, is very difficult, and this explains tbe 
paucity of evidence of it. The peripheral 
degeneration is found most commonly in the 
legs, but is met with also in the arms when 
these are the seat of symptoms. The change 
in the nerves bears no relation to that in the 
spinal cord in degree, or even in existence, 
for extreme alterations have been found in 
the nerves when the cord was quite normal. 
On the other hand, in some cases, the nerves 
have been healthy. 
The optic nerves, when atrophied, present 
wasting of the nerve-fibres, and usually a 
remarkable increase in the interstitial con- 
nective tissue, which constitutes thick tracts, 
of gelatinous aspect. Degeneration of the 
ascending or descending roots of the fifth 
nerve has been repeatedly found (first by 
Westpbal in 1864) in cases in which symptoms were present in the 
Fig. 124.—Osseous lesions 
in tabes. (After Charcot.) 
A. Atrophy of the head 
of the femur. B. Exces- 
sive formation of callus 
after so-called “ sponta- 
neous” fracture of the 
ulna and radius. 
* The first observation was made by Westphal, but the extent and significance of 
the change in the nerves was pointed out by Pierret (1880), and his observation was 
soon after confirmed and extended by Dejerine and Pitres, 
t Schmaus, * Deut. Arch. f. kliu. Med.,’ 1890. LOCOMOTOR ATAXY. 
425 
area of its distribution. Similar changes in the roots or nuclei of 
other cranial nerves have also been found. 
Pierret has described, as common in cases with vaso-motor and 
visceral symptoms, a degeneration of the intermedio-lateral tract and 
adjacent nerve-fibres in the upper part of the cord, traceable up the 
medulla oblongata in the region of the so-called “ slender column,” 
adjacent to the accessory, glosso-pharyngeal, and pneumogastric nuclei, 
from which it is supposed that the chief visceral and vaso-motor 
influences are exerted. The sympathetic has been examined in several 
cases, and found healthy, with one exception, in which the sympa- 
thetic on the left side of the neck was degenerated in association with 
left exophthalmos. 
In the diseased bones or joints conspicuous changes are found 
after death. There is occasionally an extraordinary wasting of the 
articular ends of the bones, which seems to begin by rapid erosion of 
the cartilages, extending quickly to the bone beyond, the extremity of 
which may be much reduced in size and altered in form. In the hip- 
joint, for instance, in a case recorded by Charcot, the edges of the 
acetabulum had been removed, and the whole of the head of the femur 
and most of the trochanter had disappeared (Pig. 124). 
Similar changes have been found in most of the larger joints. In 
the bones, the compact tissue has been found thinner and more porous 
than normal. At the seat of old fractures a large amount of bony 
callus is formed (Pig. 124), and sometimes new bone is found in the 
capsule of joints that have been injured. 
Pathology.—The great fact of the pathology of tabes is that it is 
a neural degeneration in the sensory nervous system, peripheral and 
central. In both peripheral nerves and spinal cord, the incidence of 
the disease is almost exclusively on the structures concerned in affe- 
rent conduction. The cerebral system suffers in far less degree than 
the spinal, and in more irregular manner, but in the occasional peri- 
pheral degeneration of the optic nerve, and the central changes in the 
roots of the fifth, we may trace the same law of distribution. It is 
less dominant, however, than in the spinal system, since some of the 
cranial nerve symptoms are exclusively motor. The motor character 
of the leading symptom, ataxy, is, as we shall see, only an apparent 
and not a real exception to the general sensory character of the 
malady. 
The degeneration commences in the nerve-elements themselves; 
the overgrowth of connective tissue, which gives to the lesion its 
obtrusive character, is secondary. This fact has been obsefved in 
the peripheral nerves; as regards the spinal cord it rests on inference 
scarcely less certain. That it is rrue of the spinal cord has, indeed, 
been doubted, chiefly on the ground of the thickening of the walls of 
the vessels seen in some cases, and the manner in which the increase of 
tissue seems to start from them. But the “ system ” character of a 
d-isease, the limitation of a wide-spread lesion in its early stage or slight 426 
SriNAL COED. 
degree to structures having a common function, is probably in all 
cases proof of its neural origin, i. e. its origin in the nerve-elements 
themselves. In tabes the evidence thus afforded is corroborated by 
the disease of .the peripheral nerves, which unquestionably commences 
in the nerve-fibres, and by the partial character of the sensory loss, 
which means the limitation of the chief lesion to fibres of one sensory 
function. There is every gradation, moreover, between the cases in 
which the perivascular disease is great, and those in which it is so 
slight that there is nothing to suggest a primary interstitial process. 
The change in the vessels may reach a high degree in the poste- 
rior median columns when their degeneration is purely secondary, 
and certainly commences in the nerve-fibres; a similar thickening of 
the vessels has also been met with in secondary degenerations in 
other parts. It is most important to remember that the over- 
growth of the neuroglia is a pathological process of growth distin- 
guishable (and to a large extent distinct) from the degeneration of 
the nerve-fibres that excites it. It may vary in degree in different 
cases, and, even in the secondary degeneration of peripheral nerves, 
may assume an independent inflammatory character. Once excited, 
the energy of tissue-growth may be in some degree independent of its 
cause. Secondary vascular disturbance may attend it, and thus a sub- 
inflammatory condition (or even true inflammatory condition) is 
probably sometimes developed, which may invade the pia mater, and 
through this may spread widely. 
The chief causal fact regarding the disease is its common relation 
to syphilis. Tabes is generally, although not invariably, a post- 
svphilitie disease; certain elements of the nervous system degenerate 
in consequence of the influence on them of previous or present 
svphilis. But these elements have a special liability to degenera- 
tion, which causes their nutrition to fail from other causes, and 
may also constitute their special susceptibility to suffer from the 
virus of syphilis. The usual symmetry of tabetic lesions indicates 
that the mechanism by which syphilis affects the nervous system is a 
blood-state. The manner in which the peripheral nerves suffer in 
many cases, brings tabes, in spite of its chronicity, into analogy with 
the more acute forms of peripheral neuritis, such as succeed acute 
specific diseases at a variable interval. The long interval, moreover, 
and the common slowness of the process in tabes when a sequel of 
syphilis, are only in proportion to the chronicity of the causal malady, 
compared with the acute specific diseases that have neuritic sequelae. 
Further, the considerations mentioned in the account of multiple 
neuritis, which suggest that its immediate cause, when it is due to 
an acute blood disease, is a product of the growth of the organisms 
of the primary malady, rather than the organisms themselves, hold 
good also in the case of syphilis and tabes. The degenerative changes 
in the nervous system differ from the lesions of active syphilis, both 
in character and in time, in such a way as to make the assumption LOCOMOTOR ATAXY. 
427 
reasonable that they depend upon some product of the growth cl the 
syphilitic organisms, a product which may possibly be a chemical 
substance—a suggestion first made by Strumpell, and widely held 
regarding other analogous maladies. Recent research is bringing into 
ever greater prominence the important part played by such products 
in the generation and course of diseases. In the specific diseases 
that have these sequelae, there may be more than one such product of 
their organisms, causing more than one kind of consequence. The 
differences between such nerve degenerations as those of tabes, and 
other late effects of syphilis, is at least not difficult to comprehend 
on this hypothesis; neither is the fact—which has been so great a 
difficulty to many —that the treatment which has so speedy an effect on 
syphilis itself, is generally without influence on the degenerative pro- 
cesses that sometimes follow it. 
Tabes is probably a rare sequel, when regarded from the side of 
syphilis. But the occurrence of such consequences in some instances, 
and not in others, has analogies in the case of almost all the acute 
specific diseases that have similar sequelae, and must be taken as 
evidence of variations in the precise character of the primary disease. 
The virus of the primary malady is doubtless organismal, and such 
variations are familar to us in the case of other diseases. They some- 
times have, and at other times have not, consecutive effects upon the 
nervous system, as in the familiar instance of diphtheria. The varia- 
tions in the character of the organisms, and in their effects, may be 
relatively great, although entirely beyond our present powers of 
observation. 
These considerations receive a notable emphasis from the occur- 
rence of tabes in children who are the subjects of inherited syphilis, 
to whom the disease in early life is probably confined. The fact 
also shows how potent must be the part played by the agent, 
compared with the susceptibility that is, as it were, the causal comple- 
ment—a fact seen also in the raritv of cases of tabes in which syphilia 
can be absolutely excluded. 
The pathological facts already known enable us to understand many 
of the symptoms of the disease. There may be an interruption of the 
sensory path in one or both of two places, in the peripheral nerves, 
and in the posterior root-fibres as they enter the cord, and an 
interruption of the fibres in either place will explain the loss of 
sensibility which is so frequently present. The pains may reasonably 
be ascribed to the molecular changes in the nerve-fibres and their 
altered function, either in the periphery or in the cord. The intensity 
of a sensation is no measure of that of the process that causes it. 
Whether the affection of the sensory cells of the cord* takes part 
* In disease of the nerve-roots of the cauda equina there is always ascending 
degeneration of the posterior median columns, but not of the antero-lateral ascend- 
ing tract. Hence tlie root-fibres from which the path is continued by this tract 
must end in nerve-cells in the posterior cornua, and the degeneration of this tract 428 
SPINAL CORD. 
in the production of the anaesthesia and pains, we cannot tell. It 
is noteworthy that the affection of the peripheral nerves must involve 
the structures by which the nerve-impulses of sensation are normally 
generated by mechanical and other processes. The long persistence 
of pains without any increase in the symptoms, shows that they 
may be due to the action of structures that are changed, but not 
changing. The loss of reflex action from the skin is explained 
by the interruption of the sensory path, and an increased irrita- 
bility of the sensory nerves, the result of the commencing degene- 
rative changes, sufficiently explains both the hyperaesthesia and the 
increase of reflex action sometimes observed. Whatever theory of the 
nature of the so-called “ tendon-reflex ” action is held, the loss of the 
knee-jerk must be explained by an interruption of the sensory path. 
On the theory I have advanced, the arrest of impressions from the 
afferent muscular nerves abolishes the muscle-reflex action on which 
the local irritability depends. Many other facts of disease show that 
this irritability is easily lost, and that a very slight change in any 
part of the reflex arc, too slight to cause other symptoms, is sufficient 
to arrest the knee-jerk.# Hence we can understand that this loss 
should be constant and early. It is not improbable, moreover, that 
these nerves suffer in special degree. The muscles may be insensitive 
to pain, e. g. that of electrical stimulation. Pressure and extension, 
which in health are painful, sometimes cause no sensation, even when 
the skin is sensitive. 
The mechanism of the muscular inco-ordination, which is the 
obtrusive symptom of the disease, has been the subject of much dis- 
cussion. Two fundamental facts, however, limit the problem. First, 
the ataxy cannot be primarily due to the loss of cutaneous sensibility. 
Disease of the conducting path in the cord may cause absolute 
anaesthesia of the skin without the least ataxy. Although this does 
not prove that interruption of the sensory path in the nerves, between 
the skin and the reflex centres, may not cause inco-ordination, this 
element seems to be excluded by the fact that there is no relation 
between the ataxy and the loss of feeling in the skin. There may be, 
in tabes, much ataxy without any cutaneous anaesthesia, and vice 
versa. The second fact is that ataxy may exist in considerable degree 
when the lesion is solely one of the peripheral nerves, and the pos- 
terior columns of the cord are free from disease.f These two facts, 
taken together, seem to show that the ataxy may be produced by one 
in tabes is proof of the degeneration of these sensory cells. See the * Lancet,’ 
June 19, 1886. 
* JE.g. its loss after diphtheria when there are no other symptoms, 
f Apart from the evidence of this from cases of true tabes, a very instructive case 
has been recorded by Dr. Hughes Bennett, in which all the symptoms of tabes were 
present in a case of multiple tumours of the posterior nerve-roots (‘Clinical Soc. 
Transactions,’ vol. xviii). Ataxy has also resulted from other processes, such as 
injury, that have caused extensive damage to the posterior roots alone. LOCOMOTOR ATAXY. 
429 
mechanism, even operating alone, the disease of the afferent muscle- 
nerves. If the loss of the knee-jerk in tabes is to be taken, as I 
believe it may, as an indication of the disease of these nerves, the con- 
stancy of the loss shows the constancy of the presence of this element, 
in some degree. As just stated, a very slight degree of disease may 
abolish the knee-jerk; it is probable that a greater degree is needed 
to cause inco-ordination, and a still greater change to produce actual 
insensibility to pressure or extension. 
In unilateral lesions of the spinal cord, as we have already seen (p. 
229), there may be loss of the sense of posture, with intact cutaneous 
sensibility, on the side of the lesion, and no loss of this sense on the 
opposite side, on which cutaneous sensibility is lost. In such a case 
marked ataxy has been observed on the side on which the sense of 
posture was lost, when motor power returned.* Whatever effect in 
causing ataxy is produced by disease of the path of muscular sensi- 
bility in the spinal cord must also be produced by interruption of the 
path between the muscles and the cord. The latter must also arrest 
whatever reflex action depends upon these muscle-nerves,f and it is 
possible that such reflex action takes some part in the mechanism of 
muscular co-ordination. 
In this connection it is important to note that the fibres that pass 
up by the posterior median columns probably constitute the path from 
these nerves. The root-fibres to the columns seem to pass up, as the 
path is proved to do, without decussating, and they may be diseased 
in intense degree when there is no loss of cutaneous This 
tract is affected in almost all cases of tabes in which there is a lesion 
in the cord, and in all such cases in which there is ataxy. This 
fact suggests that the lesion of the root-fibres is first and chiefly of 
those from the muscles.§ 
The posterior median columns (extensively connected with the cere- 
bellum) and the direct cerebellar tract probably conduct to the cere- 
bellum the impressions from the sensory muscle-nerves. If so, the 
disease of these tracts and nerves must interfere with the co-ordinating 
* Gilbert; see foot-note, p. 229. 
f In a case in which the inco-orilination was much greater in the right leg than 
in the left, and cutaneous sensibility was equally impaired in the two, a strong trac- 
tion on the calf muscles, by forcible passive flexion of the foot, produced a distinct 
sensation in the extended muscles of the left leg, and no sensation in those of the 
right. In another case, in which the skin was sensitive to the slightest touch, the 
patient was unconscious of a vigorous extension of the toes produced by faradic 
stimulation of their short extensor. 
£ This posterior tract is most diseased on the side opposite to that on which there 
is most degeneration of the antero-lateral ascending tract, which probably con- 
ducts sensations of pain. 
§ The opinion that the ataxy depends on impairment of the muscular sense was 
put forward in 1855 by Dr. Eussell Reynolds; see p. 398. Dejerine has also asso- 
ciated the ataxy with the degeneration of the peripheral sensory muscle-nerves 
(‘ Archives de Physiologic,’ 3rd series, vol. iii, p. 231). 430 
SPINAL COED. 
action of the cerebellum, and cause some part of tbe loss of function 
■which results from disease of the cerebellum itself. 
There is another mechanism which may co-operate in increasing 
ataxy. The vertical fibres of the postero-external column have only 
a short course, and some probably connect the posterior grey matter 
at adjacent levels. The affection of these fibres seems to be proved by 
the fact that the comma-shaped bundle of fibres in the front of the 
post.-external column may be specially degenerated. This lesion may 
impair the association of the sensory structures, and so cause a want of 
harmony in the central mechanism. The theory that the ataxy was 
due to this cause was advanced by Todd in 1847. It is not probable 
that, if effective, it has more than an intensifying influence, since ataxy 
may exist when the posterior columns are throughout unaffected. The 
discovery that ataxy may result from alcoholic peripheral neuritis 
confirms the view of its origin above stated. 
Although cutaneous anaesthesia cannot, alone, produce ataxy, it may 
reasonably be assumed to increase that which already exists. Sensa- 
tions from the skin furnish important guidance to the motor cerebral 
centres, and are probably also concerned in such reflex muscular actions 
as that of standing. Similar guidance to the cerebral co-ordinating 
centres is also afforded by visual impressions, the loss of which distinctly 
augments the defect of co-ordination. The varying characters of the 
ataxy in different cases probably depend on the local variations in the 
degree of change in the muscle-nerves. The special effect of the 
disease of other elements of the cord, related to the posterior roots 
(as the posterior vesicular column), has still to be ascertained. The 
degeneration of the antero-lateral ascending tract is perhaps con- 
nected with loss of sensibility to pain. 
It is probable that co-ordination is chiefly an automatic process, 
depending partly on muscle-reflex actions, and on the connection of 
neighbouring sensory structures in the spinal cord, but chiefly on the 
function of the cerebellum, determined by the connection of the 
muscles with it, and that the interruption of this connection is the chief 
element in the inco-ordination of locomotor ataxy. It is probable also 
that the automatic processes are in part under cerebral control, guided 
by sensory impressions which do enter the sphere of consciousness, and 
that the derangement of this control will intensify inco-ordination, 
though incapable of producing it. We do not at present know to what 
extent, in any given case, the symptoms are due to the cord disease or 
to the peripheral nerve lesions. Apparently pains, ataxy, and anaes- 
thesia may be due to either. The question can only be decided by the 
comparison of symptoms and pathological changes in a large number 
of cases. That anaesthesia may be due to the peripheral changes 
is proved by the observed correspondence of the two in distribution 
(Dej&rine). 
The trophic changes in the skin, bones, and joints are probably due 
to the process of degeneration in the peripheral nerves. The degenera- LOCOMOTOR ATAXY. 
431 
lion Las been found in all cases of the kind in which it Las been looked 
for, and found also in the nerves of diseased joints. The pathology of 
the muscular wasting has been already mentioned. 
The pains in the region of the fifth nerve are explained by the lesions 
in its root, especially in its ascending root, which,coming up from the 
medulla, is homologous with the posterior spinal roots. This nerve, 
indeed, as Pierret has pointed out, represents the sensory roots of 
almost all the motor cranial nerves. The degeneration of the optic 
nerve is fairly comparable with that of the peripheral spinal nerves. 
Considering the special character of the optic nerve, the absence of 
degeneration of the retina does not seem to destroy the analogy between 
the two. Regarding the pathology of the visceral crises we know but 
little. The changes observed by Pierret in the neighbourhood of the 
centre for the pneumogastric may be, as Buzzard has suggested, an 
indication of the cause of the disturbances that occur within the 
range of this nerve, especially of the gastric and laryngeal crises. 
The transient motor symptoms in the limbs, and in the eyeball 
muscles, are apparently of functional origin. They must be distin- 
guished from the lasting palsies, which are probably due to degene- 
rative processes in the nerves or nuclei; the loss of function of the 
internal ocular muscles, being persistent, must be ascribed to degene- 
ration of the related centres. But even the light-reflex may return 
after it has been absent for years, and its loss must therefore depend, 
at least sometimes, on molecular changes capable of recovery. It is 
indeed important to remember that tabes is a disease which begins as 
a derangement of molecular nutrition, which is probably only to be 
discerned when relatively great in its degree. If we also remember 
that this derangement is the result of some toxic material or virus 
circulating in the blood, we can understand better the leading facts of 
the disease, and especially the variations in its course, its degree, and 
the precise character of the symptoms. 
Diagnosis.—The diagnosis of tabes rests on the combination of 
symptoms already described. In the early stage, the loss of the knee- 
jerk, together with pains, or unsteadiness on standing with the feet 
together and the eyes closed, justifies a diagnosis of the commencing 
affection, provided we can exclude toxic peripheral neuritis (especially 
that due to alcohol), diabetes, diphtheritic palsy, and also a lesion of 
the anterior cornua or nerve-roots by the absence of wasting of the 
muscles and change in their irritability. The diagnostic value of the 
loss of the knee-jerk can hardly be overrated. It is probably never 
absent in health. If there is doubt as to its loss, the precautions 
recommended on p. 15 should be adopted. When it is lost, and reflex 
action is in excess, a true reflex movement may sometimes simulate 
the jerk ; the distinction is that the tap sometimes causes a movement 
and sometimes does not; that an interval, brief but appreciable, 
elapses before the movement occurs ; that a similar movement is 
caused by a prick on the skin, and that the delayed contraction some- 432 
SPINAL CORD. 
times occurs in the otter leg, or in the adductors of tott legs.* In 
cases in whict the knee-jerk is present, the diagnosis of tabes is only 
justified by distinct and characteristic inco-ordination. Jn the few 
cases of this kind that have come under my own observation, the knee- 
jerk has been either unequal on the two sides, or has been lost on one. 
Such abnormality is probably the rule in these cases, and the diagnosis 
is thus facilitated. In a case with lightning pains, but neither inco- 
ordination nor loss of knee-jerk, a suspicion of tabes would be justified 
by the presence of some other symptom, such as retention or incon- 
tinence of urine, loss of sexual power, or loss of the iris-reflex. But, 
as we have seen, it is probable that cases occur in which these 
pains exist alone,—a condition that may be termed “tabetic neu- 
ralgia.” 
The loss of the iris-reflex is of great diagnostic importance. It 
shows that a degenerative process is at work in the nervous 
system, and it suggests, therefore, that other symptoms are also due 
to degeneration. But since the iris-reflex is not always lost in tabes, 
the negative significance of a normal reflex is far less than is the posi- 
tive significance of its loss. The practical value of this symptom can 
hardly be overrated. It puts the observer, so to speak, on the track 
of nerve degeneration. Its loss is, moreover, so often due to preceding 
syphilis, that it should always suggest this antecedent. 
There are certain diseases with which tabes is especially liable ta 
be confounded. One of these is multiple alcoholic neuritis. The 
ordinary form of this disease is readily distinguished by the symme- 
trical paralysis which is its chief manifestation. But the variety 
which closely resembles locomotor ataxy is the “ alcoholic pseudo- 
tabes ” (p. 125), and in this the diagnosis may be very difficult. This 
is not surprising, because it resembles tabes pathologically ; the lesion 
is a “ parenchymatous neuritis,” a subacute degeneration, beginning 
in the nerve-fibres, and similar to the peripheral form of tabes. It 
often affects, however, in some degree, the motor as well as the sen- 
sory nerves, and there is then some weakness in the distal portions of 
the limbs. An altered electrical reaction may be found in the muscles 
(never in the weakness sometimes met with in early tabes), and there 
is generally marked muscular tenderness, scarcely ever present in 
tabes. The pains have not the “lightning” character, and the 
sphincters escape. The pupils act normally, but this is not an 
absolute distinction, since they may be unaffected in tabes. A history 
of alcoholism may help the diagnosis, and so may improvement when 
alcohol is withdrawn. By attention to all these points, a diagnosis 
can generally be made without much difficulty. 
"When the symptoms and lesion of tabes are combined with those 
of general paralysis of the insane, it may be doubtful in which cate- 
* It is impossible to exaggerate tbe difficulty presented by some patients in ascer- 
taining whether the knee-jerk is or is not lost, and tbe care needed, and repeated 
observations that are desirable, in doubtful cases. LOCOMOTOR ATAXY. 
433 
gory a case should be placed. The question is rather one of the pre- 
ponderance of the symptoms of one or the other malady than of 
absolute distinction between them. In most cases, however, in which 
this combination exists, the symptoms of general paralysis become 
more pronounced as time goes on, and the spinal symptoms, which at 
first were the most conspicuous, pass into the background. 
All common forms of paraplegia are distinguished by the early 
loss of power, and by the persistence of the knee-jerk, often 
emphasized by its excess and by the occurrence of a clonus in the 
rectus or the calf muscles. If weakness supervenes in tabes, it is 
usually late in the cource of the disease, and the other symptoms 
have been and are well marked. If the knee-jerk has been once 
lost in this disease, it is not reproduced by secondary lesions of 
the cord which ordinarily increase the knee-jerk. The same distinc- 
tions usually suffice for the diagnosis from the combined form of 
paralysis and inco-ordination that I have termed “ ataxic paraplegia.” 
In this the knee-jerk is excessive, and there is foot-clonus, while pains 
and anesthesia are absent; spasm supersedes ataxy. In other forms 
of combined disease of the cord the diagnosis depends chiefly on the 
recognition of union. 
Acute lesions of the cord, probably situated in the postero-external 
column, may produce inco-ordination and pain, but the suddenness of 
the onset, the limitation of the symptoms, and their tendency to sub- 
side, usually suffice for the distinction. Symptoms from this cause 
are far more common in the arms than in the legs. Ataxy in one limb 
may also be produced by a tumour growing in the posterior column, 
but other symptoms indicate the invasion of adjacent structures, as 
was conspicuous in the case figured in the chapter on tumours of the 
cord. All these cases present the characteristics of a focal lesion with 
random consequences, rather than of a system disease with limitation 
to a special function. 
In diphtheritic paralysis occurring long after the sore throat, or in 
which the nature of this was not recognised, the loss of the knee-jerk 
may cause tabes to be suspected; but the nature of the case is almost 
always rendered clear by the paralysis of accommodation and of the 
palate which precedes the ataxy, and should be suggested by the 
absence of pains and the presence of weakness. If true tabes follows 
diphtheria, the sequence is too rare to be of practical importance. 
When the dorsal region of the cord is chiefly affected, the severity 
of the pains in the trunk may lead to a suspicion of disease of the 
vertebral bones, but in the latter the pain is local and fixed, and this, 
with the charact eristic increase of pain when the patient moves, should 
prevent error. It is still more frequent to mistake such cases for 
neuralgia of the intercostal nerves, but even if there are no pains in 
the legs to suggest tabes, the knee-jerk and the light-reflex of the iris 
are lost in tabes. Experience shows that the most frequent errors in 
diagnosis are due to a mistake as to the nature of the pains, which 
VOL. I. 434 
SPINAL CORD. 
are mistaken for rheumatism, especially when influenced by weather, 
or for sciatica when referred to the region of the sciatic nerve, or for 
some form of gout if the disease exists in the patient or his family, 
or in the mind of the physician.* 
The only organic intra-cranial disease that may be mistaken for tabes 
is tumour of the cerebellum. In some cases of tabes the unsteadiness 
resembles that of cerebellar origin. Loss of the knee-jerk is strongly 
in favour of tabes; in cerebellar tumour, increase of the jerk is the 
rule, and loss is only to be regarded as not absolutely incompatible. 
Anaesthesia and lightning pains are conclusive evidence of the spinal 
disorder, while in cerebellar tumour severe occipital headache is almost 
invariable, and considerable optic neuritis is extremely common. Optic 
nerve atrophy is primary in tabes, post-neuritic in tumour. 
The various visceral crises are often mistaken for primary disorders 
of the deranged organs. Recurring attacks of the character described 
should always arouse suspicion of their possibly tabetic nature, and an 
examination of the knee-jerk will usually decide the point. 
Prognosis.—The prognosis in tabes corresponds with the facts 
stated as to the course of the disease. It does not, as was once 
thought, deserve the epithet “progressive,” given to it before the pre- 
ataxic stage was known and before the disease had been widely 
observed. Arrest is frequent, and considerable im provement is not rare. 
The earlier the stage of the disease, the better is the prognosis. In the 
first stage, the disease often becomes stationary. When ataxy is deve- 
loped, the prospect of arrest is less than in the first stage, but is still 
considerable. Occasionally, even in the typical form of the disease, the 
amount of improvement is very great. One patient was scarcely able to 
walk across the room, in consequence of the inco-ordination, when he 
came under treatment, and at the end of six months his gait was scarcely 
distinguishable from that of a healthy person. When the third stage 
is reached the possibility of improvement is far less, but is not quite 
absent. A woman suffering from pure tabes, when admitted to 
hospital, had been unable even to stand for six months, on account of 
the extreme ataxy; but she improved so much that in a few months 
she was able to walk about the room without help, and has continued, 
now for six years, to do her household work without difficulty, and 
even to walk some miles with the aid of a stick. On the other hand, 
in some cases the malady increases in spite of every effort, and even 
when there is permanent arrest or improvement it' is rare for all 
symptoms to disappear. The knee-jerk generally remains absent, and 
often attacks of pain continue to occur. It is difficult to find any 
trustworthy indications to guide the prognosis in an individual case. 
The fact of preceding syphilis has little influence on the prognosis. 
* In one case, in which tabetic trunk-pain was chiefly felt at the level of the 
epigastrium, a physician of repute not only made a diagnosis of gastric gout, but 
refused to modify his opinion when loss of the knee-jerk was discovered, and the 
patient became unsteady in gait. LOCOMOTOR ATAXY. 
435 
Only when the symptoms have developed rapidly and the syphilis is 
recent is there some ground to anticipate good from antisyphilitic 
treatment. In all cases, however, in which the onset of symptoms is 
acute there is more prospect that they will pass away than if they de- 
velop slowly. In most cases the only trustworthy guide to prognosis 
is the observed tendency of the individual case. 
Of special symptoms, the pains are often the most distressing, and 
unfortunately they are the most obstinate symptom of the disease. 
They may persist in undiininished severity when other symptoms 
lessen ; and, on the other hand, they may become trifling when the 
disease increases. Diminution of the pain is a good sign if other 
symptoms are stationary, but not if these increase. It is often, how- 
ever, a solace to the patient to know that persistence of the pains do 
not mean progress in the disease. The optic nerve atrophy is usually 
progressive, but not invariably, as is often asserted. In a few cases 
I have known its progress to be permanently arrested. Strange to 
say, the occurrence of optic nerve atrophy makes the prognosis as to 
the spinal symptoms better; in most cases of atrophy the spinal lesion 
remains in the first stage. 
Treatment.—The disease is one in which treatment often has a 
very clear influence, not only in relieving suffering, but in determining 
the arrest or diminution of the disease. This is true especially of 
treatment by drugs. But the first care should be to secure freedom, 
as far as possible, from all influences capable of causing the disease, 
and from whatever is likely to depress the nervous system. Excessive 
mental work, anxiety, and physical fatigue are all harmful. In 
severe and acute cases, absolute rest for a week or two is often useful 
at the onset of treatment. If the patient walks about, exercise should 
always stop short of fatigue. Care should be taken to avoid the risk 
of falls; a severe concussion of the spine will sometimes excite to 
fresh activity a stationary disease. Exposure to cold is also injurious ; 
a severe exposure may cause acute mischief. If practicable it is well 
that the winter should be spent in a warm and dry climate. A sea 
voyage is sometimes useful, combining, as it does, a maximum of 
fresh air with a minimum of exertion ; it has, however, less actual 
effect than might be expected. If there is much ataxy, the risk of 
falls from the motion of the ship must be taken into consideration. 
It is the most useful in cases that are already stationary ; such 
patients often return with a diminution in all their symptoms. 
When the disease is advancing, a voyage often does harm rather than 
good. 
The digestive organs should be kept in careful order; an attack 
of indigestion or constipation is often attended by lightning pains, 
which cease when an aperient has acted. Food should therefore 
be light in quality, and easily digestible. The change from an active 
to an inactive life, which tabes often causes, may lead to the develop- 
ment of gout in an individual predisposed to it, either by inheritance 43 G 
SPINAL COKD. 
or by bis previous mode of life; and the tendency must, as far as 
possible, be obviated by regulation of diet and by frequent aperients. 
Smoking should be either avoided or limited to a small amount. 
Alcoholic excess is especially harmful; it sometimes excites a very 
severe exacerbation of the symptoms ; this is not surprising, since, 
as we have seen, chronic alcoholism may cause a disease resembling- 
tabes in its symptoms and pathology. Sexual excess is also most 
injurious. Many patients are preserved from this danger by the 
disease itself, but it is not always so. Excess seems to have a special 
influence on the optic nerve atrophy. Several very painful instances 
of this Lave come under my notice. A man in the early stage of tabes, 
with slight atrophy, some peripheral limitation of the fields, but little 
impairment of acuity of vision, started on a voyage from Australia to 
England. The day before he started he married, and when he reached 
this country he was quite blind. 
The influence of drugs on the disease is unquestionable in many 
cases, and if they are used wisely, the more a physician sees of the 
disease, the more highly is he likely to esteem them. There is no 
specific for the malady, and in some cases the morbid tendency over- 
powers every influence that can be brought to bear upon it. Moreover, 
the influence of drugs is variable ; that which seems to do much good in 
one case has no influence on another, and this is true also of the same 
case at different jjeriods. Hence the therapeutic statements that have 
been made by various observers are somewhat discordant. 
The first question is the influence of antisyphilitic agents. In 
tabes such influence is distinct only in rare cases, chiefly under the 
conditions mentioned in the section on prognosis. In those circum- 
stances full doses of iodide of potassium should be given, and if the 
interval since the primary disease is short, mercury may be rubbed in 
until the gums are slightly affected. In cases of slow development, 
several years after primary syphilis, such treatment seldom does good, 
and sometimes does harm. But so widely spread is the opinion that 
every consequence of syphilis is amenable to treatment, that it is often 
well to avoid the suspicion of neglect, and even to clear the therapeutic 
ground, by a course of iodide of potassium for five or six weeks. 
Very small doses of mercury, such as grain of the red iodide, may 
also be given for a longer time, and may often be conveniently com- 
bined with other drugs. It seems sometimes to have a tonic influence, 
and perhaps may lessen the secondary subinflammatory process in the 
cord and pia mater, which, as we have seen, sometimes constitutes 
part of the morbid process. But in such late cases, and in all the 
late nerve degenerations that follow syphilis, energetic mercurial treat- 
ment only does harm. Its depressing influence often increases the 
degenerative tendency, and hastens the progress of the disease. 
Of drugs that have been recommended for tabes, those that are 
most useful are arsenic, iron, quinine, aluminium, nux vomica and 
strychnia, nitiate of silver, Calabar bean, belladonna, ergot, phos- LOCOMOTOR ATAXY. 
437 
phorus Of these arsenic is certainly that which most frequently does 
distinct good. Most of the cases in which I have known the greatest 
improvement to occur, have been taking it at the time. In several of 
these cases there was no other change in the conditions of life to 
which the improvement could be ascribed. The form in which arsenic 
is given matters little ; it\v or Tl\vij of the Liq. Arsenicalis maybe given 
in a mixture, or TV gr. of arseniate of soda in a pill. Iodide of arsenic 
has no special advantage, and is not so well borne. This or any 
other drug must be continued for at least six weeks before an opinion 
of its influence can be formed. Rapid improvement can never be 
expected in so chronic a disease. But it is not well to continue any 
drug for more than about three months at a time. Most good is 
effected by alternating two or more ; the return to one that had ceased 
to do good is often beneficial. In connection with the influence of 
arsenic, it is interesting to note the well-known effect of the drug in 
improving the nutrition of the skin, and the frequency with which 
the cutaneous nerves are degenerated in tabes. Quinine, or the 
extract of nux vomica, may be usefully combined with arsenic; or a 
small dose of mercury may be also given, ti\xv of Liq. Hyd. Bichlor. 
with rrpv of Liq. Arsenicalis, or gr. of the red iodide with TV gr. of 
arseniate of soda in a pill. Occasionally arsenic seems to irritate the 
nerve-centres, but a very small dose may then be borne with advan- 
tage. Nitrate of silver and phosphorus are less useful, but may 
sometimes be given alternately with arsenic. The chloride of alumi- 
nium is another agent that I have found of distinct service, 2—4 gr. 
twice or three times a day. 
Calabar bean has been recommended by Ringer as producing tem- 
porary improvement in many chronic spinal diseases. Its influence 
in tabes is not great. Ergot has been esteemed highly by some, but 
is seldom distinctly effective ; it is most likely to be useful if the 
svmptoms suggest that there is a secondary subinflammatory process. 
Belladonna is sometimes useful, and strychnia often produces marked 
improvement, especially combined with a small dose (2-5-0 gr.) of nitro- 
glycerine, which causes the blood containing the tonic to pass more 
freely to the nerve-centres. 
Counter-irritation to the spine, by blisters or the actual cautery, is 
sometimes useful, chiefly in the cases just mentioned, in which the dis- 
ease develops, or the symptoms increase, rapidly, or in Avhich there 
is spinal pain or tenderness. It is not probable that it influences the 
process of degeneration, but it may lessen any secondary inflammation. 
Of special symptoms that require treatment, the pains are the 
most important. Unfortunately they are often very obstinate, and 
their variability renders it difficult to estimate the influence of treat- 
ment upon them. Severe paroxysms may yield only to hypodermic 
injections of morphia, but this should be reserved for the most intense 
attacks, since its use is undesirable for a recurring symptom which may 
continue for years. Indian hemp is often effective; gr. 5 or 5 should 433 
SPINAL CORD. 
be given every three or four hours during an attach. But the most 
useful agents for relieving a paroxysm are antipyrine and acetanilide. 
One or the other of these seldom fails; should they do so, exalgin or 
phenacetiu may succeed. Hypodermic injections of cocaine generally 
arrest, for several hours, pains that are superficial in character, 
especially if accompanied by hyperaesthesia of the skin. The injec- 
tion should be of to of a grain, at the upper part of the region 
to which the pain is referred. Cocaine has no influence over the 
deeper pains. Superficial pain is also relieved by the local applica- 
tion of chloroform sprinkled on spongio-piline (or lint and oiled 
silk). Occasionally the pains are lessened by a warm bath. Counter- 
irritation to the spine, as by repeated sinapisms, may give some relief. 
These measures, however, only relieve paroxysms, and do not prevent 
recurrence. This is sometimes effected by a course of chloride of 
aluminium. 
Paroxysmal visceral symptoms often yield to antipyrine or aceta- 
nilide, but when severe, morphia alone mitigates their intensity. 
Slight gastric crises may be relieved by simultaneous sinapisms 
to the epigastrium and neck. Laryngeal spasm is usually at once 
relieved by nitrite of amyl or nitro-glycerine; the local application 
of cocaine is also useful. Weakness of the bladder is sometimes 
lessened by nux vomica or strychnia. The latter may be given by 
hypodermic injection, as recommended in the chapter on muscular 
atrophy. .Nocturnal passage of urine is occasionally arrested by 
belladonna. 
Blisters or sores on the feet should receive careful local treatment 
until they are well. If neglected they may become very troublesome. 
The patients should be cautioned never to cut a corn; a perforating 
ulcer is often set up by a corn being cut too deeply. The epidermis 
should be softened with an alkali and rubbed off with pumice-stone. 
Attention to the bladder is one of the most important elements in the 
treatment of tabes, as in that of all diseases of the spinal cord, chronic 
and acute. If there is any reason to believe that the bladder is imper- 
fectly emptied, a catheter should be passed; and if residual urine is 
found, the bladder should be emptied perfectly and washed out every 
day or every other day. No hesitation need be felt in the use of the 
catheter in these cases. Many patients die every year from want of 
the catheter, because it is thought that all is right since they pass 
urine freely. The residual accumulation, or the slight cystitis, sets up 
chronic pyelo-nephritis, which develops insidiously, and is unsuspected 
until mysterious febrile disturbance occurs, chronic or acute, and leads 
to death. It is probable that the onset of the final acute disturbance 
is sometimes determined by the passage of a catheter, just as this will 
cause a rigor or transient hsematuria in a healthy person. I have seen 
many melancholy instances of death from the consequences of un- 
suspected retention, and I have never seen any case in which the 
early and frequent use of the catheter did harm. It is especially LOCOMOTOR ATAXY. 
439 
important to insist on the danger that the practitioner may be misled 
by the patient, who thinks that because he passes urine freely he 
necessarily empties his bladder perfectly. 
Electricity has little influence on the chief symptoms of tabes. The 
voltaic current is powerless over either the pains or the ataxy, whether 
it be applied to the spine or the limbs. Faradisation of the skin by 
the wire brush has been recommended for the defect of cutaneous 
sensibility, but it has little if any influence. Temporary improvement 
in gait, and sometimes a little permanent improvement, may be 
obtained by faradisation of the muscles; the stimulation of the 
afferent muscle-nerves is probably the mechanism of its action. 
When the bladder or its sphincter is weak, faradisation from the 
hypogastrium to the perineum may be employed, and occasionally 
seems to do some good. In secondary wasting of the muscles an 
attempt may be made to maintain their nutrition bv stimulating them 
with whatever current they respond to, but the central cause usually 
renders local treatment ineffective. 
Nerve-stretching was fashionable a few years ago, the operation 
being usually performed on the sciatic nerve. In the first case in 
which it was employed (by Langenbuch) the procedure was followed 
by remarkable and mysterious improvement, not only in the pains, but 
also in the inco-ordination. The patient subsequently died under 
chloroform, administered in order that the nerves of the arms might 
be stretched. The spinal cord was found by Westplial to be healthy. 
Although the nerves were not examined, there can be little doubt that 
it was one of the cases in which the nerves alone are diseased. The 
operation has since been performed in a large number of cases, but 
without results that have secured its survival, and it is passing 
into merited disuse. Its place has been taken by extension of the 
spinal column. In this procedure the patient is suspended in such 
a manner as to allow the weight of the body to rest on the head and 
shoulders, and head alone, alternately, and the ligaments of the spinal 
column are supposed to be so stretched that the spinal cord and its 
nerve-roots are elongated. The chief effect is produced on the liga- 
ments of the upper part of the spine, but the actual amount of 
elongation of the spine is exceedingly slight and in significant, as has 
been proved by experiments on the dead body. It is difficult to conceive 
anv mechanism by which it can do the good in tabes which was at 
first ascribed to it; and the careful observations by Bussell and Taylor 
on a large number of cases at the Queen Square Hospital* seem to 
show conclusively that it has no real powt r of influencing the disease. 
It will also probably before long be forgotten. 
* Russell and Taylor, ‘ Brain/ Summer Number, 1890, vol. xiii, p. 20G. 440 
SPINAL COED. 
PRIMARY SPASTIC PARAPLEGIA 
(primary lateral sclerosis). 
The morbid state thus designated is one that has been, and still is, 
the subject of much discussion. Its relations are complex, and a 
somewhat lengthy pathological introduction is necessary. 
General Pathology.—We have seen that in every kind of trans- 
verse lesion of the spinal cord, provided this is situated above the 
lumbar enlargement, the paralysis of the legs is soon accompanied by 
excess of myotatic irritability (increased knee-jerk, foot-clonus), and 
that the muscle-reflex action, on which this irritability (and muscular 
tone) seems to depend, gradually increases to tonic spasm, so that a 
condition develops to which the term “spastic paraplegia” is applied. 
A condition quite similar to that which is thus secondary to a trans- 
verse lesion often develops gradually, without any indication of a 
primary focal disease, and without any sensory symptoms to indicate 
that the mischief extends beyond the purely motor elements of the 
cord. We have also seen that these symptoms indicate disease of the 
upper segment of the motor path, the cortico-spinal segment (p. 176), 
which extends from the motor cortex through the pyramidal tracts, 
and ends in the grey matter of the cord, doubtless by a subdivision and 
ramification of the nerve-fibres in the fibrillary network of the spongy 
substance. From the gradual onset and limitation of the symptoms 
in these cases, it has been assumed that the disease consists of a 
primary sclerosis of the pyramidal tracts, i. e. in a degeneration of the 
fibres of this upper segment. Since these tracts run chiefly in the 
lateral columns, the disease has been termed “ lateral sclerosis.” 
The clinical features presented by these cases, and their probable 
significance, were first pointed out bv Erb * Degeneration of the 
pyramidal tracts had been already observed, by Tiirclc (1856) and 
Charcot (1865). Erb’s inference as to the nature of these cases 
was supported by the independent (and indeed previous) researches 
of Charcot on cases of muscular atrophy; he showed that in such 
cases muscular rigidity coincides with degeneration of the pyramidal 
tracts. Pathologists have since been searching for confirmation of the 
hypothesis—for evidence that the symptoms, in their pure form, 
without muscular atrophy, depend on degeneration limited to the 
pyramidal tracts. Such degeneration in slight degree, associated 
with slight symptoms, has been found in cases of general paralysis of 
the insane (by Westphal and others); but in all other cases that have 
been examined, either other parts of the white substance have been 
degenerated, or the disease has involved also the anterior cornua.f 
* In 1875, ‘ Berlin, klin. Wocliensclir.,’ No. 26 ; 1877, ‘ Virchow’s Archiv,’Bd. lxx. 
f In a case recorded by Stofellu no other part than the pyramidal tracts could PRIMARY SPASTIC PARAPLEGIA. 
441 
In some cases, as one published by Dreschfeld (of which a figure is 
given at page 447), the change in the anterior cornua has been so 
slight that the required conditions are nearly fulfilled. 
Although absolute demonstration has not yet been furnished, the 
indirect evidence of the correctness of the pathological hypothesis 
is very strong, and the only open question is whether, when there 
is no disease of the motor nerve-cells of the anterior cornu, the 
degeneration is so limited to the pyramidal tracts as to constitute 
a system disease in the strict sense of the word. It is not sur- 
prising that demonstration of the nature of the pure cases is not 
lorthcoming, since, as we shall see, the disease has little tendency to 
shorten life. 
It should, moreover, be noted that cases which present this group 
of symptoms may be very various in nature. We have seen (p. 212) 
that, in each segment of the motor path, the same symptoms are 
produced by disease of any part of the segment. In the upper 
segment, with which we are now concerned, the symptoms are the 
same, whether the disease is in the cortex of the brain, the internal 
capsule, the pyramids of the medulla, or the pyramidal tracts of the 
cord; and they must also be the same if the disease is limited to the 
termination of the segment in the grey matter of the cord. In 
cerebral hemiplegia the state of the arm closely resembles that present 
when primary spastic paraplegia involves this limb. The leg in hemi- 
plegia presents a less close resemblance to its condition in spinal 
disease, because the leg is innervated from both cerebral hemispheres, 
and the supplementary influence of the hemisphere of the same side 
lessens the effect of the disease of the hemisphere of the opposite side. 
But if there is disease of the leg-centres in both hemispheres, the 
state of the legs may be identical with that resulting from disease of 
the spinal cord. Such bilateral disease often results from injury 
dui'ing birth,—meningeal haemorrhage over the upper part of the 
central convolutions. This resulting condition is termed “ congenital 
spastic paraplegia.” (See vol. ii.) 
On the other hand, it is extremely probable that degeneration begins 
in the termination of the fibres in the grey matter, just as it does in 
the extremities of the peripheral nerves. It may even be limited to 
these terminal parts, as the extremity of the lower segment is para- 
lysed alone by many agents. In such disease the white columns would 
be found normal, as in one recorded case in which the symptoms of 
spastic paraplegia existed during life, and no anatomical change was 
discovered after death. The detection of the disease of the terminal 
portion in the grey matter is extremely difficult, perhaps impossible, 
because the structure must consist of nerve-fibrilhe that interlace with 
others that are unaffected. This view is supported by the fact that 
in other cases some degeneration has been found in the lateral pyra- 
be seen diseased on naked-eye observation, but no microscopical examination was 
made. 442 
SPINAL CORD. 
midal tracts in the lumbar region, slighter than the intensity of 
the symptoms suggested, and gradually lessening, to cease higher 
up the cord. Such a condition is comparable to the degeneration of 
the lower portion of the second segment of the motor tract in some 
cases of peripheral (degenerative) neuritis, in which there is a degene- 
ration of motor nerve-fibres, greatest in their extremities, extending 
for a variable distance up the nerves, but lessening long before the 
spine is reached. It is highly probable that the toxic agents which 
cause latliyrism and pellagra (q. v.) act on the extremities of the 
pyramidal fibres, as curara does on the nerves; among the spinal 
symptoms of lathyrism are paralysis of the legs with rigidity and 
contractures, and increase of myotatic irritability—foot-clonus, &c.# 
Both clinical and pathological evidence shows that the morbid state 
often occurs also as part of a more extensive degeneration. Degene- 
ration may occur in both lateral and posterior columns, giving rise to 
combined paralysis and ataxy—“ataxic paraplegia,” sufficiently definite 
in its clinical characters and course to make its distinction convenient; 
it is therefore separately described. The following account of the 
clinical features of spastic paraplegia is founded on cases in which the 
motor paralysis and spasm existed alone, with no definite sensory loss, in 
which they came on gradually, with nothing in the state of the patient 
or the history of his symptoms to suggest either a focal lesion or an 
acute process. 
Causes.—An inherited neuropathic tendency is to be traced occa- 
sionally in this as in other chixmic spinal diseases. Thus in one case 
there was a history of insanity in uncle, aunt, and two cousins. The 
disease affects both sexes in almost equal frequency, presenting in this 
a contrast to posterior sclerosis. The period of life at which it most 
frequently begins is between twenty and forty; about three quarters 
of the cases begin in these two decades, and about an equal number 
in each. Cases frequently commence, however, in the second decade 
of life, chiefly in its latter portion. After forty they become much 
less common ; the latest age at which I have known a typical case 
to commence is sixty-one. 
The disease sometimes follows syphilis in a way to suggest a causal 
relation, even when all cases are excluded in which there is any reason 
to suspect a focal lesion. In one case the symptoms commenced six 
months after the primary disease.f But this antecedent is not fre- 
quent, and in this respect also the disease contrasts with posterior 
sclerosis. Proximate causes are to be traced only in a minority of the 
cases. The most frequent is concussion of the spine, such as a fall 
on the back. Some time, often two or three years, elapses between 
the fall and the first pronounced symptoms of the disease, and hence 
focal lesions due to the fall can be excluded. Next in frequency 
* See Marie, ‘ Prog. Med./ 1S83, No. 43. 
t The cord lesion was found to be sclerosis, but the direct cerebellar tract 
was also degenerated (Minkowski). 443 
PRIMARY SPASTIC PARAPLEGIA. 
is repeated exposure to wet cold. Very rarely the symptoms have 
slowly followed some acute illness. In several cases the disease has 
succeeded prostration after childbirth or abortion, or has commenced 
during lactation. In one case an attack of arthritis in the knee aud 
ankle of one leg was the immediate antecedent, and this leg was the 
first to become weak. In another case the symptoms followed sub- 
acute arthritis of both knee-joints, apparently rheumatic in nature. 
The possibility that a joint inflammation may be of spinal origin must 
be borne in mind in considering the significance of such cases, but it is 
on the whole probable that a primary joint affection is an occasional 
cause of the spinal disease.* (Acute arthritis, certainly of spinal origin, 
has only been observed in severe myelitis.) The cause of the congenital 
form is always injury to the brain during birth, in most cases menin- 
geal haemorrhage, causing compression of the motor cortex. 
Symptoms.—Weakness of the legs, of very gradual development, 
is the first symptom. The patient finds that he gets tired more 
readily than before, and that the legs feel heavy; sometimes one leg 
becomes weak before the other. The progress of the weakness is very 
variable, but it is slow in all characteristic cases. In many instances 
the patient is still able to walk a mile or two, even after the disease 
has lasted for several years, slowly increasing. On the other hand, 
walking power may be almost lost at the end of six months. It is 
doubtful whether more acute cases belong to this category. The early 
weakness is often accompanied by slight unsteadiness, chiefly subjec- 
tive. When the patient seeks advice, it will generally be found that 
there is very distinct loss of power in the flexors, often greatest in the 
flexors of the hip, but considerable also in those of the knee and ankle, 
and occasionally much greater in the last than elsewhere. The 
knee-jerk is excessive and quick; the rectus contraction can be 
obtained, as the patient lies, by tapping the depressed patella, and a 
rectus-clonus is often obtainable by sudden depression of the patella. 
The foot-clonus is usually also obtained with readiness. In rare 
cases, in which the upper part of the legs suffers most, there may be 
a rectus-clonus, but only slight indications of a foot-clonus, two or 
three movements quickly ceasing. The tendency to spasm is at first 
noticeable as slight stiffness of the legs on first rising in the morning, 
but it gradually increases in degree as power lessens, until at last the 
legs, whenever extended, pass into a condition of strong extensor 
spasm, rigidly fixing them to the pelvis, so that, as the patient lies, if 
one leg is lilted from the couch by the observer, the other leg is 
moved also. The spasm may be such that the knee cannot be pas- 
sively flexed by any force that can be applied to it until the spasm has 
become less. When flexed the limb is comparatively supple ; but 
if it is then extended, the spasm instantly returns, making the limb 
rigid, and often completing the extension, just as the blade of a knife 
opens out under the influence of its spring, “ clasp-knife rigidity.” 
See ‘Arthritic Muscular Atrophy.’ 444 
SPINAL CORD. 
The spasm is, roughly speaking, proportioned to the loss of power, and 
its extensor character may enable the patient to stand, the legs being 
fixed and rigid, when muscular power is quite insufficient to support 
the body when it is unaided by the spasm. In a still greater degree a 
voluntary effort may only excite general spasm of the limb instead of 
causing a definite movement. Occasionally there are also paroxysms 
of brief flexor spasm causing the legs to draw up. This occurs 
chiefly when the patient is in bed, and especially during sleep. When 
the spasm is great, a paroxysm may pass into violent clonic spasm, but 
this is mei’ely the same clonus that can be produced by passive exten- 
sion, excited by tbe tension of the spontaneous spasm (see p. 222). 
Reflex action from the skin is also usually excessive, and the stimulus 
excites an attack of spasm. 
The gait of the sufferers from spastic paraplegia is very character- 
istic. The legs seem to drag behind the patient, and, in walking, 
each is hauled forwards as a rigid "whole, the toes catching against the 
ground, and, when the ball of the foot rests on the ground, the limb 
may shake from the clonus develojied by tbe extension of the calf 
muscles. When the patient sits, a similar trepidation occurs until the 
patient pushes the leg forwards so that the heel rests also on the 
floor. The muscles of the legs are usually large and well nourished. 
They often seem, indeed, to be hypertrophied, and perhaps are really 
so: the contraction of spasm constitutes a physiological stimulus to 
growth, just as does voluntary effort. But they are uot always large ; 
they are sometimes moderately vrasted. The electric irritability is 
usually perfectly normal, but in the muscles that present the slight 
wasting just mentioned, there may be a trifling diminution of irrita- 
bility, to faradism and voltaism alike. When the patient ceases, or 
almost ceases to walk, contracture sometimes occurs in the calf muscles. 
An active contracture is indeed common, preventing at first passive 
flexion of the ankle beyond a right angle ; but if the pressure is main- 
tained, the muscles yield and full flexion is possible. But in some 
cases there is the fixed contracture described on p. 214 (form 3). 
Flexor contraction at the hip or knee may occur also in the same cases 
under the influence of posture, but is on the whole rare, the tendency 
to it being counteracted by the extensor spasm. 
The arms are often unaffected, but they suffer in some cases, and 
present the same progressive weakness and excess of myotatic irrita- 
bility. Vigorous contractions are elicited by a tap on the tendon of a 
muscle, or on the bone to which the tendon is attached, provided the 
muscle is extended. A clonus can sometimes be obtained in the flexors 
of the fingers. There is less paroxysmal spasm than in the leg, but 
much rigidity of the limb, from active muscular contracture, flexing the 
elbow and flexing the fingers at all the joints, as in the “ late rigidity ” 
of hemiplegia. The difference in the form of spasm in the arm and leg 
is no doubt connected with existence of a reflex extensor mechanism, 
in the lumbar centres, concerned in the act of standing. The muscles PRIMARY SPASTIC PAKAPLEGIA. 
445 
of the arm are often as well nourished as those of the leg. The affec- 
tion of the two arms is very rarely equal; it is common for one arm 
to be almost normal when the other is much affected and both legs 
are equally involved. Sometimes, however, the arm and leg on one 
side are paralysed, and the limbs on the other side are so slightly 
involved that, in comparison with the palsied members, they seem 
normal; the patient often believes that they are unaffected, but 
examination always reveals some weakness and an abnormal degree 
of myotatic irritability. 
The muscles of the trunk may also suffer. A subjective “feeling of 
weakness ” in the back is often complained of early, but seems to be 
as much a sensory as a motor symptom. Painful spasm of the 
abdominal muscles may occur in severe cases, and I have even known 
attacks of tetanoid rigidity of the back to be produced by attempts to 
move. 
It is not common, in typical cases, for the symptoms to extend into 
the region of the cranial nerves, but, in rare instances, difficulty of 
swallowing and of articulation has existed, due to a similar palsy of 
the bulbar nerves. Excessive myotatic irritability has also been 
observed in the muscles of mastication, so that a tap on the chin 
causes a vigorous elevation of the depressed jaw (Beevor). 
Sensory symptoms are often entirely absent, with the exception of 
slight dull pains in the legs, or more frequently in the back. The 
sensation of weakness in the back, already mentioned, occasionally 
reaches an intense degree. Rheumatoid pains may be troublesome, 
but sharp pain is rare, except in untypical cases to be presently 
mentioned. In such cases also there may be very slight defect of 
sensibility—such, for instance, as blunting of tactile sensibility on the 
finger-tips. Subjective sensations of “ numbness,” tingling, formi- 
cation, are more common. They may exist for years without the 
development of any other anaesthesia, in spite of the progress of the 
motor symptoms. 
The sphincters are sometimes affected, occasionally very early; 
often, however, they escape even to an advanced stage. Sexual power 
may be lost, or may remain, even when the spastic paraplegia has 
reached a high degree. The nutrition of the skin and joints under- 
goes no change. 
Ocular symptoms are rare, with the exception of nystagmus, which 
will olten be found if searched for. The action of the pupils is 
usually perfect, aud I have only once seen optic nerve atrophy in an 
uncomplicated case. 
The infantile form may resemble very closely that which occurs in 
adults. There are the same extensor spasm and increase of all forms 
of reflex action. As the child sits on the knee or a chair any sensory 
stimulus will make the legs shoot out in spasm (Eig. 125). But the 
rigidity does not reach the extreme degree often attained in the common 
form. The excess of the knee-jerk is always distinct, but a foot- 446 
SPINAL CORD. 
clonus is not often to be obtained, perhaps because the muscle-reflex 
mechanism related to the calf muscles has not received the functional 
development that must result from the process of walking, with its 
Fig. 126. 
Fig 125. 
Fig. 125.—Congenital spastic paralysis (cerebral). Extensor spasm in 
the legs excited by a sensory impression.* 
Fig. 126.—Infantile spastic paralysis of cerebral origin: cross-legged 
progression. (Drawn by Dr. Spencer, from a photograph.) 
recurring sequence of tension and contraction. Tlie active contracture 
in the calf muscles, which most cases present, is a serious hindrance 
to walking even when the muscular power is sufficient, and it is long 
before the attempt overcomes the contracture. In most cases, how- 
ever, the child ultimately gains the power of walking, although much 
later than normal, and often with some peculiarity of gait, sometimes 
a tendency to “ cross-legged progression," in which one foot gets over 
or in front of the other (Fig. 126), or with a swinging oscillation of 
the body, which may persist to adult life. The growth of the legs is 
often hindered. 
The arms do not present tonic spasm such as is seen in adult cases. 
There may be a choreoid disorder of movement, spontaneous irregular 
movements with inco-ordination, but in the cases that can fairly be 
called “ spastic paraplegia ” the arm symptoms are slight. When 
considerable the condition is often termed “ double athetosis.” Its 
characters are described in vol. ii. 
Transitional forms are met with which constitute gradations between 
primary spastic paraplegia and other degenerations of the spinal cord. 
Slight inco-ordination may co-exist in cases approximating the “ ataxic 
paraplegia ” described in the next section. Cases may begin as pure 
* Drawn by Dr. H. R. Spencer, from a photograph by Mr. Hyde Marriott. PRIMARY SPASTIC PARAPLEGIA. 
447 
tabe3, and indications of lateral sclerosis may be superadded. Slight 
muscular wasting in tbe arms may be associated with indications of 
lateral sclerosis in the legs, and. constitute a transition to the form of 
spinal muscular atrophy to which the name “ amyotrophic lateral 
sclerosis ” has been given by Charcot. Yerv rarely considerable mus- 
cular wasting succeeds spasm in the same part. 
Lateral sclerosis of the spinal 
cord (like posterior sclerosis) 
often forms part of the morbid 
process that underlies general 
paralysis of the insane. In some 
cases of this character the 
mental symptoms are extremely 
slight, and the case may have 
the aspect of a primary spinal 
disease, with slight mental 
failure complicating it. 
The course of characteristic 
cases of primary spastic para- 
plegia is thus very chronic. The 
malady may, at any stage, cease 
to advance. Slight symptoms 
may remain stationary for twenty 
years. Often, however, arrest 
only occurs when the disease 
has reached a considerable de- 
gree. It is perhaps the least 
dangerous to life of any chronic 
spinal disease. Even secondary 
kidney trouble scarcely ever oc- 
curs ; perhaps the excessive re- 
flex action may save the bladder 
from injurious over-distension. 
It is when other elements of 
the cord suffer that dangerous 
complications ensue. 
Pathological Anatomy.—In 
the fact j ust stated we probably 
have an explanation of the silence of morbid anatomy on the subject of 
uncomplicated lateral sclerosis. “ Nee silet mors,” the apt motto of the 
Pathological Society, is true chiefly of disease that kills. Complete 
degeneration of the pyramidal tracts, anterior as well as lateral, is 
met with chiefly in cases in which the anterior ganglion-cells and motor 
nerves are also diseased, although in some instances the amount of 
this disease is small, and limited to the cervical region. An instance 
Fig. 127.—Sclerosis of the lateral and (in 
the cervical region anterior) pyramidal 
tracts, with slight degeneration of the 
anterior cornua. A, cervical; B, dor- 
sal ; C, lumbar sections.* 
* I am indebted for these sections to Dr. Dreschfeld, who has published the case 
(‘ British Med. Journal,’ Jan. 29th, 1881). 448 
SPINAL CORD. 
of such degeneration is shown in Fig. 127. The degeneration in the 
lumbar enlargement is usually limited to the lateral tract, but the 
anterior tract may be affected higher up the cord, as in 127, a. The 
lateral sclerosis is bounded externally, in the dorsal and cervical 
regions, by the normal direct cerebellar tract, and internally by the 
narrow “lateral limiting layer” which intervenes between the pyra- 
midal tract and the intermediate grey matter. There is the usual 
increase of connective tissue and wasting of nerve-fibres. In many 
cases granule-cells are abundant in the affected area. They are 
always present in cases of short duration, and indicate the stage 
rather than the nature of the process. The degeneration probably 
begins in all cases in the nerve-elements themselves. In most cases 
many nerve fibres can still be seen, scattered through the sclerosed 
area; most of them are fibres which lie in the pyramidal tract, 
but do not belong to it. The degeneration of the tract has been 
traced through the medulla, pons, and cerebral hemispheres to the 
motor cortex, in which indications of degeneration have also been 
found. This degeneration through the brain was traced in one case 
in which the disease of the anterior cornua was slight, the wasting 
was limited to the hand muscles, and the spastic paralysis began in 
the legs and then invaded the arms.* Such a case is almost a pure 
degeneration of the whole of the first segment of the motor path. 
FlO. 128.—Sclerosis of the pyramidal tracts, lateral and anterior: dorsal 
region. From a case of muscular atrophy. 
The degeneration of the pyramidal tracts is well shown in Fig. 128, 
from a case of progressive muscular atrophy. The anterior and 
lateral tracts are entirely degenerated, and the sclerosis stops ab- 
ruptly at the outer margin of the lateral, but in front extends for- 
* Kojewnikoff, ‘Arch, de Neurologic,’ 1883, No. 18. PRIMARY SPASTIC PARAPLEGIA. 
449 
■wards, probably in the short fibres that connect the anterior cornu 
at different levels. In other cases, in which the anterior ganglion- 
cells were normal, the sclerosis has not been limited to the pyra- 
midal tracts; the anterior columns have been also sclerosed in the 
lumbar region of the cord.* The direct cerebellar tract and pos- 
terior vesicular columns have been also found degenerated with the 
pyramidal tract, and an annular sclerosis of the periphery of the 
antero-lateral column has been found in several cases.f More frequent 
still is a combination with degeneration of the posterior columns, 
described more fully in the next section. In most of these combined 
cases the degeneration has lessened in the upper part of the cord. In 
one case, at least, the white columns of the cord have been found 
healthy. The probable significance of this fact has been already 
stated. It should be remarked, however, that there seems sometimes 
to be a tendency for the morbid process to extend beyond the pyra- 
midal tracts in a manner that suggests a greater tendency for the 
secondary connective-tissue changes to take on an independent 
invasive activity than in other system diseases. (See also Ataxic 
Paraplegia.) Another point that deserves mention is the occasional 
occurrence of lateral sclerosis in association with insular sclerosis. In 
some cases of this character the degeneration of the pyramidal tracts 
is purely secondary, the result of the damage to the pyramidal fibres 
by an islet of sclerosis situated in some part of their course. But it 
does not appear that this explanation can be given of all cases. In 
some instances the sclerosis of the pyramidal tract appears to be inde- 
pendent and coincident. A similar association of insular and posterior 
sclerosis has also been observed; and such combinations receive 
additional emphasis from the fact that insular sclerosis may be 
accompanied by a primary atrophy of the optic nerve, precisely 
such as occurs in tabes. These facts make it probable that lateral 
sclerosis, although a system disease, is often one of less strict features 
than tabes, having some tendency towards chronic myelitis. We 
shall see that this is true also of ataxic paraplegia. 
The probable mechanism of the symptoms that give the dominant 
characters to the malady have been considered in the general account 
of the symptoms of disease of the spinal cord. The most important fact 
is that the degeneration, whatever its upward extent, always involves 
the lowest part of the pyramidal segment, because it seems to begin 
in this and ascend the fibres. Hence the intra-cornual termination 
must always be involved. This, it is assumed, is the structure that 
controls the muscle-reflex centre, and the consequent loss of control 
* As in a case recorded as one of spastic paraplegia by Hopkins (‘ Brain,5 Oct., 
1883), but this was an example of combined lateral and posterior sclerosis (ataxic 
paraplegia). An illustration of the changes in this case is given in the next 
section. 
t Direct cerebellar and pyramidal tracts in a case by Minkowski, in which the 
disease rapidly succeeded syphilis; annular sclerosis by Westphal (see “Ataxic 
Paraplegia 
VOL. I. 450 
SPINAL CORD. 
explains the excess of myotatic irritability and the progressive spasm, 
progressive by what may be termed a functional hypertrophy result- 
ing from continuous over-action. When there is the rare consecutive 
wasting of muscles, we must conceive that the degeneration involves 
also the ganglion-cells and lower segment of the motor path ; when 
there is coincident wasting of other muscles than those that are the 
seat of spasm, it would seem that some elements of this lower segment 
are the seat of a primary degeneration. The slighter muscular wast- 
ing without, or with only ti'ifling, change in electrical irritability, is 
the expression of a sl ghter alteration in the nutrition of the cells and 
fibres, without actual destructive degeneration. 
Diagnosis.—The diagnosis rests on the combination of weakness, 
excess of myotatic irritability, and spasm,—on the gradual onset of 
these symptoms,—and also on the absence of indications of a focal 
lesion. An acute onset, occupying a few days or weeks, is primd 
facie evidence of a lesion that takes the case out of the category 
of degenerative disease. In most acute cases there is other evidence 
of a focal lesion, extending, at some level, beyond the limits of the 
motor path. Such indications are initial impairment of sensation, 
or a girdle-pain. The latter indicates irritation of the posterior 
root-fibres at a certain level, and proves that at that level the disease 
extends beyond the limits of the pyramidal tracts. Spastic paraplegia 
is common after such lesions, but is secondary and not primary. 
Although marked sensory symptoms, in a case that presents the 
symptoms and course of primary lateral sclerosis, are thus evidence 
that the sclerosis extends beyond the motor tracts, and that the case 
is not one of pure lateral sclerosis, it is doubtful what significance 
is to be attached to very slight sensory symptoms, such as slight sub- 
jective sensations of dull pain, formication, &c., when they exist alone. 
It is possible that they are due to functional disturbance in the sen- 
sory nerve-elements, and do not imply structural disease outside the 
motor area. They are not followed by any more pronounced sensory 
symptoms. 
The absence of objective unsteadiness is the chief distinction from 
ataxic paraplegia (q. v.). When this is slight, it may be difficult to say 
in which class a case should be placed. There are no doubt intermediate 
cases in which there is a very slight degree of the additional lesion that 
exists in ataxic paraplegia, but the distinct objective character of the 
ataxy is the best criterion. Considerable muscular wasting in any part 
is commonly regarded as bringing the case into another category, that 
of “ amyotrophic lateral sclerosis but some cases of the kind, in 
which the wastiug is confined to a few muscles, resemble more closely 
the cases we are now considering than they do those with wide-spread 
and extreme muscular atrophy. These cases are further considered 
in the account of progressive muscular atrophy. 
Primary spastic paralysis is not uncommon in those who are at the 
age and of the sex at which hysteria prevails, and there is no form of PRIMARY SPASTIC PARAPLEGIA. 
451 
cord disease that is so often mistaken for hysterical paraplegia. The 
mistake is facilitated by the perfect muscular nutrition. But the 
mistake ought not to occur, as the peculiar extensor character of the 
spasm, lessening with flexion, is distinctive ; nothing resembling it 
ever occurs in hysterical paraplegia. When the spasm is trifling or 
absent, as in slight and early cases, the diagnostic difficulty is much 
greater, and is increased by the fact that slight excess of myotatic 
irritability occurs in some cases of so-called hysterical paralysis. But 
this scarcely ever reaches the degree necessary to give rise to a true 
foot-clonus or a rectus-clonus. There may be a slight clonus pro- 
duced through a voluntary depression of the foot of the patient in 
response to the passive flexion of the ankle, and readily recognised ; 
or a true clonus may be obtainable during hysterical contracture, but 
apart from such contracture a true foot-clonus or a rectus-clonus 
deserves the greatest weight, as all but conclusive evidence of organie 
disease. I have known many mistakes in diagnosis, in which lateral 
sclerosis was mistaken for hysterical paraplegia owing to disregard of 
the evidence afforded by this symptom, but I have never known the 
opposite error from undue regard to this symptom. Moreover, 
an excess of myotatic irritability in so-called hysterical paralysis must 
depend on more than functional disease. There must be changes in 
nutrition, and consequent persistent defective control of the muscle- 
reflex centres. On the hypothesis that I have advanced, this control 
is exerted by the termination of the pyramidal fibres, i. e. of the upper 
motor segment, by the structures degeneration of which probably 
causes spastic paraplegia. A case is actually on record (the case of 
lateral sclerosis described by Charcot in 1865) in which an initial 
hysterical paraplegia, cured suddenly and relapsing on emotion, passed 
ultimately into lateral sclerosis. 
When the arm and leg suffer on one side only, the disease may be 
mistaken for cerebral hemiplegia. There is not, however, any affection 
of the fa«e, which, although theoretically conceivable, is, as a matter 
of fact, always absent. The limbs on the other side are never quite 
normal, but present slight symptoms—weakness and an excess of 
myotatic irritability—similar to those on the affected side, which 
indicate the nature of the malady. 
The diagnosis of the congenital infantile form is only difficult when 
the observer is unaware of the occurrence of these cases. A slight 
degree of inco-ordination in the hands will usually be found if they are 
carefully watched while the patient takes hold of some object. The 
wide separation and irregular movement of the fingers is very charac- 
teristic. Chronic primary cord diseases are almost unknown in young 
children. Caries of the spine is, in them, the chief cause of para- 
plegia ; and the definite onset of the paralysis, in a previously healthy 
child, is an absolute distinction from the cases of birth-palsy. Other 
diagnostic indications are described in vol. ii (Infantile Meningeal 
Haemorrhage). A definite onset also distinguishes glioma of the 452 
SPINAL CORD 
pons, which may likewise cause spastic paralysis of arms and 
legs. 
Prognosis.—In primary lateral sclerosis there is some prospect of 
arrest, and even of improvement, if the disease has not reached an 
advanced stage. Actual recovery is rare, hut does sometimes occur in 
early cases. When the spastic state is well developed and has lasted 
for some time, it is very rare for more than arrest to he obtained. 
This is perhaps due rather to the tendency of the disease than to its 
degree, since a similar condition that is secondary to a focal lesion 
often recovers perfectly ; and many facts show that it is not likely that 
there is anything in the nature of the lesion to preclude the restoration 
of a normal condition, until dense connective tissue has replaced the 
nerve-elements. In the cases that improve most, it is possible that 
the disease is limited to the terminal structures. We have not, at 
present, any guide to the prognosis in an individual case, besides its 
duration and degree, except its observed tendency, especially under 
treatment. The prognosis of the infantile form is considered in vol. ii. 
Treatment.—So far as drugs are concerned, the treatment is, to a 
large extent, the same as that of posterior sclerosis, already described. 
The drugs most useful are the same, but, unfortunately, their influence 
is less frequently appreciable. Nux vomica and strychnine have* 
however, to be given with caution, and in very minute doses, as they 
have a tendency to increase the spasm. In severe cases this is a most 
distressing symptom, and often not amenable to any influence. 
Bromide sometimes lessens it slightly, but even large doses of 
bromide have but a trifling effect. Indian hemp, belladonna, and 
calabar bean maybe tried, but seldom have a distinct influence. One 
of them may be combined with arsenic, or whatever metallic agent is 
employed. Absolute rest is sometimes of service, and occasionally 
seems to produce improvement, which all treatment failed to effect 
while the patient was walking about. The avoidance of fatiguing 
exertion is a very important element in treatment, and often seems to 
permit medicines to do good, which before were counteracted. Rub- 
bing is also beneficial in some cases. Its influence on the spasm is often 
very distinct during the process, and a long course of rubbing bas 
produced a permanent improvement in the spastic condition. Upward 
rubbing seems to have more influence than kneading the muscles. If 
there is contracture of the calf-muscles, tbe foot should be pressed up 
while these muscles are rubbed. When there are facilities for it, the 
rubbing may advantageously be combined with sweating in the Turkish 
bath. In one case, of moderate degree, almost all the symptoms 
passed away after a long course of Turkish baths, arsenic being also 
given. The patient, who could at first walk scarcely half a mile, 
became able to walk several miles without fatigue, and the improve- 
ment was permanent. Electricity is useless in the pure disease. 
Faradism and all painful applications are harmful, stimulating 
further the already excessive excitability of the reflex centres. I he ATAXIC PARAPLEGIA. 
453 
constant current to the muscles, or from the spine to the muscles or 
to the feet in water, has no distinct influence in either lessening the 
spasm or improving the strength. 
In the infantile form, drugs are useless. Rubbing is desirable, and 
can be efficiently performed by the nurse or mother. Carefully planned 
gymnastic exercises are also useful. The tendo Achillis is sometimes 
divided for the contracture of the calf-muscles, but the operation is 
useless and ought never to be performed. Supports help the child to 
walk somewhat sooner than it would without their aid, and so hasten 
improvement, but they should only be employed when there is suffi- 
cient power and control to make them useful by enabling the will 
to effect ordered movements. 
ATAXIC PARAPLEGIA 
(combined lateral and posterior sclerosis). 
Tlie term ataxic paraplegia seems the most accurate clinical de- 
signation for a disease of the spinal cord which presents a combination 
of the symptoms of paraplegia and ataxy, and consists in combined 
disease of the posterior and lateral columns. Although its clinical 
features present some varieties, and may approach those of each of its 
constituent forms of disease, yet in the majority of cases the symptoms 
are uniform, and sufficiently characteristic to justify the distinction of 
the disease and its separate description. A few pathological obser- 
vations have been published. The following account is based on 
these and on a series of cases that have come under my own observa- 
tion, and of which the clinical characters were well marked * 
Causes.—Neurotic heredity is to be traced only in a small proportion 
of the cases—about one tenth. A history of syphilis is as rare as it is 
frequent in pure tabes. Males suffer much more frequently than 
females. The disease usually commences between thirty and forty, 
but I have known it to begin as early as nineteen and as late as 
fifty-two, while commencement at fifteenf and at sixty-onej is on 
record. Exposure to cold is to be traced occasionally as an exciting 
cause. In one young lady the symptoms commenced after a season 
* See Prevost, *Areh. de Physiologie/ t. iv; Pierret, ib.; Babesieu, ‘ Virchow’s 
Arcbiv,’ Bd. Ixxvi; Kabler and Pick,4 Arch. f. Psychiatric/ Bd. viii; Westphal, ib., 
Bd. viii and x ; Dana, 4 New York Med. Record/ July 2, 1887; and Clarke, * Brain/ 
1890- The condition was described by Dejerine in 1884 under the name of “ataxo- 
paraplegic tabes;” see Ladame, ‘Brain/ 1890, part lii, p. 530. I have not seen 
Dejerine’s description, and did not know of it when the above chapter was written. 
f Oppenheitn, ‘ Near. Cent./ 1888, p. 647. Such early cases are generally isolated 
forms of “ Hereditary Ataxy.” J Suckling, ‘ Lancet,’ 1886. 454 
SPINAL COED. 
of balls, at which when heated she would habitually sit at open 
windows, and often sleep in clothes saturated with perspiration. In 
a few cases, severe exertion, such as excessive athletics, has been the 
apparent cause. A severe concussion of the spine lias sometimes pre- 
ceded the first symptoms by a few months. The disease may also 
follow great sexual excess. In many cases no cause can be traced, 
immediate or remote. Its general etiology thus resembles that of 
simple spastic paraplegia. 
Symptoms.—The onset of the disease is usually slow and gradual, 
two or three years passing before walking power is much impaired ; it 
is rarely subacute, so as to reach a considerable degree in two or three 
months. The early symptoms resemble those of spastic paraplegia, 
with the addition of ataxic unsteadiness, which may be at first the 
most prominent symptom. The legs suffer first, often alone, or the 
arms may also be involved. The patient finds that he tires more 
readily than before, and also becomes unsteady on turning or walking 
in the dark, and these symptoms gradually increase. The weakness 
may be slight, but if all the movements are tested, a defect in power 
will be found in some, often most in the flexors of the knee and hip, 
and frequently more in one leg than the other. The patient is unsteadv 
when he stands with feet together, and he tends to fall if the eyes 
are then closed. If the feet are bare, the irregular action of the 
muscles is shown by the movement of the tendons on the dorsum of 
the foot, as in tabes. In early cases, the inco-ordination is revealed 
by the patient’s gait, which is distinctly unsteady. There is rarely 
the high movement and sudden descent of the feet often seen in 
tabes, but (as in many cases of tabes) the patient is unsteady, reels 
on turning, and has often to bring his foot suddenly to the ground to 
maintain his equilibrium. He may even have to steady himself with 
a stick, or to catch hold of some adjacent object, to save himself from 
falling. The ataxy is equally evident when he lies, and attempts, his 
eyes being closed, to touch some object with his foot. 
The sensory and reflex symptoms present a marked contrast to those 
of tabes. Lightning pains are almost always absent; I have only met 
with them in one case, and in this they were a transient symptom. 
Sometimes there is a slight dull pain in the legs, felt especially on 
fatigue. Dull pain in the sacral region or in the spine is not 
uncommon, and is often an early symptom. The sacral pain, indeed, 
is sufficiently frequent to deserve special note. A girdle-pain is met 
with only in rare cases. As a rule there is no loss of sensation either 
on the legs or trunk. Hvpersesthesia is equally rare. Keflex action 
from the sole may be normal or increased; less commonly it is 
diminished. The cremasteric and abdominal reflexes are sometimes 
lost. The most striking difference from tabes, however, is in the con- 
dition of myotatic irritability, which, in the vast majority of cases, is 
greatly increased. The knee-jerk is quick and extensive; it can be 
obtained from above (see p. 16), and there is generally a distinct 455 
ATAXIC PARAPLEGIA. 
rectus-clonus. The foot-clonus is also commonly to be obtained. 
This myotatic excess persists and increases, and when the arms are 
involved they present symptoms similar to those in the legs—inco- 
ordination, weakness, and marked excess of the myotatic ii-ritability. 
There may be conspicuous ataxy of the hands, and a tendency to 
cramp-like spasm on an attempt to use them. The muscles in both 
arms and legs are usually well nourished. 
Sexual power is often lost early in the disease. The sphincters may 
be impaired, sometimes early, but they also often escape. As in 
other diseases, inability to empty the bladder is apt to develop 
insidiously, without the patient’s knowledge, and the organ may thus 
become habitually distended. 
The iris usually acts to light, but I have seen loss of the light-reflex 
in two or three cases, and have once known accommodation to be lost,, 
the action to light being normal. These symptoms occur chiefly in 
cases following syphilis. Optic nerve atrophy occurs only in rare 
cases, far less frequently than in tabes ; I have seen one case in which 
there were indications of a retro-ocular axial neuritis. The external 
ocular muscles are unaffected as a rule, except for nystagmus, which 
often exists on movement of the eyes, but seldom when they are at 
rest. 
Slight impairment of articulation is not uncommon ; sometimes there 
are irregular tremulous movements of the face resembling those of 
general paralysis, and this in cases in which there is no mental change. 
Westphal has observed marked ataxy of the facial muscles. As a rule 
the mental state is either normal, or there is merely slight failure of 
memory. 
As the disease increases, the muscular weakness and reflex spasm 
become more and more considerable; while the ataxy, after reaching a 
certain degree (not sufficient to prevent locomotion), necessarily sinks 
into the background as the paralysis increases. With the increased 
weakness, the aspect of the patient comes to be that of spastic 
paraplegia, described in the last section. Indications of unsteadiness 
may still be observed in isolated movements. The arms, if previously 
free, may begin to suffer, but sometimes they escape altogether. The 
motor weakness may go on to complete paralysis. This is quickly 
reached in some cases, but so slow is the usual progress of the disease 
that one patient, in whom the disease was at no time absolutely 
stationary, was still able to stand, after eight years. In spite of the 
progress of the weakness, sensation remains unimpaired, and the 
cranial nerves do not suffer. 
The symptoms present, in some cases, variations from this type. 
Sensation on the legs may be impaired, and the knee-jerk may be lost- 
These cases are, however, very rare, and are probably cases of true 
tabes with lateral sclerosis added. Other cases occur in which a girdle- 
pain, impaired sensation, &c., suggest extensive changes in the cord,, 
although the state of the legs is that common in the disease. Such 456 
SPINAL COED. 
cases, as we shall see, are probably examples of chronic myelitis, or are 
intermediate between that and the disease now under consideration. 
Ataxic paraplegia has little tendency to cause death. Indeed, the 
fatal cases have, for the most part, been untypical, and do not convey 
an accurate idea of the characters of the disease. The chief danger 
to life is from the accidents common to all chronic spinal affections, 
—bedsores, and especially kidney disease from undiscovered or 
untreated imperfect action of the bladder. 
Among complications the most important are mental changes 
resembling those of general paralysis of the insane, of which indeed 
this combined sclerosis may form part. Slight muscular atrophy 
sometimes occurs. Arthritis of doubtful significance has been once 
observed. A patient of Westphal’s presented derangement of the 
sympathetic, and died from peculiar spasm of the muscles of respira- 
tion. Yisceral crises, however, are practically unknown. 
Pathological Anatomy.—In all cases the spinal cord has presented 
sclerosis of both posterior and lateral columns ; but the precise extent 
and degree of the degeneration are subject to considerable variations. 
As a general rule, the sclerosis of the posterior columns diffei’s from 
that of tabes in two particulars. First, it is not more intense, and 
often it is less intense, in the lumbar than in the dorsal region of the 
cord. Sometimes, indeed, as in the case shown in Fig. 129, in the 
middle and lower parts of the lumbar region, the posterior columns 
may be free from sclerosis, although it is considerable in the dorsal 
region and at the junction of this with the lumbar enlargement (n). 
The second difference is that the sclerosis has not that special intensity 
in the root-zone of the postero-external column which characterises 
the lesion of tabes. In rare cases the whole posterior column in the 
lumbar region is diseased. The part of the external column near the 
commissure and near the neck of the posterior horn usually remains 
free. Sometimes the degeneration does not extend up to the posterior 
surface of the cord ; for instance, as in the case figured, it affects chiefly 
the middle three fifths of the posterior columns. When the degene- 
ration is considerable, the posterior median columns, in the upper 
part of the cord, may present the usual ascending degeneration of 
secondary origin. When the lesion is slight in degree in the lower 
half of the cord, there may be only a diffuse degeneration of the 
columns in the cervical region, similar to that below, and not the more 
intense limited affection of the median part which occurs when there 
is a typical ascending degeneration from a considerable lesion of the 
column lower down. 
The degeneration in the lateral columns is also variable in extent 
and position, and is often not strictly “ systemic ” in character, 
i. e. is not strictly limited to a single system of fibres, although 
the pyramidal tracts are chiefly affected. In one or two cases, 
indeed, the whole pyramidal tract, and this alone, has been dege- 
nerated; but more often the sclerosis, while intense in this tract, ataxlo paraplegia. 
457 
also extends in front of it into 
the mixed zone of the lateral 
columns (Fig. 129, a, b). A 
similar extension, however, is 
usually met with in the sclero- 
sis that attends degeneration 
of the anterior cornua; com- 
pare Fig. 127. The lateral 
limiting layer, between the 
pyramidal tract and the grey 
matter, may be also invaded. 
The direct cerebellar tract 
often escapes, as in Fig. 129, a 
(b is below its level of origin), 
but it is affected iu some cases. 
Occasionally a zone of sclerosis 
has existed in the whole peri- 
phery of the cord, extending 
deeply into the lateral column 
in the position of the pyra- 
midal tract. This tract has 
been found diseased, in some 
degree, in all cases, and in 
several the extent of its de- 
generation has been greater 
in the lower part of the cord 
than in the upper. The direct 
(anterior) tract may be affected 
as well as the lateral, and is 
commonly involved when the 
lesion is considerable in the 
upper part of the cord. As in 
most other degenerative diseases 
of the cord, there may be some 
increase of connective tissue in 
the unaffected columns. As a 
rule no morbid change has 
Fig. 129.—Ataxic paraplegia, combined 
lateral and posterior sclerosis. A, upper 
dorsal; B, last dorsal; C, mid-lumbar. 
The posterior columns are free from 
sclerosis in C, except in their anterior 
parts; in B the disease involves the 
middle and anterior parts of both post.-med. and post.-ext. columns except in the 
neighbourhood of the neck of the horn ; in A the sclerosis is slighter and is con- 
fined to the middle three fifths of these columns. The sclerosis of the lateral 
columns in C is limited, on the right, to the pyramidal tract, on the left it extends 
in front of this; in B it is very dense in the whole lateral column, involving m t 
only the pyramidal tract but the limiting layer, and part of the “ mixed zone ;” in 
A it is similar in extent but slighter in degree. There is some increase of tissue 
throughout the anterior columns, and a focus of sclerosis near the anterior fissure, 
on the right in A and B, on both sides in C.# 
* I am indebted to Mr. J. Hopkins for the opportunity of drawing these sections. 
The patient was a man aged twenty-one, in whom weakness of the legs commenced 
at twenty, after a wetting, improved, and then slowly increased. He was admitted 458 
SPINAL CORD. 
been recognised in tbe grey matter or in the membranes. In one case 
only was there slight meningitis. Disease of the ascending root of the 
fifth has been found in some cases ;* in one there was also atrophy of 
the cells of the oculo-motor nucleus, and the case thus differed con- 
siderably from the type. The muscles have been found normal. 
Pathology.—The double lesion in the posterior and lateral columns 
supplies an explanation of the two sets of symptoms which characterise 
the disease. The inco-ordination must be referred to the disease of 
the posterior columns, which, greatest in the dorsal region, involves 
there the fibres that conduct impulses from the muscles, probably 
to the cerebellum.f The effect must be to lessen the cerebellar 
guidance, and this explains the resemblance of the inco-ordination 
to that in cerebellar disease. The fact that the disease does not 
extend into the lumbar root-zone accounts for the integrity of the 
muscle-reflex action, and enables us to understand this marked differ- 
ence from tabes. Disease of the direct cerebellar tract probably has an 
influence similar to that of the posterior median columns (see p. 215). 
That interruption of the conducting path in the cord will produce 
inco-ordination is, as we have seen (p. 205), well established. The 
sclerosis in ataxic paraplegia occupies also the region of the cord in 
which the short vertical fibres run, connecting the posterior grey 
matter at different levels, and it is possible that the damage to these 
fibres may contribute to the ataxy. 
The only recognisable lesion that can be regarded as the cause of 
the paralysis is the degeneration of the pyramidal tract. The state- 
ments made regarding spastic paraplegia apply also to the disease, and 
need not be repeated. The lesion has been found greater on the side 
on which one leg was weaker than the other. The variations in the 
amount of disease, which does not always correspond to the degree of 
palsy, are probably due to the fact that the latter may be caused by 
degeneration of the termination of the fibres, which may be much 
greater t ban that of the fibres higher up the cord. In most cases that 
have been examined, the visible disease was greater in the lower than 
a year after the onset, with considerable weakness of the legs, a reeling, unsteady 
gait, increased knee-jerlc, foot-clonus, but with no anassthesia, wasting of muscles, 
pains, or affection of the arms. The symptoms slowly increased, paraplegia became 
ab-olute, and the spasm very intense, sometimes flexor and sometimes extensor. 
There was a doubtful impairment of sensibility to touch on the legs, but no loss to 
pain. The sphincters became affec ted, bedsores formed, and the patient died two 
years after the onset. Fuller details will be found in ‘ Brain,’ October, 1883, p. 383. 
* Oppenheim, ‘Neur. Cent.,’ 1888, p. 647. 
f Much evidence lias been obtained of the connection of the posterior median 
columns with the cerebellum through the grey matter of its bulbar nucleus, and 
also of the effect of interruption of these columns in the dorsal cord, in causing 
inco-ordination like that of cerebellar disease. Besides the experiments of Bech- 
terew on the latter point already mentioned (p. 215), a recent important inve>tiga- 
tion into the connections of the cerebellum fully confirms that with the post.- 
pyramidal nucleus (Biosset, ‘Contrib. h l’etude des Connexions du Cervelet/ Paris, 
1891). ATAXIC PARAPLEGIA. 
459 
in the upper part of tlie cord, increasing from above downwards, a 
fact which, suggests that the maximum lesion is at the lowest part—• 
in the terminal ramification within the grey matter. 
The chief pathological difficulty arises from the fact, which we have 
already considered in connection with spastic paraplegia, that the 
morbid process often extends beyond the limit of the tracts chiefly 
diseased. It tends to assume a diffuse character, so that it has 
been regarded by some as rather a chronic myelitis than a system 
degeneration. It may occupy an intermediate position, and illustrate 
the fact that there is a close connection between the primary decay of 
nerve-elements and the growth of the connective-tissue elements that 
replace the former. In a pure secondary degeneration this growth is 
limited to the tract affected, but even in tabes it may manifest some 
degree of independence, which seems to be still greater in ataxic 
paraplegia. Sometimes, indeed, the primary morbid tendency may be 
double, involving both the nerve-elements and interstitial tissue. If 
it so far preponderates in the latter as to cause considerable changes 
outside the tracts specially diseased, and marked symptoms, such as 
a girdle-pain or loss of sensation, the condition is really one of chronic 
myelitis, and the cases should be so classified. This is probably the 
true solution of the problem, which has been much discussed, whether 
the malady is or is not a system disease. It is so in typical cases, 
but it is on the border of the group of system diseases, and inter- 
mediate cases connect it with diseases of diffuse character and non- 
systemic nature. 
Diagnosis.—The diseases from which ataxic paraplegia has to be 
distinguished differ according to the stage of the disease at which the 
diagnostic problem presents itself. The dominant symptom in the 
early period is the inco-ordination ; in the later period, the spastic palsy. 
Hence the disease in the early stage is liable to be confounded with 
pure locomotor ataxy, but the condition of the knee-jerk, lost in the 
one, excessive in the other, is distinctive. In the rare cases of 
early tabes in which it is not lost, it is never increased. In tabes, 
there is not the loss of power which will always be found in ataxic 
paraplegia, and when a clonus and extensor spasm are added, there 
should be no risk of confusion; but it is necessary to emphasize the 
distinction, because cases with much unsteadiness are frequently 
described as tabes with preserved knee-jerk. From primary spastic 
paraplegia the diagnosis depends on the presence of inco-ordination, 
or in a history of it, if voluntary power has become too slight to be 
susceptible of derangement. Ataxic paraplegia is spastic paraplegia 
'plus inco-ordination. If the ataxy is considerable, as it often is, the 
distinction is easy enough, as experience shows that it is chiefly with 
tabes that such cases are confounded. If slight, it may be difficult to 
sav in which class the case should be placed; the best criterion is 
that mentioned in the account of spastic paraplegia, the distinctly 
objective character of the unsteadiness. The so-called “hereditary 460 
SPINAL COED. 
ataxy ” presents a close resemblance to ataxic paraplegia, and is, 
indeed, as we shall see, intermediate between this disease and true 
tabes. It is distinguished by its occurrence in several members of 
the same family, and by the common loss of the knee-jerk ; while the 
presence of nystagmus, of some impairment of articulation, and of 
other symptoms described in the account of the disease, distinguish 
the isolated cases that are sometimes met with. 
The distinction from diffuse or focal chronic myelitis depends chiefly 
on the extent of the symptoms in the former, and their limitation in 
the latter. The subacute forms of myelitis are also distinguished by 
their more rapid onset.* The greatest difficulty is presented by cases 
which have a subacute onset, and the distinction from a local myelitis 
involving the posterior and lateral columns may be very difficult. It 
depends chiefly on the progressive tendency of the symptoms, which 
■contrasts with the regressive tendency of myelitis. It is possible that 
when there is a degenerative tendency, a focal myelitis may set up a 
progressive degeneration in the columns concerned, as it certainly may 
set up a degeneration limited to the posterior columns. 
A tumour in the middle lobe of the cerebellum may cause unsteadi- 
ness, closely resembling that of some cases of ataxic paraplegia, and 
it may also cause weakness of the legs with increased knee-jerk, from 
the pressure on the pyramidal fibres as they pass through the pons. 
In such cases, indeed, we probably have the two elements of the 
disease, produced iu a different manner, by lesions of different posi- 
tion. We have a degeneration of the lateral columns which is secon- 
dary instead of primary, and we have disease of the co-ordinating 
centre instead of interruption of the path to it. But the weakness 
in the legs is never great in cerebellar tumour, and special symptoms 
of this are never absent. Occipital headache, vomiting, and optic 
neuritis are present in most cases. In a case in which the pons is 
compressed, some cranial nerves are usually also damaged. 
Prognosis.—The prognosis in ataxic paraplegia is similar to that in 
the spastic form, and depends on similar considerations, which need 
not be here repeated. 
Treatment.—The treatment of ataxic paraplegia is the same as that 
of the allied diseases, and especially of spastic paraplegia, to the account 
of which the reader is referred. 
PELLAGRA. 
Pellagra is an endemic malady which, though fortunately unknown 
in this country, deserves mention here on account of the incidence of 
its effects on the spinal cord. Its chief anatomical lesion seems to be 
* For some instructive notes on this point in diagnosis see Dreschfeld, f Brain,' 
January, 1888. “ HEREDITARY ATAXY.” 
461 
a degeneration of the lateral and posterior columns of the cord, 
corresponding closely to that of ataxic paraplegia, and, as in that 
disease, with a greater affection of the lateral than of the posterior 
columns. It differs, however, in the fact that some atrophy of the 
large nerve-cells of the anterior cornua is common, and also in the 
constancy with which chronic inflammation of the pia mater is met 
with, sometimes accompanied by the formation of bony plates in the 
arachnoid. 
The Cause of the disease appears to be the action, on the elements 
of the spinal cord, of an organised virus (or of some product of 
this) which is taken into the system with diseased maize. The virus 
has been thought by some (as Loinbroso) to be a fungus growing in 
the maize; by others to be sj)ecific micro-organisms of other than 
fungoid nature, present in the maize, which develop in the system 
and produce there the toxic agent that has a special action on the 
nerve-elements (Belmondo). 
The Symptoms resemble very closely those of ataxic paraplegia. 
There is weakness in the legs, with increased myotatic irritability 
going on to spasm; unsteadiness of movement, especially iu the early 
stages, sometimes accompanied by tremor. Sensibility may be normal, 
or the perception of touch or pain may be increased or lessened. 
Belmondo, from an important series of investigations,* has arrived at 
the conclusion that the symptoms depend on a primary systemic 
degeneration of the nerve-elements of the pyramidal tracts and 
posterior columns, determined by the influence of the toxic agent. 
The course of the disease is chronic, but sometimes an intensely acute 
stage comes on, with symptoms of spinal meningitis,—a condition to 
which the term “ typhus pellagrosus ” has been applied. After death 
in this state there are often found commencing acute myelitis, in 
addition to the inflammation of the membranes, and also swelling of 
the intestinal lymphatic glands, with signs of enteritis,—indications 
of an acute blood state which justifies the view that the affection is, 
p lima rily, a toxsemic malady. 
"HEREDITARY ATAXY” 
(friedreich's disease, hereditary ataxic paraplegia). 
The so-called hereditary ataxy is a form of ataxy, or rather of ataxie 
paraplegia, depending on combined posterior and lateral sclerosis, 
which occurs in families, and differs further from the common forms 
of tabes and of ataxic paraplegia in the early age at which it always 
commences, and in tLie presence of certain additional symptoms. It 
is often termed “Friedreich’s disease,” because this physician first 
‘ Rev. Sperimeiit./ 1889-90, xv and xvi. 462 
SPINAL COLD. 
described the characteristic features of the malady and the lesion in 
the posterior columns.* 
The dependence of the disease on a congenital tendency is clearly 
shown by its usual occurrence in families. But direct inheritance has 
been traced in only a few instances. In one, the mother of the family 
affected, and her mother, both suffered from the disease. That a 
general neuropathic inheritance is also sometimes effective is shown 
by cases in which there is a history of other neurotic diseases, such as 
insanity or epilepsy, in collaterals or ancestors. Two brothers who 
were affected had another brother epileptic, and a sister suffered from 
repeated attacks of chorea. Alcoholism in parents has been supposed 
to be influential, but the evidence of this is not strong. Consanguinity 
of parents has existed in some instances, and has doubtless intensified 
the morbid tendency in these cases. 
The family tendency of the disease is shown by the affection, in most 
instances, of brothers and sisters. Thus sixty-five cases were distri- 
buted in nineteen families, giving an average of rather more than three 
to each. The number affected in one generation has varied from two 
to eight. In the case in which the mother and grandmother suffered, 
an uncle and seven children were also affected, making ten in one 
family. Few isolated cases have been recorded, but they certainly 
occur. Probably the nature of the affection has not been suspected 
on account of the isolation. In many of these cases (to judge from my 
own observations) this feature extends beyond the disease ; the patient 
is au only child, or the only one of the sex in the family. Thus one 
patient was the only daughter, and her four brothers were healthy. 
The two sexes present nearly equal liability; males slightly pre- 
ponderate (thirty-five males to thirty females). In some families the 
two sexes have suffered equally, but in others the disease has shown a 
marked tendency to affect one sex. Thus in one family of nineteen, 
the two males suffered, and the seventeen females escaped. In 
another instance, recorded by Musso, a brother and sister (the off- 
spring of a melancholic mother) married healthy individuals; the 
brother had three daughters affected out of seven living children ; and 
of the sister’s children three sons were diseased. A curious fact is that 
three of the brother’s and four of the sister’s children were born dead. 
The age at which the first symptoms are recognised has varied 
between two and twenty-four years.f The seventh and eighth years 
* Friedreich’s first accouut was given to a medical society in 1861, and published 
in ‘Virchow’s Arcliiv’ (Bd. xxvi and xxvii) in 1863. Further cases were published 
by him in 1876 (ib., Bd. lxviii and lxx), and a collection of 57 cases is given by Dr. 
Everett Smith, * Boston Med. and Surg. Journal,’ Oct. 15, 1885. See aEo Ormerod, 
‘Brain,’ Jan., 1888; Dejerine, ‘Med. Moderne,’ 1890, No. 25, and ‘La Sem. Med.,’ 
1890, Nos. 11, 12; and especially Soca, ‘ These de Paris,’ 1888 (who has collected 
165 cases—many, however, doubtful), and Lada me, * Brain,’ 1890, pt. lii, where a 
full bibliography will be found. 
f In the family recorded by Everett Smith, the father presented symptoms of 
ataxic paraplegia at the age of sixty-six, coming on gradually after an attack of “ HEREDITARY ATAXY.” 
463 
of life are those in which disease most often begins; and next comes 
the period of puberty, from twelve to sixteen. In isolated instances 
the onset is generally later than in the grouped cases. It begins 
somewhat earlier in males than in females, and often commences about 
the same period in the same family. 
Immediate causes can rarely be traced; preceding acute diseases 
may have facilitated the onset, but can scarcely have done more. 
Symptoms.—The first and chief manifestation of the disease is a 
gradual impairment of co-ordination, first in the legs and afterwards 
in the arms. Initial pains scarcely ever occur. The ataxy is shown 
by unsteadiness in standing and. walking, at first slight, but slowly 
increasing, until the feet have to be placed wide apart in standing, and 
the patient reels in walking like one under the influence of alcohol. 
The feet are not often raised too high, unless when an unusually long 
step is taken. Closure of the eyes causes a considerable increase in 
the unsteadiness in some cases; in others it has but little influence. 
Children often first show the affection by the readiness with which 
they stumble and fall. The impairment of movement in the arms is of 
a similar character, but usually commences some time after that of the 
legs. There is irregularity in the voluntary movement of the arms and 
fingers, and the ataxy has often a distinctly jerky character. In most 
eases the power of the muscles is at first unimpaired; their nutrition 
is good, but the myotatic irritability is lost. In most cases the knee- 
jerk has been found absent as soon as the patient came under obser- 
vation; in one case it disappeared after the other symptoms had set 
in; in another it was normal on one side, absent on the other. In 
several there has been no change long after all the other charac- 
teristic symptoms had manifested themselves; very rarely it has been 
increased, chiefly in untypical cases. 
As the disease progresses, some jerky irregularity develops in the 
movements of the neck and head, so that the head presents slight 
unsteady movements, sometimes like an irregular tremor, when it is 
supported by the muscles. Speech is also impaired ; syllables are 
elided, and there may be, with this, an occasional hesitation. There 
is no twitching of lips, but occasional jerky movements have been 
noted in the tongue. The affection of speech is not often an early 
symptom. It may not be noticed until three, five, or ten years after 
the onset of the other symptoms. In most cases (but notin all) there 
is nystagmus when the eyes are moved laterally or upwards. Some- 
times the movement is slower than in most forms of nystagmus, and 
it is rarely present when the eyes are at rest, directed straight 
forwards. This symptom may come on after those in the limbs, but 
careful examination will often reveal it in the early stage. Paralysis 
rheumatism produced by exposure to cold. In the age of the sufferer this case 
stands alone in the history of the disease, and is not included in the figures given. 
The case may he a mere coincidence, or may show that a latent predisposition may 
persist through life. 464 
SPINAL CORD. 
of the ocular muscles is very rare ; in one case there was strabismus 
with double vision,* and slight diplopia sometimes exists for a time and 
passes away. Optic nerve atrophy never occurs. The pupils are usually 
normal, but several cases have been recorded in which there has been 
loss of the light reflex. Whenever this condition exists, evidence 
of hereditary syphilis should be most carefully sought for, as it is 
probable that many of the cases in which this loss was met with were 
cases of true tabes, with some involvement of the lateral columns, 
occurring in young persons, and should not be classed with the disease 
in question. 
Sensory symptoms are very variable. Lightning pains and any 
severe pains are extremely rare, though in one or two recorded in- 
stances they have been severe ; but slight dull or rheumatoid pains in 
the legs are not uncommon. Sensibility has been quite normal in 
many cases even of severe degree ; in others there has been slight 
anaesthesia in the legs, early in some instances, late in others. In one 
case there was delay of conduction, such as is met with in tabes ;f 
rarely sensibility to pain and temperature is impaired. The sense of 
posture of the limbs has been found normal in several cases in which 
it has been examined. The electro-sensibility of the muscles is said 
to be sometimes lessened. Increased sensitiveness to pain is occa- 
sionally met with. Reflex action from the sole is usually preserved, 
but may be lost when there is anaesthesia. The cremaster reflex is 
often lost. On account of the age of the patients little is known of 
the condition of sexual power, but it is certainly often absent. 
Menstruation usually becomes irregular and ceases. The sphincters, 
as a rule, are unaffected. There is no tendency to trophic changes in 
the skin or joints. 
Although muscular power is commonly normal at first, and may be 
normal even when the ataxy is considerable, it usually becomes impaired 
as the disease progresses, and sometimes weakness comes on, with the 
ataxy, at the onset of the disease. The loss of power is always 
greatest in the legs, and may be confined to them. The flexors suffer 
more than the extensors, and the weakness in the flexors of the ankle 
may permit some degree of talipes to occur. The loss of power may 
be ultimately great, although it rarely amounts to absolute paralysis. 
Slight wasting of the muscles may occur in the later stages of the 
disease, attended with only trifling depiession of the electrical con- 
tractility ; in two recorded cases, however, a brother and sister, there 
was great atrophy of muscles with altered electrical reactions.f 
Lateral curvature of the spine, and talipes equinus or equino-varus 
of the feet, are common as later results of the muscular weakness, 
developing under the influence of posture; and contraction of the 
flexors of the knees has also resulted. 
* Charcot, ‘ Prog. Med.,’ 1887, No. 23. 
f Dejerine, * Mod. mod.,’ 18U0, No. 25. “ HEREDITARY ATAXY.” 
465 
Visceral crises do not occur. Frequency of pulse lias been noted, 
however, in many cas s, and curious vaso-motor symptoms (flushing, 
oedema, sweating, polyuria, and salivation) were present in one of 
Friedreich’s cases. There is no mental change that can be regarded 
as part of the disease, although imbecility has co-existed (Power).* 
The isolated cases may correspond closely to the type, presenting 
the same nystagmus, weakness, and unsteadiness; many of these 
cases, however, differ somewhat, although sufficiently characteristic 
in their main features to justify their inclusion. Speech more often 
escapes. I have once met with a congenital lisp. In some the sym- 
ptoms are slight, and have developed late. A difficulty in micturition 
may precede other symptoms. There are also cases, sporadic and 
grouped, in which coarse tremor is conspicuous, and the condition might 
be regarded as one of simple tremor, were it not for the presence or 
development of other symptoms. For instance, one man had clipping 
speech “all his life;” between forty and fifty, difficulty in writing 
came on, owing to a peculiar spasmodic tremor in both arms, brought 
on also in the legs by exertion; at fifty, unsteadiness on walking was 
added. There was a history of a similar affection in several relatives. 
The rate of progress of the malady varies much, even in different 
members of the same family. One, in whom the disease commenced 
last, may be unable to walk while another who suffered sooner may 
be still in the early stage of the disease. Now and then the disease is 
stationary for many years. The duration of the malady is corre- 
spondingly variable. It is always long, even more than thirty years, 
and in mauy instances it has not apparently shortened life. On 
the other hand, death may occur at the end of ten or twelve years. 
The end has generally come from intercurrent affections, rarely from 
exhaustion. Acute myelitis has also caused death (Everett Smith). 
Pathological Anatomy.—The lesion in hereditary ataxy is that 
of ataxic paraplegia and of tabes combined. There is degeneration in 
the lateral column, often also in the anterior column, such as occurs 
in ataxic paraplegia ; but the sclerosis of the posterior column is more 
intense than in that disease, and it is also more extensive, especially in 
the lumbar region. It is similar to the degeneration of tabes, and 
agrees wuth this also in that the posterior nerve-roots are usually 
affected, whereas in ataxic paraplegia they almost invariably escape. 
The distribution of the lesions shows a close correspondence in 
different cases, as will be seen by a comparison of the figures here 
given, which are from three different cases of the disease. The sclerosis 
of the posterior columus may be complete throughout the cord, with 
the exception of a narrow band near the neck of the cornu, which 
always remains but little damaged. In the lumbar region it is usually 
intense up to the head of the horn and the posterior surface of the 
cord ; occasionally, however, it is somewhat less intense in this region 
* An excellent analysis of the symptoms, &c., is given by Crozier Griffith (‘Trans, 
Coll. Phys. Pniladelpliia,’ 1888); and by Ladame (‘ Grain,’ 18'JO, pt. 52). 
VOL. I. 466 
SIMNAL COED. 
than it is higher up, extending, nevertheless, into the root-zone. In 
the cervical region the sclerosis may also be general, or it may be 
greatest in the root zone and in the posterior median columns. The 
cervical root-zone never escapes, as it often does in 
tabes. 
The degeneration of the lateral columns always 
involves the pyramidal tracts, and is most intense 
m Ui?ir position. It is not, however, limited to tnem. 
It usually extends outwards to the periphery of the 
cord, even where the pyramidal tract does not reach 
the surface, thus involving the direct cerelel'ar 
tract; and it also extends forwards at the surface, so 
as to constitute a band of annular sclerosis, which 
varies in thickness in different parts of the cord and 
in different cases (Figs. 130, 132). In the inner 
part of the anterior column there may be a distinct 
Fig. 131.—Hereditary ataxy; section of spinal cord 
at first lumbar segment. Sclerosis of tbe whole of 
the posterior columns except a narrow zone adja- 
cent to the neck of the horn. Degeneration also 
of the lateral pyramidal tracts, and, in front of 
this, slight degeneration in the superficial layer of 
the lateral column. Adjacent to the anterior 
median fissure there is also a zone of sclerosis of 
the anterior pyramidal trait, which extends, in this 
cord, into the lumbar region.* 
Fig. 130.—Heredi- 
tary ataxy; dis- 
tribution of de- 
generation in the 
white columns, 
indicated by the 
dotted shading. 
(After Fried- 
reich.) 
* I am indebted for this section to Dr. Everett Smith, who has published the ease 
in the ‘ Boston Med. and Surg. Journal,’ Oet,. 15,1885. The patient was one of three 
sisters affected with the disease, the brothers being healthy. The father suffered 
from ataxic paraplegia late in life, as mentioned on p. 462. In the case from which 
the drawing is made, the inco-ordiuation began in the legs at the age of nineteen, 
and in the arms soon afterwards, and was quickly followed by loss of power, which 
gradually increased to almost universal paralysis, with muscular contractures (talipes 
equino-varus, &e.) and considerable loss of sensation. There was nystagmus, affec- 
tion of articulation, and some mental dulness. Death occurred at the age of forty. “ HEREDITARY ATAXY.” 
467 
area of degeneration in the 
position of the anterior 
pyramidal tract. This is 
seen in Fig. 131, in which 
this tract extends unusu- 
ally low in the cord, and is 
distinctly degenerated in 
the upper part of the lum- 
bar enlargement. Atrophy 
of the posterior vesicular 
column has been found 
associated with that of the 
direct cerebellar tract. 
Slight abnormal appear- 
ances have been seen in 
the nerve-cells of the ante- 
rior cornua in some cases, 
but, as a rule, these are 
normal, and the grey 
matter presents no other 
disease. It is very likely, 
however, that future obser- 
vations will reveal the oc- 
currence of changes in the 
nerve-cells of the posterior 
horns, such as are met with 
in tabes. 
The pia mater over the 
posterior columns has been 
found thickened. -The pos- 
terior nerve-roots usually 
present some degeneration 
of their fibres; this may be 
partial (Fig. 133, b), or may 
amount to total destruction 
of the fibres (as at c). The 
peripheral nerves in the 
limbs have been found 
normal.* 
Some general shrinking 
FlGt. 132.—Hereditary ataxy. A, cervical; B, 
dorsal; C, lumbar regions of the cord. The 
posterior columns are sclerosed in their whole 
extent, except in the vicinity of the neck of 
the horn in the cervical and lumbar regions, 
the degeneration being rather less intense in 
the lumbar than in the other parts. In the 
antero-lateral columns there is an annular zone 
of sclerosis in the periphery of the cord, widen- 
ing in the region of the pyramidal tract. In 
front of this tract the zone is widest in the 
dorsal region, and trifling in degree in the lum- 
bar. The grey matter is but little affected.f 
* Friedreich, ‘Virchow’s Ar- 
chiv,’ I3d. lxx, p. 145. 
+ For the sections from which the drawing is made I am indebted to Dr. Pitt 
•(who prepared them) and the late Dr. Moxon, under whose care the patient died in 
Guy’s Hospital. The case (full details of which will be found in a recent volume of 
the ‘Guy’s Hospital Deports’) is one of a series of five cases (four brothers and a 
sister) which I reported some years ago to the Clinical Society (‘ Clin. Soc. Trans.,* 
vol. xiv, 1881, p. 1). 468 
SPINAL CORD. 
and induration of tbe pons and medulla were found by Friedreich, 
with atrophy of tbe cells of tbe post pyramidal nucleus and some 
degeneration of tberes- 
tiform bodies, but none 
of tbe anterior pyra- 
mids. Corpora amy- 
lacea were present in 
the hypoglossal nerves. 
Atrophy of tbe cere- 
bellum was found in 
one ease ; tbe cells of 
Purkinje were dimin- 
ished in numbers, but 
showed no sign of 
atrophy or degene- 
ration* 
Pathology.—Tbe 
disease apparently oc- 
cupies a clinical and 
pathological position 
between the combined 
sclerosis described as 
ataxic paraplegia and 
simple tabes, resem- 
bling the former in the 
common affection of tbe 
lateral and posterior 
columns, and the consequent weakness with ataxy—resembling it also 
in the imperfect limitation of the changes, and in the intensity of those 
m tbe middle of the posterior columns in the dorsal region ; but it 
differs from this, and resembles tabes, in the degree of affection of the 
posterior columns in the lumbar regions, the extension in slight 
decree into tbe root zones, and the affection of the posterior roots; 
with these the loss of the knee-jerk and tbe affection of sensation are 
apparently connected. The isolated cases, occasionally met with, 
present tbe same combination of spinal symptoms. Tbe precise 
origin of the affection of articulation and of the nystagmus has not 
yet been traced. 
The age at which the disease commences, long before the period at 
which ordinary degenerations occur, and its family grouping, 
suggest that its ultimate cause is a congenital tendency of develop- 
ment, by which tbe affected elements have a briefer period of vital 
endurance than the other tissues of the organism. Mdbius has 
suggested that there is an actual arrest of development of these 
structures, but it is evident that their development suffices for perfect 
function during the early part of life, and that their functional 
FlO. 133.—Hereditary ataxy; degeneration of poste- 
rior nerve-roots (from the same ease as Fitr. 124). A, 
normal ant' rior root, for comparison. B, posterior 
root, partially deirenerated ; a few norma! nerve- 
fibres are seen, but mo-tof the spaces which should 
contain nerve-flares are empty. C. posterior root, 
totally degenerated, probably by a more acute pro- 
cess than that of B, since there is some destruction 
of the septa and increase of amorphous connective 
tissue, 'l lie products of degeneration are rendered 
invisible by the mode of preparation. (Compare C 
with the similar changes in a totally degenerated 
peripheral nerve shown in Fig. 54, B, p. 132.) 
# P. Menzel, ‘Arch. f. Psych./ Btl. xxii, II. 1, p. 1G0. “ HEREDITARY ATAXY.’* 
469 
capacity undergoes subsequent failure, which can only be due to a 
process of structural change. It is possible that we have here, again, 
a double morbid process, and that a tendency to early degeneration in 
the nerve-elements is associated with a converse tendency to over- 
growth of the interstitial tissue, analogous to that which we have in 
the muscles in Pseudo-hypertrophic Paralysis (q. v.). In this con- 
nection it is important to note that, in one case, the neuroglial over- 
growth suggested a pure increase of the normal tissue, rather than a 
result of inflammation; and the peripheral sensory nerves, although 
not degenerated, contained a considerable number of embryonal 
nerve-fibres in the fasciculi.* Dejcrine would regard the neuroglial 
increase as the sole element in the morbid process; but the fact last 
mentioned, as well as the preponderant affection of certain tracts, 
makes it improbable that this exclusive view is correct. 
Diagnosis.—In most cases the inco-ordination is sufficiently pre- 
dominant to suggest that the disease is a form of ataxy, and the 
unsteadiness of the head, the affection of articulation, the nystagmus, 
aud the age at onset, suffice for the distinction from ordinary tabes. 
The common form of ataxic paraplegia bears a close resemblance to 
this disease, a resemblance that is more than superficial, although the 
excessive knee-jerk and foot-clonus, almost always present in ataxic 
pai'aplegia, are usually absent in hereditary ataxy; much spasm is 
always absent, and nystagmus is common. The difference in the state 
of myotatic irritability is, as we have seen, not absolute; cases of 
combined lateral and posterior sclerosis occur, of tabetic type, in 
which the knee-jerk is lost, and in at least one case of hereditary 
ataxy the knee-jerk has been excessive. The age of onset and family 
multiplicity may decide the question, but the isolated cases, which 
are by no means rare, commencing soon after puberty, are not dis- 
tinguishable from the hereditary disease ; they seem to be analogous to 
the isolated cases of pseudo-hypertrophic paralysis. A greater difficulty 
is presented by cases of slight tabes in children, the subjects of 
inherited syphilis, in whom it is not uncommon for some weakness of 
the legs to co-exist, or speech to be disordered, in consequence of some 
•early lesion of the brain. The loss of the iris-reflex should suggest 
inherited syphilis, and other indications of this will often decide the 
nature of the case. 
Disseminated sclerosis presents inco-ordination, nystagmus, and 
impaired articulation, but the ataxy of the arms differs in the wide 
range and violent character of the disordering jerks which characterise 
this disease; while simple unsteadiness of the legs is very rare, and 
the course of the malady is more rapid. The affection of speech 
differs from that of hereditary ataxy in being simply “ staccato,” with 
undue separation of syllables, which are rarely run together. The 
cases are always isolated. 
Cerebellar tumour aud hereditary ataxy can hardly be confounded, 
* Anscher, ‘La Semaine Med.,’ 1890, No. 32. 470 
SPINAL CORD. 
in spite of the fact that the unsteadiness in walking is very similar in 
the two diseases ; the common affection of the arms in the one, and 
the conspicuous head symptoms (severe pain, optic neuritis, &c.) of 
the other, sufficiently distinguish them. It is very common for the 
tremor of the head to be at first ascribed to mere “ nervousness,” and 
also for the isolated form, in girls, to be regarded as hysterical. Tho 
presence of nystagmus should at once decide the question ; it is 
absolute proof of definite disease. 
Prognosis.—The prognosis in every case is very serious, since the 
disease, being a developmental affection, is essentially progressive ; but 
life may be prolonged for many years, and in slight cases the malady 
may interfere comparatively little with the patient’s occupation. 
Thus I have known a man, with very marked symptoms, follow his 
business as a tradesman for many years. The only guide ta 
individual prognosis is the observed rate of progress, which has little 
relation to the age at which the symptoms commence. 
Treatment.—As in other diseases that depend on a congenital 
tendency, treatment is almost powerless. The measures recommended 
for ordinary locomotor ataxy (apart from those suggested by the 
special symptoms of tabes) arc those most suitable to the hereditary 
form. Arsenic, phosphorus, and nitrate of silver deserve a trial; now 
and then they seem to check the progress of the disease for a longer 
or shorter time, but its individual tendency determines its course, 
almost irrespective of treatment. 
SIMPLE SENILE PARAPLEGIA. 
Tliis name seems the most unobjectionable for a condition, somewhat 
rare, which appeal’s hitherto to have been unrecognised.* It is con- 
fined to late life, occurring in those over 40, and especially over 50. Its 
characteristic is simple weakness of the legs, with some slowness of 
movement, but without wasting, sensory disturbance, or reflex altera- 
tion. The knee-jerk is normal, and there is no foot-clonus. The 
malady develops very gradually and is slowly progressive, although it 
seems seldom to attain such a degree as to prevent standing. The con- 
dition of the legs resembles that in cases of paralysis agitans without 
tremor, in which the malady is manifested only by weakness, and stiff 
slowness of movement of the limbs, face, and trunk. Cases are met 
with in which the condition of the legs above described is associated 
with slight symptoms in the arms and face, such as characterise these 
cases of paralysis agitans. This senile paraplegia is probably a partial 
development of the morbid process of that disease; instead of being 
general, it is limited to the structures for the legs. If, as the condition 
Beems to suggest, paralysis agitans depends on peculiar changes in the 
* A note upon it by myself appeared in tbe * Centralbl. f. Nerveukr.,’ 1890. nutrition and function of the motor cells of the cortex cerebri (which 
impair the power and alter the action of the cells, but do not usually 
go on to such destructive alteration as entails secondary degeneration 
of the pyramidal fibres), we can readily conceive that such a process 
may be sometimes limited to the leg-centres, and may cause the 
symptoms. If so, the malady is a cerebral and not a spinal one, but 
it is mentioned here on account of its paraplegic features, and their 
resemblance to those of disease of the spinal cord. Degenerative 
changes may, however, be various in kind and degree, especially in 
late life; cases occur, similar to these, but with myotatic excess con- 
necting them with the destructive changes of lateral sclerosis, while 
others present such symptoms as nystagmus or impeded articulation— 
evidence that the altered nutrition is Avider in its range. 
CHRONIC. MUSCULAR ATROPHY. 
471 
CHRONIC SPINAL MUSCULAR ATROPHY 
(PROGRESSIVE MUSCULAR ATROPHY; WASTING PALSY; AMYOTROPHIC 
LATERAL SCLEROSIS ; CHRONIC POLIO-MYELITIS). 
The disease which has long been known by the names “progressive 
muscular atrophy” and “wasting palsy” is characterised by slow 
wasting of the muscles, beginning in some one part, and usually 
spreading aud increasing until it is wide in extent and extreme in 
degree. The changes in the muscles depend on changes in the spinal 
cord, a slow degeneration of the ganglion-cells of the anterior cornua, 
accompanied by a similar degeneration in the motor nerve-fibres which 
spring from the cells. With this degeneration of the cells and peri- 
pheral fibres there is usually also associated a degeneration of the 
pyramidal tracts in the cord, sometimes, at least, to be traced up to the 
motor cortex of the brain. 
Chronic muscular atrophy was separated from primary paralysis by 
Sir Charles Bell, and was afterwards described more fully by Aran and 
Cruveilbier. Bell and Cruveilhier regarded it as a spinal disease. 
Aran (who first called it “progressive muscular atrophy”) thought 
that it was primarily a disease of the muscles, a view that was after- 
wards held by Duchenne, and subsequently also bv Friedreich. This 
opinion was supplemented by a theory that the wasting was due to a 
disturbance of the sympathetic. Lockhart Clarke first discovered the 
disease of the grey substance of the spinal cord, and Charcot specially 
associated the atrophy with the wasting of the ganglion-cells. When 
the constancy of the spinal lesion was demonstrated, it was thought 
that every form of chronic muscular atrophy was of spinal origin ; but 
this view has proved erroneous, and it has been shown that there are 
forms of muscular atrophy which are purely local and idiopathic. The 
morbid process is not confined to the spinal cord. Atrophy of the 
nerve-cells from which the motor bulbar nerves arise often accompanies 472 
SPINAL COED. 
that of the spinal cells, and “ progressive bulbar paralvsis ” is Iht u 
associated with “progressive muscular atrophy:” it often comes on 
after the disease has existed for some time, and ends life ; occasionally 
it initiates the malady. 
Two varieties of the disease have been distinguished by Charcot, 
who has been followed in this by most subsequent writers. In the 
one variety the disease is manifested only by the wasting of the mus- 
cles; in the other there are, in parts otter than those much atrophied, 
the indications of degeneration of the pyramidal tracts of the cord. 
En the latter cases, Charcot regarded the degeneration of the pyramidal 
tracts as the primary lesion, and the affection of the cornua as secon- 
dary. He therefore termed the cases of the first class “ protopathic,” 
and those of the second class “ deuteropathic,” and gave to the latter 
the name “amyotrophic lateral sclerosis.” In Germany, however, and 
especially by Leyden, doubts have been expressed as to the validity of 
the distinction between the two classes of cases, and as to the sequence 
of the lesions in the second class. These doubts are not without foun- 
dation. The subject will be discussed when the pathology of the 
disease is considered, and reasons will then be given for the course 
here adopted of considering the two varieties together as essentially 
one disease. 
But cases are also met with (although not frequently) that present 
every gradation to subacute polio-myelitis in one direction, and perbaps 
also to polyneuritis in another. Attempts are being made to classify 
these, but types may be multiplied indefinitely from the intermediate 
forms, and many more pathological and clinical observations are neces- 
sary before a useful classification of the cases can be made. In the 
following description the common forms are chiefly considered. 
Causes.—The disease is more frequent in males than in females, the 
proportion being about three to one. It is cbieflv a disease of adult 
life, commencing usually between twenty-five and forty-five. I have 
known it to begin at fourteen and as late as seventy, and a case is 
recorded in which it began at twelve ;* there was wasting and rigidity in 
the limbs, tongue, lips, and lower face. But most cases of muscular 
atrophy in early life are idiopathic, and not spinal. Heredity is to be 
traced only in less than half the cases, and generally as an indirect 
neuropathic disposition. Rarely there is direct inheritance of the 
disease. Among instances that I have met with are a lady whose 
mother died from a similar atrophy, and another case (from which 
Fig. 135 is taken) in which a brother had died from some chronic disease 
of the cord, attended with wasting; but three cases with bulbar symp- 
toms have been recorded, two of whom were cousins, the children of two 
sisters : the third, who had had syphilis, was a cousin, but his affection 
was untypical.f Direct inheritance seems to be most common in cases 
that occur late in life. When many members of a family suffer from 
* H. Blumenthal, “Inaugr. Digs.,” ‘Neur. Ceut.,’ 1831, p. 376. 
+ ‘ Virchow’s Arcliiv,’ 1889, p. 115. CHRONIC) MUSCULAR ATROPHY. 
473 
muscular atrophy, the malady is nearly always idiopathic and not 
spinal. The affection occurs in all clashes of society, and it is doubt- 
ful whether workers with the muscles furnish a larger proportion of 
the eases than can bo accounted for by their greater exposure to certain 
exciting causes. 
Of these more direct causes one of the most frequent is mental distress 
and anxiety, and this is especially met with in females and in late life. 
A severe fright has been thought to excite it. Anolher cause is ex- 
posure to wet cold, which is also a cause of many other chronic spinal 
diseases. Sometimes the exposure has been habitual; sometimes a 
single exposure has been effective, and some neuralgic pains, indicative 
of the deleterious influence on the nervous system, have followed 
the exposure and connected it with the later wasting. The pain 
has been either in the part afterwards wasted, or in some other, 
more common, seat of neuralgia. Thus one patient, after remaining 
in wet clothes for twelve hours, suffered for six weeks from severe 
neuralgia in the left side of the face, and then the muscles of the left 
shoulder began to waste. Although excessive use of individual 
muscles may cause them to waste, it is doubtful whether this influence 
produces general muscular atrophy. Injury to the cord, such as results 
from concussion of the spine, is a rare cause. It more often produces 
disseminated myelitis, which may be manifested by muscular wasting 
combined with other symptoms.* In a few instances I have known 
progressive atrophy, of typical characters, to slowly follow a concussion, 
as if this had set up a perversion of the nutrition of the nerve-elements. 
Still more rarely a fall, injuring one limb, has been followed by 
muscular atrophy commencing in this limb and becoming general. 
Thus a woman fell downstairs, and pitched on her kft hand and 
wrist; she had pain in the arm for a long time; two years after 
the fall this arm began to waste, and the atrophy ultimately became 
general. The relation might be passed as an accidental coincidence, 
were it not that in other central diseases—even, for instance, in para- 
lysis agitans—the symptoms may commence in an injured limb. In 
rare cases, the disease develops, during adult life, in a subject of old 
infantile palsy (polio-myelitis), and may start from the most affected 
part (see p. 364). 
The disease sometimes succeeds syphilis, and no other cause may 
be traceable. As with other degenerative diseases, an interval of 
years elapses between the primary disease and its nervous sequel. 
The cases that I have seen after syphilis have been typical in course, 
and evidently degenerative in nature. That syphilis has some share 
in the causation of these cases is probable from its relation to other 
diseases, such as tabes; but it is noteworthy that in one case the 
wasting commenced during, and in another directly after, an energetic 
* In one unusual case the wasting (ultimately general) began in the de’t ids a 
month after a fall, which probably fractured the base of the skull (Manor, ‘Alienist 
and Neurologist,’ 1886, p. 430). 474 
SPINAL CORD. 
mercurial course. This relation is intellig'ble if the disease is due to 
a product of the syphilitic virus, and not to the organisms themselves 
(see Tabes). Occasionally syphilis and a neurotic heredity can both 
be traced. In the cases in which atrophy has followed an acute 
specific disease, especially measles, and has begun in early life, it is 
probable that the malady is a chronic neuritis and not the central 
affection now under consideration. Such cases are known as of the 
“ Peroneal type,” from the muscles in which wasting is first obtrusive, 
and are separately described at a later page. General muscular 
atrophy may result from lead poisoning, but this form is not, as a. 
rule, progressive in character when its cause has ceased to act. It 
resembles the ordinary form of progressive muscular atrophy, however, 
in seat and features, and thus differs from the common atrophic palsy 
of the extensors that is produced by lead. In many cases of progres- 
sive muscular atrophy no cause for the disease can be traced. When 
obtrusive symptoms have followed some adequate cause, it is not 
uncommon for this to have been preceded by slight symptoms, which 
show that the malady already existed. A careful inquiry for such 
symptoms should never be neglected. 
Symptoms.—The definite symptoms of the disease are often preceded 
by aching pain in the part afterwards wasted, rarely severe. Sometimes 
there is such pain in the spine or elsewhere, especially, as already 
stated, in the cases that are due to exposure to cold. Rarely some 
sensation other than pain precedes the local symptoms. Thus in one 
case a sense of coldness preceded the atrophy in each limb that was 
attacked. Weakness and wasting usually come on together, but 
either may first attract the attention of the patient. In the shoulder 
and back, the loss of power is usually first noticed, and in such 
covered parts the wasting may become considerable before it is 
observed. In the hand the wasting is often first noticed, but some- 
times it is the impairment of some delicate action, such as writing, 
that draws attention to the part. The affected muscles lose their 
proper shape, and there is flattening, or even a depression, where there 
should be a prominence. If a patient is fat, however, the wasting may 
cause at first very slight alteration in the external aspect. 
The disease commences in the arm in nine tenths of the cases, and 
as frequently in one arm as in the other. It begins with almost equal 
frequency in the hand and in the shoulder muscles. From the part 
first affected the disease spreads to other parts of the same limb. 
Before it has attained a considerable degree in one limb, it usually 
shows itself in the corresponding limb on the other side; often in 
the muscles corresponding to those in which it commenced, sometimes 
in those affected second in order of time. As the muscles waste, 
paralysis results of various character and degree, corresponding to the 
atrophy. In the hand, the thenar muscles and interossei are usually 
the first to suffer. The thenar eminence becomes flattened, and the base 
of the first metacarpal bone becomes prominent. Of the interossei. CHRONIC MUSCULAR ATROPHY. 
475 
the atrophy of the abductor iudicis is especially conspicuous; the 
normal prominence gives place to a bollow beside the metacarpal bone 
when the thumb is abducted. Depressions 
form between the metacarpal bones on the 
back of the hand, and. also between the 
flexor tendons in the palm in consequence 
of the wasting of the lumbricales. The 
forearm muscles may be next involved, the 
flexors usually before the extensors; and with 
the flexors the supinators may suffer, or they 
may escape until the biceps is involved. 
Occasionally the disease begins in the fore- 
arm, and then especially in the extensor 
FlO. 134. — Progressive 
muscular atrophy. 
Wasting of the mus- 
cles of the back and 
arms; in the forearm 
scarcely any muscular 
tissue can be recog- 
nised, and in the hand 
all the muscular pro- 
minences have van- 
ished. (Drawn by Dr. 
H. It. Spencer.) 
Fio.135—Progressive muscular atrophy. 
Waiting of right trapezius complete 
(the rhomboids remaining), of the left 
trapezius partial. On each side the 
tipper part of the trapezius is wasted, 
and the contour of the neck is ror- 
respom ingly changed. Both deltoids 
are also atrophied. (Drawn by Dr. 
Spencer.) 
muscles of the fingers, sometimes in those of the thumb, especially of 
its phalanges. The several parts of the long finger muscles may suffer 
unequally; the ulnar extensors usually suffer most. Of the shoulder 
muscles, the deltoid is generally the first to manifest the disease, and 
in some cases which begin in the hand the deltoid suffers before the 
forearm muscles. The rounded contour of the shoulder becomes 
changed (Figs. 7, 134, 135), and the head of the humerus can be 
recognised beneath the acromion. It is not rare for part of the del- 476 
SPINAL COItD. 
toid to suffer and part escape: we have seen (p. 30) that the several 
portions have different functions and associations, and this probably 
involves a relation to separate groups of nerve-cells. The wasting of 
the deltoid is soon followed by that of the other muscles of the upper 
arm and of the scapula. The triceps usually suffers less and later 
than the biceps, but sometimes the reverse is the case. The supi*a- 
and iufra-spinati are often affected with the deltoid. In exceptional 
instances the deltoid or hand muscles escape, and there are cases 
(perhaps a special group) in which the upper arm and shoulder 
muscles waste even to an extreme degree, and the forearm and hand 
muscles escape entirely. 
In most cases, the wasting early involves the muscles of the back, 
and it sometimes begins in them. The middle and lower parts of the 
trapezius usually suffer first; the rhomboids and erectors of the spine 
at a later date. The affection of the trapezius is readily recognised 
if the patient tries to put the shoulder back (Fig. 135). The highest 
part of the trapezius presents a remarkable indisposition to atrophy ; 
it often remains intact to the last, and then may contrast with the 
wasting below it, standing out on each side, like a cord passing from 
the occiput to the shoulder. Hence Duchenne termed this part 
the ultimum moriens. I have, however, seen several otherwise typical 
cases (beginning either in the deltoids or in the hands) in which the 
highest parts of the trapezii suffered before the middle parts. The 
levator anguli scapulae also generally escapes, even when all the mus- 
cles about it are wasted. The serratus, latissimus, and pectoralis 
major are usually affected later. They may escape wholly or in part; 
isolated bundles of the 
pectoralis may waste, the 
intervening parts escap- 
ing, or either the upper 
or lower part of the 
muscle may atrophy 
alone. According to the 
affection of the muscles 
that are attached to the 
scapula, the position of 
the bone changes, and it 
becomes rota ed under 
the influence of the 
muscles that are unaf- 
fected and unopposed 
(Fig. 7, p. 28). The 
muscles that extend the head on the spine often suffer in con- 
siderable degree, and from this there results a difficulty in the 
carriage of the head (Fig. 136). It is habitually inclined back- 
wards, so as to balance it cn the spine with but little muscular 
exertion; if moved forwards, it falls so that the chin touches the 
FlG. 136.—Progressive muscular atrophy. Weak- 
ness of the muscles of the neck. A, habitual 
p-istnre of the head inc’ined backwards. B, posi- 
tion into which it tails if the patient attempts to 
keep it iu the normal balance. (Drawn by Dr. 
Spencer.) CriRONIO MUSCULAR ATROPHY. 
477 
chest. It can be brought back into its former position only with diffi- 
culty ; the patient has to incline the trunk backwards, so as to bring 
the head nearly into the vertical position, and then, with a sudden 
contraction of the sterno-mastoids, and a jerk, the head goes back into 
its former posture. The increased innervation of the weak extensors 
of the head often causes a synergic over-action of the frontalis muscles, 
which are normally associated with the extensors (so that the eye- 
brows are raised when the head is put back to look upwards). The 
skin at the back of the neck lies in transverse folds when the neck is 
extended. The patient may be unable, when lying in bed, to move the 
head from side to side. The sterno-mastoids also are often wasted 
either the sternal or clavicular part may be most affected. In striking 
contrast to the general wasting of the neck is the condition of the 
platysma myoides, which always escapes, and may become hypertro- 
phied in a vain attempt at compensation. 
The muscles of respiration suffer in the majority of cases, and their 
impairment constitutes a grave source of danger to life. The inter- 
costals rarely escape altogether ; the diaphragm is involved in many 
cases, and respiration is then carried on by the intercostals and 
superior thoracic muscles. On the other hand, the intercostals may 
suffer much and the diaphragm remain free; respiration is then 
purely abdominal, and the walls of the thorax may be almost motionless 
in breathing, or there may be merely a slight movement of elevation of 
the upper ribs. The chest becomes flattened in front, and narrow from 
before back, from the influence of atmospheric pressure on the ribs, 
unopposed by the intercostals. Either the upper or lower intercostals 
may suffer most. When the diaphragm is paralysed, the upper chest 
muscles often suffer more than the lower, and a compensatory increased 
movement of the lower ribs carries forward the abdominal wall, and 
may suggest that the diaphragm is acting when it is not. A careful 
examination will always prevent the error. The muscles of the abdo- 
minal wall occasionally waste, but far less frequently than those of 
the thorax. 
Wasting in the legs is much less common than in the arms, and if 
it occurs is usually slighter in degree ; but occasionally ilie disease first 
manifests itself in the legs, and is more intense in them than elsewhere. 
The glutei, extensors of the knee, and the muscles in the front and 
on the outer side of the lower leg, are those that are most affected. 
We shall presently see, however, that the legs are often paralysed 
when they are not wasted, and sometimes they are the seat of wasting 
which differs in certain features from that which is the special 
characteristic of the disease. 
The face almost always escapes the general atrophy, and its normal 
appearance may present a striking contrast to the rest of the body. 
In many cases, however, the lips are paralysed as part of the bulbar 
palsy that so often accompanies the spinal disease. A remarkable 
case in which the face shared the atrophy of the limbs, and the tongue 478 
SPINAL COLD. 
escaped, Las been recorded by Langer ■* on the other hand, the tongue 
has been the first part to suffer, the arms being affected a month 
later.f 
As the wasting progresses, the appearance of the parts in which it 
is most advanced becomes extremely changed. All trace of muscle 
may disappear from parts of limbs or even from an entire limb 
(Fig. 134); and there is usunlly a wasting of the adipose tissue as well 
as of the muscle, so that the bone seems to be covered only by fascia 
and skin. The transverse processes of the vertebrae may be felt in 
the hollow beside the spine, and the bony prominences about the 
shoulder may be almost as conspicuous as in a skeleton, so that 
beneath the acromion there may be a groove, into which the finger 
can be placed, in consequence of the descent of the head of the humerus 
from the glenoid cavity. The unequal affection of antagonistic 
muscles leads to various contractions and deformities. In the hand, 
especially, distortion is apt to occur ; from preponderant paralysis of 
the interossei and contraction of the long flexor and extensor muscles, 
the “claw-like hand” develops in extreme degree (Figs. 19 and 20, 
p. 36). If all the muscles of a part are equally and simultaneously 
affected, no deformity results unless an unsupported part yields to 
the influence of gravitation (Fig. 134). Lordosis is very common 
in cases in which the trunk and hip muscles are involved. It is often 
the indirect result of the weakness of the extensors of the hip-joint, 
in consequence of which the pelvis is unduly inclined forwards, and 
carries with it the lower lumbar vertebrae ; the upper part of the trunk 
has then to be inclined backwards, to bring the centre of gravity over 
the base of support; it disappears when the patient sits, and the pelvis, 
resting on the ischial tuberosities, is no longer inclined. This was 
the case, for example, in a woman with extreme lordosis from 
progressive muscular atrophy, in whom, when standing, a plumb-line 
from the seventh cervical spine fell three inches from the sacrum and 
an inch and a half from the buttock. Sitting, her spine was perfectly 
straight. 
The electrical irritability of the wasted muscles presents changes 
which vary in character in different cases. When the wasting is 
slow, there is usually a diminution in both faradic and voltaic irri- 
tability, similar in character to each current. The irritability fails 
with the muscular nutrition, and when the wasting is great only a 
slight contraction can be obtained, even with a strong current. 
When the wasting is extreme, irritability at last becomes extinct, 
but the voltaic irritability of the muscular fibres persists long after 
the faradic irritability has disappeared. It may be normal in degree, 
or lowered, but is seldom increased in such cases. The quality 
of the voltaic m-itability may also be normal, but sometimes ACC 
(anodal closure contraction) occurs as readily, or more readily than 
* Vienna Medical Soriety, March 17th, 1882. 
f Birdsall, ‘ Journal of Nerv. and Ment. Dis.,* 1887, xiv, p. 250. CHRONIC MUSCULAR ATROPHY. 
479 
KCC. Tetanic contraction during the passage of the current is pro- 
duced with undue readiness compared with the closure contractions, 
and opening contractions are often caused by currents but little 
stronger than those that cause closure contractions. Thus there may 
be the qualitative change of the reaction of degeneration without the 
voltaic increase (see p. 56). When there is the rapid and considerable 
paralysis described on p. 483, either at the onset or during the course 
of the disease, the palsy being followed by rapid wasting, there may 
be quick extinction of faradic with actual exaltation of voltaic irrita- 
bility, and the reaction of degeneration may be present in all its 
characteristics. Between these forms every intermediate condition 
may be met with, including the mixed reaction described on p. 26. 
The mechanical irritability of the muscles is considerably increased; 
a tap causes a local contraction of the fibres struck. Moreover, 
spontaneous flickering contractions of parts of the muscles are very 
common, now of one bundle, now of another, conspicuous to the eye, 
although scarcely felt by the patient. This “ fibrillation,” as it is 
termed, is so frequent as to be characteristic, but it is not invariable, 
nor is it confined to this disease. It may sometimes be observed in 
muscles that are not yet invaded by the wasting, but where it is 
observed atrophy usually follows. 
In the parts affected by the characteristic wasting, all reflex action is 
abolished, clearly in consequence of the damage to the motor part of 
the reflex arc ; the afferent portion of the arc is unaffected, for, as we 
shall see, there is no loss of sensation. The myotatic irritability 
(“ tendon-reflex action ”) is also lost, and lost early. The knee-jerk, 
for instance, disappears as soon as there is even a slight diminution in 
the bulk of the thigh muscles, in cases in which the legs are the seat 
of primary wasting. The muscles are flaccid and toneless—a condition 
that may be conveniently termed “ atonic atrophy.” To this common 
rule, however, exceptions are sometimes met with; there may be from 
the first rigidity of the affected muscles. Wheu this is the case, the 
wasting does not go on to the entire destruction of the muscle ; it is 
often trifling, but may be considerable. With this rigidity there is a 
preservation of myotatic irritability. We may term this, “ tonic 
atrophy.” It is generally associated with spastic paralysis, without 
wasting, in some other part. For instance, in one case the forearms 
and hands were the seat of this tonic atrophy, and in the legs there 
was simple spastic paraplegia. We shall presently consider the 
pathology of this condition.* 
Sensory symptoms are usually slight and always subordinate. They 
* Ifc should be noted, however, that, in the muscles that are the seat of toneless 
wasting, when the atrophy has attained an extreme degree, slight rigidity may 
develop, accompanied by considerable tenderness of the muscle. It is probable that 
this rigidity is idiopathic, and due to the structural changes in the muscles presently 
to be described. This condition, which should be distinguished from the initial 
rigidity, is rare: the early relaxation is usually maintained to the last. 480 
SriNAL CORD. 
are confined to pain, usually dull and rheumatoid in character, felt 
chi. fly in the limbs in which the malady is most active. Such pains 
are common at the onset, as we have already seen, and they may recur 
from time to time during the course of the disease. Sometimes vague 
feelings of “numbness” or “deadness” are complained of, but cuta- 
neous sensibility is never impaired. (When anaesthesia accompanies 
muscular wasting, both symptoms are due eitherto chronic meningitis, 
damaging the nerve-roots, or to disseminated focal myelitis or multiple 
neuritis ) Nor do the muscles lose such sensibility as they normally 
possess. Perception of posture persists, and the muscles are not only 
sensitive to pressure, but are often more sensitive than in health both 
to pressure and to extension. 
When the arms are the seat of such atrophy as has been described, 
the legs, if not also wasted, may be normal, or they may be slightly 
affected, the thighs thin, and the knee-jerks lost. Often they are the 
seat of gradual loss of power without wasting, and with an increase of 
myotatic irritability. The knee-jerk is excessive ; a clonus can readily 
be obtained, and the reflex over-action of the muscles may increase to 
actual rigidity and spasm, so that there is the condition of spastic 
paraplegia described in a preceding chapter. It is rare, however, for 
the spasm to reach the higher degree of intensity, and for the muscles 
to present the massive firmness that characterises the simple form of 
spastic paraplegia. On the other hand, there is often some diminution 
in the size of the muscles, and thus we have a gradation to the condi- 
tion of tonic atrophy just described. In this condition, moreover, there 
is usually only a moderate diminution in electrical excitability, which 
does not go on to extinction. The one condition does not seem to pass 
into the other; the state of ligidity and myotatic excess does not give 
place to muscular relaxation ; atonic atrophy does not succeed the 
tonic wasting. In very rare cases, of which I have seen a few instances, 
there is a similar condition in the hands when the shoulders are the 
seat of simple atonic atrophy. The forearms are then rigid, moderately 
wasted, with myotatic excess, while the muscles of the shoulders are 
extremely wasted and absolutely flaccid. In still more rare cases the 
whole arms are thus affected, are thin and rigid, and in no part is 
there atonic atrophy. In one remarkable case of this character, the 
muscles of the trunk participated in the spasm ; after coughing or 
yawning, respiration would be checked for a few seconds by general 
spasm, and whenever the patient was raised from the bed, the arms, 
legs, back, and neck became stiff in tetanoid rigidity, the head being 
bent backwards. 
The combinations of the ordinary atonic wasting and loss of power, 
without wasting and with increased myotatic irritability, are exceed- 
ingly numerous and variable. The most frequent, as already stated, 
is flaccid atrophy in the arms and spastic paralysis in the legs ; but I 
have twice seen atonic atrophy below the knees, with weak but 
well-nourished thigh muscles and much increased knee-jerk. The CHRONIC MUSCULAR ATROPHY. 
481 
variable combination of these conditions gives rise to differences that 
are more apparent than real, and may easily be allowed undue weight 
in classification. 
The extreme emaciation of the most affected parts shows that the 
adipose tissue wastes as well as the muscles. The atrophied limbs are 
usually cold, and may be livid or pale, but there is no tendency to acute 
vaso-motor disturbance in the ordinary form of the disease. I have 
known the skin of the face to become thin and smooth, so that, in one 
instance, the dark iris could be seen through the closed eyelids, but 
such a change is quite exceptional. In another patient there was a 
very remarkable form of local atrophy. Certain areas of muscles 
underwent wasting, the rest being normal; the affection commenced 
by a livid discoloration of the skin, and the wasting seemed to involve 
the skin, subcutaneous tissue, and muscle, causing local depressions. 
Considerable tracts of the trapezii were thus affected, and smaller 
spots in the arms and legs. The patient was a single woman of 
thirty-five, and the disease, which did not show a strongly pro- 
gressive tendency, is probably a special affection, perhaps of local 
nature. 
The functions of the sympathetic are not, as a rule, deranged. Dila- 
tation or contraction of one pupil has been frequently observed, chiefly 
in association with atrophy of the muscles that are supplied from the 
lower part of the cervical region; and it no doubt depends on the dis- 
ease of the spinal cord, and not of the sympathetic itself. The reflex 
action of the iris is usually normal, and optic nerve atrophy never 
occurs.* Nystagmus is present in rare cases. 
The visceral functions are usually little disturbed. Sexual power is 
often lost. The sphincters rarely suffer, even when the wasting is 
general and extreme; occasionally they are involved, and they may 
even suffer early. In other cases, in which the legs become weak after 
the wasting sets in in the arms, the affection of the sphincters may 
coincide with that of the legs. In the composition of the urine, slight 
changes have been found, but not constantly. Urea has been increased 
in some cases, lessened in others.f The quantity of lime has been 
* I have once met with a remarkable reflex fixation of the eyeballs in a case of 
advanced progressive muscular atrophy. If the patient, looking to one side, was 
suddenly told to look at an object on the other side, his head was instantly turned 
towards the second object, while the eyes remained fixed on the first, by a movement 
corresponding to that of the head but in the opposite direction, and then, after a 
few seconds, they were slowly moved towards the second object. The phenomenon 
continued to the end of the patient’s life. As I pointed out in an account of this 
curious condition (‘ Brain,’ vol. i), it is interesting evidence of a normal reflex 
mechanism in the fixation of the eyes; this was, as it were, isolated by disease, 
which lessened voluntary' control over it. 
f In a patient who weighed 7 st. 13 lbs., and whose urine varied between 760 and. 
960 cubic centimetres, I found the daily excretion of urea to vary between 107 and 
15 grammes, the average being 13 grammes. This is just half the normal average 
for a man of that weight, which would be (according to Parkes), 24 grammes. 
VOL. I. 482 
SPINAL CORD. 
found to be increased (Fromman), that of kreatin diminished, even to 
one tenth of the normal (Rosenthal, Langer). Glycosuria has been 
observed in association with bulbar symptoms.* The lungs may 
suffer from the impairment of breathing power, when the intercostals 
and diaphragm are weakened. 
Varieties.—The chief varieties of the disease depend on the relative 
distribution of the three conditions: (1) atonic atrophy, becoming 
extreme; (2) muscular weakness with spasm, but without wasting, or 
with only slight wasting; and (3) tonic atrophy, rarely extreme in 
degree, with myotatic excess. The commonest condition is to have 
atonic atrophy in the arms and upper part of the trunk, with simple 
weakness and spasm in the legs. Atonic atrophy in both arms and 
legs is less common, and the least common is tonic atrophy alone, in 
the arms, or universal. The last is, indeed, extremely rare. It is 
important to note, however, that these conditions may coexist in every 
degree and combination ; between universal atonic atrophy on the one 
hand, and universal spastic paralysis without wasting on the other, 
there is every gradation. The latter does not come into the category 
now under consideration, but similar cases are met within which there 
is atrophy of a few muscles (as, for instance, of the hands only), which 
complete the series. The varieties due to the different combinations 
of atrophy and paralysis have been already alluded to. 
A peculiar form of muscular atrophy has been mentioned, first 
conspicuous in the peroneal regions and spreading thence to other 
muscles of the leg and to the hands. It is characterised by occurrence 
in early life, and often in several members of the same family, and 
has been termed the “ peroneal type ” by Dr. H. Tooth. It is pro- 
bably not dependent on the spinal cord, and is considered more fully at 
a subsequent page. 
Complications.—Progressive muscular atrophy is occasionally accom- 
panied by the symptoms of some other degenerative disease of the 
spinal cord. The paralysis with spasm, already described, can 
scarcely be regarded as a complication; it is rather part of the disease, 
and its relation to the other symptoms will be considered when we 
discuss the pathology of the affection. In rare cases, muscular atrophy 
in the arms is accompanied by the symptoms of locomotor ataxy in 
the legs. By far the most frequent complication is bulbar paralysis, 
weakness of the lips, tongue, pharynx, and often of the laryngeal 
muscles. It is the expression of a degenerative process in the medulla, 
similar to that which, in the spinal cord, causes the affection of the 
limbs. It may come on at any stage of the disease, may precede the 
spinal symptoms, or only come on when these have attained a con- 
siderable degree. In characters, the bulbar palsy may resemble 
perfectly that which occurs in isolated form, and will be described 
among the diseases of the brain. Frequently, however, there is but 
little paralysis of the tongue, even when swallowing and articulation 
* Rovighi and Melotti, ‘Riv. Sper./ 1888, p. 315. CHRONIC MUSCULAR ATROPHY. 
483 
are much impaired. There may also be slight interference with 
articulation when there is no marked bulbar palsy. A minor compli- 
cation is the neuralgic pain, wliich, as already stated, is sometimes 
troublesome in the early stage of cases that are due to cold. In several 
patients I have known headache to be frequent and severe throughout 
the course of the disease. General paralysis of the insane has been 
met with as an exceptional complication.* 
Course.—The malady, in most cases, is steadily progressive, as its 
name implies, but in the rate of its progress it varies in different cases, 
and in the same case at different periods. It may, moreover, become 
stationary (sometimes as the result of treatment) at any period in its 
course, and when once actually arrested, it does not usually again 
become active. Unfortunately, the tendency to cessation is greatest 
in the later stages of the disease, when there is little except life to be 
preserved. Sometimes progress ceases at an earlier stage, and chiefly, 
I think, in those cases in which the atrophy is strictly symmetrical, 
and develops simultaneously, or almost simultaneously, on the two 
sides. Thus I have met with several cases in which there was 
symmetrical wasting in the two bauds, or in certain muscles of the two 
forearms or of the two upper arms, and in which the atrophy, after 
attaining a considerable degree in its limited seat, had become 
stationary and continued so. Occasionally some symptom (as weak- 
ness of the sphincters) may pass away, although the atrophy pro- 
gresses. 
When the progress at the commencement is rapid, it usually 
continues rapid, until the disease has attained a wide extent, although 
the acute local onset mentioned below may be followed by slow 
extension. When it begins slowly, it is usually slow throughout. 
Although the disease sometimes commences in the second arm very 
soon after its onset, it more commonly makes some progress in its 
primary seat before beginning on the second side, and the interval that 
elapses varies with the rate of extension. It often happens that a 
year intervenes between the affection of the two arms, and I have 
known, in a very chronic case, the atrophy to slowly progress in one 
arm for seven years before it showed itself in the other. It is not 
common for the arms to be reduced to practical helplessness in less 
than two or three years, but the hands may become useless in as short a 
time as six months, while in one case the wasting, commencing at the 
shoulder, had invaded the whole arm in the course of a month. The 
shortest time in which I have known a patient to reach the last stage 
of the disease is nine months. 
With any rate of general progiess, the otherwise uniform course of 
the disease may be broken by the occurrence of almost sudden palsy 
in a certain group of muscles. Considerable loss of power, it may be 
absolute paralysis, comes on in a few days, or even in a few hours. It 
may occur at the onset of the affection. The extensors of the wrist 
* Tainbroni, * Riv. Sper. de Fren., &c.,’ 1887, xiii, p. 184. 484 
SI'INAL CORD. 
and fingers are the muscles most commonly thus affected. The weak- 
ness is usually followed by a well-marked degenerative reaction in the 
muscles. I have seen several cases which began by such subacute 
or even acute paralysis of the extensor muscles, first in one arm and 
soon afterwards in the other ; the initial condition closely resembled 
the paralysis from lead-poisoning, even to the escape of the supinator 
longus and ext. ossis met. pol. This cause was, however, excluded, 
and soon the muscles of the shoulder and back presented commencing 
slow progressive atrophy, followed by wasting of the interossei until 
a typical state was reached. In another case, the quick loss of power 
was confined to the extensors in one arm, which were already weak 
and slightly wasted, most of the other muscles of the upper limbs 
having been long atrophied. When there is weakness of the legs, 
without wasting, the onset of this may coincide with the atrophy of 
the arms, or may succeed it at any interval. In one case five years 
elapsed, after the arms began to waste, before the legs became weak.. 
It is very rare for the paraplegic weakness to occur first. 
The chief danger* to life is from pulmonary maladies, rendered 
grave from the weakness of the muscles of respiration. The common 
complication of bulbar paralysis is another frequent cause of death, 
either by the interference with swallowing and nutrition, or by the 
laryngeal paralysis. Less commonly, death results from bedsores and 
septicaemia, or from intercurrent maladies. 
Pathological Anatomy.—The wasting of the muscles is as evident 
after death as during life. They are reduced in size and pale in 
colour. Sometimes there is little in the tint of what remains to 
suggest muscular tissue. Parts of a muscle may be hardly dis- 
tinguishable from adjacent fat. On the other hand, the bulk of the 
muscle may be dark, and pale streaks in it may mark the position of 
local degeneration. Under the microscope, the fibres present various 
changes, and of these four are well defined. (1) There may be simple 
narrowing of the fibres, without any considerable change in their 
striation (Fig. 137), although the striae often seem to be further apart 
than normal, and sometimes the fibrillary segmentation is unusually 
distinct. (2) Simple fatty degeneration, in which the transverse 
striation gives place to a granular appearance (Fig. 138), the granules 
becoming larger and fewer (Fig. 137) until ultimately distinct globules 
are scattered through the sheath. Where the muscle resembles fatty 
tissue to the naked eye, the microscope may show only sarcolemma 
sheaths containing groups of globules. (3) Muscular fibres are seen 
in which the sheath contains only a clear material enclosing a few 
fatty globules, and a few transverse strise, faint, as if fading away. It 
is probable that this is not the result of fatty degeneration, but of a 
different process, which has been termed “ vitreous degeneration,”—a 
sort of dissolution of the striae, indicated by the appearance of such 
fibres as are shown in Figs. 137, 139, 140. (4) A longitudinal 
striation develops in the fibre, and at first coexists with the traus- CHEONIO MUSCULAE ATEOPHY. 
485 
verse striation ; but ultimately the latter becomes indistinct, and the 
fibre looks like a fasciculus of longitudinal connective-tissue fibres 
{Fig. 140). Sometimes, with the longitudinal striation, the fibre 
presents a transverse striatiou very much finer than normal, the stria3 
being narrower and nearer together, as if from a division of the 
sarcous elements.” This change may sometimes be seen alone, and 
Fig. 137. 
Fig. 138. 
Fig. 139. 
Fig. 140. 
Fig. 137.—Narrowed fibres with nearly normal striation; others clear, containing 
a few fat globules, and a few faint transverse striae, and some longitudinal striation: 
large globules of fat lie in the interstitial tissue in front of one narrowed fibre. 
Fig.138.—Granular degeneration: a fibre with normal transverse striation presents 
also indications of longitudinal striation. Increase of nuclei of interstitial ti-sue. 
Fig. 139.—Two normal fibres and one presenting the clear homogeneous aspect, 
with a few fat globules and some faint striation. 
Fig. 140.—Several fibres similar to that of the last figure, with globules of fat 
between them. On the right is a fibre which has undergone complete longitudinal 
striation, the normal striae having disappeared, so that it resembles the adjacent 
interstitial fibrous tissue. Other fibres in the same muscle were in intermediate stages 
of degeneration, some transverse striation coexisting with the longitudinal striation. 
Fibres of Wasted Muscles in Progressive Muscular Atrophy. 
may be present in only one part of a fasciculus. Thus at one place 
the number of striae in ToVo' iu°h was only seven, while in another 
region of the same fasciculus seventeen were to be counted in the same 
space. A tendency to transverse Assuring has also been described, 
but this is probably artificial. Fatty globules accumulate between the 
fibres (Fig. 140), accompanied in some cases with granules and masses 486 
SPINAL COED. 
of reddish-brown pigment. There is often also an increase of the 
nuclei (Fig. 138), and sometimes of the fibres of the interstitial tissue. 
Two or three rows of nuclei may lie between the fibres. The capil- 
laries may be dilated and distended. It is very common to see 
muscular fibres that are much altered side by side with others that 
present a nearly normal appearance. Ultimately the sheaths become 
empty, and shrink-, and may be scarcely distinguishable from the 
interstitial fibrous tissue. 
The peripheral nerves contain many degenerated nerve-fibres, and 
the terminal branches for the muscles a still larger number. If the 
nerves are traced up to the cord it is found that the degenerated fibres 
come only from the anterior roots. These are conspicuously changed 
to the naked eye, small and grey. They may resemble fine threads of 
connective tissue, and under the microscope no nerve-fibres may be 
found in them, or only a few may remain of normal aspect, the rest 
being in various stages of degeneration, or represented only by their 
empty sheaths. The degree of affection of the anterior roots corre- 
sponds to the wasting in the parts supplied by them. The posterior 
roots are normal. 
The spinal cord is often softer than natural at the affected part, and 
the white substance of the lateral columns may be grey and translucent 
in aspect, especially in the cervical enlargement. Under the micro- 
scope morbid changes are seen in the anterior cornua, and also, in 
most cases, perhaps in all, in the antero-lateral white columns. The 
change in the anterior cornua corresponds in its intensity to the 
origin of the nerves to the most affected parts, and since the latter 
are usually the arms, the disease is generally most intense in the 
cervical enlargement. In stained sections the grey matter of the horn 
is less deeply tinted than normal, but in some parts it may stain more 
deeply, especially in the circumference of the cornu and tbe processes 
of grey matter which project into the white column. Occasionally, 
larger areas have a dense aspect and stain deeply, but the central part 
of the cornu is generally pale and wasted in aspect. Most of the large 
nerve-cells have disappeared; many entirely, while others are repre- 
sented only by small angular bodies. Not a single large cell mar be 
seen in a section which, in a normal cord, would contain a considerable 
number. Frequently, however, a few large cells can still be seen, but 
most of these have lost their processes and are more globular than 
normal. The interstitial tissue is also changed. The nerve fibrillre 
waste with the cells, and there is an increase of the small, angular, 
and stellate cells and other connective-tissue elements. The larger 
vessels are dilated and surrounded by unduly wide spaces, but there 
is no considerable distension of the capillaries. The cornu as a 
whole is not usually changed either in size or shape. Similar altera- 
tions may be traced through the dorsal region. In the lumbar 
enlargement, the grey matter may be normal, even when it is much 
altered in the cervical region; but if the legs are wasted, there are CHRONIC MUSCULAR ATUOPUY. 
487 
changes similar to those already described. When the atrophy 
begins in the legs, the disease may be more intense in the lumbar 
than in the cervical enlargement; but more often any degeneration 
that exists is slighter, and a larger number of normal or slightly 
Fig. 141. 
Fig. 142. 
FiG.141.—A normal anterior cornu for comparison with the next figure. 
Fig. 142.—Progressive muscular atrophy; anterior cornu, cervical region. 
(From drawings by Dr. H. It. Spencer.) 
changed cells can be seen. Sometimes certain groups of cells are 
little affected while others are much atrophied. The degeneration 
may involve to some exten. the intermediate grey matter between the 
cornua, but here it ceases; the posterior horn is always normal. 488 
SPINAL CORD. 
There is distinct degeneration 
of the anterior root-fibres passing 
from the cornu through the an- 
terior column. A few fibres may 
remain, but whole fasciculi appear 
to be replaced by fibrous tissue. 
There is also degeneration of the 
fibres of the anterior commis- 
sure, in consequence of which it 
stains much more deeply than 
normal, in the regions in which 
the grey matter is considerably 
diseased. 
In the white columns there is 
usually considerable, and often al- 
most complete, degeneration of the 
pyramidal tracts, anterior and 
Fig. 143.—Progressive muscular atrophy; 
degeneration of the anterior cornua and 
pyramidal tracts. A, medulla oblongata, 
complete degeneration of the anterior 
pyramids A P; B, at the upper part of 
the decussation of the pyramids; d, the 
decussation of the degenerated fibres; 
A P, the pyramids, still incomplete. C, 
cervical, D, dorsal, E, lumbar sections. 
The degeneration of the anterior cornua 
is complete in C, but in E a few cells 
remain, for the most part without pro- 
cesses. In C and D the degeneration 
of both anterior and lateral pyramidal 
tracts is conspicuous; in E the anterior 
tract has ceased, and the lateral tract 
extends up to the surface of the cord, 
from which it is separated in C and l3 
by the undegenerated direct cerebellar 
tract. In C and D the degeneration 
extends forwards in front of the lateral 
pyramidal tract, but gradually ceases. 
The fibres of the anterior commissure 
are also degenerated.* 
* In this case the arms were greatly 
wasted and flaccid; the legs were para- 
lysed, rigid, with moderate wasting. The 
muscles of the back were also atrophied. 
In the arms the weakness and wasting 
came on at the same time, in the right 
arm some time before the left. The 
shoulder-muscles suffered first, but the 
atrophy quickly spread, and was ulti- 
mately extreme in the muscles of the 
shoulders, forearms, and hands. The dis- 
ease ran a rapid course; death occurred 
two years after the gradual onset. CHRONIC MUSCULAR ATROPHY. 
489 
lateral.* The area of sclerosis, 
resulting from the degeneration 
of the two tracts, varies in ex- 
tent according to the size of the 
anterior tract, and to the dis- 
tance which it extends down the 
cord. In Fig. 144 this is illus- 
trated in an unusual manner, in 
consequence of an inequality in 
the decussation of the pyramids 
at the medulla, fewer fibres of 
Fig. 144.—Progressive muscular atro- 
phy. A, medulla oblongata; degene- 
ration of the anterior pyramids A P. 
B, cervical, C, first dorsal, D, first 
lumbar, E, mid-lumbar sections. The 
nerve-cells have disappeared from 
the anterior cornua, except in E, in 
which a few remain. There is com- 
plete degeneration of the pyramidal 
tracts, anterior and lateral. The de- 
cussation at the medulla was unequal 
in this case; of the left pyramid 
fewer fibres crossed than of the right, 
and hence the left anterior pyramidal 
tract is larger, while the right lateral 
tract is smaller than normal, and, 
moreover, has ceased at the middle of 
the lumbar enlargement, to which 
the left anterior tract extends. + 
* 1 have not yet met with a single 
case of progressive muscular atrophy 
in which the pyramidal tracts were 
unaffected. Such cases are extremely 
rare, but one has been published by 
Striimpell (‘Zenker’s Zeitsch.,’ 1887, 
and ‘ Neur. Centralbl.,’ 1888, p. 139) 
which was characterised by the general 
wasting of the arm, a very slow course, 
and the absence of leg symptoms. 
The spinal nerve-cells and motor 
nerves were degenerated. Striimpell 
suggests that the affection may have 
begun in the peripheral motor nerves, 
and have ascended these to the cord. 
If so, the case belongs to a separate 
class. 
f The patient was a man forty-eight 
years of age. The disease followed a 
severe exposure to cold. The wasting 
of the arms was extreme, and they were 
absolutely powerless. The legs were 
much less wasted than the arms, but very weak, the loss of power being out of 
proportion to the wasting. 490 
SPINAL CORD. 
tlxe left pyramid having crossed than of the right, so that the left half 
of the cord contains more than its proper share of the fibres, and the 
anterior tract extends into the lumbar region even further than does 
the lateral tract. Where the direct cerebellar tract exists, this, always 
unaffected, limits the sclerosis of the lateral tract on the outer side. 
On the inner side, the “ lateral limiting layer ” (see p. 182) is usually 
much less degenerated than the pyramidal tract, and intervenes be- 
tween the latter and the grey matter; but this layer suffers in some 
degree, perhaps by the affection of outlying pyramidal fibres con- 
tained in it. The sclerosis does not usually cease at the anterior 
extremity of the pyramidal tract, but extends forward in the “ mixed 
zone ” of the lateral column, lessening in intensity, and ceasing 
usually opposite the outer part of the anterior cornu. It is here 
most intense close to the grey substance, and ceases before it reaches 
the surface of the cord, the antero-lateral ascending tract being 
unaffected. This sclerosis may be due to the degeneration of 
the short vertical fibres that pass between adjacent regions of the 
anterior cornu, and which share the degeneration of the nerve-cells. 
Occasionally it extends, in slighter degree, into the anterior columns. 
The posterior columns are always free from definite degeneration, but 
there may be some general increase of connective tissue throughout 
the whole cord. The degeneration of the pyramidal tracts is usually 
considerable in degree ; often most of their fibres seem to have perished. 
If it is incomplete in the cervical region, it may be slight in the lower 
part of the cord, the degenerated fibres being chiefly those that end 
in the cervical enlargement and dorsal region. When the sclerosis is 
intense, it is not confined to the cord ; it can be traced up through the 
decussation (Fig. 143, b) and through the medulla oblongata, in which, 
as Figs. 143 and 144 show, the whole of both pyramids may be degene- 
rated, so that they stain deeply, and no nerve-fibres can be dis- 
tinguished in them. The degeneration of the pyramids has been 
found in several cases to extend through the pons and crus to the 
internal capsixle, and even through the white substance to the cortex. 
Above the capsule, however, the pyramidal fibres are so mingled with 
others that their degeneration is no longer recognisable by the deeper 
staining of a definite tract; but it has been detected by the presence 
of abundant products of degeneration in the path of the fibres. In 
the motor cortex, the large ganglion-cells have been found fewer than 
normal, and distinctly degenerated, many having lost their processes, 
and, in the interstitial tissue, the spider cells and other connective- 
tissue elements are increased in number.* But the degeneration of 
the pyramidal tracts has also been found to cease at the crust and at 
the decussation.t 
* Koschewnikoff, ‘Archives de Neurologic,’ 1883, No. 18j and ‘Centralbl. f. 
Nervenkr.,’ 1885, p. 409; Marie, Neur. Centralbl.,* 1884, p. 61. 
f Rovighi and Melotti, loc. cit.; Dornblutk, ‘Neur. Centralbl.,’ 18S9, p. 377. 
J Moeli, ‘Arch. f. Psycli.,’ x, 718. CHRONIC MUSCULAR ATROPHY. 
491 
In cases in which the symptoms of bulbar paralysis were present 
during life, the motor nuclei of the medulla have presented changes 
corresponding to those of the grey matter of the spinal cord, with a 
similar degeneration of the nerve-cells. In other instances, tho 
degeneration of these nuclei has been slight, but in such cases the 
degeneration of the pyramids has been intense, and doubtless involved 
the fibres connecting these nuclei with the cortex of the brain. 
The sympathetic nerves and ganglia, when examined, have been 
found normal, or have only presented such changes as are common 
apart from symptoms of disease of the nervous system. 
Pathology.—The theories, according to which the disease was 
regarded as primarily one of the muscles or of the sympathetic nerves, 
have now only an historical interest. The constancy of the changes 
in the ganglion-cells of the spinal cord, the degeneration of the motor 
root-fibres, and the analogous effects of acute lesions of the anterior 
cornua, leave no doubt of the relation of the muscular wasting to the 
disease of the grey matter, and essentially to that of the ganglion-cells, 
and the fibres proceeding from them. The slowness of the change 
causes the impairment of the nutrition of the muscular fibres to pro- 
ceed pari passu with that of the nerve-elements, and the interference 
with motor conduction to be proportioned to both. We are thus able 
to understand the condition of electrical excitability, and its slow 
failure, as nerve and muscle degenerate together. It is only when the 
slow degeneration is varied by a more acute process of destruction of 
cells and more rapid degeneration of fibres that the muscular tissue is 
for a long time less damaged than the nerve-fibres, and presents 
paralysis in excess of the wasting, with a voltaic irritability in excess 
of the faradic irritability of the nerve-endings (p. 24). Thus the 
essential lesion of the disease is a slow decay of the lower segment of 
the motor path, the segment which consists of the ganglion-cells and 
their prolongations in the axis-cylinders of the nerve-fibres (see p. 176)- 
To this the conspicuous symptom, the muscular wasting, is secondary. 
It is perhaps better thought of as a degeneration of the whole segment 
than as simply a lesion of the ganglion-cells, although the latter 
being the element on which the nutrition of the segment depends, the 
two views are merely different modes of stating the same fact.* 
But the disease is rarely limited to the lower segment of the motor 
path. The case mentioned in the note on p. 489 is an almost isolated 
example of such limitation—an “ exception that proves the rule.”f 
* In a few anomalous cases, degeneration of the motor cells of the cord has been 
met with when no degeneration could be detected in the peripheral mixed nerves (see 
Kronthal, ‘Neur. Centralbl.,’ 1891, p. 133). The interpretation of these cases is, at 
present, uncertain. Possibly, complete disappearance of some fibres left the rest 
apparently normal, although the skill of the investigators renders this explanation 
difficult to accept. Many more observations, however, are needed to justify a. 
modification of current views. 
f Moreover, the fact that these cases may not be primarily spinal must be borne’ 
in mind. 492 
SPINAL COPD. 
We have seen that the pyramidal tracts are commonly degenerated, 
and it is probable that the degeneration often extends through their 
entire extent, and involves the motor cells of the cortex * Thus the 
upper segment is often degenerated as well as the lower segment. In 
the presence of that complete degeneration of the lower segment 
which causes the atonic atrophy of the muscles, the degeneration of 
the upper segment can cause no symptoms. The loss of power 
that it would produce is also caused by the degeneration of the lower 
segment, and the latter abolishes the myotatic irritability, excess of 
which is the characteristic indication of disease of the upper segment. 
Hence the degeneration of the upper segment of the motor path for 
the muscles that present the atonic atrophy cannot be recognised 
during life, for it cannot produce its characteristic symptoms. 
What is the relation between the degeneration of the two segments, 
between the lateral sclerosis and the affection of the ganglion-cells P 
We cannot assume (as some have been inclined to do) that the affection 
of the upper segment is secondary to that of the lower, because a 
primary lesion of the grey matter, such as occurs in polio-myelitis, 
does not cause ascending degeneration of the related pyramidal fibres. 
Moreover, even a complete interruption of the pyramidal tracts is 
followed by no degeneration of their upper parts. Hence the intense 
degeneration met with in progressive muscular atrophy cannot be 
regarded as secondary. Neither, when there is atonic atrophy, can 
we consider the affection of the upper segment to be the primary lesion, 
and to be the cause of that in the lower. In the seat of slight atrophy 
there are, as a rule, no indications of the preceding degeneration of 
the upper segment, which would certainly exist if this lesion were the 
primary change. Moreover, degeneration of the upper segment does 
not necessarily cause any degeneration of the lower. It is a matter of 
•everv-day observation that intense degeneration of the termination of 
the upper segment may occur, from dorsal myelitis, for instance, with- 
out any considerable wasting of the legs, and such degeneration has 
never been known to excite the complete degeneration of the lower 
segment which causes atonic atrophy. Hence the only adequate 
explanation of the facts is that the degeneration of the upper and 
lower segments is simultaneous, or if not simultaneous, at least so far 
independent that neither is the cause or consequence of the other; 
both are the results of the same tendency to degeneration of the 
motor path. Atonic muscular atrophy is thus, at least in manv 
cases, the visible expression of a tendency to decay of the whole 
motor path from the cortex of the brain to the muscles. 
The weakness of some parts, as the legs, with excessive myotatic 
* At the same time, we have seen (p. 213) that the nutritional stability of nerve- 
fibres is less in their lower than in their upper parts, and that their isolated degenera- 
tion may be greatest in the lower parts. That this may sometimes also be the case 
in these pyramidal fibres is suggested by the fact already stated that the degene- 
ration may extend no higher than the decussation or the crura cerebri. CIIItONIC MUSCULAR ATROPHY. 
493 
irritability, often going on to spasm, is explained by the degeneration of 
the pyramidal fibres for the legs, the lower segment being unaffected. It 
is easy to understand that the affection of the upper segment, and 
escape of the lower, or the affection of both, may vary much in relative 
extent, and give rise to the multiform varieties already mentioned. In 
such a case, the nerve-cells for the part thus paralysed are normal. 
This weakness of the legs usually succeeds the wasting in the arms, 
and in most cases in which spastic paraplegia is followed by atrophy 
in the arms, the latter have not shared the spastic palsy. When tins 
condition is associated with slight wasting of the legs, without con- 
siderable change in electrical irritability, the condition exists that we 
have more than once considered, in which we must assume that the 
motor nerve cells of the cord, while structurally intact, undergo slight 
changes in nutrition. In this condition there are many nerve-cells of 
normal appearance in the grey matter ; the alterations in nutrition are 
too slight to cause changes in aspect, or if there are such changes we 
have not yet learned to detect them. They are perhaps results of the 
degenerative changes in the termination of the upper segment; when 
such degeneration is secondary to a focal lesion of the cord or brain, 
the changes in nutrition of the cells seldom attain such a degree 
as to arrest the myotatic irritability, or to cause wasting such as 
attends the destruction of these cells. 
In some cases, however, the muscular wasting may be great, although 
the increase of myotatic irritability persists. In these cases, as we 
have seen, there is considerable rigidity of the muscles throughout the 
whole course of their wasting, the condition that we have termed 
“ tonic atrophy.” In such a condition it is common to find that many 
nerve-cells have disappeared or are very small, but others remain 
normal or slightly changed in aspect. Apparently, in addition to 
the degeneration of the upper segment and to the nutritional changes 
just mentioned, we have then a considerable degeneration of many, 
but not destruction of all, the elements of the lower segment. We 
cannot regard this as simply secondary to the degeneration of the 
upper segment, for the reasons already given. It must be the 
expression of a distinct pathological tendency similar to that which 
elsewhere causes the atonic atrophy and total wasting, but slighter 
in extent and later in time—insufficient to prevent the less affected 
cells from causing rigidity under the influence of the degeneration 
of the upper segment. It is doubtful whether the tonic atrophy ever 
goes on to atonic atrophy. Theoretically conceivable, it is certain 
that if it ever occurs it is extremely rare. Nor does it seem that atonic 
atrophy ever gives place to tonic atrophy, with excessive myotatic 
irritability. The rigidity of tonic atrophy is due to the degeneration 
of the upper segment, but the effect is not produced if the lower 
segment is already the seat of such extensive degenerative changes as 
abolish myotatic irritability. The pyramidal fibres for the parts that 
are the seat of atonic atrophy are constantly found degenerated, 494 
SPINAL CORD. 
although the muscles have been flaccid to the last. In the rare cases 
{mentioned on p. 480) in which muscles, with atonic atrophy, 
become rigid towards the end of the process, it is probable, as the 
tenderness suggests, that the rigidity is idiopathic, due to the changes 
in the muscles, and is not dependent on the central nervous system. 
It may be the result of the increase in the interstitial connective tissue, 
and the longitudinal division and fibrillation by w'hich the muscular 
fasciculi come to resemble bundles of connective-tissue fibres. It is 
also possible that similar idiopathic muscular changes may ultimately, 
in tonic atrophy, maintain and increase the rigidity that is primarily 
■dependent upon the spinal cord. 
It has been mentioned that the cases in which the legs present 
the simple palsy and spasm, or the tonic atrophy, which indicate 
degeneration of the pyramidal tracts, have been separated by Charcot, 
and termed “ amyotrophic lateral sclerosis,” the separation being based 
on the assumption that in such cases the primary lesion is the degene- 
ration of the pyramidal tracts, and that the affection of the grey 
matter is secondary or “ deuteropathic,” even where the atrophy is 
atonic. We have seen also that this assumption is unwarranted so far 
as the atonic atrophy is concerned. It is probable that the pyramidal 
tracts are degenerated, if not constantly, at any rate in such a very 
large proportion of the cases of progressive muscular atrophy, that 
Charcot’s distinction is, in effect, giving a new name to an old disease, 
and that the sequence is not that indicated by the name. Whether 
there are indications of lateral sclerosis or not, depends on the 
■circumstance whether the degeneration of the pyramidal fibres is or is 
not more extensive than the complete degeneration of the nerve-cells 
that causes atonic atrophy. If the latter is universal, the pyramidal 
tracts may be totally degenerated, and yet there may be none of the 
■characteristic indications of such degeneration. On the other hand, 
both arms and legs may be the seat of the spastic paralysis that 
indicates pyramidal degeneration, and atonic atrophy may be limited 
to a few muscles of the hands. Between these we have every grada- 
tion, in degree and distribution, of atonic atrophy, spastic paralysis, 
and tonic wasting. 
The process in the grey matter has been regarded by some as a 
chronic inflammation. The occasional rapid increase in the symptoms 
may be thought to be justification for this view ; but the process in 
general is at the degenerative extremity of the series of nerve-lesions. 
The principle involved in this question has been already discussed, 
and we have seen that, whatever be the nature of the primary process, 
we must recognise secondary tissue changes of independent energy, and 
that a distinct process of inflammation may occasionally form part of 
these (see p. 396). The significance of the occurrence of inflammation 
may therefore easily be overrated, so far as concerns the question of 
the process, and the tissue-elements in which the disease begins. 
Diagnosis.—The simultaneous and gradual onset of weakness and CHRONIC MUSCULAR ATROPHY. 
495 
Masting, the slow but progressive increase and extension of the sym- 
ptoms, render the diagnosis of the developed malady simple and easy. 
At the onset, when only a single muscle or group of muscles is 
affected, the question arises whether the atrophy is local or is the 
commencement of a wider affection. Local atrophy is said sometimes 
to occur from great over-use of a muscle, especially one of the small 
muscles of the hand, but such a cause is extremely rare, and only to 
be suspected on the clearest indications. 
As a rule, the local atrophy from which the affection has to be dis- 
tinguished is that due to disease of the nerves. The wasting from 
disease of single nerves or at a plexus (as the brachial) is sufficiently 
distinguished by its limitation, coupled with its rapid onset and 
associated sensory symptoms. Much more difficult is the distinction 
of some forms of multiple neuritis. The difficulty presents itself 
chiefly in two forms:—(1) When the spinal affection begins as sub- 
acute atrophic palsy (see p. 483). (2) When neuritis affects chiefly 
motor branches, as in the arms in lead-poisoning, or in the legs in 
alcoholism, &c. In the first case it is necessary to wait for signs 
of slower wasting in other parts than those first affected before 
a diagnosis can be made. In the second, a careful search will generally 
reveal other symptoms of neuritis, and a known cause is usually 
obtrusive. 
In pachymeningitis of the cervical region, with considerable 
damage to the nerve-roots, the wasting in the arms may resemble that 
of progressive muscular atrophy, and there is often weakness with 
rigidity in the legs, but the wasting is less chronic in onset, and is 
always accompanied by distinctive sensory symptoms,—by acute pains 
and usually by anaesthesia, irregular in distribution. The same dis- 
tinctions suffice for the diagnosis in diseases of the nerve-roots of the 
cauda equina, as by a tumour. This may cause slow wasting in the 
legs, but there is always severe pain and loss of sensibility. Chronic 
disseminated myelitis may cause wide-spread muscular atrophy, but is 
distinguished by the presence of symptoms of irregular damage to 
other structures in the cord. The diagnosis from syringo-myelia will 
be considered in the account of this disease. 
From primary muscular atrophy, “ idiopathic atrophy,” “ muscular 
dystrophy,” as it has been termed, the diagnosis is sometimes easy, 
sometimes very difficult. It is easy in the pseudo-hypertrophic form, 
and often also in the atrophic variety (the cases in which no muscles are 
large); on account of its characteristic distribution, its course, the age at 
which it begins, and the tendency to affect many members of a 
family, and males more than females—features that will be presently 
described. Whenever several cases of muscular atrophy occur in a 
family, or during childhood or youth, the probability is great that they 
are idiopathic and not spinal. Indeed, the idiopathic form is to be 
suspected whenever muscular atrophy begins under twenty, unless 
there are distinctive spinal symptoms. But cases are sometimes met 496 
SPINAL COED. 
with in which idiopathic atrophy begins in adult life, and the distinc- 
tion of such cases may be very difficult, and will be better understood 
after a perusal of the account of this disease. 
Prognosis.—The progressive character of the malady renders the 
prognosis, in every case, grave and uncertain. The chief guide is the 
observed tendency of the morbid process, both the fact of its actual 
advance and the energy it manifests. At the same time, there is a 
possibility of arrest, greater in middle life than in old age. Some in- 
crease of atrophy in the parts already affected may occur for a short time 
after the process in the cord has ceased to spread—the muscular wasting 
going on until it corresponds to the changes in the nerves that have 
already taken place. The prospect of arrest seems to be greater in tko 
cases in which the wasting is strictly symmetrical and nearly simul- 
taneous on the two sides, than in those in which it is irregular, and 
attacks the second side when it has attained a marked degree in the 
first. Spontaneous cessation unfortunately seldom tends to occur 
until an advanced stage is reached ; but, as the result of treatment, 
arrest may take place at any stage. The danger to life is chiefly 
proportioned to the interference with the muscles of respiration, and 
to the indications of implication of the medulla. Bulbar symptoms 
increase the gravity of the prognosis, especially when definite weakness 
can be recognised. Slight vague difficulty in articulation may remain 
stationary for years, and does not necessarily render the prognosis 
worse, especially if the atrophy elsewhere does not increase rapidly. 
If the malady ceases to advance, the prospect of any recovery depends 
on the rate at which the disease has progressed. Recent rapid loss of 
power may be to some extent recovered from, especially when the 
muscles present the degenerative reaction. Wasting that has existed 
for six months will probably persist unchanged. In a typical chronic 
case there is little hope of any actual recovery of tissue or power. 
The effects depend on a slow destruction of nerve-elements, the renewal 
of which seems to be impossible. 
Treatment.—The first important element is to secure favorable 
conditions of life, and to maintain the general health as perfect as 
possible. Fresh air and gentle exercise are important, but all 
fatiguing exertion should be avoided, and likewise all mental strain. 
When the patient becomes helpless, great care is necessary. Bedsores 
in this disease mean inattention, and may always be avoided. 
Only one method of treatment has, in my own experience, shown 
itself capable of arresting the disease, not indeed in all, but in more 
than half the cases in which it has been employed.* It is the admin- 
* At first I regarded the apparent result with doubt, hut careful and repeated 
observations have made it impossible to consider the arrest of the disease as other 
than tiie direct effect of the treatment. It may be asked, Why should not a larger 
dose by the mouth be equally effective? A large dose involves risk of over-stimu- 
lating the nerve-elements, and doing harm rather than good; it is quite different 
from a small dose acting suddenly. CHRONIC MUSCULAR ATROPHY. 
497 
istration of strychnia by hypodermic injection. In seven almost con- 
secutive cases, in middle life, this treatment has been followed by 
arrest within a month of its commencement, and the arrest has been 
permanent in all the cases but one. In the senile cases the treatment 
has failed, bnt in most of them the disease was in an advanced stage, 
and the lumbar cord had begun to suffer. In some of the cases 
in which the result was prompt and distinct, strychnia given by 
the mouth had failed. It is conceivable that the different result is 
due to the fact that the agent is brought into more rapid contact with 
the nerve-elements, perhaps in purer form. Its action may possess 
greater momentum, as it were, and may thus exert an influence on the 
nutrition of the nerve-elements much more considerable than when it 
is slowly absorbed from the alimentary canal. One injection daily 
has been given, at any convenient place. The nitrate is the most con- 
venient salt, one hundredth of a grain at first, quickly increased to 
one fortieth. It is not wise to give a larger quantity, lest the nerve- 
elements should be over-stimulated; although, in their damaged 
state, they may be unable to manifest the influence, it may yet do 
harm. When the malady is apparently arrested, it is well to intermit 
the injections for one week in three or four. Other nervine tonics 
seldom exert a distinct influence, but those that are useful in other 
degenerative diseases, as tabes, may be given by the mouth at the 
same time as the injections are employed. In a malady so grave, it is 
desirable to neglect nothing that may possibly exert a beneficial in- 
fluence. 
Local treatment of the muscles has very little influence on the 
wasting, as may, indeed, be expected from its nature. The most 
sedulous and skilful use of electricity, voltaic or faradic, fails, as a 
rule, to produce alone any effect on the course of the disease. If the 
malady is progressing at the same rate in each arm, and the muscles of 
one arm are regularly treated with electricity, while those in the other 
arm are left alone, no difference can be detected in the rate of wasting 
on the two sides. It is possible, nevertheless, that electricity some- 
times does a little good. In cases iu which a rapid loss of power has 
occurred, and weakness is out of proportion to the wasting, some re- 
covery is possible, and there is no doubt that the excitability of the 
muscular tissue is maintained for a longer time by galvanism, although 
the bulk of the muscle may not be influenced. In other cases, all that 
can be said is that the influence of electricity, properly applied, is in 
the right direction. Moreover, the disease is one of those in which 
patients find it hard to believe that electricity cannot help them, and 
the probability is that their conviction will be fostered by some 
medical adviser. It is one of the diseases in which unjustifiable 
assertions are too often made that early electrical treatment would 
have been successful. It may be well, therefore, if only to satisfy 
the patient that nothing has been left untried, that a careful course 
of electrical treatment should be adopted. Faradism may be used 
VOL. 1. 498 
SPINAL CORD. 
if the muscles are sensitive to it, but if they present any greater irri- 
tability to voltaism, it is better to use this. It is immaterial whether 
the application is confined to the muscles or whether one electrode is 
placed over the affected part of the spinal cord. The latter method 
has no disadvantages, but my own observations have failed to confirm 
the confident statements sometimes made regarding its superiority. 
It is very important that the current-strength employed should be 
moderate. Strong applications often cause much subsequent pain, 
and even increased disability, and should be carefully avoided. I 
have known a rajnd increase of weakness follow a strong application, 
in a way that convinced the patient at least that the two were con- 
nected. 
Rubbing and massage of the muscles have been frequently em- 
ployed, and of this treatment also it may be said that its influence is 
in the right direction, although usually inappreciable so far as the 
muscular atrophy is concerned. Combined with passive movement, 
the influence of rubbing in preventing and diminishing deformities is 
more distinct. No special bath treatment is of service. When the 
disease occurs in the subjects of syphilis, specific treatment invariably 
fails, and I have even known the progress of the disease to be dis- 
tinctly accelerated by an energetic course of treatment both by iodide 
and by mercury. It is important that all treatment should be pur- 
sued in moderation, and that its effects should be carefully watched. 
Arthritic Muscular Atrophy. 
Articular inflammation is almost invariably attended witli rapid 
wasting of tlie muscles that move tlie joint. This occurs equally, what- 
ever be the cause of the inflammation, and whether this is spontaneous 
or traumatic. It attends chronic as well as acute inflammations, and 
occurs in animals if joint-inflammation is produced in them.* 
The muscles that waste are chiefly those which extend the affected 
joint. The atrophy is well seen in the muscles in front of the thigh, 
when the lcnee is inflamed. If the ankle is affected, the calf muscles 
chiefly waste ; if the hip, the glutei; if the wrist, the extensor muscles of 
the forearm ; the triceps when the elbow is affected ; the deltoid when 
the shoulder-joint is inflamed. In rheumatoid arthritis of the finger- 
joints, such wasting is usually very conspicuous in the interossei, and 
especially in the abductor indicis. The atrophy, however, sometimes 
involves the flexors as well as the extensors, and rarely muscles of the 
limb that are near but do not move the affected joint. In very rare 
cases all the muscles of a limb have presented some wasting. Cases 
* Valtat, ‘Archives Generales,’ 1877, tome xxx, pp. 159 and 321. The subject has 
been discussed by Vulpian (‘ Lemons sur l’App. Vaso-moteur,’ 1875, t. ii) and by Paget 
(‘Lancet,’ 1873, vol. ii, p. 727, in a lecture republished in ‘Clinical Lectures and 
Ks>ays,’ 1875, p. 20S). ARTHRITIC MUSCULAR ATROPHY. 
499 
In which the atrophy is unusual in distribution, and especially when 
it is on the distal side of the affected joint, must be regarded with 
some suspicion, because inflammation may have spread from the joint 
to a nerve, and distant wasting may have been thus produced. It is said 
that there is sometimes, at the onset, a considerable weakening of 
the muscle, interfering with movement more than can be accounted 
for by the pain in the joint which movement causes, and that such 
initial palsy is transient (Yaltat, Duchenne). But the pain, by its 
inhibitory influence, usually obscures such palsy, which is indeed con- 
fessedly rare. 
The atrophy, on the other hand, may be regarded as almost con- 
stant. If the onset of the joint affection is acute, the wasting occurs 
rapidly ; in a week or ten days, a difference in the circumference of 
the limb may be detected by measurement. However long the affected 
muscle may be, the wasting involves the whole length of it, and not 
merely the part in the neighboui’hood of the diseased joint. The 
degree varies; usually moderate, and sometimes slight, it is occasionally 
considerable, so that the femur may be readily felt when the quadriceps 
femoris is the seat of the wasting, or the head of the humerus may be 
distinct, aud the acromion prominent, if the deltoid is affected. 
Although the whole length of the affected muscle is always involved, 
if the muscle is a wide aud compound one, some parts may suffer 
chiefly. Thus in the thigh all parts of the extensor may waste equally, 
or the rectus or vastus internus may suffer more than the other parts. 
The wasting increases during two or three weeks, then becomes 
stationary, but continues as long as the joint disease lasts. When the 
joint has recovered, the muscles in most cases slowly regain their 
normal size. Occasionally, especially when the arthritis has lasted a 
long time, the wasting may continue for months or years after the 
joint disease is at an end. 
The electrical irritability of the atrophied muscles may be normal, 
but is often slightly lowered, equally to faradism and voltaism. The 
change is trifling, to be recognised only by comparison with the other 
side. There is generally a distinct, and sometimes a considerable, local 
increase in myotatic irritability; the knee-jerk is excessive if the 
thigh muscles are affected, and a rectus-clonus can sometimes be 
obtained. A foot-clonus may be elicited when the ankle-joint is 
affected. Occasionally the increased irritability extends beyond the 
region of atrophy, so that, for instance, a foot-clonus may be obtained 
when the knee-joint and thigh muscles are affected, although there is 
no wasting below the knee. As an example of this, which illustrates 
also the occasional persistence of the atrophy, may be mentioned the 
ease of a young man who jumped over a hoarding and twisted his left 
leg in doing so. He felt immediately severe pain in the knee, the joint 
quickly swelled, and became the seat of an acute inflammation which 
lasted for several weeks, and then slowly subsided. During the 
inflammation, the thigh wasted. I saw him two years after the onset, 500 
SPINAL CORD. 
and there was still considerable wasting, involving the whole of the 
extensor of the knee. The minimum circumference of the left thigh 
above the knee was three quarters of an inch less than that of the 
right, although there was no difference bet ween the two legs below the 
knee. There was a slight diminution in faradic and voltaic irritability 
in the affected muscles. The knee-jerk was much more considerable 
on the left than on the right side, and there was a well-marked foot- 
clonus in the left leg, but none in the right. A year and a half later 
the symptoms were unchanged. Very rarely some contracture occurs 
in the opponents of the atrophied muscles. Sensory symptoms are as 
a rule absent, but there may be slight tingling in the skin during the 
acute stage ; it is said that areas of anaesthesia sometimes develop, but 
probably in such cases, inflammation has extended to a nerve in the 
vicinity of the joint. 
Pathology.—Few facts have been ascertained regarding the con- 
dition in man. In one case, carefully investigated, the only change 
was in the muscles, and consisted merely in a narrowing of the fibres, 
one half of which were below the normal average, while no less than 
84 per cent, fell short of a standard which, in health, only 21 percent, 
failed to reach.* A few presented longitudinal striation (as in 
Fig. 140), and some of normal width were unduly tortuous ; otherwise 
their aspect was normal. The sheath nuclei were proliferated in 
places, and, apart from this change, the intermediate substance pre- 
sented local increase in quantity, especially where the fibres were 
narrower than normal. This observation agrees with those that have 
been made on animals, in which the condition has been produced, and in 
them, moreover, the motor nerves have been found normal (Valtat).f 
Indications of inflammation have been found in the joint-nerves.J as 
might, indeed, be expected, whatever the mechanism of the atrophy. 
Visible changes in the spinal cord have never been discovered, but 
this does not exclude nutritional changes. 
We may, therefore, exclude from the possible causes all forms of 
motor neuritis, both simultaneous, due to the cause of the joint 
inflammation, and consecutive, communicated to the adjacent nerve 
from the joint. The latter (a secondary extension of inflammation 
to the nerve) would manifestly not explain the affection of the 
whole of a muscle on the proximal side of the affected joint—as, 
for instance, atrophy of the w hole ext nsor in arthritis of the knee,— 
although the extension does occur and must be recognised as an 
occasional event. § We must also recognise the possibility of a simul- 
taneous neuritis, with acute changes in the nerve-fibres, manifested 
by the reaction of degeneration in the muscles. The event is, how- 
* Darkschewitsch, *Neur. Cent.,’ 1891, p. 353. 
t Valtat, ‘De l’Atrophie Muse., &c.,’ Paris, 1877. See also Deroche, ‘Etude 
clin. et exp.,’ Paris, 1890. X See Duplay and Cazin, ‘Arcli. Gen.,’ January, 1891. 
§ E.g. to the ulnar, in rheumatoid arthritis of the hand (Bury, ‘Med. Chron.,* 
1888, p. 1S2). See on this subject A. E. Garrod, ‘ Med.-Chir. Trans.,’ lxxi, 2u5 ; also 
Pitres and Vaillard, ‘ ltev. de Med.,’ 1887, No. 6. ARTHRITIC MUSCULAR ATROPHY. 
501 
ever, exceptional. It is certainly separable and to be separated from 
the common arthritic atrophy ; but it is not easy to keep apart the 
two varieties of neuritis—the simultaneous and the consecutive— 
when a case is seen only long after the onset, because a neuritis that 
arises by extension may travel along the nerve and present an ultimate 
distribution quite different from that which it possessed at the onset. 
For ordinary arthritic atrophies we must seek some other explana- 
tion. The nature of their cause long ago suggested to Paget a “ reflex 
influence” on the muscles as the probable mechanism, and Yulpian 
and Charcot have suggested a similar hypothesis, assuming a derange- 
ment of the nutrition and influence of the motor cells of the cord, to 
be determined by the morbid impulses from the joint-nerves, and to 
determine the alterations in the muscles. The theory receives impor- 
tant support from the fact that the wasting of the muscles is pre- 
vented by previous division of the posterior spinal roots (Raymond), 
which amounts, indeed, to an indirect demonstration of the fact that 
a reflex process* underlies the phenomena. It is doubtful whether 
we can go much further than this. By preceding hemisection of the 
cord, it is increased on the side of the operation ; but the conditions 
are here more complex, and the demonstration of the reflex relation 
less simple, than in the result of division of the roots. 
The increased knee-jerk, &c., that attend the wasting, and the 
curious fact that arthritis may set up a degeneration of the spinal 
cord, apparently beginning in the termination of the pyramidal fibres 
(see p. 443), should be kept in mind. They are certainly significant, 
and suggest that the influence from the joint-nerves acts on the “con- 
trolling structure ” of the muscle-reflex centre (see p. 201), but more 
facts are needed before a valid hypothesis can be framed. 
Diagnosis.—The moderate degree of the wasting, with correspond- 
ing change in electrical reactions, coupled with the wide extent of 
the alteration, embracing the whole of the muscles involved, constitute 
a distinctive characteristic—distinctive, at least, when taken in con- 
nection with the preceding joint affection which is the cause of the 
atrophy. A primary neuritis, causing secondary arthritic adhesions, 
has its own features—their wider range, so far as function is concerned, 
and especially their limitation to nerve distribution. Hardly any other 
malady is likely to be confused with it, except some graver disease, 
while still in an early stage, but such an affection can only be dis- 
tinguished by waiting until the nature of the malady has had time to 
show itself. 
Prognosis.—When the inflammation of the joint is brief in dura- 
tion, recovery of the muscles may be anticipated with confidence. 
In children, even after prolonged joint disease, the muscles usually 
regain their normal bulk. In adults the wasting often lasts for a long 
time after the joint is well, and a cautious prognosis should be given 
if the arthritis has lasted long. Even if slight wasting is persistent, 
* Raymond, ‘ Rev. de Med.,’ 1S90, 374. 502 
SPINAL COLD. 
normal power is usually recovered, but, as the case mentioned above 
shows, the symptoms sometimes continue for years. The prognosis 
should be especially cautious where there is a marked increase in myo- 
tatic irritability, or if the atrophy shows a disposition to involve 
other muscles of the limb than those concerned in moving the 
affected joint. 
Treatment.—The chief treatment is local; electrical stimulation 
of the muscles, and gentle rubbing. It is doubtful whether drugs 
have any influence on the condition, but small doses of strychnia may 
be given, or added to whatever agent is given for the joint affection. 
As long as the joint is inflamed, treatment rarely causes any increase 
in the bulk of the muscle. It is of great importance to secure the 
early recovery of the joint, and to avoid all influences that cause pain 
in it, since, as we have seen, it is apparently through the sensory 
nerves that the joint affection exerts its injurious influence. When 
the arthritis has ended, the muscles usually recover slowly without 
assistance, but it is probable that the local treatment accelerates the 
process. The form of electricity is of little consequence ; either fara- 
dism or voltaism may be employed, but should only be used in suffi- 
cient strength to cause gentle contraction. The muscles act readily 
to faradism, and a mild faradic current is, as a rule, the best to 
employ. All painful stimulation of the sensory nerves should be 
avoided. 
Muscular Atrophy from Over-use. 
Muscles that are much used sometimes waste. The effect is 
seen most frequently in the small muscles of the hand, especially 
in persons of weakly constitution, who use these muscles unduly. 
Thus a young lady devoted many hours a day to “illuminating/' 
during several years, and then some muscles of the thenar eminence 
began to waste, and became considerably atrophied. Such wasting 
is scarcely ever met with in the larger muscles, but has been observed 
in the biceps, consecutive to hypertrophy, in Sheffield smiths 
(Frank-Smith). The electric irritability is gradually lowered in this 
local wasting, equally to both currents, as it is in progressive mus- 
cular atrophy. We do not know whether this wasting from over use 
is purely local, or whether the related ganglion-cells of the spinal 
cord fail first, and the muscular wastiug is secondary to their 
atrophy. As Gull said many years ago, “ it is as reasonable to 
infer a lesion of the grey matter from overwork as of the muscles.”* 
The wasting often persists when the over-use of the muscles is discon- 
tinued. Hypertrophy from over-use does not usually give place to 
atrophy. These two facts are somewhat in favour of the view that 
the lesion is primarily of the nerve-cells. The wasting in these cases 
* Hosp. Reports/ 18G2, p. 24G. IDIOPATfllC MUSCULAR ATROPUY. 
503 
shows no tendency to extension beyond its original limits. The 
treatment is, first, the cessation from the excessive exertion of the 
muscles ; secondly, the improvement of the general health, and the 
administration of nerve tonics, especially of strychnine; and thirdly, 
the gentle electrical stimulation of the muscles by either faradism or 
voltaism. 
IDIOPATHIC MUSCULAR ATROPHY 
(myopathic atrophy; MUSCULA.R dystrophy). 
Idiopathic atrophy, which is primarily muscular, although it is not 
one of the diseases of the nervous system, is commonly described with 
them, because it frequently presents so close a resemblance to the 
spinal atrophy just described as to be distinguished with some diffi- 
culty. Moreover, even the varieties that do not present this close 
resemblance were for a time, and indeed until lately, believed to be of 
central nature, to depend on the spinal cord, and to be rightly included 
among its diseases. Hence the custom of thus describing them has 
become established, and has now to be followed, although we know 
that it is based on a mistaken theory. At the same time, not only 
has the method the advantage of convenience, but it has also some 
m aisure of scientific justification. The muscles are more closely 
allied to the nerves than to any other structures, as regards both 
physiological properties and pathological susceptibility, and it is 
doubtful whether any other association would better befit these 
diseases. 
The idiopathic myopathies have received a great amount of atten- 
tion during the last seven years, and more facts have been ascertained 
than can yet be used. The difference of opinion regarding the relation 
of the several forms is still considerable. For the present, it seems 
better, therefore, to leave unchanged the method of describing them 
which was first adopted, and which is not without its advantages. 
Before long, it may be possible to recast the description of these 
diseases on lines of greater accuracy.* The following account of them 
may, however, be more intelligible to the reader if it is preceded by 
a brief sketch of their general pathology. Any points of interest in 
connection with their history, &c., are left to be mentioned when the 
varieties ar-e described. 
All the diseases of this class seem to depend on a defective tendency 
of development of the germinal tissue which forms muscles ; they are 
* A treatise upon them by Erb, who made a special study of the subject, is now 
iu course of publication, and cannot fail to make our knowledge far more precise 504 
SPINAL CORD. 
essentially congenital diseases. Although they are, in most cases, 
merely potential maladies at the time of birth, and sometimes for 
years afterwards—even occasionally, during a considerable part of 
life—the morbid tendency does sometimes attain actual development 
in the earlier years. But we know nothing, or almost nothing, at pre- 
sent, of any other cause than this developmental tendency ; we know 
nothing of these diseases as acquired maladies, the result of influences 
acting on a healthy and normal organism. 
Another fact of their general pathology is analogous to that which 
we have already considered in connection with developmental diseases 
of the central nervous system. It depends on the double constitution 
of muscular as of nervous organs, on the presence of interstitial 
connective tissue between the contractile elements, and on the relation 
of both to trophic tendencies. An overgrowth of the interstitial 
tissue may concur with wasting of the fibres, and this overgrowth may 
be abnormal in its features. Hence Erb has chosen the term “ muscular 
dystrophy,” as a more precise designation for the class; we have yet 
to see whether it will obtain general acceptance. The important fact 
to recognise is that there may be either a simple defect in the growth 
of the fibres, ultimately leading to their disappearance, or there may 
be, with this, an overgrowth of the connective tissue, either a simple 
hyperplasia, or a perverted growth in which fat-cells form. These 
cells increase its bulk, but are ultimately removed. The muscular 
fibres are thought sometimes to present hypertrophic enlargement, but 
simple wasting is the most common change. 
The symptoms by Avhich these changes are manifested vary accord- 
ing to the nature of the alteration. In all cases, muscular power fails 
as the contractile fibres waste. The chief difference in aspect, however, 
depends on the seat of the affection and the effect of the interstitial 
changes, and especially on the frequent enlargement of muscles from 
the formation of fat in the fibrous tissue. This produces the semblance 
of hypertrophy that has led to the name “ pseudo-hypertrophic para- 
lysis ” being applied to the cases in which it is present. The amount 
of enlargement varies much ; the fibrous tissue alone may cause none, 
but it is sometimes great and wide-spread in the cases in which fat 
is formed. In all, however, a primary shrinking of the muscles is 
due to the wasting of their proper fibres, the result mainly of a 
defective tendency of vital endurance or growth, and only in a slight 
degree to the influence of the interstitial tissue, when this is increased 
in quantity. 
Thus certain varieties are constituted by the external manifestation 
of the muscular changes. Even in the class in which pseudo- 
hypertrophy occurs, there may be no change, or only diminution 
in the size of the muscles, but with increased firmness, as the 
accompaniment of the lessened poAver. When there is enlargement, 
this may or may not correspond in time to the loss of poAver, since the 
muscular fibres may Avaste either during interstitial groAvth, or aftei PSEUDO-HYPERTROPHIC MUSCULAR PARALYSIS. 
505 
this tissue has undergone the atrophy which ultimately supervenes. 
Thus we may have two classes of cases belonging to this type, 
one with enlargement of muscles, few or many, the other with only 
wasting of muscles, the two corresponding in position and in the 
general course and relations of the affection. 
In another form there is never an interstitial growth of fat, and, 
probably, no considerable increase of fibrous tissue; simple atrophy 
of tue fibres is its pathological characteristic, while primary shrink- 
ing of the muscles is its external manifestation. The shoulder muscles 
are prone to suffer most, and in some cases there is a peculiar affection 
of the face. These cases are also more variable in the time of life at 
which the symptoms begin. But these varieties, as we shall see, are 
connected by cases which to some extent combine the various features. 
Such combined forms forbid the separation of the types, which, never- 
theless, frequently maintain so distinct a course in many members 
of a family, even through several generations, that we are compelled 
to recognise their distinctness, although we cannot divide them 
altogether. 
The essential element in the disease has been spoken of as a “quali- 
tative” defect, which entails an imperfect development, manifested 
sooner or later by the defective vitality of the proper elemeuts of the 
tissue. But there is reason to believe that the defect is not always 
merely qualitative. In some cases the defect in certain muscles is so 
absolute at so early a period, as to make it almost certain that these 
muscles or parts of muscles are congenitally absent, and that the 
germinal defect is thus quantitative as well as qualitative. The 
muscles in which this apparent failure is observed vary in the several 
forms, and will be mentioned in the account of these. 
The peculiar form of atrophy, which differs from the others in the 
■early affection of the muscles supplied by the peroneal nerve, is 
separately described, and its features are not included in these 
remarks. 
PSEUDO-HYPERTROPHIC MUSCULAR PARALYSIS (LlPOMATOUS 
Muscular Atrophy, &c.). 
Tlie affection thus designated usually manifests itself during the 
later developmental period of childhood, and clearly depends on a 
morbid developmental tendency, which, is often present in several 
members of the same family. It is characterised by a progressive 
change in the size, and diminution in the power, of many muscles. 
The apparent cause of the change has been already mentioned 
Isolated cases, which can now be recognised as examples of this 
disease, were recorded in England in 1830 (Sir Charles Bell) and in 
1847 (Partridge), and in Italy in 1838. A series of cases was 
described by Mery on in 1852, and Oppenheim in 1855, but enlarge- 506 
SPINAL CORD. 
ment of the muscles was not conspicuous in these.* Several remarkable 
examples had already come under the notice of Duchenne, who was 
busy exploring the field of muscular paralysis with the aid of 
“ localised electrisation.” He recognised its novel features, and pub- 
lished an account of it in 1861, under the name by which it has since 
been generally known. 
Etiology.—Our knowledge of the causes of the disease is limited 
to a few general facts. Males furnish the majority of the cases ; they 
suffer at least four, and perhaps seven times as frequently as females. 
In the latter, moreover, the malady is slighter in degree, later in 
development, and less frequently causes death. 
The disease occurs rather less commonly in isolated cases than in 
family groups. The number in a family has varied from two to eight. 
As many as eight brothers suffered and died in the family described 
by Meryon, while all the daughters escaped. In a family known to 
me, four sons have suffered and none of the daughters ; in another 
instance two daughters are affected and no sons. Thus there may be 
a tendency in a family to the affection of one sex, and not the other; 
but, on the other hand, children of both sexes may suffer in the 
same family. In many instances in which several members of one 
generation are affected, no antecedent cases can be traced in the family ; 
the malady, while congenital, is not hereditary. In other families 
antecedent cases can be traced, and these are invariably on the mother’s 
side. The disease is thus transmitted by women who are not them- 
selves its subjects. In a case in which four brothers suffered, the 
mother’s brother and sister were likewise affected. Again, a brother 
and sister were diseased, one daughter of a second sister, and three 
daughters of a third sister. In another instance, a boy suffered, and 
his sister, unaffected, had two sons diseased and a daughter free, of 
whose children two sons were the subjects of the malady. Thus the 
congenital tendency is exclusively due to the maternal element in the 
embryo. This is also shown by a fact many times observed, that the chil- 
dren of the same women, by different husbands, suffer in the same way. 
Indirect hereditary tendencies, such as are indicated by the occur- 
rence of diseases of the nervous system, can be traced so rarely that 
it is doubtful if they have any influence. Neither the age of 
parents, nor their intemperance, appears influential, and their con- 
sanguinity becomes effective only when raised in energy by repetition. 
Thus in a family known to me, the intermarriages during five genera- 
* Nevertheless, Meryon’s cases (‘Med.-Chir. Trans.,’ 1852) certainly belonged to 
this variety. Conclusive proof of the fact is afforded by cases in collaterals which 
have come under the writer’s observation in near and distant branches of the same 
family. Other evidence of the fact is described in a * Cliuical Lecture on Pseudo* 
hypertrophic Paralysis’ (London, Churchill, 1879). The chief literature is referred 
to in that lecture; the numerous papers that have appeared since have added 
chiefly to our knowledge of the characters of the allied forms of idiopathic atrophy, 
&c., and the relations of these to the pseudo-hypertrophic variety, and are referred 
to on a later page. PSEUDO-llYPERTEOPHIO MUSCULAR PARALYSIS. 
507 
tions were very numerous, and of eight children in the present family, 
five are albinoes, and two of these are the subjects of pseudo-hyper- 
trophic paralysis. 
The disease always manifests itself during the period of development, 
sometimes in the early stage of growth, at the close of infancy, often 
only during mid-childhood, rarely not until growth is nearly ended. 
In a third of the cases, the first symptoms are noted when the child 
first attempts to walk, which is usually a little later than in healthy 
children ; very rarely indeed, the child has never walked. In about 
another third the child seems well until it is four, five, or six years 
old, and then impairment of power attracts attention. In three 
quarters of the cases, the disease manifests itself before the tenth 
year. Barely, the patient is conscious of no symptoms until after 
puberty, at the age of eighteen or twenty, but in such apparently late 
onset, there has been enlargement of muscles long before power 
becomes impaired, and the disease began much earlier than it seemed 
to do. One patient, for instance, in whom weakness was only noticed 
when she was twenty, had been often “ chaffed,” when a young girl at 
school, on account of her “ tea-kettle calves.” Neither social state 
nor general constitutional condition seems to influence the occurrence 
of the disease, but its manifestation has sometimes been apparently 
accelerated by influences that disturb the general health; it has been 
first noticed, for instance, during convalescence from some general 
illness. 
Symptoms.—Impairment of power usually atti’acts attention before 
any change is observed in the size of the muscles, or if these are 
noticed to be large, it is with feelings of parental pride rather than 
with suspicion, in spite of the fact that the children often walk 
clumsily, fall with ease, and rise with difficulty. The act of going 
upstairs is especially difficult to them; the child has to take hold of 
the banisters and pull himself up. 
The muscles may at first present nothing unusual, especially in slight 
cases, or if the child is fat, as is frequently the case. But at the 
age of five or six years an unnatural enlargement of certain muscles 
is usually conspicuous, especially when there is a contrast between 
these and other muscles which are small. If enlargement is almost 
universal, it is usually great and conspicuous. The enlarged muscles 
usually for a time become still larger in comparison with the others, 
but afterwards they cease to increase and ultimately become smaller, 
first relatively and then absolutely. This change occurs earlier in 
some muscles than in others, and it may give place to a condition of 
distinct atrophy. 
Among muscles that are most frequently large, those of the calf 
take the first place. They sometimes attain a remarkable size. I have 
measured a calf 14| inches in circumference in a boy of twelve. The 
muscles in front of the lower leg are less frequently enlarged, but 
sometimes project beyond the edge of the tibia. The extensors of the 508 
SPINAL OOIiD. 
Fig. 145. 
Fig. 146. 
Fig. 147. 
Figs. 145 nnd 146.—Two brothers, aged four and s?ven, suffering from 
pseudo-hypertrophic paralysis. 
Fig. 147.—Partial enlargement of rectus, the vasti being small. 
knee are often big; occasionally the rectus or vastus internus is alone 
increased in size (the rectus in Fig. 147), and the other parts may be 
normal or small; less frequently all parts are small. The flexors of the 
knee commonly escape. The glutei are frequently conspicuously large ; 
the flexors of the hip are, of course, inaccessible to observation, but 
they are usually feeble, and no doubt diseased ; there is generally 
enlargement of the lumbar muscles, and disease of a peculiar and 
important character in those of the shoulder. 
Of all the muscles of the body, next to those of the calf, no one is 
enlarged more frequently or in greater relative degree than the infra- 
spinatus. It often stands out so conspicuously that its edge is apt 
to be mistaken for that of the scapula (Figs. 148 and 149). The 
supraspinatus is sometimes also prominent, but its condition is usually 
concealed by the trapezius, which is little involved. The deltoid is also 
frequently large ; the serratus rarely. The pectoralis is never enlarged, 
but, on the other hand, its lower half is wasted or absent (see p. 518) 
in a large proportion of the cases, and with this the latissimus dorsi, 
which has the same action in depressing the raised arm (see p. 26). 
The teres major may share the wasting of the latissimus. 
The other muscles of the arm suffer in diminishing degree and fre- 
quency from above downwards. The triceps and biceps are sometimes PSEUDO-TTYPERTROPEIO MUSCULAR PARALYSIS. 
509 
enlarged, the former more frequently than the latter, but occasionally 
only in one part. Both these muscles are sometimes wasted. The 
forearm muscles suffer in 
only a email minority of 
the cases, and the intrinsic 
muscles of the hand usually 
escape altogether. 
This escape of the intrinsic 
muscles of the hand affords 
a very marked contrast to 
spinal muscular atrophy, in 
which they suffer early; but 
Fig. 149.—Wasting of latissimus 
dorsi and serratusj enlarge- 
ment of infraspinatus, supra- 
spinatus, and deltoid; atrophy 
of biceps and triceps. (By Dr. 
H. R. Spencer, from a photo- 
graph.) 
Fig. 148.— Pseudo-hvpertrophic paralysis. 
Absence of latissimus dorsi, enlargement 
of infraspinatus. (From a photograph.) 
no rule is free from exception, and although the escape of the hands 
in the idiopathic affections is almost constant, it is not quite invariable; 
slight (or commencing) implication of the intrinsic muscles has been 
met with in very rare instances that were otherwise typical,* and quite 
distinct from the “peroneal type” to be presently mentioned. 
The muscles of the neck are very seldom affected, but I have noted, 
in a few cases, wasting of the clavicular part of the sterno-mastoid. 
Those of the face do not suffer except in extremely rare cases 
* JE.ff. Sachs, ‘New York Neurol. Soc.,’ Oct. 2nd, 1888; Baumler, ‘ Sudwest. 
Neurol. Versamml.,’ Freiburg, 1888. I have once met with wasting of the 
extensors of both phalanges of one thumb, and enlargement of the abd. indicis has 
been observed (Taylor, Clin. Soc., April 24th, 1891), and fatty growth in the thenar 
muscles (Berger, ‘Arch. f. Psych.,’ Bd. xiv). 510 
SPINAL CORD. 
intermediate between this and the third type (see also Westphal, 
* Charite Annalen,’ 1887, xii, p. 447), but in the patient shown in 
Mg. 152 there was considerable enlargement of the masseters. The 
tongue has been increased in size in a few instances. The other 
muscles supplied by the cranial nerves always escape. 
The diseased muscles are weak, but the impairment of power is to 
some extent irrespective of the change in size. The muscles that are 
abnormally small are generally weaker than those that are abnormally 
large ; and in the latter the weak- 
ness increases with the wasting. In 
the legs, the greatest weakness is in 
muscles that are inaccessible to ex- 
amination—the flexors of the hips; 
next in order of weakness come 
Fig. 150.—Mode of obtaining extension of hips 
in pseudo-hypertrophic paralysis. F, ful- 
crum of the lever formed by the femur. P, 
mean position at which the power is applied 
by contraction of the quadriceps femoris. 
W, position of weight in the ordinary mode 
of rising, w, the place to which part of 
the weight is transferred by putting hands 
on knees. 
Fig. 151.—Mode of rising from the 
ground in pseudo-hypertrophic 
paralysis. 
the extensors of the knee, and the extensors of the hip. The muscles 
below the knee usually retain considerable power for a long time, and 
the extensors of the ankle fail before the flexors. In the upper limbs 
the depressors of the arm are usually alone weakened during the early 
period of the disease, but subsequently the shoulder muscles suffer, 
then the triceps and the biceps, while the muscles that move the hand 
commonly retain good power tp the last. 
The distribution of weakness in the legs causes certain peculiar 
defects of movement which are very characteristic, and some are even 
all but pathognomonic of the disease. The difficulty in going upstairs PREUDO-HYPERTROPHIO MUSCULAR PARALYSIS. 
511 
is especially due to the weakness of the extensors of the knee and hip 
The defect of the extensors of the hip causes the gait to have a 
peculiar oscillating character, in which the body is so inclined as to 
bring the centre of gravity over each foot, on which the patient 
successively throws his weight, because the weak gluteus medius 
cannot counteract the inclination towards the leg that is off the ground, 
unless the balance is exact. The greatest defect, however, is in the 
power of rising from the floor, and the most characteristic peculiarity is 
the mode in which this is achieved, if it be still possible, and no objects 
nre near, by which the patient can aid himself. He commonly has not 
sufficient power to extend the knees when the weight of the trunk is 
on the upper extremity of the femur, which is then a lever in which 
the power, applied between the fulcrum and the weight, acts at least 
advantage. He therefore places his hands on his knees, as in Fig. 150 ; 
and his arms thus bring much of the weight of the upper part of the 
trunk on the femur close to the fulcrum, between this and the power, 
which can then act at greater advantage. Moreover, the mere weight 
of the head, which is in front of the arms, tends to aid the extension. 
This, indeed, may effect the extension of the knee without the aid of 
the extensor muscles, as anyone may ascertain by observing the mobility 
of the patella in this attitude. When the knees are extended, the 
power of the extensors of the hip may be sufficient to raise the body 
into the upright position, or the patient may aid them by an upward 
push with the hand as he takes it off. If, however, these extensors 
are weak, the hands are often moved higher and higher up the thighs, 
grasping alternately, and thus pushing up the trunk. To get thus the 
requisite support, the knees must not be quite extended; and if their 
•extensors have no power, the device cannot be employed, and the 
patient is altogether unable to rise. In many cases, especially when 
extension of the hip is easy, the patient achieves the extension of the 
knees in another way ; he puts the hands on the ground, stretches out 
the legs behind him far apart, and then, the chief weight of the trunk 
resting on the hands, by keeping the toes on the ground and pushing 
the body backwards, he manages to get the knees extended, until the 
trunk is supported by the hands and feet, all placed as widely apart 
as possible (Fig. 151, 2). Next the hands are moved alternately along 
the ground backwards, so as to bring a larger portion of the weight 
of the trunk over the legs. Then one hand is placed upon the knee 
(Fig. 151, 3), and a push with this, and with the other hand on the 
ground, is sufficient to enable the extensors of the hip to bring the 
trunk into the upright position. 
The shortening and contraction of certain muscles lead to another 
group of symptoms,—distortions due to permanent alteration in the 
position of joints. Some of these are produced, as are distortions in 
other forms of muscular weakness, by shortening of the less affected 
opponents of the weaker muscles. Thus the knee-joints become fixed 
by the contraction of the flexors, and the elbow by the contraction of 512 
SPINAL COED. 
the biceps when the triceps has lost all power. These contractions 
only occur late, and are usually facilitated by the habitual flexion of 
the knee- aud elbow-joints. But the deformity at the ankle-joint, which 
results from contraction of the calf muscles, commences earlier, before 
their opponents are weak, and is the result of shortening of the muscles. 
As a consequence of it, the patient cannot get the heels well upon the 
ground, and the foot cannot be flexed passively beyond a right angle, 
lhe gradual increase of the contraction results in considerable 
“ talipes equinus, and as power lessens, the patient is able to walk less, 
and the consequent loss of the extension involved in the act permits 
a rapid increase in the cont rac- 
tion. The feet, as Fig. 152 
shows, soon assume a pos- 
ture of extreme extension, the 
dorsum being in a line with the 
front of the leg, or forming 
with it a convex curve. A 
subluxation of the ankle-joint 
takes place, and the articular 
surface of the astragalus, its 
anterior extremity, and that 
of the os calcis, form three 
prominences under the skin. 
When this reversal of the 
ankle occurs, the tibialis anti- 
cus can no longer act as a 
flexor. 
Another deformity, which is 
due chiefly to muscular weak- 
ness, is curvature of the spine. 
An antero-posterior curve, 
with the concavity backwards, 
is an early symptom of the 
disease, and it may become 
extreme, the upper part of the trunk being carried so far back that a 
veitical line from the scapula falls an inch or more behind the sacrum. 
It is due, not to the weakness of the trunk muscles, but to that of the 
extensors of the hip, in consequence of which the pelvis is inclined 
forwards, carrying with it the lower lumbar vertebrae ; hence the upper 
part of the trunk has to be held far back to keep the ceutre of gravity 
of the body over the feet. The proof of this mechanism is that w'hen 
the patient sits, and the pelvis is supported on the ischial tuberosities, 
the lordosis disappears. It is, indeed, replaced by an opposite curve, 
in which the back becomes convex, clearly due to the weakness of its 
extensor muscles. This curve may become very great, as in the case 
shown in Fig. 153. The weakness of the spinal muscles also permits 
the occurrence of lateral curvature 152), influenced, in its 
l’io. 152.—Late stage of pseudo-hypertro- 
phic paralysis; a boy fourteen years old, 
with muscular contraction and wasting, 
and lateral curvature of the spine. PSEUDO-HYPERTROPHIC MUSCULAR PARALYSIS. 
513 
direction, by the habitual posture and the preponderance of weakness 
on one side or the other. 
Fig. 153.—Lad, aged fifteen; late stage; wasting of 
thighs; inability to sit upright in consequence of 
the weakness of the spinal muscles. 
The electric irritability of the muscles is only altered when distinct 
weakness or wasting has set in, when it is lowered alike to faradism 
and voltaism. There is never any ti’ace of degenerative reaction. 
The knee-jerk may be at first normal, but as the extensors of the 
knee become feeble, it is always lessened and gradually disappears. * It 
is never excessive, and in all advanced cases it is lost. Sensation is 
unaffected, and so also are the sphincters in the vast majority of cases. 
Yery rarely there has been, towards the end, a slight difficulty in the 
retention or expulsion of urine, to be regarded, perhaps, rather as a, 
complication than as an effect of the disease. All other functions of 
the nervous system are commonly normal, including those of the 
sympathetic. The mental development of the subjects of this disease 
is generally beyond that of other children of the same age, doubtless 
on account of the indirect influence of a malady which withdraws them 
from active amusements; mental defect is a pure complication. 
The rate of progress of the disease and its duration vary much. 
After some years, often between ten and fourteen, the power of standing 
becomes lost in consequence of the increasing weakness and the con- 
traction of the calf-muscles. When the patient ceases to walk, the 
muscular disease make::, more rapid progress, deformities become 
greater, and the patient may become almost helpless, except in the 
hands, and yet live on for several years. Death is sometimes due to 
some intercurrent malady, as an acute specific disease, but generally 
the lessened respiratory power causes come chest affection to develop, 
or one that should be trifling, to become grave. Life is thus ended bjr 
acute pneumonia or bronchitis, or by chronic lung disease,— a form of 
vol. r. 514 
SPINAL CORD. 
pneumonic plitliisis or broncho-pneumonia, which develops gradually, 
with little febrile disturbance. There is never suflicient paralysis of 
the respiratory muscles to cause death directly, l lie duration of the 
stage of helplessness depends very much on the care which the patient 
can obtain. 
In the cases in which muscular power remains good until after 
puberty, the progress of the disease is generally slow. The patient 
may reach the age of thirty before power is much impaired. It is possible 
that, in some cases, the disease never attains a considerable degree. 
More frequently, however, after slight symptoms have lasted for some 
years, a rapid increase occurs, and very few patients reach the age of 
forty. The course of the disease is slower in girls than in boys, and 
females furnish a relatively large proportion of the late cases. 
Varieties.—The chief varieties of the disease depend on the age at 
which it commences, and on the condition of the muscles, whether they 
are large or small. In rare cases a single muscle may be large, and 
the rest small, as in Fig. 154, in which only the 
vast! were increased in size. Or everywhere and 
from the first the muscles are smaller than nor- 
mal, and they progressively waste. Such cases 
are not uncommon ; in the first group of cases 
described (by Meryon), enlargement of muscles 
was inconspicuous. Many cases in which all 
muscles are small belong properly to the form 
considered in the next section. The cases 
described by Meryon must be regarded as ex- 
amples of the pseudo-hypertropliic form (see 
p. 505), but they present many points of resem- 
blance to the “simple atrophy” described further 
on. 
Complications.—Congenital mental weakness, 
due apparently to defective development of the 
brain, sometimes complicates pseudo-hvpertrophic 
paralysis. In rare cases there have been indica- 
tions of some other morbid condition of the 
central nervous system, such as epilepsy. It 
is uncertain in what light the slight occasional affection of the 
bladder is to be regarded, whether as an invasion of the vesical 
muscles or as a central complication. Vigoroux has recorded a case in 
which the symptoms of pseudodrypertrophic paralysis were combined 
with the peculiar rigidity of Thomsen’s disease. Of course the subjects 
of the disease are liable, like other children, to various affections of the 
nervous system ; I have seen both chorea and polio-myelitis as merely 
accidental complications. 
Pathological Anatomy.—It is rare, at the time of death, for any 
muscles to be actually larger than natural, and most of those that are 
affected are usually below the normal size. They are pale and 
Fig. 154.—Enlarge- 
ment of the vasti 
and not of the 
rectus. In this case 
all other muscles 
were below normal 
size. PSEUDO-HYPERTROPHIC MUSCULAR PARALYSIS. 
515 
yellowish in colour, and often, to the naked eye, resemble perfectly 
masses of adipose tissue. The resemblance is not merely one of aspect. 
As seen under the microscope, it may be difficult for the observer to 
realise that he is not looking at a fatty tumour. Nothing may be at 
first visible but fat-cells, precisely like those of adipose tissue. Among 
the cells, however, are tracts of nucleated fibrous tissue, and a closer 
examination of these shows that the tracts contain also muscular fibres 
(Fig. 155), most of them much narrower than normal. They are also 
irregular in width; a broad fibre, for instance (as in the figure), sud- 
denly becoming narrow. 
Fl3. 155.—Gastrocnemius muscle; muscular fibres, irregularly nar- 
rowed and in part degenerated, lie among tracts of nucleated fibrous 
tissue, separated by adipose tissue. 
The fibres for the most part preserve their transverse striation, but 
where they are narrowest this may have in part disappeared, either by 
granular degeneration, or, more commonly, by a simple fading of the 
striae. In the narrowed fibres the striae are sometimes farther apart 
than normal. In other parts broad fibres may be seen, normal or 
nearly normal in aspect (Fig. 156) coursing among the fat cells, aud 
accompanied by a smaller amount of fibrous tissue. Fibres occasion, 
ally present fatty degeneration, a longitudinal striation or Assuring, 
vitreous (“waxy”) degeneration, or vacuolation, but these are rare. 
Some empty sarcolemma sheaths maybe seen where the narrowing of 
the fibres is greatest. In muscles that still preserve some red tint, 
the amount of fat is less, and there is often a relatively larger amount 
of interstitial fibrous tissue. Very rarely, in some part of a muscle, 
there has been only wasting of the fibres, without the interstitial 
change, present elsewhere (Singer, in the triceps). 516 
In some of these the interstitial tissue may be almost entirely 
fibrous, a few fat cells only being visible here and there. In such 
muscles it is common to find the fibres more damaged than in 
those in which the growth is partly fatty. It is chiefly in the latter 
that many normal fibres are seen. Muscular fibres larger than normal 
are seldom found after death, but such fibi-es have been seen in frag- 
ments removed during life by excision, or by a “ harpoon-trocar; ” 
it is possible that the increased size was due to a vital contraction 
under the mechanical stimulus involved in the extraction, but enlarge- 
ment has sometimes seemed unquestionable (See note, “Muscular 
Hypertrophy ”). 
SPINAL COIiD. 
Fig. 156.—Gastrocnemius muscle; two nearly normal muscular fibres, 
accompanied by fibrous tissue, surrounded by fat cells. 
The motor nerves, when examined, have been found normal. The- 
condition of the sensory muscle-nerves (which terminate in the 
interstitial tissue in which the primary morbid process occurs) has not 
been ascertained in any instance. The spinal cord has been found 
perfectly normal in most cases in which it has been examined. In 
a few there have been slight and irregular degenerative changes. 
They have not been so marked in any other case as in one examined 
by Lockart Clarke and myself,* but the anterior grey matter was 
unaffected, and the changes were probably merely associated, and 
not the cause of the symptoms. Haemorrhages have been occasionally 
found. Probably they have occurred late in life in the degenerated 
* * Med.-Cliir. Trans.,’ vol. lvii, p. 247. In this case the cervical and dorsal 
regions were normal, with the exception of here and there slight accumulations, at 
the bottom of the fissures, of products of degeneration, probably derived from the 
perivascular erosion common at all ages. At the last dorsal segment, however, there 
was an area of granular disintegration in the intermediate grey substance on each 
side, in front of the posterior vesicular tract. This part was unduly translucent for 
half a centimetre in vertical extent, and in the middle of this area the disintegration 
had produced an actual cavity, across which the fibres for the cerebellar tract ran 
unchanged. PSEUDO-HYPERTROPHIO MUSCULAR PARALYSIS. 
517 
tissue. The neuroglial cells have been found increased in number, 
and the fibres of the white substance have been found irregularly 
changed, in a few cases, without any constancy in the seat of the 
alteration. 
Pathology.—The common integrity of the anterior grey matter of 
the cord, and especially of the motor nerve-cells, seems conclusive evi- 
dence that the disease of the muscles is not due to a primary lesion of 
the spinal cord. The slight irregular changes occasionally found 
are probably consecutive to the long inaction of the coid and 
deformity of the spine. Pseudo-hypertrophic paralysis is not there- 
fore, as was at first thought, merely a form of spinal muscular atrophy 
with a special muscular change. The significance of the pathological 
anatomy is that the malady is a primary disease of the muscles, 
consisting in an overgrowth of the interstitial connective tissue, in 
which fat may or may not be deposited, and that the wasting of the 
muscular fibres is secondary to the interstitial growth. The indi- 
cation of the conditions under which the disease occurs is that the 
disease is congenital, the result of a perverted tendency of growth, 
inherent in the embryo, and derived from the germ from which the 
embryo proceeds. In this connection it is instructive to note that 
there is one form of congenital tumour, the structure of which is almost 
exactly the same as that of the muscles in pseudo-hypertrophic 
paralysis. Pig. 157 might be a fragment of a muscle in this disease, 
Fig. 157.—Section of a myolipoma which was attached to the spinal 
cord of a man suffering from locomotor ataxy, for comparison with 
Figs. 155 and 156. 
but it is a section of a myolipoma, the congenital character of which 
is emphasised by the fact that it was attached to the conus medullaris 
of the spinal cord of a patient whose muscles were healthy. (The 
tumour is shown also in Fig. 163). It must have been due to the 
misplacement of some of the embryonal elements from which muscular 518 
SPINAL CORD. 
tissue is developed, and it shows that, from such elements, tiie 
structural condition found in pseudo-hypertrophic paralysis may arise. 
The points of chief importance in the general pathology of the disease 
have been mentioned in the introductory remarks. The difficult 
question of the precise mechanism by which the muscular fibres 
suffer must be regarded as an open one. We may assume a defective 
vitality in them, but the conspicuous lesion is the growth of connec- 
tive tissue, and by this the fibres are doubtless damaged, whether 
fatty tissue is formed or not. Indeed, the fibres seem to suffer more 
when there is only fibrous tissue than when there is the fatty deposit, 
although it is chiefly the fat that causes the enlargement of the 
muscles. There seems to be a tendency to the formation of fat in 
the early stage of the disease, and to its removal in the later stage, 
since in the former the muscles may often be observed to increase 
in size, and in the latter they become smaller, partly from some 
removal of fat and partly from the increasing atrophy of the muscular 
fibres. It is then that the greatest impairment of power occurs. 
In the cases in which the muscles are small from the first, the 
tendency to the deposit of fat seems slight, and the condition is 
an almost pure muscular sclerosis. The late shortening which occurs 
seems to be due to the contraction of the interstitial fibrous tissue, 
and it often coincides with the shrinkage from the removal of some of 
the fat, and the atrophy of the muscular fibres. 
If it be true that the latissimus dorsi and lower half of the 
pectoralis are sometimes congenitally absent in pseudo-hvpertrophic 
paralysis, the fact is quite consistent with the explanation of the nature 
of the disease given above. These two muscles stand perhaps lowest, 
in functional importance, among the muscles of the body, being used 
chiefly for the rare depression of the arm against a resistance (see 
p. 26). It is readily intelligible that a defect in the embryonal tissue 
of the muscular system should be quantitative as well as qualitative. 
The loss of the knee-jerk is sufficiently explained by the lesion of 
the muscles. According to the theory that the irritability on which 
the jerk depends is due to a muscle-reflex action, the loss is readily 
intelligible, since the afferent impulse is due to the stimulation, by 
tension, of the sensory muscle-nerves, and these end (or begin) in the 
interstitial tissue, which is the seat of the primary morbid process in 
this disease. But the wasting of the muscular fibres must also be 
capable of abolishing the knee-jerk when the atrophy reaches a 
considerable degree, and it is also possible that the motor nerve- 
endings share this structural damage. On any theory of the nature of 
the knee-jerk, this will explain its loss. It is only when the muscular 
changes have attained a considerable degree that the loss occurs. The 
fact therefore does not, in itself, suggest any lesion of the spinal 
cord. If the malady is thus one of a morbid developmental tendency, 
it is not surprising that a tendency to analogous developmental 
diseases should be sometimes present in the nervous system, and that psEUDO-nYPEirmopino muscular paralysis. 
519 
thus imbecility and epilepsy on the one hand, or albinism on the other, 
should be occasionally associated with the disease. 
Diagnosis.—The diagnoses of the disease is usually easy, if its 
characters are known. The peculiarity of gait and the mode of rising 
from the floor, the age of the patient, and the progressive character of 
the impairment, are in themselves sufficient to suggest the affection, 
and examination reveals enlargement and often contraction of the calf- 
muscles, and a change in the size of others, which confirm the diagnosis. 
The mode of rising is not absolutely pathognomonic, audit has misled 
even good observers; it is occasionally acquired in other diseases in 
which there is a gradual weakening of the extensors of the hip and 
knee. It is met with equally in the simple idiopathic atrophy, but is 
so rare from any other cause as to be of very great diagnostic 
suggestiveness. 
Of the condition of the muscles, that which is most characteristic 
is the combination of enlargement of the infraspinatus with a 
wasting of the latissimus and lower part of the pectoralis. I pointed 
out some years ago* that this condition, which is seldom absent, is of 
very high diagnostic importance, and subsequent observations have 
fully confirmed the opinion. Next in importance is the enlargement 
of the calf-muscles, especially in combination with contracture that 
cannot be overcome. In general, the enlargement and diminution of 
neighbouring muscles is very significant, but it must be remembered 
that they may be gravely diseased, and yet of normal size, or from 
the first smaller thau normal. In such cases they are often hard, 
and the distribution of the affection is the same as that of the double 
change in typical cases. Such cases illustrate the relation of this 
form and the simple atrophy described in the next section. 
The disease with which confusion is most common is the so-called 
“ congenital spastic paraplegia ” (p. 441). Both diseases affect 
children ; in both there are weakness of the legs and contraction of the 
calf-muscles, and in both the muscle§ are frequently large. The chief 
distinctions have been already mentioned. The most important are 
the preservation and excess of the knee-jerk in spastic paraplegia, the 
tendency to spasm of the legs,—the facts that the contracture is active 
and can be overcome, that the patient does not rise from the ground 
in the way peculiar to pseudo-hypertrophic paralysis,—and the oppo- 
site tendency of the two diseases. Spinal muscular atrophy is only 
likely to be confused with the simple atrophy. 
Between the two forms of idiopathic atrophy, the distinction is 
scarcely one of diagnosis proper; it is rather a question of the category 
in which a case should be placed. The most important distinction is 
the freedom of the calf-muscles from enlargement in the atrophic form. 
The face is not affected in pseudo-hypertrophy as it so often is in 
idiopathic atrophy, except only in some intermediate instances. If 
more than one member of a family is affected, some of the sufferers 
* ‘ Pseudo-hypertrophic Muscular Paralysis,’ London, 1879. 520 
SPINAL CORD. 
will usually present characteristic symptoms of the special form, for it 
is remarkable with what constancy the two types generally remain 
distinct (see p. 403). 
Prognosis.—In the case of any child with pseudo-hypertrophic 
paralysis, the prognosis is most grave. It is almost certain that each 
year will bring increasing disability, and that the patient will not 
reach adult life. It is only when the disease develops late, and the 
symptoms do not become considerable until after twenty years of age, 
that there is a possibility that the disease may not attain its ultimate 
degree, but even in such cases this hope is seldom realised. In any 
case, and at any age, it is unlikely that the patient will live more than 
seven years after the power of standing is lost. 
Treatment.—As a congenital developmental malady, pseudo-hyper- 
trophic paralysis is one of those diseases in which medicine is neces- 
sarily powerless to cope with the essential elements of the process. 
As may be, therefore, expected, no drug has been found to exert an 
influence on the course of the affection, although such nervine tonics 
as phosphorus and arsenic have been thought sometimes to retard for 
a time the progress of the weakness. The stimulation of the muscles by 
electricity has been emplo}red and advocated, but, however sedulously 
employed, no distinct result follows the use of either faradism or 
voltaism. It must be remembered, moreover, that electricity is a very 
feeble agent in stimulating the growth of muscular fibres, compared 
with the physiological stimulus of voluntary effort. Muscular exercise 
may reasonably be looked to in order to make up, in some degi'ee, 
what is lacking in this disease, and does seem to have some influence 
in retarding the failure of power. It may perhaps induce further 
growth, or greater power in the muscular fibres that have not yet 
suffered, or actually supplement the defective trophic energy. When 
muscular exercise is stopped, there is certainly a quicker failure of 
strength. Hence it is desirable that the patient should carry out 
carefully planned gymnastic exercises, so arranged as to call into 
action the muscles that most need help. These, thoroughly per- 
severed in, have seemed, more than any other means, to retard the 
disease. Although they have not in any case arrested it, the trouble 
that is necessary to arrange the method is certainly well spent. 
Rubbing and massage improve the circulation, and tend, especially 
when combined with passive movements, to lessen the tendency to 
muscular contraction and consequent deformities. 
The influence of muscular exercise renders it very important to 
maintain locomotion as long as possible. The ability to stand and 
walk is generally lost, through the contraction of the calf-muscles, 
some time before the muscular weakness would take the patient off his 
feet. In such cases, tenotomy may restore the power of walking for 
some years, and when the contracture returns, its removal has, a 
second time, enabled walking to be resumed. The operation is thus 
distinctly beneficial, and should be performed as soon as the actual SIMPLE IDIOPATHIC MUSCULAR ATROPHY. 
521 
need for it arises, and division of the tendon is far better than any 
imperfect substitute. 
During the later stages of the disease great care is required to 
preserve the patient from catarrh, which helps to excite the pulmonary 
mischief that so often ends life. Similar care is also needed during 
any intercurrent malady which the patient may contract. 
Simple Idiopathic Muscular Atrophy.* 
The cases in which there is no muscular enlargement, in which 
wasting is manifest from the first in the size of the muscles, are much 
more rare than the pseudo-hypertrophic disease. They belong to 
several types, more or less distinct, of which the most common is that 
to which Erb has given the name of “juvenile,” and of which most 
instances are probably the pseudo-hypertrophic disease without mus- 
cular enlargement; others are more special since the lower leg 
muscles have suffered but little. A more striking variety is that 
which is characterised by the affection of the muscles of the face 
in addition to those of the shoulder girths—the “ facio-scapulo- 
humeral type ” of Landouzy and Dejerine. In a third variety the 
affection begins in the legs and is peculiarly slow in course. Some 
other types may ultimately be differentiated, but it is important 
to recognise the fact that even those that we can now distinguish, as 
the most pronounced in their features, do not keep entirely distinct. 
They are connected, by intermediate forms, not only with each other, 
but even with the pseudo-hypertrophic disease.f But these are very 
rare ; as a rule the two latter types remain distinct in the families in 
which they occur, and this is the justification for their separate 
description. In those families in which simple muscular atrophy 
occurs, however numerous the cases, however different the distribu- 
tion of the disease, and however various the ages at which it begins, 
cases rarely present the distinctive characters of pseuclo-hypertrophic 
paralysis. 
* The most important writings on the subject (besides those specially quoted) are 
those of Duchenne in ‘ Electrisation Localise ’ (,p. 60 of Poore’s translation, published 
by the New Sydenham Society) ; Barsickow, ‘ luaug. Dissert.,’ Halle, 1872 ; Leyden, 
* Klin. d. Ruckenm. Krank./ Bd. ii, p. 525; Mobius, “ Hered. Nervenk.,” Volkmann’s 
* Klin. Vortrage,’ No. 171; Landouzy and Dejerine, ‘ Revue de Med./ 1885, pp. 81 
and 251; Marie and Guiuon (a series of cases observed at the Salpetriere), ib., 1885 ; 
Sachs, ‘New York Med. Journ./ Dec. 15th, 1888; Hitzig, ‘Berlin klin. Woclien- 
schr./ 1888; Singer, * Zeitsch. f. Heilk./ Bd. viii. Especially valuable are the 
papers by Erb, ‘ Deut. Archiv f. klin. Med./ Bd. xxxiv, 1884, and ‘Neurol. Cen- 
tralbl./ July 1st, 1886, with numerous later writings. Bibliographical references, 
&c., will be found also in Tooth’s ‘Thesis on the Peroneal Type/ and in my Lecture 
on Pseudo-hypertrophic Paralysis (1879), and in Sack’s article (loc. cit.). 
f E.g., case described and collected by Marie and Guinon (loc. cit.), connecting 
the pseudo-hypertrophic form with both the juvenile and the facial. 522 
There is less constant separation between the simple “juvenile” 
and the facial forms. Although they often keep distinct, the affection 
of the face has been absent in a few cases in a family in which it 
was the first part to be affected in most sufferers. Thus a man with 
simple atrophy, beginning at fourteen in the shoulder- and thigh- 
muscles, whose face was unaffected, had a daughter who began to 
suffer at eleven, and in whom the face, scapular, and arm muscles 
were involved.* The peculiar “peroneal type” is not included in 
this outline, and the statements here made do not apply to it. 
Causes.—We are able to trace no cause beyond the congenital 
tendency, already considered, shown by the occurrence of many cases in 
the same family, and in more than one generation. In one remarkable 
series recorded by Barsickow, twenty-four cases were distributed 
through five generations, and the disease was also traced through five 
generations in a group described by Landouzy and Dejerine. It is 
very rare for the disease to be confined to one generation, far more 
rare than for pseudo-hypertrophic paralysis to be so confined. But, as 
in the case of most congenital hereditary diseases, cases that are 
apparently isolated are occasionally met with. Such isolated cases 
are rare,—more so, probably, than in the pseudo-hvpertrophic form; 
although wider observation may show that they are more frequent 
than we now suspect. In the families of the patients shown in Figs. 
158-61 and 162 no example of analogous disease could be heard of. 
Both sexes suffer; in a few families, females chiefly; in others,, 
males ; in most, both have been affected. The age at which the disease 
first manifests itself is extremely variable. It may begin as early as 
twof or threej and as late as sixty years. But the onset is seldom 
during childhood ; in the majority of cases the disease shows itself 
between fifteen and thirty-five; that is, during the later period of 
growth and the early period of adult life. Even in the same family, 
the variations may be extreme ; in that described by Barsickow the 
date of the onset of seventeen cases was known, and was as follows :— 
in one at 12; in four between 15 and 20; in seven between 20 and 30; 
in three between 30 and 40; in two after 40. A woman, aged fiftv-two, 
began to suffer at 30, but her son at 3 yeai's of age.§ Sex lias no 
influence on the date of onset, nor, as a rule, can any relation be traced 
between the date and the place at which the wasting begins. When the 
wasting begins in the face, the disease more frequently commences in 
childhood than when the first symptoms are in the limbs, but, in some 
instances, the atrophy has commenced in the face late in life, and this 
in the same family in which other sufferers have been young. Thus 
in the sexual proclivity, and in the date of onset, there is a marked 
difference between this form and pseudo-hvpertropliy; the latter 
SPINAL CORD. 
* Troisier and Guinon, ‘ Itev. de Med.,* 1889, p. 48. See also Singer, ‘Zeit. 
f. Heilk.,* viii, p. 229. 
f Kreske, ‘ Muncli. Med. Wochensclir.,* 1886. 
J Landouzy and Dejerine, loc. cit. § Ibid. SIMPLE IDIOPATHIC MUSCULAR ATROPHY. 
523 
showing a stronger tendency to affect males, and to manifest itself in 
childhood. The “juvenile ” form, as a rule, presents less difference. 
As a rule, no direct exciting cause can be traced. In a few instances 
the onset has succeeded some other morbid process, such as chlo- 
rosis, acute disease, or rheumatic affections due to exposure to cold; 
and the depression of general health resulting from these may have 
determined the time of onset, but is not likely to have done more. 
In other individuals of the same families the disease has developed 
without the aid of any exciting influence. 
Symptoms.—The onset is always gradual. Weakness and wasting 
come on together, and are noticed simultaneously, unless the com- 
mencing atrophy is concealed by subcutaneous fat. The atrophy 
generally begins in the upper arm and shoulder-muscles, having, in 
the most common “juvenile” form, a similar distribution in these 
parts to that of pseudo-hypertrophic paralysis. In the facial form, 
however, this part usually suffers first, as in the lad figured on p. 406. 
In rare cases the wasting not only begins in the legs, but remains 
limited or almost limited to them. In the part first affected the dis- 
ease slowly increases, and thence it usually spreads. The onset may 
be symmetrical on the two sides, or one side may suffer some time 
before the other. 
Of the arm-muscles, the weakness and wasting are noticed first in 
the biceps and triceps, and with these the supinator longus often 
suffers. But examination generally shows that the lower part of the 
pectoralis and latissimus dorsi are greatly wasted, a loss of which the 
patient may be little aware, on account of the relative unimportance of 
these muscles. Sometimes the upper part of the pectorals, and even 
the pectoralis minor, are also affected (Fig. 159). The tendency to 
atrophy of the lower part of the pectoralis and latissimus is a character 
which, as already stated, is common to this disease and pseudo- 
hypertrophic paralysis, but not invariable in either. The deltoids are 
rarely involved; in many cases they ai*e normal; sometimes they 
have been thought to be unduly large; in a few instances they have 
been wasted (Fig 162). The serratus magnus is often affected 
(Fig. 161), but may escape, even in a severe case. The supraspinatus 
and infraspinatus may also suffer, but are often normal or even 
enlarged; the trapezius and rhomboids have been affected in many 
cases, sometimes much atrophied (Fig. 161), especially in the 
“ juvenile ” form. 
The forearm-muscles generally escape, with the exception of the 
supinator longus. Occasionally there has been some weakness of the 
long extensors or flexors of the fingers, with or without slight visible 
wasting. In the case mentioned on the next page, the extensors of 
the phalanges of the thumb were involved on the left, and the radial 
extensor of the wrist on the right side. Rarely the forearm-muscles 
have been much atrophied. In several instances there has been some 
atrophy of the small muscles of the hands, the thenar and interosseal 524 
SPINAL CORD. 
muscles, or the interossei only, as in the case of Landouzy and 
Dejerine; but in the majority the integrity of these muscles is a 
marked feature of the disease, and a contrast to the spinal form. 
The affection of the face is peculiar. There is commonly a failure 
of the zygomatic muscles, and, in consequence, a loss of the naso-labial 
furrow, and a curious alteration in the smile ; instead of the angles of 
the mouth being drawn outwards and upwards, they are moved 
upwards by the elevators of the upper lip and angle of the mouth. 
The orbicularis oris is also affected, and, in consequence, the lips are 
habitually separated, the lower lip projects, the patient cannot 
“pout,” and the articulation of labials is imperfect. The face has a 
■dull expression and the aspect is very peculiar; it has been termed, 
by Landouzy and Dejerine, the “ myopathic face.” In one case, 
observed by them, the face was unequally involved on the two sides. 
Rarely (as in Fig. 159) the frontales have been involved, and the 
orbicularis palpebrarum has been weak. Weakness of the eyelids 
was supposed to be the cause of distinct exophthalmos present in one 
woman.* In the case described by Kreske, inability to close the eyes 
was noted at three, and at ten the paralysis of the face was absolute. 
Wasting of the muscles may be indistinct, because the contour of the 
face is only to a slight degree influenced by the substance of the 
muscles. The projecting lower lip may, indeed, appear to be thicker 
than normal. In many cases the buccinators have been affected, in 
some instances they have been normal, and then have drawn out the 
angles of the mouth in smiling. The tongue has been always un- 
affected, and so also have the pharynx, larynx, muscles of mastication, 
and the eyeball-muscles.f 
The muscles of the spine have sometimes been normal, sometimes 
* Landouzy and Dejerine. 
f In a singular case under my care some years ago, an affection of the facial 
muscles, similar to that of idiopathic muscular atrophy, was associated with paralysis 
of ocular muscles. The patient was a girl twenty-seven years of age; there were no 
indications of syphilis, nor could any history of muscular atrophy in the family be 
ascertained. The ocular palsy commenced gradually at twenty-four, and increased 
until the movements of both eyes upwards, of the left eye inwards, and the right out- 
wards, were lost, and all other movements were weakened. The eyelids drooped 
slightly; the internal ocular muscles were normal. The affection of the face followi d 
that of the eyes; the zygomatic muscles were powerless, so that the smile consisted 
only in elevation of the upper lip; the orbicularis was weak. The palate, pharynx, 
and larynx were normal. The arms became feeble, and the flexors of the hips 
almost powerless. There was no visible change in the nutrition or electrical irrita- 
bility of the muscles; the knee-jerk was normal. If the case was central, as it 
appeared to be, the peculiar affection of the lips and zygomatics is not confined to 
idiopathic muscular atrophy. If the disease was muscular, the eyeball-muscles do 
not invariably escape. With this case may be noted one recorded by Oppenlieim 
(‘Charite Annalen,’ xiii) as the “juvenile” form, with derangement of the lateral 
movement of the eyes, nystagmus, and some laryngeal palsy. The shoulder- and 
thigh-muscles suffered chiefly, but, below the knee, the perouei—a noteworthy 
aberration from the typo. SIMPLE IDIOPATHIC MUSCULAR ATROPHY. 
525 
they have been considerably atrophied.* The intercostals are often 
affected in the later stages, but rarely in extreme degree. The 
diaphragm also sometimes suffers, as in the case shown in Fig. 158. 
The abdominal muscles have been involved in only a few instances. 
In the legs the muscles most commonly affected are the flexors of the 
hip, the extensors of the knee, and less frequently the glutei. The 
muscles below the knee have escaped in many cases ; when they have 
suffered, the atrophy has often been general. When the peroneal and 
anterior tibial muscles have been specially affected, as in the case 
shown in Fig. 162, the case has generally been of the peculiar 
“peroneal” type to be presently mentioned, although it is possible 
that some instances of the kind are on the borders of the group now 
under consideration. 
The electric irritability of the affected muscles is usually lessened 
in proportion to the wasting, and equally to both currents. Indeed, 
the diminution seems sometimes out of proportion to the wasting, and 
great when the atrophy is slight. There is no trace of degenerative 
reaction, and there is not even the longer persistence of voltaic than 
of faradic irritability which occurs in the more chronic cases of spinal 
atrophy. Fibrillation is almost always absent, but not quite in- 
variably ; hence its absence cannot be made distinctive, still less 
its presence. Myotatic irritability is lessened or lost; it is never 
increased. Some shortening of muscles has been occasionally noted, 
frequently in the calf-muscles, rarely in the biceps. 
All other functions of the nervous system are unaffected. Sensi- 
bility is normal. In a few cases transient rheumatoid pains have 
accompanied a rapid development of the disease in the arms, but in 
the vast majority of cases the disease is painless. The sphincters are 
unaffected, and there is no tendency to trophic or vaso-motor dis- 
turbance. 
As the muscular atrophy progresses, the form of the affected parts 
becomes changed just as in spinal atrophy. Deformities may also 
occur, chiefly from the shortening of less affected muscles, but these 
rai-ely reach the considerable degree common in other forms of muscular 
wasting. Lordosis occurs in the upright posture, and is probably 
due to the same mechanism as in pseudo-hypertrophic paralysis, 
ceasing, as in that disease, when the patient sits (compare Figs. 158 
and 161). When the muscles of the lower leg are involved, talipes 
may develop. 
The course and duration of the disease are exceedingly variable. 
The atrophy may remain limited to the part in which it begins. The 
face alone has been affected in some members of a family, although in 
other members the limbs subsequently suffered. In cases in which 
* Atrophy began in the back-muscles at forty-four in a case recorded by Musso 
(‘ Riv. Clin.,’ June, 1887), and twelve years later had involved also the legs. The 
patient’s mother, two brothers, sister, and maternal uncle suffered in the same way 
at the same age. 526 
SriXAL CORD. 
the wasting spreads, years may intervene before the extension takes 
place. In one case, for instance, the right arm became affected at 
nineteen, the left at twenty-five, the legs at thirty. In another the 
arms began to waste at thirty-five, power of standing was only lost at 
Fig. 159. 
Fig. 159. 
Fig. 160. 
Figs. 158 to 161.—Idiopathic muscular atrophy affecting the face. Fig. 158 
shows the wasting of the deltoid upper-arm muscles and supinator longus 
(while the forearm-muscles are not wasted), and the rotation of the scapula 
from the loss of the trapezius and rhomboids. Fig. 159 shows the habitual 
appearance of the face, and Fig. 160 the greatest possible movement of the 
facial muscles in c’o-dng the eyes and smiling, and also the wasting of the 
deltoids and pectorals. The general distribution of the atrophy and ptojec- 
tion of the scapulae are seen in Fig. 161.# 
* The patient was a lad sixteen years of age. The following is an abstract of 
the notes of his case. In his family no history of any similar affection can he 
a-certained. There is conclusive evidence that lie had a hard chancre at the age 
of three, followed by secondary symptoms. The muscular wasting began gradually 
during childhood; even when very young there was little movement in the face, and 
that ceased at the age of six or seven. Walking became difficult about three years 
ago. The face is almost motionless: an effort to smile causes only a just perceptible 
movement of the left cheek, the amount of which is fairly indicated by the difference 
between Figs. 159 and 160. It is accompanied by a distinct movement of the ears. 
The lips are full and can be brought together, hut not shortened. The eyelids cannot 
be made to meet, even with a strong effort, being then £ in. apart. Forehead 
absolutely motionless. Eyeballs prominent, movements normal. AJasseters, tongue, 
pharynx, and larynx unaffected. In the neck the sterno-mastoids are very small and SIMPLE IDIOPATHIC MUSCULAR ATKOPUY. 
527 
fifty-five, and the patient lived till seventy-five. Even when the malady 
begins in childhood its progress is sometimes vei'y slow. Thus in one 
case tbe affection of the face was first noticed at five, at twelve the 
arms began to suffer, and a few years later 
the flexors of the Lip became weak, but the 
patient was still able to walk at the age of 
forty. The disease may increase until deve- 
lopment is over and then remain stationary, 
as in a case in which, at forty-four, there 
had been no change since the age of twenty. 
The patient’s daughter was more severely 
affected.* On the other band, the progress 
of the disease may be more rapid and uni- 
form, and the atrophy may reach its widest 
distribution in eight or ten years. In most 
cases, even of severe type, the wasting does 
not become universal, but remains limited to 
the muscles mentioned above, but occasionally 
hardly any muscles of the body may escape. 
The duration of the disease varies from ten 
to fifty years. Death has never occurred as 
the direct result of the malady. In the cases 
of most severe degree and rapid course, tbe 
patient has usually died from phthisis, pro- 
bably related to the deficient breathing power, 
just as in the sufferers from pseudo-hypertro- 
phic paralysis. In most cases, however, death 
has been due to other maladies, and has not 
been in any degree the consequence of the muscular disease. 
Pathological Anatomy.—In general, the condition of the mus- 
cular fibres resembles that met with in pseudo-hypertrophic para- 
feeble, the omo-liyoids large and strong. The following muscles seem quite gone— 
trapezius (except, perhaps, a little of the middle part of the right), rhomboids, 
deltoid pectorales, latissimus dorsi, serrati, biceps, brachialis, triceps, supinator 
longus. The lev. ang. scapulae, supra- and infra-spinatus are unaffected ; the latter 
is large but probably only hypertrophied from over-use. The supinator longus is 
feeble on the left, powerless on the right side. The extensors of the phalanges of 
the thumb are lost on the left side, and the extensor carpi radialis on the right. All 
the other forearm- and hand-muscles appear to be unaffected. The erectors of the 
spine are small and feeble; intercostals strong, diaphragm powerless, abdominal 
muscles weak. In the legs the glutei and flexors of the knees seem normal, the flexors 
of the hips weak, extensors of the knees small and feeble, muscles of the lower leg 
rather small and feeble, but only the peronei are powerless, right-angled contracture 
of ankle-joint with tendency to varus. Knee-jerk absent. Circumference (in 
inches) of upper arms (middle), R. L. 5|; of forearm (maximum), each 8; of 
thighs (minimum inches above patella), R. 10£, L. ; calves (maximum), 
R. 10f, L. 11. Electric irritability much lowered in all affected muscles to each 
current; in most, no contraction can be obtained. Sensation, the sphincters, and 
the visceral functions are unaffected. # Landouzy and Dejerine, loc. cit. 
Fig. 161. 528 
SPINAL CORD. 
lysis, the increase of interstitial tissue "being wanting except in those 
cases that really belong to this form, but in which the characteristic 
enlargement is absent, because no fat cells are developed in the tissue. 
A multiplication of nuclei is, however, sometimes seen. The chief 
change is sometimes a simple narrowing of the fibres, with an ultimate 
disappearance of the transverse striation. Degenerative changes are 
frequently met with, indistinct striation or granular, fatty, or “ waxy ’* 
transformation being seen here and there, alike in narrowed or 
enlarged fibres, and in those that retain their normal calibre ; occa- 
sionally fibres present longitudinal striation, Assuring, or vacuolation ; 
but in other cases, or in some muscles (especially in the “juvenile ” 
form), a remarkable increase has been found in the size of fibres in 
excised fragments,* even of muscles that are below the normal size. 
It seems to show pathological enlargement, although allowance has 
seldom been made for the influence of excision, mentioned in the 
chapter on Hypertrophy. 
The statements made regarding the spinal cord in the pseudo- 
hypertrophic form, are strictly applicable also to this variety. It is 
normal as a rule, to which exceptions are so rare that they can have 
no relation to the malady, save that of secondary indirect consequences. 
The nerves also are normal, if the cases are eliminated in which the 
symptoms indicate the peroneal form. 
Thus the facts ascertained regarding this type do not suggest any 
special addition to the general conclusions intimated in the introduc- 
tory paragraphs. The affection appears to be the result of a primary 
developmental tendency, involving the muscular tissue only, aud cannot 
be regarded as a secondary result of the interstitial changes, except in 
a trifling, occasional, and unimportant degree. Still less is it a conse- 
quence of changes in the spinal cord. If it is in any measure the result 
of failure in the nutrition of the terminal structures of the nerve-fibres 
(by which the nervous and muscular tissues are connected, and which is 
perhaps to be regarded as intermediate between the two), the fact has 
yet to be demonstrated, and its significance ascertained. 
Diagnosis.—The two most important diagnostic indications are the 
affection of more than one member of the same family, and the onset 
of the disease before adult life is reached. The former is practically 
conclusive; and the latter should always suggest the probable idiopathic 
nature of the case. In isolated cases the diagnostic difficulty is much 
greater, and no indication is actually conclusive, except, perhaps, the 
affection of the face. Commencement during childhood is also of great 
weight. It is most unlikely that progressive muscular atrophy, 
beginning under ten, is of spinal origin, but I have known such 
atrophy, certainly spinal, to commence at the age of fourteen. The 
peculiar affection of the zygomatic muscles is very characteristic, but 
we cannot yet say that it is pathognomonic (see note on p. 405), and 
* See especially Schulze, * Ueber den mit Hypertropliie verbundenen Muskel- 
sehwund,’ Wiesbaden, 1886, and Hitzig, loc. cit. SIMPLE IDIOPATHIC MUSCULAR ATHOP1IY. 
529 
the affection of the lips must be carefully distinguished from that due 
to the bulbar palsy so commonly associated with spinal atrophy. Of 
the distribution of the wasting, that of the latissimus and lower half 
of the pectoralis, and the escape of the hand-muscles, are the most 
important characteristics, although they are not, by themselves, con- 
clusive, since they are sometimes met with in spinal atrophy. 
But the most important distinctions between spinal and idiopathic 
atrophy, whenever they are available, depend upon the symptoms of 
a lesion of the cord, or of the bulbar nuclei. Especially significant 
is the excess of the knee-jerk which results from lateral sclerosis, a 
conclusive indication of spinal disease, rendering the spinal origin of 
the atrophy all but certain. The distinction from the pseudo-hyper- 
trophic form has been already considered ; that from the peroneal type 
will be presently mentioned. 
Prognosis.—The extreme variations in the course of the disease 
render the prognosis in any individual case both uncertain and 
difficult to formulate. Speaking generally, chronicity favours arrest, 
i\nd the later the symptoms appear, the slower will be their progress. 
The prognosis is distinctly less grave in the simple atrophy than in the 
“juvenile” atrophic variety of the pseudo-hypertrophic disease, and in 
a considerable number of cases, perhaps one half, the malady has not 
appeared to shorten life. Even in cases that begin during youth it is 
therefore possible that the patient may reach old age. It seems also 
to be better in the cases that do not involve the facial muscles. 
Treatment.—It is not yet clear that idiopathic muscular atrophy 
can be influenced by treatment in any considerable degree. Most 
published records of cases are almost silent on the subject, and the 
disease is so rare that few individuals have an opportunity of forming 
an opinion. It might be assumed that the essential cause of the 
disease, a congenital tendency, withdraws it from the range of thera- 
peutics, but the course of the malady is very different from that of 
some other diseases which own a similar cause. The extreme varia- 
tions in the date of onset, the fact that the disease may not be mani- 
fested until late in life, and the long period that may intervene between 
its onset and extension, all suggest that other influences co-operate 
with the congenital tendency in determining the development of the 
malady. It is quite possible, therefore, that the first inference from the 
history of the disease may not be altogether correct, although it must 
be admitted that we have not as yet any evidence that the disease 
is susceptible of influence from drugs. Electrical treatment and mas- 
sage have been thought to do good and even to produce arrest (Erb), 
but the variable tendency of the malady renders the evidence of arrest 
insufficient. If voluntary exercise is practicable, this is a far more 
efficient stimulus to muscular growth than any electrical application, 
and it is probable that such exercise, carefully persevered in, may do 
something to prevent the occurrence of the malady in those pre- 
disposed to it, and even to retard its progress in those who are 
VOL. I. 530 
SPINAL CORD. 
already attacked. In this connection it is noteworthy that very few 
of the sufferers have been engaged in occupations that involve active 
muscular exertion. Over-exertion should, however, be carefully 
avoided. The general health should be attended to, and anv defect 
removed as speedily as possible, both in those who suffer and in those 
who are related to sufferers, since, as we have seen, depressing 
influences may apparently excite the development of the disease, and 
it is therefore reasonable to suppose that they may accelerate its 
course, and lessen any tendency there may be for the morbid process 
to become stationary. 
The Peroneal Type of Family Amyotrophy. 
The name “ peroneal type ” has become current as the most con- 
venient designation for the variety of muscular atrophy, occurring in 
early life, to which it was applied by Dr. Howard Tooth in a Thesis 
published in 1886 * This was the means of calling general attention 
to the form, of which, however, an account had been published 
shortly before by Charcot and Marie,f and many cases had been pre- 
viously described, in most instances without recognition of their special 
character. J The cases of this form present certain resemblances to 
the idiopathic atrophies just described—resemblances sufficiently 
important to have led to the description of these cases in association 
with the primary myopathy, embracing, as they do, the age of the 
sufferers, the occurrence of the disease in members of the same family, 
its gradual onset, and its very slow but progressive course. Yet this 
position must be regarded as provisional only, and probably erroneous. 
The distribution of the wasting involves a constant difference from 
the idiopathic muscular affections, and some of the cases, otherwise 
inseparable from the rest, present features that indicate neuritis. The 
disease may have, as an antecedent, an acute specific disease—a circum- 
stance that has the same significance. The facts ascertained con- 
cerning this form must, therefore, be carefully excluded from our 
generalisation regarding the idiopathic atrophy. 
In this form, males suffer about twice as frequently as females. 
It generally begins in the second half of childhood, and very seldom 
after twenty, although cases have been described beginning as late 
as forty. It is occasionally hereditary, and still more frequently 
collaterals suffer, several brothers and sisters being affected. The 
wasting is first apparent in the extensor longus pollicis, or extensor 
communis digitorum, or in the peronei muscles. According to Tooth, 
it very often begins in the latter, and occasionally in the gastrocnemius, 
* 1 The Peroneal Type of Progressive Muscular Atrophy/ London, Lewis, 1886. 
f * Revue de Med/ 1886, p. 97. 
J By Friedreich, Eichhorst, Oppenheimer, Ormerod, and others. A table of 
thirty collected cases (some doubtful) is given by Tooth. PERONEAL TYPE OF AMYOTROPHY. 
531 
but it is probable that it occurs simultaneously, or even earlier, in the 
small muscles of the foot, where it readily escapes observation. Such 
oarly atrophy in the feet has, indeed, been actually found in some cases 
that came under observation at an early stage.* The calf-muscles 
suffer subsequently, and still later those of the thigh, especially 
the vastus interims. The unequal affection of the muscles of the 
leg causes the early development of club-foot, which, especially in 
children, becomes a characteristic symptom.f The arms are only 
invaded, in most cases, some years after the legs, so slow is the course 
of the disease. The intrinsic muscles of the hands (thenar, hypo- 
thenar, and interosseal muscles) are first attacked, and subsequently 
those of the forearm ; sometimes the extensors and sometimes the 
flexors suffer first and most; while the supinator longus remains 
normal, and so do the muscles of the shoulder, neck, back, and face. 
The atrophy is often symmetrical, but occasionally the muscles on one 
side waste first and most. The claw-like deformity of the fingers may 
result from the affection of the intrinsic muscles of the hand. This 
is so rare in early life from any other cause, that its significance is 
considerable, and almost distinctive when combined with the deformity 
of the feet just mentioned. The case shown in Fig. 162 was probably 
an example of this type.J 
Fi<J. 162.—Advanced muscular atrophy, probably of the “peroneal type.” 
(Drawn by Dr. Spencer, from a photograph.) 
The affected muscles (especially in the hand) occasionally present 
slight fibrillation. Their electric irritability is diminished sooner, and 
* Hoffmann, ‘Arch. f. Psych.,’ xx, p. 660; Joffroy, ‘ Gaz. Hebei.,’ 18S6, No. 18. 
t See Sachs, * Brain,’ Winter part, 1889. 
J It was given in the last edition as an example of simple atrophy. The patient 
was a man aged twenty-seven at the time of his death (in University College 
Hospital). No history of any analogous case in his family could be ascertained. 
The affection began at the age of fourteen, when his feet began to turn in so that 
he walked on the outer side of the foot, and soon he noticed gradual wasting of 
the legs, which slowly progressed, and about the age of twenty-four the arms also 
began to suffer. When first seen, a few months before his death, the muscular 
atrophy was universal, and the subcutaneous fat had also disappeared. Even the 
hands were greatly wasted; there was a hollow in the position of the thenar 
eminence, just as in progressive muscular atrophy, and the interosseal muscles were 
also greatly wasted. There was slight fibrillation. The intercostals were paralysed. 
The wasting of the legs was extreme; the maximum circumference of the calf was 532 
SPINAL COED. 
in greater degree, than in the ordinary idiopathic atrophy, while a still 
greater difference is presented by the fact that faradic irritability may 
early become extinct, and that there may be a distinct reaction of 
degeneration. In connection with this, should be noted the important 
fact that cutaneous sensibility, though often normal, is sometimes 
impaired or lost, especially over the region in which the atrophy is 
greatest, or upon the soles of the feet. Pains occur in some cases, 
and so also do spontaneous spasmodic contractions, especially in the 
muscles of the thigh. The muscle-reflex action is lessened or lost in 
the affected regions, but there may be extensive atrophy below the 
knees, without loss of the knee-jerk, if the thigh-muscles are pre- 
served. Cutaneous reflex action presents considerable variations, and 
is preserved more often than would be expected. Vaso-motor dis- 
turbance sometimes occurs (Sachs). 
The nature of these cases has still to be demonstrated. Their very 
slow course, the time of life at which they begin, and the affection of 
several members of the same family, are features analogous to the 
idiopathic atrophy, but a marked contrast to this is presented by the 
tendency of the malady to succeed an acute specific disease, measles, 
and this also may appear as a family tendency. This feature re- 
sembles the causation of multiple neuritis, and the electrical reaction 
of degeneration is conclusive proof of preponderant changes in the 
motor nerves, while anaesthesia demonstrates that, in some cases, the 
sensory fibres are also affected. In such cases, a peripheral neuritis, 
motor or total, of extremely chronic course and peculiar origin, must 
be recognised as the only possible lesion, and it was actually found, 
in one. case, by Friedreich, and in another by Gombault. If this is 
the cause of the symptoms in some instances, the question arises 
whether it is not the lesion in all the cases of this peroneal type. 
Such a lesion is conceivable; the degenerative form of neuritis 
presents every degree of chronicity, and may be limited to the motor 
fibres and to certain muscles. This pathology was advocated, as the 
probable one, by Tooth, who pointed out that it would also enable us 
to understand the occurrence of fibrillation, which is extremely rare 
in the idiopathic atrophies. It is, indeed, asserted by Hoffmann that 
not only are the peripheral nerve-fibres the seat of a primary degene- 
ration, but that this change ascends the nerves to the anterior and 
posterior roots, and involves, in a secondary manner, the elements of 
the spinal cord, especially the fibres of the posterior median columns 
(which continue the path from the muscles) and the motor cells of 
the anterior cornua. But we do not know how far the premature 
only seven inches; the feet were everted, the sole hollowed, and the toes flexed. The 
patient died from diarrhoea. The muscles were found to be small and pale. The 
chief microscopical change was interne granular and fatty degeneration of the fibres. 
A very few normal fibres were seen in some muscles. There was no iucrease of 
interstitial tissue. Microscopical examination revealed no morbid changes in the 
spinal cord. The nerves, unfortunately, were not examined. PERONEAL TYPE OF AMYOTROPHY. 
533 
failure of nutrition is a secondary process, transmitted from below, 
or how far it is the result of a defect in vital energy, shared by the 
central as well as the peripheral nerve elements. 
The intimate relation between the motor nerves and the muscular 
fibres should also be kept in view in this connection. There may 
be a morbid tendency in the nerves similar to that of the muscles, 
including a liability to early slow degeneration, analogous to that 
which the muscles present, and equally prone to occur in several 
members of a family. But it is desirable that the neuritic 
nature of the affection should be placed on a broader basis of 
ascertained fact before it is allowed expression in the name given to 
the disease. 
It should also be remembered as possible that the atrophy may be 
idiopathic in some cases, while in others it may be secondary to such a 
neuritis as above mentioned. There is nothing difficult, or even anoma- 
lous, in the conception of a congenital tendency to premature failure 
of nutrition in the peripheral neiwe fibres, like that which, in the pyra- 
midal fibres, seems to underlie “ hereditary ataxy,” or which, on the 
other hand, in the muscles, is the apparent cause of idiopathic atrophy. 
Further,if the lesion is really neuritic, we can understand that an acute 
specific disease like measles should occasionally be its excitant, although 
its occurrence in families shows that a congenital tendency must be 
called into activity by the virus, and the cases must be distinguishedfrom 
those in which a pure neuritis is induced by the influence of the poison 
of the specific disease. An acute specific disease, the virus of which 
is known to be capable of inducing the degeneration of “ parenchyma- 
tous ” neuritis, may readily excite this state in each of several mem- 
bers of the same family, if a congenital tendency to it exists in them. 
It may readily evoke that which it could, even alone, produce. Ac- 
cording to this theory, a tendency to nerve degeneration, acting alone, 
may lead to the early failure of nutrition of the nerves, while the 
wasting of their muscular fibres may be either a consequence or a 
concomitant, in part or altogether. Thus, the muscles may atrophy 
because the nerves have degenerated, or because they also have a 
tendency to atrophy, or from both causes combined. Nerve and 
muscle may alike share the congenital imperfection in some cases, 
while in others its primary incidence is on the nerves alone, the 
muscles suffering in consequence of the changes in the nerves. The 
congenital association may sometimes be even more extensive, and a 
tendency to the early failure of structures in the central nervous 
system may be conjoined, giving rise to cases of complex aspect and 
character. 
It is especially important to note, in this connection, the occurrence 
of cases that occupy an intermediate position, and combine the 
characters of this and the myopathic types. Such combined cases are 
usually partial only, but such partial cases, when combined, ultimately 
cover the whole intermediate ground. For instance, the condition of 534 
SPINAL CORD. 
the legs in the “ peroneal type ” has coexisted with that of the arms 
in the “juvenile form ” in several recorded cases.* 
Thus, the possibility must be recognised that the cases of this type 
vary, even more than their characters suggest, in the degi’ee in which 
the morbid tendency acts upon nerve or muscle, or both, as well as 
the degree in which its activity is spontaneous or induced. Hence, 
the cases may here be only partly out of place, some perhaps not at 
all; and their position, as forms of “neuritis,” might be equally open 
to exception. 
The progressive character of the cases of this type is commonly 
pronounced, and, even if slow, it renders the prognosis gloomy, and 
the scope for treatment small. So far as anything can be done, it is 
by the measures already mentioned in the account of the treatment of 
the maladies to which the cases approximate, the primary disease of 
the nerves on the one hand, and of the muscles on the other. 
Muscular Hypertrophy. 
The occurrence of a true hypertrophy of muscles, as a condition of 
disease, is exceedingly rare. In most cases in which the muscles are 
enlarged, the increase in size is due to a growth of interstitial tissue, 
fatty or fibrous, such as has been described in the chapter on pseudo- 
hvpertrophic paralysis. We have seen that muscular fibres larger 
than normal have been described in that disease, and also in some 
cases of simple atrophy. When this increase in size has been met 
with only iu excised fragments, it is possible that the condition may 
have been due to a vital contraction excited by the process of excision, 
and such evidence of hypertrophy is certainly inadequate ;f only when 
it is found after death, can its occurrence be regarded as beyond ques- 
tion. Nevertheless, true hypertrophy of fibres is a change that may 
be expected to be occasionally met with in cases that are due to a con- 
genital tendency, and its presence, even in muscles that are the seat 
of atrophy, need, therefore, excite no surprise. It was met with by 
* E.g. by Hoffmann, ‘Berlin, klin. Wochensehr,’ 1887, No. 22; and Eisenlohr, 
‘ Neur. Ceutralbl.,' 1889, p. 565. 
f Since the above was written, the donbt there expressed has been confirmed by 
an observation made for me by Dr. H. R. Spencer. A fragment of the gastrocnemius 
of an amputated leg was excised immediately after the amputation, and the fibres 
were compared with those of the muscle twenty-one hours later. In order to 
ascertain more definitely whether a vital contraction persisted as an apparent 
increase in size, a part ot the excised fragment was separated and faradised. The 
average size of the fibres in the muscle was inch, in the fragment excised 
inch, in the fragment faradised inch. Since the division of the nerve 
during the amputation may have caused some contraction, it is possible that the 
difference in size produced by excision may be even greater than these figures 
represent. [I leave the above note unchanged because, since it appeared in the first 
edition, the observation and doubt have been fully confirmed by various observers,. 
e.g. by Oppenheim and Siemerling, ‘Med. Centralbl.,’ 1889, No. 39.J 535 
MUSCULAR HYPERTROPHY. 
Brack in a remarkable case of general muscular enlargement in an 
idiotic child, in whom it apparently developed after birth. The affec- 
tion first showed itself in the tongue, but the muscles presented 
spasmodic contractions, and the case, like most of the kind, was 
evidently anomalous in its features. Muscular hypertrophy has 
been found in the singular malady described in the next sec- 
tion (Thomsen’s disease). It has also been met with, in very rare 
instances, as a widespread or partial condition, usually associated, 
strange to say, with either diminished power or with a morbid readi- 
ness of fatigue.* The muscles most frequently affected have been 
those of the shoulder and upper arm, or of the thigh and calf, on 
one side or on both. It has also been observed in the glutei, spinal 
muscles, and trapezii. The causes are obscure, but it has been 
ascribed to over-exertion. The diameter of the fibres has been increased 
to double the normal, a maximum of rJ-5th inch having been met with 
(Eulenberg), whereas the normal maximum may be taken as 
inch. An increase of the nuclei has been observed, without any over- 
growth of the interstitial tissue. 
The condition is manifested by an increase in the size of the 
muscles, which are also firm. The circumference of the limb is 
greater than normal, and when the change is unilateral, the difference 
between the limbs of the two sides may be very striking. The 
maximum circumference of the calf has been as much as seventeen 
inches. The muscles are soon exhausted, and have been weak in 
some cases, while in others there has been abnormal strength for brief 
exertion. The electrical, mechanical, and myotatic irritability of the 
muscles has usually been found unaltered. 
The disease may be suspected if a marked increase in size in an 
adult is accompanied by impaired power of sustained exertion; if the 
muscles are firm, and the patient does not manifest other indications 
of pseudo-hypertrophic paralysis. The diagnosis can, however, only 
be made with certainty by the microscopical examination of an excised 
fragment, and even then subject to the reservation mentioned on the 
previous page. The meagre facts regarding the course of the disease 
suggest that it usually persists without getting either better or worse. 
Treatment appears to have but little influence upon it. 
A singular case has been reported by Eulenberg,f which differs in 
many particulars from the form of disease above described, and 
illustrates the complex relations of enlargement of the muscular fibres 
and its connection with degenerative processes. A man, aged thirty- 
six, presented an enormous enlargement of the muscles of the left 
* Auerbach, ‘ Virchow’s Archiv.,’ Bd. liii, pp. 234 and 397; Berber, ‘ Deut. Archiv 
f. klin. Med./ Bd. ix, 1872, p. 363; Friedreich, ‘ Ueber Prog. Muskelatrophie, &c./ 
1873; Eulenberg, ‘ Real-Encyclopadie/ Bd. ix, p. 354. A very similar case is 
described by Pal, ‘ Wien. klin. Wocbenschr./ 18S9, No. 10. 
f ‘ Ueu'.scb. Med. Wochenschrif c,’ 1885, No. 12. 536 
SPINAL CORD. 
leg, which were soft and flabby and weak, with lowered irritability. 
The condition had slowly developed after a fall on the back at ten, 
which caused imperfect paraplegia, motor and sensory. A year later, 
during pleurisy, he had thrombosis of the left femoral vein. In an 
excised fragment of the gastrocnemius, the muscular fibres were 
large, the maximum being of an inch ; they presented fatty and 
vitreous degeneration, and fat was seen between the fasciculi. The 
muscles of the other leg were somewhat wasted, but the fibres were also 
enlarged and degenerated. It would appear as though the condition 
had resulted from a traumatic lesion of the spinal cord, and had been 
intensified in the left leg by the influence of the thrombosis and 
resulting vascular disturbance. 
THOMSEN’S DISEASE; MYOTONIA CONGENITA. 
The malady thus designated may be considered here, notwithstanding 
the obscurity of its nature, because it agrees with the diseases last 
described, in that the symptoms are muscular, and that the disease 
seems often congenital and occurs in families. It has been named after 
the physician whose description gained for it general notice, and who 
is himself its subject, but it had been previously described by Leyden, 
and hinted at, long ago, by Sir Charles Bell.* It is not always con- 
genital, and “ Transient Myotone ” would be a more exact name. 
The disease is characterised by a peculiar rigidity of the muscles, 
which comes on when they are first put in action after a period of rest. 
The rigidity is transient, and when it has passed off, it does not return 
as long as exertion is continued. The malady is often hereditary, 
and usually affects several members of the same family. Iu that of 
Thomsen, cases can be traced through five generations. It appears 
to be more common in Scandinavia and Germany than in France 
* Bell’s * Nervous System,’ Case 184, p. 436. The objections to cognominal 
nomenclature of disease are certaiuly reduced to a minimum when the first describer 
of a rare disease is also its subject. The most important papers on the disease are 
those of Leyden, ‘ Klinik der Ruckenmarkskr.,’ 1874, Bd. i, p. 128 ; Thomsen, ‘Arch, 
f. Psychiatrie,’ Bd. vi, 1876, p. 702, also ‘ Centralbl. f. Nervenkr.,’ 1885, p. 193; 
Bernhardt, ‘Virchow’s Arcliiv,’ Bd. lxxv, 1879, p. 516, and ‘Centralblatt f. 
ervenkr.,’ 1885, p. 122; Ballet and Marie, ‘Arch, de Neur.,’ 1883, No. 13; 
Mobius, ‘Schmidt’s Jahrb.,’ Bd. cxcviii, 1883; Ringer and Sainsbury, ‘Lancet,’ 
1884, pp. 767, 816, and 860; Erb, ‘Die Thomsen’sche Krankheit,’ Leipzig, 1886, 
also ‘ Deut. Arcliiv f. klin. Med.,’ 1890, xlv, p. 529; Seifert, ib., xlvii; Marie, in 
‘Encycl. des Sc. Med.,’ 1886; Hale White, ‘Brain,’ April, 1886, and ‘ Guy’s Hosp. 
Rep.,’ vol. xlvi (a very valuable paper, with bibliography); Jacoby, ‘ Journ. of 
Neur. and Ment. Dis.,’ xiv, p. 23; Jolly,‘Siidwest. Neurol.,’ Baden, June, 
1890; Buzzard, * Lancet,’ 1887. thomsen’s disease. 
537 
or England, but it is a rare disease ;* and although a considerable 
number of clinical cases have now been recorded, there has been 
no post-mortem examination. There is little to attract attention in 
the slighter forms, and the rarity of these may ultimately be found 
to be less than at present appears. 
Both sexes suffer. In most cases the symptoms have been first 
noted in childhood, between four and ten years of age, sometimes even 
in the cradle. They increase during the period of muscular deve- 
lopment, and then remain stationary. A few patients have seemed 
free until about the period of puberty, but even in such instances it 
is probable that the tendency was congenital in origin, since the cases 
occurred in families, other members of which suffered earlier. But 
in a few cases symptoms apparently identical with those of the con- 
genital disease have come on in early manhood after some exciting 
cause —in one case a lightning stroke, in another a sudden alarm + 
Severe and prolonged exertion during two years preceded the onset 
of very characteristic symptoms in a man of twentv-fiye, without 
heredity.]; In such cases the disease has been apparently acquired. 
The characteristic symptom is tonic spasm of the muscles when 
they are put in action after a period of rest. As soon as the patient 
attempts to move, the muscles become rigid. The rigidity ma • make 
movement impossible while it lasts, or may merely lessen the p >ssible 
range of movement. After a few minutes, or less, the spasm passes 
away, to be renewed, but in slighter degree, by a fresh attempt. If 
the movements are continued, the spasm soon becomes trifling, and 
does not return until after a period of rest. The longer the rest, 
the more troublesome is the spasm. The subject can walk for hours 
without fatigue when it has passed off. The rigidity is sometimes 
iessened by alcohol and increased by attention and by fear of it; the 
more the sufferer tries to overcome the stiffness, the less is he able to 
do so. It is also worse in cold and damp weather. In a severe case, a 
slight impulse will make the person fall, and it may then be impossible 
for him, for some minutes, to rise from the ground. The arms are 
usually less affected than the legs, but in some cases, the rigidity fixes 
the fingers for a short time on an attempt to use the hand. The 
muscles of the face are usually free; mastication may, however, be 
interfered with by the spasm in the muscles of the jaw. Barely, the 
tongue or face has been affected ; still more rarely the muscles of the 
eyeball, interfering with its movement and retarding the descent of the 
upper lid.§ Most voluntary muscles, indeed, seem liable to suffer, 
even the muscles of the larynx and pharynx; those concerned in the 
* In England cases have been observed by Buzzard, Herschcll, Hale White, 
Banham, and Chapman. 
f ‘ Engel, ‘ Phil. Med. Times/ 18S3, p- 412; Schonfeld, * Berlin, mod. Wochenschr./ 
1883, No. 27. 
J Moyer, * Med. News,’ 1890. 
§ Raymond, * Gaz. Med. de Paris/ June, 1891. 538 
SPINAL CORD. 
processes of respiration, defsecation, micturition, and coitus have also 
been involved. Sometimes the spasm is greater on one side of the 
body than on the other. 
The muscles are always well nourished; they are often, indeed, above 
the normal size, and possess more than normal strength, but they 
are sometimes less strong than is normal, even when large. Thomsen 
believes that the more the muscles are employed the less severe is 
the spasm, and that a life of active exertion produces some per- 
manent amelioration in the disease. The malady is, however, a 
source of some disability, and of considerable annoyance; in the words 
of Thomsen, “it casts a shadow over the lives of the sufferers,” and 
may have caused the mental irritability and hypochondriacal tendency 
that have been conspicuous in some cases. 
Careful investigations of the muscular phenomena have been 
made by several observers and that by Erb is especially instructive. 
In his case a single brief effort caused tonic contraction which lasted 
for twenty-five seconds. Momentary electrical stimulation of the nerves 
caused only a momentary contraction of the muscles, but continued 
stimulation always causes a prolonged contraction, the “myotonic 
reaction” of Erb. In certain muscles, moreover, an uninterrupted 
current caused peculiar wave-like contractions, about one per second, 
passing from the negative to the positive pole (Erb).* Any strong 
stimulation of the muscle itself caused a prolonged after-con traction, f 
The irritability of the nerves is generally normal in degree ; that of 
the muscles is normal or increased to voltaism. In some cases the 
anodal closure contraction has occurred with undue readiness, and the 
“latent interval ” alter stimulation has been found unchanged (Hale 
White) or increased.J The muscles are remarkably sensitive to 
mechanical stimulation, and firm pressure may cause a tonic contrac- 
tion lasting from twelve to twenty seconds. 
In all undoubted cases of this disease sensibility has been intact, 
and the superficial reflexes have been unaltered. Myotatic irritability 
is normal or increased. 
Once developed, the condition seems to persist, with little change, 
through life, but in one case, a female (in whose family were other 
cases) considerable improvement is said to have followed marriage.§ 
In some instances, the symptoms are slight, and remain so, even when 
they begin in early life and occur in the same families as severe 
cases. Such cases, when isolated, may readily be overlooked. 
Pathology.—An examination of the central nervous system has 
yet to be made, but it is unlikely to yield results of novelty or im- 
* Although Erb, Seifert, and others have noted this, some observers (as Hale 
White) have failed to obtain the phenomenon. 
f Jolly has found that repeated stimulations by either current, without too long 
an interval between the succe-sive stimulations, tend to render the after-contraction 
less and less evident, until it ceases to occur (‘ Neur. Centralbl.,’ 1890, p 438). 
X ‘025 or -03 sec. instead of "01 (Blnminau, * Near. Cent.,’ 1883, p. 679). 
§ Herschell, ‘ Lancet,’ Eeb. 1, 1890. Thomsen’s disease. 
539 
portance. The state of the muscular fibres has been ascertained from 
excised fragments—a method which, however, involves the fallacy, 
already mentioned (p. 534, note), of possibly stimulating the fibres to 
contraction. At the same time, the evidence of hypertrophy appears 
conclusive. Where the minimum width was the same as in health, the 
maximum diameter was double the normal (Erb). In other cases the 
maximum or even average diameter in fragments excised under chloro- 
form was double that observed after death in unaffected persons ; and 
that the size was pathological was rendered probable by the aspect 
of the fibres, which presented indistinct striation, fewer “ sarcous 
elements,” irregular, non-parallel edges, and sometimes vaeuolatiou. 
An increase of the nuclei and of the interstitial connective tissue has 
been found.* 
The manifestation of the disease is in a disorder of the functions of 
the muscles, and most writers on the subject have followed Leyden in 
regarding the malady as essentially muscular in nature, as consisting 
in an altered functional condition of the muscular tissue. This 
opinion is strongly supported by the frequent alteration in electrical 
excitability (which can hardly be otherwise interpreted than as an 
indication of a change in the mode of action of the contractile muscular 
protoplasm), by the structural changes, and also by the interesting 
experiments of Ringer and Sainsbury, who found that certain salts, 
such as sodium phosphate, are capable of causing in the frog tonic 
spasm bearing considerable resemblance to that of Thomsen’s dis- 
ease, and that such spasm persists not only after the nerve has been 
di vi d ed, b ut after the in tra- m uscul ar nerve-e n dings h ave been paralysed 
by curara. This does not prove that Thomsen’s disease is muscular 
in origin ; it is a proof that a similar state may be due to the mus- 
cular tissue, but no proof that this is the sole element in Thomsen’s 
disease. We must remember that the malady has apparently resulted, 
in rare cases, from influences acting on the nervous system in adult 
life, and also that, in the congenital cases, the sjjasm only develops, 
as a rule, after some years of voluntary action. It may thus be an 
acquired disease, and the case related at the end of this chapter 
shows that similar spasm may be due to a primary affection of the 
cord. The spasm is a transient consequence of rest. But “ rest” is 
not inactivity, either in the nerve-cells or muscles. Muscular “ tone ” 
and adaptation to posture mean an unceasing flow of nerve-force 
from the cells, an overflow perhaps, due to the perpetual elaboration 
of energy which keeps the cells ready for instant response to the 
voluntary stimulus. The tonic activity then ceases, or at least does 
not interfere with the different action excited by the will. But the 
phenomena of Thomsen’s disease suggest that the cells respond 
abnormally to the voluntary stimulus, that this causes at first an 
increased tonic activity, slowly ceasing as their energy is lessened by 
* Erb, Seifert, and also Nearonow, ‘St. Petersburg psych. Gesellsch.,’ 1889 j see 
*Neur. Cent.,’ 1S39, p. 239. Hale White found no increase in the nuclei. 540 
SPIXAL COKD. 
action. Wide as is the difference between the jnuscular and ner- 
vous tissues, we must remember that they have some conditions 
in common. The dependence of the nutrition of the muscles on 
that of the motor nerve-fibres and cells is a very remarkable fact, 
and so also is the influence of the functional activity of the cells 
and fibres in 'causing a similar condition in the muscular tissue. 
To say that the two structures are connected is hardly an explanation 
of the fact. Whatever is the nature of the relation between them, it 
is at least conceivable that an abnormal functional state, congenital 
in origin, may be common to the two, and that the peculiar over-action 
in the muscles may be accompanied by a similar over-action in the 
ganglion-cells of the spinal cord, and even in the pyramidal,cells of 
the cerebral cortex. It is even conceivable that the condition of the 
nerve-cells may be the primary change, and that of the muscles may 
be secondary, although, when produced, it is in some degree inde- 
pendent, and may be excited independently by local stimulation. Such 
a theory enables us to understand the two facts above mentioned 
—the influence of emotion and the acquisition of the disease, each of 
which seems to be inconsistent with a purely muscular pathology. 
Treatment.—No treatment, properly so called, appears to exert 
any influence on the disease. The congenital malady persists through 
life; in the cases in which a similar condition has apparently been 
acquired, it has also been persistent. The only influence that has 
appeared to Thomsen to ameliorate the condition is a life of active 
muscular exertion. But it is possible that the influence of thera- 
peutics is not yet exhausted. 
Congenital Paramyotone.—Under this name Eulenberg has de- 
scribed* a strange family affection, allied to Thomsen’s disease in its 
general character, although differing very much in its special features, 
and equally obscure in nature. The malady was widely spread in the 
affected family, aud could be traced through six generations, but 
appears now to be dying out. Its congenital character was shown not 
only by its multiplicity, but also by the fact that in some individuals it 
was manifested immediately after birth. The symptom was tonic 
spasm, lasting from a quarter of an hour to several hours, excited 
chiefly by cold, although often by merely slight cold. The rigidity was 
followed for a time by weakness. The facial muscles were very prone 
to become thus rigid, especially the orbiculares palpebrarum and oris ; 
and while the contraction lasted the patient was often unable to speak 
or to open the eyes. The rigidity was slighter in the legs than in the 
arms, but the subsequent weakness was equally marked. Warmth 
removed the spasm. There was no persistent loss of power, and no 
increase of mechanical irritability. The electrical excitability of the 
nerves was normal; that of the muscles was lowered to each current, 
• * Neurologisches Centralblatt,’ 18S6, p. 2G5. TIIOMSIiN’s DISEASE. 
541 
and there was an abnormal tendency to tetanic contraction during the 
passage of the current. Eulenberg speculates that the symptoms 
may be due to reflex vaso-motor spasm in the muscles, because the 
diminution of the blood-supply to muscles renders them weak ; but 
it is clearly equally possible that the two certain phenomena, the 
sensory impression and the muscular contraction, may be directly 
connected. 
Ataxic paramyotone seems the best provisional designation for an 
acquired condition of which one case has come under my notice. 
Persistent tonic spasm, like the transient spasm of Thomsen’s disease, 
was associated with distinct ataxy, and also with weakness and some 
anaesthesia. The symptoms commenced gradually in the legs, in a 
healthy man, aged 40, without neurotic heredity ; it invaded the arms 
six months later, and increased more rapidly in the arms than in the 
legs. At his state was this. A well-built man, with well-developed 
muscles, unduly firm in all parts except the neck and head. The 
firmness was due to tonic spasm, which never ceased. It was present 
on waking in the morning, and through the day interfered with all 
movements, making them slow and stiff. He rose from a seat 
slowly and with difficulty ; when standing there was slight unsteadi- 
ness, increased by closing the eyes, and a slight impulse or stumble 
in walking would cause a fall, chiefly because the spasm prevented 
the needed quickness of movement to save him. Prolonged exertion 
had no influence on the tonic spasm, which opposed passive, as much 
as active, movement. Power in arms and legs was lessened, but not 
considerably. The grasp = 50 and 55 ko. The extensors of the 
fingers were weaker than the flexors, but could act perfectly although 
involuntary flexion followed the slow extension. The electrical 
irritability of the muscles seemed to be normal. Inco-ordination was 
especially marked in the hands; with eyes shut, buttoning his coat 
was almost impossible ; the attempt was made with thumb and fore- 
finger, the others being flexed, and he could touch his nose only after 
many wandering failures. On the palms, from the wrist to the tips 
of the fingers, sensibility was lost to touch, slightly delayed to pain, 
little changed to temperature. Slight tactile loss extended to the 
back of the last phalanges; on the back of the hands it was normal. 
A similar but slighter loss existed on the soles; he often felt as if 
walking on a rounded surface. The size and weight of objects 
placed in the extended hand could not be recognised. No trace of 
the knee-jerk or other evidence of myotatic irritability could be 
elicited, but the spasm was enough to explain the failure, and its real 
condition is uncertain. Mind, special senses, and cranial nerves 
were unaffected. 
Unfortunately, the course of the affection could not be observed. 
Its symptoms must have been due to disease of the spinal cord, and 542 
SPINAL CORD. 
they are instructive as showing that muscular spasm, like that ot 
Thomsen’s disease, may be thus produced. The time may not have 
been sufficient for the production of changes in the irritability of the 
muscles, but we must also remember that differences in the influence 
on the muscles may be connected with the defective power. 
TUMOURS OF THE SPINAL CORD. 
Morbid growths within the spinal canal may spring from the 
membranes, or may grow in the substance of the cord itself. The 
difference in seat entails some difference in symptoms, but it is never- 
theless convenient to consider the two classes together, because they 
have many symptoms in common, and it is often impossible to carry 
the diagnosis farther than the existence of an intra-spinal tumour. 
Etiology.—The general causes of these growths correspond, for 
the most part, to those concerned in their production in other situa- 
tions, and present few peculiarities that merit special mention. 
Fatty growth outside the dura mater occurs early in life ; malignant 
tumours develop late. Of tumours within the dural sheath, 
myxomata are chiefly met with in middle life, tubercular growths 
occur occasionally in childhood, but generally between fifteen and 
thirty-five (Herter*); lipomata are congenital. Males are a little 
more prone to suffer than females.f 
Of the diathetic conditions which give rise to tumours elsewhere, 
only two, syphilis and tubercle, are effective in causing growths 
which commence within the spinal canal. Parasitic tumours occur, due 
to the same influences which produce them in other situations. A 
few rare growths appear to be congenital in origin, due to the 
abnormal development of germinal tissue, while the more common 
gliomata within the cord arise from embryonal tissue, which has 
suffered an arrest of its normal development. Of the causes of 
other forms of tumour we know practically nothing. Injuries, 
such as a blow on the spine, have been supposed to be occasional 
causes, and their influence in rare instances has seemed possible, 
but the evidence is not so strong as it is in the case of tumours 
in some other situations. In many cases the first symptoms have 
immediately followed some exposure to cold and wet, and it seems 
* Ilerter, ‘ Journ. of Mental Dis.,’ 1890, has analysed twenty-six cases, 
f A collection of facts relating to these points, by Mr. Victor Horsley, will he 
found in the paper written by him and myself on the case of successful removal of 
a tumour from the spinal cord, ‘ Med.-Chir. Trans.,’ 1889; but the numerical basis is 
far too meagre to supply more than statistical suggestions. It will be necessary tc 
wait for a considerable time before adequate data are obtained. TUMOUHS. 
543 
probable that this influence may have excited secondary processes 
in the nerve-elements which were already deranged by the growth, 
and may thus have frequently excited the first symptoms of the 
tumour, but it can have had no share in the production of the 
growth itself. Traumatic haemorrhages may, however, result in 
cystic formations, which have been mistaken for new growths. 
Pathological Anatomy.—The growths within the spinal canal 
may develop outside the dura mater, inside the dura mater, or within 
the substance of the cord. The extra-dural tumours may spring from 
the membrane, or from the tissue between the membrane and the 
bone, or may grow into the canal from the outside, through the 
intervertebral foramina. Subdural tumours may proceed from the 
inner surface of this membrane, from the arachnoid, or from the pia 
mater (Fig. 165). The growths in the cord may spring from the pia 
mater, or may develop in the substance of the cord. They sometimes 
proceed from the peculiar tissue which surrounds the central canal. 
The forms of extra-dural tumours are lipoma, from an overgrowth 
of the fat which normally exists between the membranes and the bone ; 
and parasitic tumours, chiefly echinococci ; but all are rare.* Growths 
also occur that spring from the bones or intervertebral tissue —enchon- 
droma, sarcoma, and cancerous tumours, which have been already 
considered. Far more frequent are collections of inflammatory pro- 
ducts from bone disease, but these do not come into the category of 
morbid growths. 
Fig. 163.—Myolipoma of the spinal cord. A, transverse section of the tumour 
and of the conus medullaris of the spinal cord, to which the growth was 
attached, and of which the grey matter is represented by the dotted shading 
CM. n, sections of nerve-roots, partly enclosed in the tumour; m, bundles ot 
muscular fibres. B, part of the tumour more highly magnified, showing the fat- 
cells, of which it was chiefly composed; p.m. pia mater of the cord, of which 
l c. is part of the lateral column. C, part of the tumour, still more magnified, 
showing striated muscular fibres, fibrous tissue, and fat-cells (see also Fig. 157, 
p. 517). The tumour had caused no symptoms. 
* An adeno-sarcoma has also been met with (Hodenpyl, ‘ Am. Journ. Med. Sc.,* 
1888). 544 
SPINAL COED. 
The tumours which begin within the dura-matral sheath are chiefly 
syphilomata, sarcomata, and myxomata, sometimes containing cysts or 
“ brain-sand.” Tubercular and parasitic tumours are rare, but both 
echinococci aDd cysticerci have been met with, developing in the 
meshes of the arachnoid. Fatty tumours have been found in a few 
instances, and may contain muscular fibres. They are congenital and 
sometimes associated with spina bifida (q.v.). Fig. 163 represents 
such a tumour, a myolipoma consisting of fatty tissue and striated 
muscular fibres, which had grown from the pia mater or meshes of 
the arachnoid, and was found in a case of tabes.* Neuromata occur 
on the nerve-roots, and may compress the cord.f 
The growths within the substance of the cord itself are more 
diverse in character. Syphiloma and glioma are the most common ; 
sarcomata, myxomata, and tubercular tumours also occur, containing 
the characteristic bacilli, and always associated with tubercle else- 
where. A cysticercus has once been met with. Some growths have 
a compound character, and have been termed myxo-sarcoma, glio- 
sarcoma, and fibro-sareoma. Sarcomata and gliomata are sometimes 
very vascular, and have been termed “ angio-sarcoma ” and “angio- 
glioma.” It is far more common for the tumour to spring from the 
pia mater or from the peri-ependymal tissue around the canal than 
for it to begin among the nerve-structures, but tubercular growths 
usually begin in the grey matter on one side. 
Extra-dural growths are always single; those within the dura mater 
are often single, but sometimes two or three co-exist; or the growth 
may be diffuse, as in a sarcoma of the pia mater, which extended 
as high as the sixth pair of cerebral nerves, and as low as the cauda 
equina.J Neuromata or sarcomata on the nerve-roots are often 
multiple, and sometimes are very numerous. Tumours within the 
spinal cord are also usually single, even those of tubercular nature, 
but occasionally more than one growth is found. 
The size attained by growths outside the cord is necessarily moderate, 
in consequence of the limitation of the space in which they grow. 
They vary from the size of a pea to a width of one and a length 
of two inches, which is rarely exceeded, and chiefly by extra-dural 
tumours. Those that develop from the pia mater are usually smaller 
than those that spring from the dura mater. Multiple tumours on 
the nerve-roots are generally small. Adhesions often form between 
the growth and the membrane from which it does not arise. The 
tumour compresses the nerve-roots and the spinal cord (Figs. 164, 
167). The compression produced by tumours within the dura mater 
is always greater than that by tumours outside this membrane. 
* See * Path. Soc. Trans.,’ vol. xxvii, 19. Another rare case is one of lymph- 
angeioma of the pia mater (Traube, ‘Neur. Cent.,’ 1887). 
f Myxo-fibromata may also form on the nerve-roots, and even extend on to the 
cord. See Bruce and Mott, ‘ Brain,’ July, 1887. 
J Pasteur, ‘ Brit. Med. Journ.,’ July, 1887. TUMOURS. 
545 
164. 
Fig. 165. 
Fig. 166. 
Fig. 164.—Tumour growing from the inner surface of the dura mater, and 
compressing the spinal cord in the mid-dorsal region. The tumour, 3 cm. long, 
was a sarcoma in which the cells were arranged in concentric groups, the centres 
of which had undergone calcification. The spinal cord was softened and dark in 
tint at the compressed part.* (Alter Lancereaux.) 
Fig. 165.—Sarcoma growing between the arachnoid and pia mater in the mid- 
dorsal region of the cord. The tumour had sprung from the meshes of the arach- 
noid, and was only slightly adherent to the pia mater. The spinal cord was 
compressed and softened. In the figure the dura-matral sheath has been laid open, 
except at the top, and the arachnoid has been opened over the lower half of the 
tumour, which, 5 cm. long, lies on the posterior and (right) lateral aspect of the 
cord.f (After Lancereaux.) 
Fig. 166.—A tumour (T) growing from the dura mater, and compressing the right 
side of the spinal cord at the origin of the 4th, 5th, and 6th cervical nerves. The 
tumour was a spindle-celled sarcoma springing from the arachnoid.J (After Leyden.) 
* The patient was a woman seventy-one years of age, paraplegic, with strong 
flexor contracture of the legs, loss of power over the sphincters, and considerable 
impairment, but not absolute loss, of sensibility. The symptoms came on gradually 
six years before death. (Lancereaux, ‘ Atlas d’Anat. Path./ p. 444.) 
f The patient was a woman twenty-eight years of age. The first symptom was 
pain, radiating over the upper part of the abdomen on the right side, and after- 
wards extending to the leg and to the left side. After a few months, weakness of 
the legs gradually came on, and became absolute, with loss of sensation and of 
power over the sphincters. Extensive bedsores were the immediate cause of death,, 
which occurred eighteen months after the onset. (Lancereaux, * Atlas/ p. 447.) 
$ The patient was a man aged thirty-five. At twenty-eight pain commenced in. 
YOL. I. 546 
SPINAL CORD. 
Fro. 167. 
Fig. 168. 
Fig. 169. 
Ftg. 167.—Tumour of dura mater opposite the upper part of the lumbar enlarge- 
ment, compressing nerve-roots and spinal cord. (From a preparation in University 
College Museum. Drawn by Dr. H. R. Spencer.) 
Fig. 168.—Tumour of the cauda equina surrounding and enclosing many of the 
nerve-roots. The cord itself was unaffected. The structure of the tumour wras 
that of a fihro-sarcoina.* 
Fig. 169.—Neuromata of the cauda equina. (After Lancereaux.) The growths had 
apparently given rise to no symptoms. 
the rig-lit forearm, and continued, intermitting, for some years, until, at thirty-four, 
it extended through the whole arm to the neck beside the spine, where it was 
increased by movement. Similar pain afterwards came on in the left arm. Then 
followed weakness in the right arm, slight spasm in the right leg, and tingling 
in the left. The arm became almost powerless and wasted, the right leg weak, 
and flexion of the neck caused severe local pain. These symptoms continued and 
increased, and pain in the left leg came on. The cervical spine became tender, and 
movement of the head to the right was limited. Then both legs became weak, and 
sensibility was lost as high as the nipples. The paraplegia became absolute, bed- 
sores formed, and the patient died seven years after the onset of the symptoms. 
Softening of the spinal cord extended down into the dorsal region. (Leyden, * Klin, 
der Riickenmarkskr.,’ Bd. i, p. 450.) 
* The patient was a man aged twenty-eight, whose symptoms commenced nine 
months before death, and consisted in severe pains in the legs and progressive weak- 
ness, the power of standing being lost about tour months after the onset. A little 
power in the flexors of the hips and the extensors of the knees persisted almost to 
the last, hut the knee-jerk was lost. All the muscles of the legs wmsted, those below 
the knee extremely, and even when the patient was first seen, electrical irritability 
was greatly lowered to both currents, without any reaction of degeneration. Tactile 
sensibility was impaired in each foot and lower leg, more in the right than in the 
left, and chiefly in the region supplied from the sacral plexus. Sensibility to pain 
w-as not affected. The bladder was affected early, and symptoms of pyelo-nephritis 
already existed. The kidney disease was the immediate cause of death, which was 
preceded by several convulsions, apparently urannic. A microscopical examination 
showed considerable damage to many nerve-roots involved in the tumour, while 
others had escaped. The muscles presented intense granular degeneration with 
some longitudinal striation, and increase of the interstitial nuclei. TUMOURS. 
547 
The amount of pressure is proportioned to the size of the tumour and 
its consistence. A soft growth outside the sheath may attain a 
considerable size, and even extend through the intervertebral 
foramina, without exerting much pressure on the cord itself. At the 
compressed part the cord is narrowed and softened, usually indented 
or flattened, because the pressure is either from one side, from the front, 
or from the back. Rarely, the degree of pressure is so great that the 
cord is reduced to the size of a crowquill, and it has even been 
apparently interrupted at the spot, the upper and lower portions being 
conical, and their poiuted extremities connected only by membranous 
tissue. The softening of the cord depends on inflammation, the 
“ pressure-myelitis ” considered in a preceding chapter (p. 345), and 
it presents the tissue-changes that have been there described. Secon- 
dary inflammation may extend clown the cord below the growth, or 
for a short distance above it, often unequally in the different elements 
—sometimes in the grey matter into the lumbar enlargement, and 
even on one side only (Francotte, see p. 552). The usual secondary 
degenerations are commonly conspicuous. 
The growths that involve the cauda equina often attain a larger size 
than those that occur higher up, because this part of the vertebral 
canal is large, and the nerve-roots occupy but a small part of it. 
Most tumours in this situation are sarcomata or fibro-sarcomata, but 
it is a not uncommon seat of syphilitic growths. They usually spring 
from the tissue of the arachnoid, and often surround and include the 
nerves (Fig. 168), the amount of damage to which is very variable. 
Multiple tumours outside the cord are sometimes very numerous. 
They are usually sarcomata, and spring from the membranes and 
sheaths of the nerve-roots. They are various in size, ranging from that 
of a hazel nut to that of a pin’s head, and many very small growths 
are often scattered among the nerves of the cauda equina. In some 
cases of this character similar growths have existed in the cerebral 
membranes. 
The tumours within the spinal cord are usually small, seldom 
exceeding half an inch in diameter, and usually less, even when they 
give rise to considerable impairment of function. But their vertical 
extent often exceeds their transverse diameter, and sometimes they 
grow through a considerable extent of the spinal cord. Gliomata, and 
especially the gliomatous growths that spring from the central region, 
and arise from embryonal neuroglial tissue (persistent by arrest 
of development, and often associated with syringo-myelia), are those 
which have most frequently a considerable vertical extent. Such a 
glioma has been known to reach from the medulla oblongata to the 
lumbar region, and often extends up from the cervical region to the 
base of the brain. 
The cord is enlarged at the seat of a tumour, and the precise 
character of the enlargement depends on the position of the growth. 
In an infiltrating glioma of the upper part of the cord, the increase 548 
SPINAL CORD. 
in size has heen so great that the wall of the foramen' magnum 
caused a constriction around tbe swollen cord. Often the abnormal 
colour of the tumour is perceptible on the surface. Tbe consist- 
ence of tbe cord may be lessened in soft growths, but tbe tumour 
is commonly firmer than the normal cord, and the difference is 
frequently increased by softening in the vicinity of the growth. If 
tbe tumour reaches the surface, the pia mater and arachnoid may be 
thickened at tbe spot, and they may even be adherent to the dura 
mater, but there is rarely any extension of the meningitis to other 
parts. On section, tbe growth is usually very distinct, since its 
aspect contrasts with that of the nerve-substance. Only glioma and 
myxoma resemble the normal 
grey substance in appearance, 
but the new tissue is usually 
distinct in position. These 
tumours in some cases blend 
with tbe substance of the 
cord, but in other instances 
they are bounded by an area 
of softening which often iso- 
lates even invading growths. 
Some tumours are sharply 
limited. It may be difficult 
to say in what structure tbe 
tumour began, but this may 
sometimes be ascertained by 
an examination of the upper 
and lower parts, where the 
growth is commonly limited 
to that part of tbe cord in 
which it first originated. 
Thus in Fig. 170, b, the 
tumour occupies a very large 
area, although the nearly 
equal extent on each side 
suggests its central origin, 
and this is clearly seen in tbe 
section through the upper 
part of the growth, in which 
the posterior commissure can 
be traced in front and behind 
the small area of growth, 
pointing to the peri-ependy- 
nal tissue as its source. Syphilitic tumours commonly originate 
from the pia mater, as they do also in the brain, and the mem- 
brane in their vicinity is often thickened. They both invade and 
compress the nerve-tissue. An instance of such a gumma of the cord 
FlO. 170.—Tumour of spinal cord, springing 
from the tissue around the central canal. 
A, upper part of the tumour in the middle of 
the cervical region; the growth is here within 
the posterior commissure. B, section through 
the largest part of the tumour, which occupies 
the whole central region of the cord. The 
vertical extent was 2 cm. It was a sarcoma 
composed chiefly of spindle-cells arranged 
in fasciculi and in concentric layers. The 
patient was suffering also from a cerebral 
tumour causing hemiplegia, and the spinal 
growth, which apparently developed rapidly 
during the final period of palsy and prostra- 
tion, was not suspected during life. TUMOURS. 
549 
is shown in Fig. 171. It probably commenced at tlie furrow opposite 
the head of the posterior cornu, which it has destroyed, and the pres- 
sure which it exerted is evident from the displacement of the posterior 
FiO. 171.— Syphiloma In the spinal cord, occupying the position of the 
posterior cornu and adjacent parts of the posterior and lateral columns, in 
the lower cervical region. The tumour presented the usual combination 
of grey translucent, and yellow cheesy areas. A second similar, hut much 
smaller tumour existed higher up. The symptoms were complicated by 
hemiplegia, &c., of cerebral origin, due to a gumma in the brain. Para- 
lysis with rigid flexor contracture of the left arm and leg was apparently 
due to the growth. The disease was certainly syphilitic, but it is note- 
worthy that it had developed during continuous treatment by full doses 
of iodide, which had entirely removed earlier symptoms, but to which the 
system bad apparently become accustomed. 
median septum. In all forms of tumour the central canal is often 
obliterated by the pressure, and may be slightly dilated higher up ; 
this dilatation is especially common from growths that begin in the 
peri-ependymal tissue. The considerable enlargement of the canal, 
termed “ syringo-myelia,” is generally associated with a peculiar 
growth in this position, probably congenital in origin; the condition is 
described in another chapter. In other forms of tumour, cysts occasion- 
ally develop, and haemorrhage may occur into such cysts, or into the 
softened tissue in the vicinity of the tumour, or even in the substance 
of a soft growth itself, especially when this is a glioma. From the 
region of the growth, secondary degenerations can frequently be 
traced upwards and downwards, but these are often slighter than the 
apparent damage would suggest, sometimes by reason of the remarkable 
tolerance of the nerve-fibres to pressure if this is slowly developed, 
•sometimes because a rapidly growing tumour has not given time for 
them to become conspicuous. As regards vertical position, growths 550 
SPINAL COED. 
may occur in any part, but are said to be most frequent beneath the 
lower cervical spines, and in the upper and lower dorsal regions, 
because (it is conjectured) there is least room at these places, although 
why the result should follow from the cause is not clear. 
Symptoms.—The symptoms produced by tumours within the spinal 
canal, whether these are within the cord or outside it, resemble in 
their general characters those which we have already considered as 
resulting from growth and caries in the bones of the vertebral column. 
The resemblance is most close in the case of extra-dural growths, and 
least so in that of tumours within the substance of the cord. The 
chief differences are the relative preponderance of symptoms of 
early irritation of the cord itself when the growth is within it, and 
the frequent indications of a transverse extension of the damage from 
one side of the cord to the other. 
In the majority of cases pain is prominent through the whole course 
of the disease. It is usually the earliest effect, severe both before and 
after the development of other symptoms. The pain may be intense 
along the course of the nerves which arise at the level of the tumour, 
and also in the parts supplied by nerves below that level, e. g. in the 
legs, but it is not felt above the growth. It may be a sharp acute 
pain, but has often a “ burning’’character, and is sometimes “stabbing” 
or “ rending.” Dull aching pain may be felt between the attacks of 
severe pain, or before them, and may then give rise to the most 
frequent of all diagnostic errors—mistaking grave organic disease for 
simple rheumatism, on account of the similarity in the character of the 
pains. The intensity of the severe pain is usually very great, and it 
has more than once led the unhappy sufferer to attempt suicide. The 
pains are often felt on one side first, in one arm, in one side of the 
trunk at a given level, or in one leg, and a considerable time may 
elapse before they extend to the other side. Occasionally the pain 
is bilateral from the first. It is generally greatest when the tumour 
compresses the cord from behind forwards, or vice versa (Horsley) ; 
this is open to more than one explanation. Pain is sometimes 
increased by movement, but rarely in the intense degree common in 
tumours of the bone. When the growth is in the lower lumbar 
region, the pain is often first referred to the soles, and seems to 
ascend. The sensory loss, due to subsequent nerve destruction, follows 
a similar course. Pain is sometimes felt iu the spine, frequently when 
the growth begins in the dura mater, rarely when it is within the 
substance of the cord. Tenderness of the spine often exists in the 
former cases, but is on the whole not common. Other subjective 
sensations may occur with the pain or in the intervals—“ numbness,” 
tingling, formication, &c., and they give significance to the pains as an 
indication of organic damage to the nerve-structures. The root-pains 
in the trunk are often accompanied by a sense of constriction, which 
may be very distressing Hyperaesthesia of the skin frequently accom- 
panies pain felt at the level of the tumour, less commonly those in the TUMOURS. 
551 
parts below. Very rarely pain is absent; chiefly in extra-dural lipoma, 
probably from the nature of the growth. 
Muscular spasm is another common symptom, most pronounced 
when the tumour springs from tbe membranes. There may be some 
rigidity of the back opposite the seat of the growth, usually associated, 
with local pain. It is most marked when the disease is at the more 
mobile parts of the spine, especially when it is in the cervical region. 
In such cases the rigidity may be painful, and the pain may be 
increased by movement. Severe spasm in the abdominal muscles is 
often associated with severe girdle-pain. Contractures may develop 
in the limbs, both in those supplied by the nerves which arise at the 
level of the tumour, and are directly irritated by it, and also, although 
less commonly, in the parts supplied from the spinal cord below the 
level of the growth. Thus the tumour in one half of the cord in the 
cervical region (shown in Fig. 171) caused persistent flexor contracture 
in the arm and leg on the side of the growth, and in the early stage 
of dorsal tumours one leg only may be rigid, or more so than the 
other. The seat of rigidity thus needs to be specially noted, as well 
as its character, if we are to obtain from it diagnostic guidance, 
because it may be due to the irritation, either of the nerve-roots or of 
the conducting tracts. Both forms sometimes occur before loss of 
power, but pain generally precedes them. 
Paralysis, of gradual onset, is almost invariably one of the sym- 
ptoms. Paraplegia is the most common form, but all four limbs may be 
paralysed by a growth in the cervical region. Yery commonly one leg 
becomes weakened before the other, and occasionally one arm and leg 
suffer before those of the other side. Tumours which are situated in the 
middle line or in the centre of the cord, however, usually affect both 
sides at the same time, and the effects of a congenital growth may 
thus accompany and complicate those of an associated syringo- 
myelia (q. v.). The proximal paits of the limbs seem, as a rule, to be 
first affected, although exceptions are occasionally met with. 
The palsy, gradual in onset, is usually also slow in its extension, the 
rate of its increase depending on the rate at which the tumour grows 
and compresses the spinal cord. This is the characteristic course of 
the paralysis produced by a tumour. But in a large number of cases 
the loss of power comes on in a subacute, or even an acute, manner, in 
consequence of the myelitis excited by the compression, which, in 
such cases, may run a course of independent rapidity. When the 
inflammation is thus in excess of its cause, the palsy may lessen as 
damage from the inflammation subsides to the degree of the damage 
from pressure. The symptoms that depend on compression slowly 
but surely increase as the tumour grows, and usually attain a high 
degree of intensity; the loss of power in the legs, for instance, becoming 
absolute and remaining so. 
Loss of sensation may come on with the loss of motor power ; 
more often after this has become considerable. It may be slight or 552 
SPINAL CORD. 
partial at first, occasionally for a long time, but tends to become com. 
plete as the damage to the cord increases, and it often ascends the legs. 
Jt corresponds in distribution to the motor palsy, when the disease 
is below the middle of the dorsal region ; but if situated higher, 
and on one side, the sensory loss is often greater on the side opposite 
to the motor paralysis. Tumours of the cord furnish a considerable 
proportion of the cases in which the crossed symptoms of a unilateral 
lesion are well marked (see p. 229). In addition to the loss of 
sensation which results from the damage to the cord itself, areas of 
anaesthesia may exist in the region supplied by the nerves which are 
damaged by the growth, and in which the severe radiating pains are 
felt. If there is crossed sensory and motor palsy, these root symptoms 
exist, chiefly on the side opposite to the anaesthesia in the limbs. 
Inco-ordination of movement is not a common symptom of spinal 
tumours, but has been occasionally met with in cases of growth in- 
vading the posterior columns, and also as a result of multiple tumours 
of the nerve-roots (see p. 428). Loss of power usually coexists and 
quickly becomes predominant when the growth is in the cord. 
The condition of reflex action depends on the position of the tumour. 
In the lumbar enlargement or the cauda equina, a growth abolishes 
reflex action in the legs, and in any position the trunk-reflexes are lost 
at the level of the lesion. But when the disease is situated higher up, 
reflex action is increased, and the excess of cutaneous reflex action is a 
very marked and early symptom of the disease ; it is lessened and lost 
only when the lower part of the cordis damaged bv secondary myelitis 
(superadded to descending degeneration and distinct from it). The 
mvotatio irritability presents also the increase that invariably results 
from damage to the pyramidal tracts, and the usual tonic spasm also 
gradually develops and often reaches a high degree. Its loss, with 
muscular relaxation, sometimes met with under these conditions, 
depends on a descending myelitis, sometimes slight and partial.* 
Muscular contracture is superadded more frequently in tumours than 
in many other diseases, and rigid spasm in the flexors of the knee and 
hip may keep the heels in contact with the nates. 
Wasting of the muscles is for the most part confined to the regions 
supplied by the damaged nerve-roots. In tumours of the lumbar 
enlargement and cauda equina, the atrophy of the muscles of the legs 
is a very conspicuous symptom. Vaso-motor disturbance sometimes 
occurs in the early stage of the disease, chiefly in the distribution of 
irritated roots, where flushing of the skin has been noted, and the so- 
called “ meningitic streak” (“ taclie spinale”) may often be produced. 
* As was found to be the case by Francotte (* Fibrome de la Dure-m&re spinale,’ 
Li£ge, ?888) in a case of tumour compressing the upper dorsal region. Slight 
descending inflammation of the right anterior cornu coincided with flaccid palsy of 
the right leg. It should have been mentioned that the connection of a similar loss 
of myotatic irritability with descending inflammation in dorsal myelitis (referred to 
at pp. 229 and 316) has been proved in two cases by Francotte (!oc. cit., p. 9). TUMOURS. 
553 
Occasionally vaso-motor oedema is a conspicuous early symptom. In 
the later stages, bedsores are very common and often severe. Dilatation 
or contraction of the pupil is common when a tumour is situated in 
the lower cervical region. Loss of control over the sphincters usually 
•accompanies motor palsy in the legs ; their state corresponds with that 
of reflex action (p. 224). 
The course of the symptoms is variable, and depends on the rapidity 
of growth of the tumour, and on the share which secondary myelitis 
takes in the production of the symptoms. As a rule, the root symptoms 
occur first, and in growths outside the cord they may exist alone for 
months, and even, in the case of a slowly growing tumour, for years, 
before the symptoms of damage to the cord itself are added. On the 
other hand, they may be entirely absent in growths which commence 
within the cord itself. In some cases the symptoms are steadily 
progressive from first to last. In others the progress is intermittent; 
periods of increase in the symptoms alternate with stationary periods. 
Their course is variable, even in cases in which the seat of the tumour 
and its nature are the same, because they depend on the secondary 
changes in the nerve-elements, and the course of these (such as the 
myelitis induced by pressure) is subject to variations, the cause of 
which is often indistinct. Thus the chronic course of the symptoms 
is often varied by periods of rapid and even sudden increase, espe- 
cially in the case of growths that involve the spinal cord itself; and 
symptoms that have thus developed with rapidity are apt (as already 
mentioned) to subside, if not completely, at least in considerable 
degree. Hence a rapid increase of the cord symptoms may be 
followed by positive improvement for a time, but scarcely ever by an 
actual disappearance of the manifestations of the disease. The most 
important element in the course of the disease is the tendency to a 
lateral extension of the symptoms, the expression of the transverse 
extension of the damage, as the several structures of the cord, at the 
same level, successively suffer. Although there is sometimes an exten- 
sion downwards of the interference with the central functions of the 
cord, when secondary myelitis descends to the lumbar enlai'gement, 
there is scarcely ever an extension upwards above the level of the 
initial interference with function. A small, slowly growing tumoui*, 
even within the cord, sometimes causes no symptoms. 
The chief differences between the symptoms of iumours of the cord 
and membranes, besides those mentioned on p. 550, are that, in 
the latter, the root symptoms are more often severe, and that the cord 
symptoms occur latex1, and are at first more limited in extent. Spinal 
pain, tenderness, and rigidity are more common. In cord tumours the 
radiating pains, due to irritation of the nerve-roots, are more often 
trifling or absent, unless the growth begins in the neighbourhood of 
the posterior horn ; then they may be pronuunced. The cord symptoms 
are often bilateral from the first, and in central tumours they may 
develop equally on the two sides. If they are unilateral at the onset 554 
SPINAL CORD. 
they extend to the other side sooner than in the case of meningeal 
growths. In the case of tubercular growths the symptoms of irrita- 
tion are usually subordinate to those of impaired conduction, and 
pain is felt chiefly in the legs (Herter). Extensive muscular atrophy 
is more common in tumours of the cord than in those of the membranes 
(except in the case of tumours of the cauda equina), because central 
tumours may damage the grey matter through a considerable vertical 
extent, and are most common in the enlargements, and also because 
myelitis spreads in the grey matter far more frequently when the 
exciting growth is in the cord itself, than when it is in the mem- 
branes. 
In tumours of the cervical region, the interference with movement 
of the neck, from the rigidity of the muscles, is often well marked, 
especially when the tumour is in the membranes. The pains due to 
irritation of the nerves are felt in the arms, and are often associated 
with muscular atrophy. The excess of reflex action in the legs is very 
great, and if the influence of the tumour is chiefly on one side, 
hemiplegic weakness, with crossed anaesthesia, is present. 
Growths in the dorsal region of the cord usually cause severe 
radiating pains in the trunk, often accompanied by an intensely painful 
sense of constriction, by hyperaesthesia, and sometimes by anaesthesia. 
The simple, merely sloping course of the dorsal nerves reveals the pre- 
cise position of the disease more clearly than do the symptoms in the 
arms when the tumour is in the cervical region. The interference with 
the trunk-reflexes often corroborates the indications afforded by the 
subjective symptoms. Spinal tenderness may be also present, but 
rigidity of the spinal muscles is not common. Reflex action in the 
legs presents the same excess that results from tumours in the cervical 
region, but sometimes, especially when the growth is near the lumbar 
enlargement, or the pressure-myelitis has been acute, the descending 
myelitis, as we have seen, may abolish the reflex action and remove 
spasm, if this previously existed. 
The symptoms produced by tumours which involve the lumbar 
enlargement, vary considerably according to the precise position of 
the growth. The characteristic pains are felt in the legs, and the 
muscles supplied from the part invaded or compressed undergo 
atrophy, and present loss of reflex action and of myotatic irritability j 
but the anaesthesia is often limited in area. A growth in the upper 
part of the enlargement may cause wasting only in the flexors of the 
hip and extensors of the knee, with loss of the knee-jerk and anaes- 
thesia in the front of the thigh, while the muscles below the knee 
present simple palsy with myotatic excess. Thus a man, who had had 
syphilis, complained of pain in the left groin and thigh, and presented 
wasting of the extensors of the knee, with anaesthesia in the front 
of the thigh ; there was loss of the left knee-jerk, and a foot-clonus* 
on each side. He recovered partially, but there was doubtless a 
small syphiloma at the upper part of the lumbar enlargement on 555 
TUMOURS. 
the left side, interrupting the reflex arc, damaging the left motor and 
sensory roots, and compressing both pyramidal tracts. A growth 
in the membranes adjacent to the middle or lower part of the lumbar 
enlargement usually causes symptoms of wide distribution, affecting 
the whole of both legs, and the early symptoms of irritation often 
involve the distribution of the upper lumbar nerves. But a growth 
at the same level within the cord may affect chiefly the muscles of the 
lower leg, and cause anaesthesia in the region supplied from the sacral 
plexus. There may also be palsy and wasting of all the muscles of 
both legs, from extensive secondary myelitis, but even then the sensory 
loss is usually limited. In lumbar tumours there is early palsy 
of the bladder and sphincters. Examination of the sphincter ani 
shows absolute paralysis, and not the pure reflex action present when 
the disease, arresting voluntary influences, is higher up the cord. 
The tendency to bedsores is commonly strong in tumours of this part. 
Growths situated in the cauda equina, which are below, and do not 
affect, the cord itself, produce symptoms very similar to those due to 
tumours of the lumbar enlargement, but the symptoms are bilateral 
from the first in the majority of cases. Barely one leg is affected alone 
at the outset. The symptoms usually begin in the lowest parts of the 
legs, which are throughout involved in greater degree than the upper 
parts, and the flexors of the hip may escape altogether. Muscular 
contraction is much less common than in tumours situated higher up. 
The anaesthesia is chiefly in the region supplied by the sacral plexus ; 
the pains, usually very severe, are first felt in the same region, and 
there may be severe pain on each side of the sacrum radiating to 
the region of the sciatic nerves. The muscles below the knee rapidly 
waste, and often (but not always) present the degenerative reaction. 
These symptoms were well marked and characteristic in the case figured 
and described at p. 546 (Fig 168), and the condition of the muscles 
suggests that the absence of any voltaic irritability in the muscular 
fibres was due to their early and intense fatty degeneration. In many 
cases the symptoms are irregular in distribution, the nerves are 
included in the growth, and are often damaged unequally, sometimes 
less than might be expected from the size of the tumour, which may 
be considerable before its expansion is arrested by contact with the 
bony walls of the canal. Hence the loss of sensation may be partial, 
and reflex action may not be completely abolished. In the case above 
mentioned, for instance, a prick on the sole caused a reflex contraction 
of the muscles in the upper parts of the legs, but of these alone. In 
many cases, however, the loss of sensation has been absolute, and reflex 
action also has been entirely lost. The tendency to trophic changes is 
great, and an affection of the sphincters is almost invariable. Cystitis 
and its consequences readily occur, and may reach a high degree, in 
consequence of residual accumulation, when the patient is conscious 
only of slight difficulty of micturition. 
Multiple tumours may give rise to very complex symptoms. If 556 
SPINAL CORD. 
there are only two tumours, they may be indicated by the successive 
development of focal symptoms, similar in character but different in 
seat. In some cases in which there are many growths, only one or 
two of the largest have caused svmptoms, and the smaller tumours 
have run a latent course. In other cases in which many tumours 
have caused slight symptoms, these have simulated closely a system- 
disease of the cord. Thus, in the remarkable case recorded by Hughes 
Bennett, multiple growths on the posterior nerve-roots produced 
the characteristic manifestations of locomotor ataxy.* When cerebral 
tumours have coexisted with multiple spinal growths, the symptoms of 
the latter have usually been lost in those of the intra-cranial disease, 
which has often preceded the spinal lesion. 
The duration of the symptoms of tumours of the cord and mem- 
branes, those of syphilitic nature being excluded, varies from three 
months to five, or even ten years. Equally variable, but shorter, is 
the time that elapses before the symptoms reach their full develop- 
ment, which depends partly on the secondary inflammation, partly on 
the rate of growth of the tumour. From the former cause, the time 
may be only a few days, when the myelitis is acute; from the latter 
it may be as short as three or four weeks, in tumours of tubercular or 
syphilitic nature. In the majority of cases, death ensues at the end 
of from one to three years from the commencement of the symptoms, 
but these last longer when the growth is outside the dura mater than 
when inside the sheath. The immediate cause of death is usually the 
direct or indirect effect of the tumour; but in syphilis death is some- 
times due to disease elsewhere, and in tubercle, frequently to general 
pulmonary tuberculosis (which usually precedes the spinal growth), 
or sometimes to meningitis. 
Diagnosis.—The evidence of a growth consists in the symptoms of 
a focal lesion of slow development, and especially in the presence of 
signs of compression and irritation (pain and rigidity), while the sig- 
nificance of these is increased by indications that the disease began at 
the surface of the cord, and sometimes by the history of a cause, as 
syphilis. Although no symptom is actually pathognomonic, yet the 
•combination of the symptoms, and their course, are in most cases 
sufficiently characteristic. Those of greatest diagnostic importance 
■are, first, the pain that is felt in the parts at the level of the tumour, 
or below it, and sometimes in the spine ; secondly, the progressive 
paralysis, motor and sensory. Of less but still considerable importance 
<ire the rigidity of the muscles of the spine, the muscular contractions 
in the limbs, and the early and marked excess of reflex action when 
the cord itself is involved. In the course of the disease the most 
important features are the steady progress of the symptoms, and 
especially their commencement on one side and extension to the other. 
Of causal indications that occasionally assist the diagnosis, the most 
important are a history of constitutional syphilis, the presence of 
* ‘ Clin. Trans.,’ 1S85. TUMOURS. 
557 
tubercular disease elsewhere, and, in rare instances, the existence in 
other parts of such multiple growths as are known to occur also within 
the spinal canal, especially multiple sarcomata and neuromata. 
The diagnosis of multiple growths depends on the recognition of the 
successive development of the characteristic symptoms in more than 
one focus. It is rare for more than two of many tumours to cause 
definite symptoms. The greatest absolute difficulty in the diagnosis 
of a spinal tumour is presented by the cases sometimes met with, in 
which an intra-cranial tumour precedes the growth within the vertebral 
column, and the symptoms of the latter are overlooked in the presence 
of the severe manifestations of the former. In most cases, however, 
the additional symptoms, which usually exist, may be detected by 
careful observation, and their significance recognised. Growths 
involving the cauda equina cause symptoms like those of tumours in 
the lumbar enlargement, save that the effects are from the first 
bilateral in even more pronounced degree, and the evidence of inter- 
ference with the nerves (loss of reflex action, nerve pain, &c.) is even 
more conspicuous. 
The differential diagnosis involves the distinction from diseases of 
the vertebral bones, of the membranes, and of the cord itself. Caries 
of the spine has many symptoms in common with tumour, but the 
root-pains are rarely very severe, and the effects of compression of the 
cord are usually bilateral, either from the first or very soon after their 
commencement; the paralysis seldom reaches a considerable degree in 
one leg before the other suffers. The signs of bone disease are rarely 
long absent, and repeated examination usually reveals tenderness and 
irregularity of the vertebral spines. From growths in the boues of 
the spinal column, the diagnosis may at first be impossible. But the 
pain of tumour is rarely increased by movement to the same intense 
degree as when the growth commences in the bone, unless the tumour 
is in the cervical region of the cord, and then the greater accessibility 
of the vertebral column renders the exclusion of bone growths 
comparatively easy by local examination. In the dorsal regiou a 
growth in the bone may long escape detection, but even here the 
influence of movement on the pain is often extreme, far greater than 
in the case of tumours within the canal. The effect of the movement of 
the vertebrae on the nerve-roots, when compressed as they pass through 
the foramina, is far greater than when they are compressed within the 
canal. Sooner or later a local enlargement may present itself 
externally, and show the nature of the case. 
“ Hypertrophic pachymeningitis,” affecting the cervical region, is 
the only meningeal disease which closely simulates the symptoms of 
tumour, but its effects are usually from the first bilateral, and they 
have a considerable vertical extent. Hence it is only with central 
tumours, which grow through several inches or more of the cord, that 
the disease is likely to be confounded. In each malady there may be 
muscular atrophy in the arms, and paralysis, without wasting, in the 558 
SPINAL CORD. 
legs But in central tumours the pains in the arms are usually 
much slighter than in the thickening of the membrane, and there is 
rarely the early and limited impairment of all forms of sensation 
which results from the damage to the nerve-roots in the latter disease. 
This is also true of syringo-myelia, in which tactile sensibility usually 
persists, although untypical cases may present much difficulty. The 
diagnosis is considered more fully in the account of that disease. 
The affection of the cord itself which most closely simulates the 
symptoms of tumour is a very chronic transverse myelitis. In such 
a case as that shown in Fig. 104, p. 338, the diagnosis may be a matter 
of extreme difficulty. The radiating pains in this case were severe 
and local, and the limitation of the symptoms, for a long time, to one 
side, with crossed sensory and motor palsy, presented an almost perfect 
analogy to the effects of a growth. But it is very rare for severe 
and acute radiating pains to result from focal myelitis, although a 
painful sense of constriction is common; moreover, in tumour, one 
half of the cord seldom suffers severely without the functions of the 
other half also being very soon impaired in some degree. The limitation 
of chronic myelitis to a single focus is also very unusual; a consider- 
able vertical extent of the cord is usually involved in varying degree. 
Hence the practical difficulty in diagnosis is not so great as, at first 
sight, might appear. Acute or subacute myelitis can only be con- 
founded with a growth in cases in which inflammation results from 
pressure, and develops with independent energy and rapidity. In 
such cases the occurrence of myelitis must be recognised, and the 
diagnostic problem is the detection of the preceding symptoms of the 
growth that excites the inflammation. This is usually easy; the 
severe pains, and commonly also the slighter symptoms of paralysis, 
which existed before the rapid increase in the loss of power, are suffi- 
cient proof of a chronic morbid process, to which the inflammation is 
secondary. 
The early pains are often thought to be neuralgic, but their constancy 
and continuance should suggest organic irritation; their seat, moreover, 
is rarely that iu which neuralgia is common. The pain produced by 
tumours of the cauda equina is often felt first in the sciatic area, and 
thought to be sciatica ; but they are commonly from the first bilateral, 
while sciatica is almost invariably one-sided, and bilateral sciatic pain 
should always suggest irritation where the sensory fibres from both 
sides are near together, and can be irritated by a single cause, i. e. 
it should suggest disease within the vertebral canal. In all cases, 
however dubious the early pains may be, other symptoms soon become 
added, and prove that there is more than a simple neuralgia. But the 
effect of the organic disease on other parts of the nervous system may 
evoke any functional derangement to which the patient is predisposed, 
and it is most important not to permit the diagnosis to be thereby 
misled, or the gravity of organic symptoms to be under-estimated.* 
* Thus the patient from whom the tumour was removed (see p. 561) had once had TUMOURS. 
559 
If the existence of a tumour is clear, two questions remain—its seat 
and nature. The interference with the elements of the cord shows 
its lateral seat, hut this is of small practical importance compared 
with the evidence of its vertical position, in any case in which an 
operation is contemplated. The latter is indicated by the level of the 
transverse symptoms, especially the upper level of the sensory 
or motor loss, or sensory irritation ; but it is of special importance to 
note that the growth is often above this, and never, or almost 
never, lower. It may be even a distance of three or four vertebra} 
above the pair of nerves corresponding to the highest level of the 
anaesthesia or pain. This discrepancy is especially noticeable when the 
growth is in the cord; it is least when the tumour is extra-dural; and 
if this is so seated as to affect a nerve on one side, there is often a 
strict correspondence between the symptoms and the situation of the 
lesion. It is explained by the upward course of many posterior root- 
fibres. 
The nature of the tumour is also of great practical importance in 
many cases. If the patient has had constitutional syphilis, the 
syphilitic nature of the growth is highly probable, and the probability 
is further raised in degree if the growth developed rapidly, so that the 
symptoms attained a considerable intensity in less that three months 
from their onset. The coexistence of a cerebral lesion also increases 
the likelihood of the syphilitic nature of the growth. Either of the 
last two considerations suggests the same conclusion in any case in 
which syphilis, although not proved, is possible; but it must be 
remembered that cerebral and spinal tumours, of other than syphilitic 
nature, may coexist. In the same way, tubercular and scrofulous 
processes suggest the tubercular nature of a tumour, and this is 
further supported bv early adult age, by rapidity of course, by the 
speedy extension of the symptoms to the second side, by the slightness 
of evidence of irritation, and, in some cases, by periods of arrest of the 
progress of symptoms that were slow in their development. Such 
arrest indicates an arrest of the growth of the tumour, which we cannot 
infer from the subsidence of symptoms that developed rapidly, and may 
have been due to secondary inflammation. When a rapid onset is due 
to this cause, irritation symptoms are usually pronounced. Tumours 
elsewhere always constitute strong evidence of the nature of one in 
the cord, but such an indication is rarely available, since the spinal 
canal is rarely the seat of secondary growths. Multiple tumours are 
some convulsive attacks, and the intense pain due to the growth having caused 
slight mental symptoms, I was asked to see him to decide the question of the 
hysterical nature of the affection. The fact is peculiarly instructive from a 
diagnostic point of view. Not less so is a case of central glioma in a girl (sent 
to me by Mr. P. B. Mason, of Burton-on-Treut), in which a central growth in the 
cervical region extended up into the medulla, and caused at last universal palsy. 
The first symptoms immediately followed severe mental disturbance; to this they 
were naturally ascribed, and thought to be functional. A similar sequence is met 
with in cerebral tumours (q. »•). 560 
SPINAL CORD. 
probably either sarcoma or neuroma. In the absence of these indica- 
tions a meningeal tumour is probably a sarcoma, perhaps fibrous or 
myxomatous, and one within the cord is probably a glioma, because 
these are the most frequent growths in those situations. A diagnosis 
founded on mere frequency of occurrence has necessarily only a low 
degree of probability, and must be sometimes wrong; but it may 
be highly probable that the growth is one of two or three kinds, and 
this may be of considerable practical value. To the surgeon the 
point is of great importance. 
Prognosis.—Unless the tumour is syphilitic, or can be removed, 
the prognosis is necessarily most grave. Of all syphilitic lesions, 
growths are those that are most amenable to treatment, and the 
effects of which most certainly pass away, if they have not reached 
an extreme degree or lasted too long a time. If, however, the damage 
has been allowed to remain unchecked for several months, recovery- 
may be imperfect. Tumours of most other kinds steadily increase, and 
the resulting damage is on the whole steadily progressive, although dis- 
course may be varied by stages of rapid (myelitic) increase in the 
symptoms, followed by stationary periods and even by transient 
improvement. In the case of growths outside the cord, the prognosis 
has been rendered much less gloomy by the progress of surgery. 
Treatment.—If the growth is syphditic, appropriate treatment 
should be energetic and prompt, so as to effect some diminution of 
the pressure as quickly as possible, since the longer this continues 
the more considerable are the degenerative changes, and the longer 
those will endure. Even the influence of a few days before treatment 
becomes effective may make a difference of weeks in the duration of 
symptoms, and lessen the degree of ultimate recovery. Whenever 
the symptoms suggest a tumour, and syphilis is possible, it is most 
important that suitable treatment should be employed; it can do no 
harm if the tumour is not syphilitic, and may save the patient’s life 
and strength if it is. Syphilis can only be excluded when there has been 
no possibility of infection. In many cases of late syphilitic lesions there 
is no history of secondary syphilis, and in others there is no history 
of a primary sore. Hence it is a priori certain that in some cases of 
late lesions a history of both primary sore and secondary symptoms 
will be absent, and, as a matter of fact, such cases are met with not 
unfrequently. Of course these cases cannot be counted as syphilitic 
in any scientific investigation into the influence of this disorder, but 
in treatment we have often to allow weight to considerations which 
are insufficient to influence scientific investigation, and treatment 
determined by the mere possibility of syphilis is often justified by its 
results. Tubercular tumours are also amenable to treatment to some 
extent, but they are too rare to be of much practical importance. 
In most other cases we can do little more than troat symptoms, 
relieving pain by sedatives, watching the state of the bladder, 
preventing the occurrence of cystitis, and guarding the patient TUMOURS. 
561 
from bedsores. We must remember that sedatives will probably be 
needed for a long time, and they must therefore be used as sparingly 
as possible, lest custom and tolerance deprive them of their power. 
Cocaine may be used in many cases as an aid in economising the influ- 
ence of morphia. 
But many tumours within the spinal canal may be removed, at 
any rate if they are outside the substance of the cord. The 
anticipation that such growths would be found removable was ex- 
pressed in the first edition of this book (1886), in words that may 
be quoted because they were soon afterwards realised:—“ Modern 
methods render the opening of the spinal canal far less formidable 
1 ban it formerly was, and the removal of a tumour from the mem- 
branes of the cord would involve less immediate danger of serious con- 
sequences than the removal of a tumour from the brain.” 
On the other hand, growths within the spinal cord are in a very 
different position in regard to surgical procedure, since the removal of 
such a tumour could hardly fail to cause a traumatic inflammation 
that would damage and perhaps destroy all the elements of the cord at 
the spot, and would probably be permanent in its effects, especially 
when these structures have already suffered from pressure. At the 
same time the early removal of a small growth might possibly be 
followed by the regeneration of conducting fibres that are on the other 
side of the organ, and the return of their function, lost only through 
the effects of pressure. 
In a man with complete paraplegia, motor and sensory, of slow 
development, accompanied by attacks of agonising spasm, a diagnosis 
of tumour led me to advise the removal of the growth. This was done 
by Mr. Horsley, and the result has been the permanent recovery of the 
patient. Although the intense spastic paraplegia showed that there 
must have been complete degeneration of the pyramidal fibres, every 
indication of this has passed away. The tumour was a myxo-fibroma, 
about the size of a split almond, which had so compressed the cord in 
the upper dorsal region as to reduce its thickness to about one half. It 
was within the dural sheath, and adherent to the cord.* It is certain 
that many growths might be removed without difficulty, and with a 
secure result, although only one instance has been since recorded. In 
this, the tumour was a lymphangioma cavernosum, situated outside the 
dura mater, over the cauda equina.f 
In connection with an operation, a question sometimes arises that 
is of very great importance, and often of equal difficulty. The sym- 
ptoms are consistent with the syphilitic nature of the growth ; and this 
cause and nature cannot be excluded, except by the disproof afforded 
by the inutility of treatment. But it is essential that this disproof 
# The details of the operation are full of instruction in reference to similar 
procedures, and are given in the account of the case in the ‘ Med.-Chir. Trans./ 
vol. lxxi, 1888. The surgical aspect of the subject is too large to be entered on here. 
■f By Laquer, of Frankfort-u.-M., ‘ Neur. Cent.,’ 1891, p. 193. 
YOL. I. 562 
SPINAL COfiD. 
should be afforded before an operation is decided on; and the question 
arises, how long should be allowed for this process of practical exclusion, 
—how long should treatment be continued without result to justify 
the last resort ? It needs to be longer when the symptoms are of con- 
siderable duration than when they are recent, since secondary changes 
of longdui'ation cannot be quickly removed. Time is needed in every 
instance to permit a trustworthy conclusion, but a month is probably 
always enough to enable a result to be reached that will justify either 
further delay on the one hand, or immediate procedure on the other. 
Finally, one injunction given by Mr. Horsley may be emphatically 
endorsed. If it is clear that the growth is not syphilitic, and that no 
good can be done by other treatment, delay in an operation can only 
cause harm—can only result in a less favorable state for the proceed- 
ing, less chance of recovery, less degree of recovery, longer and 
greater suffering, and should on every ground be avoided. 
CAVITIES AND FISSURES IN THE SPINAL CORD 
(SYRINGO-MYELIA, HYDROMYEEIA, HYDRORRHACHTS INTERNA). 
Cavities in tbe spinal cord, distended with liquid, are met with at 
all ages, and those which present certain features, aud often cause 
certain symptoms, are now known by the above terms. The following 
figures illustrate the most important facts regarding this morbid state, 
aud its somewhat complex conditions will be best understood by con- 
sidering the appearances presented in these, and their significance, 
as described in the explanations. 
The term “ Syringo-myelia ” is applied to all cavities in the cord 
with well-defined limits; but the majority of these (with the exception 
of such as exist in tumours of manifestly different nature), whatever 
their condition or form, or the changes they have undergone, are sur- 
rounded by a layer of embryonal neuroglial tissue, and outside this 
the white substance of the cord is deficient in amount. Wherever 
met with, or whatever the secondary changes the tissue presents, this 
fact of environment stamps the cavity or cavities (for there may be 
two) as congenital, because this abnormal material is due to a per- 
sistence of the embryonal tissue from which the cord is developed. 
The cavities are thus due partly to defective closure of the tube which 
is first formed (residual portions of which become distended by 
accumulation of liquid), and partly to the breaking down of this per- 
sistent embryonal tissue or to tissue formed from it by a process of 
growth. Moreover the cord sometimes suffers serious damage from 
pressui’e, owing to the distension of the cavity by the liquid which 
accumulates within it, or by growth of the adjacent tissue. The con- SYRINGOMYELIA. 
563 
dition is not rare, but is often overlooked, especially in its slighter 
forms, and is readily misinterpreted when it is associated with acquired 
disease—as in the condition illustrated in Fig. 105, p. 839, which is 
very instructive in this connection. The term “ Hydromyelia ” has 
been applied to the simpler forms,* in which the cavity is merely the 
dilated central canal; but as there is no real difference between this 
and other varieties, the designation, being unnecessary and even mis- 
leading, is falling into disuse. 
To understand the origin of these conditions it is necessary to 
remember the mode of development of the spinal cord. The sides of 
the primitive furrow of the embryo coalesce, so as to form a canal of 
relatively large size, the walls of which are thinner in front and 
behind than at the sides, and consist of elongated cells, some of which 
are arranged regularly at the inner surface of the cavity, like an 
epithelium. The anterior wall first becomes thickened, to form the 
white commissure and the front part of the grey, while an abundant 
growth of cells occurs at the sides of the tube, and extends forwards 
(i. e. downwards in the position of the embryo), thus forming the 
lateral and anterior columns; between these two projections is the 
depression of the anterior fissure. Next occurs a growth backwards 
of the now thick sides, which forms the posterior parts of the 
lateral columns and the adjacent part of the posterior columns, and 
with this the posterior roots are connected; this forms the “ root- 
zone ” of the posterior columns. The posterior median columns are 
formed later. The central canal extends backwards between these 
two rudimentary postero-external columns, being closed behind only 
by a thin layer of cells. As the posterior columns increase in thick- 
ness the posterior part of the canal becomes narrowed, and its walls 
unite near its anterior extremity so as to form the posterior grey 
commissure, and divide the canal into two parts. Of these the ante- 
rior becomes the permanent canal, while the posterior is reduced to a 
narrow fissure between the posterior columns. Ultimately this poste- 
rior narrow part becomes closed by a growth of cells which occurs 
from behind forwards, as the median parts of the posterior columns 
develop. All these parts consist first of embryonal cells, which 
afterwards undergo a transformation into the nerve-elements proper, 
and the order of transformation is the same as that in which the 
parts were formed, the posterior median columns latest. The cells of 
the grey matter are formed before the fibres of the white columns. 
Some of the embryonal elements undergo a different and slighter 
change. They may almost be said to jerdst, constituting the 
neuroglia, and the gelatinous grey substance continuous with it 
around the cord, and also massed at the posterior root fissure and 
around the central canal. 
The central canal ultimately lies in the anterior part or middle of 
the grey commissure. It may persist through life as a cavity, cir- 
* See Leyden, * Virchow’s Arcliiv,’ Bd. lxviii, p. 1. 564 
SPINAL CORD. 
cular in section, or as a slit, antero-posterior or transverse, and is 
lined with epithelium (Fig. 172). Around the canal there are 
usually many nuclear elements, especially on each side of it, and 
these frequently fill up the lumen of the canal, so that its position is 
indicated only by an oval mass of small cellular elements (Fig. 172, d). 
The obliteration of the canal often occurs quite early in life, and is no 
evidence of any morbid process. The canal may be found obliterated 
in one part of the cord, and patent in another (c, d, Fig. 172). The 
simple closure of the canal by nuclei does 
not usually cause any distension of the 
part which is above the closed portion, 
or, at any rate, not more than a very 
slight increase in size, so trifling that 
its significance is open to question. 
Syringo-myelia occurs chiefly in the 
cervical and upper dorsal regions of the 
cord. The cavity is often closed below 
by gliomatous tissue, and the excess of 
this may extend up into the medulla and 
even pons. Occasionally the cavity exists 
through the whole length of the cord. 
In the simple condition found in young 
children, or in adults when no secondary 
changes have occurred, the morbid 
change presents the two features already 
mentioned—a quantity of tissue of 
translucent aspect, which, from its struc- 
ture, is clearly persistent embryonal 
tissue in which nerve-elements have not 
developed, and a cavity due to imperfect 
contraction of the canal. The change is 
always confined to the posterior half of 
the cord, and usually to the postei'ior 
columns, which, as we have seen, are 
formed last. The persistent embryonal 
tissue may be evidently increased by 
a process of various degrees of growth, 
and the cavity enlarged by distension. 
Further, when the persistent tissue is 
considerable in quantity it may break down, and thus give rise to 
a new cavity, or enlarge that which has developed from the primi- 
tive canal. Thus the cavity may be distinct from the canal, and in 
some cases the abnormal tissue around it is very small in amount, 
and reduced even to a mere wall. It may also be separate, because it 
is the hinder part of the embryonal canal, cut off by coalescence 
of the walls. 
These conditions are shown very well in the adjoining figures, after 
Fig. 172.—Central canal in 
normal cords. It has the form of 
a transverse slit in A, a vertical 
slit in C (from the conus medul- 
laris), while in B it is circular. 
In each it is lined hy columnar 
epithelium and surrounded by 
cellular elements, rounded, or 
angular from compression, 
mingled with granules. In D, 
which is from the same spinal 
cord as C, the position of the 
canal is occupied by a mass of 
nuclear tissue. SYRINGO-MYELIA. 
565 
Leyden (Figs. 173, 174). In the first, at a, the cavity presents 
nearly the shape which it has at one period of development, before 
the formation of the posterior columns is completed, and without 
Fio. 173.—Syrmgo-myelia, from a child two years old, with encepnamcele and 
absence of cerebellum. (After Leyden.) In A, cervical region, the central canal 
is large, lined with epithelium, and from it a medial fissure extends backwards 
nearly to the periphery of the cord, limited by a layer of homogeneous tissue, 
more abundant at the posterior limit. In B, lower down, the fissure is enlarged 
to a cavity of considerable size, while in C it is still larger, and the posterior 
columns are reduced to a narrow zone between the layer of tissue which bounds 
the cavity and the grey substance. 
the separation into two parts produced by the formation of the pos- 
terior commissure. It is hounded by a narrow layer of embryonal 
tissue, which widens out behind, having nearly the shape of the pos- 
terior median columns, which are, as we have seen, the last to be 
formed. In b and c, the cavity is much larger, and the posterior 
eolumns are smaller, either by an earlier arrest of development or by 
greater distension, or, most probably, by the influence of both these 
agencies. The cavity extends up to the posterior surface of the cord, 
and is closed in there only by a narrow layer of cellular structure. 
In Fig. 174 we have somewhat more complex conditions. The 
cavity in the first section closely resembles in appearance that in A of 
the last figure, but differs in the important fact that the posterior com- 
missure has apparently been formed and the central canal developed 
in the normal manuer, although it has become obliterated by nuclei. 
This is clear, if the commissure is compared in the several figures. 
The cavity, therefore, does not, as in Fig. 173, represent the whole of 
the primitive canal, but only the posterior portion after its division. 
The adjacent tissue is much more abundant than in the other case. 
The projection into the posterior extremity of the cavity indicates a 
process of active giowth, which is also shown by the irregularity of 
the cavity in b, the large amount of tissue, and the wide separation of 
the posterior horns. In c, from the lower part of the cord, the 
embryonal tissue occupies two oval areas in the posterior column (by 
mistake, clear in the figure), while the cavity is closed or nearly so. 
(Lower down, a cavity existed in the centre of each of these areas, 
apparently due to breaking down of the tissue.) In D, again, the 
embryonal tissue occupies only the middle line, as a wedge-shaped 
area, due to the defective formation of the medial part of the posterior 
columns. It has been mentioned that the neuroglia may be regarded 
as a persistent, slightly modified embryonal tissue, and these exuberant 566 
SPINAL COED. 
masses of tissue bear considerable resemblance in structure to gliomata, 
so that the condition has been called “ gliomatosis.” In each of these 
cases the brain participated in the defect of 
development; there was internal hydro- 
cephalus, and the cerebellum was absent. 
The cavities in the adult cord present 
many varieties. The most common form 
resembles in its essential features the con- 
genital disease which we have just con- 
sidered. Between the two there are also 
differences, but the resemblance is suffi- 
ciently close, and the origin of the differ- 
ences is sufficiently clear, to make it prac- 
tically certain, as already mentioned, that 
the two forms are really the same, and 
that the form met with in adults is the 
congenital condition, persisting until later 
life. Of the characters which this form has 
in common with the congenital disease, the 
most important are the position of the cavi- 
ties and the presence of tissue in their 
vicinity of embryonal or gliomatous nature. 
The differences depend on an apparent 
increase of this tissue by a process of 
growth, on the greater damage to the other 
parts of the cord by the distension of the 
cavity, and on the extent to which the for- 
mation of new cavities or enlargement of 
old ones takes place by a process of disin- 
tegration of the newly formed or persistent 
tissue. The damage to the cord produced 
by distension of the cavity involves most 
the nearer and less resisting parts. The 
grey substance, therefore, suffers in greatest 
degree; the white columns to an extent 
that depends in part on the precise posi- 
tion of the cavities, as presently to be de- 
scribed. The latter also present, in many 
cases, the complicating changes of secon- 
dary degeneration, ascending or descending, 
as shown in Fig. 175, due to the com- 
pression of certain tracts at some specially 
affected spot. 
As the simplest condition, we may 
have a dilatation of the central canal 
surrounded by gliomatous tissue disposed as in congenital cases. 
This tissue is often more abundant, aud forms a more distinct 
Fio. 174. — Syringo-myelia, 
from a child aged two and a 
half years, with internal hy- 
drocephalus and absence of 
cerebellum. (After Leyden, 
‘Virchow’s Arch.,’ Bd. 
lxviii) A, B, cervical re- 
gion; gelatinous (embryonal) 
tissue in the posterior 
columns encloses a medial 
cavity, lined in places with 
cylindrical epithelium, and 
believed (probably wrongly) 
to be the central canal. 0, 
lower dorsal; in each poste- 
rior column is a mass of 
similar gelatinous substance 
(which, by a mistake, is 
shown in C as an open 
cavity). In D, lumbar 
region, this tissue occupies 
only the position of the pos- 
terior median columns. SYRINGOMYELIA. 
567 
mass, lower down tlie cord, 
below the cavity. A good 
example of this condition in 
slight degree is presented by 
the cord, the seat of chronic 
myelitis, represented at Fig. 
105, p. 339. In the cervical 
region (a) there is a large 
central canal, bounded by a 
thick layer of gliomatous 
tissue. In the inner part of 
this tissue, limiting the cavity, 
is a sinuous membrane, fibrous 
in structure. The origin of 
this membrane is not easy to 
explain, but it is often found 
in cavities of this character, 
and is evidence of the similar 
nature of those that differ 
much in other respects. In 
the lumbar region (b) the 
tissue, which bounds the cavity 
in the other section, forms a 
large round mass in the posi- 
tion of the canal, obliterating it. 
When a central cavity ap- 
pears not to be the canal itself, 
but to be situated behind, it is 
then apparently often due to a 
persistence of the fore-part of 
the posterior portion of the 
canal, after the posterior com- 
Fig. 175.— Syringo-myelia, from a 
case of tumours of the pons and 
cauda equina, with some diffuse 
sclerosis in the dorsal region of 
the cord. A, B, and C are sections 
of the cervical enlargement. The 
large cavity in A is perhaps the 
dilated canal, since it is lii.ed in 
front with epithelium, but in front of it, in the posterior commissure, is a group of 
nuclei like an obliterated canal. The zone of tissue around the cyst is composed of 
interlacing fibres and nuclei, and processes extend from it into tlie posterior 
columns, both in front and behind. In B, the cavity is smaller and the wall 
thicker, while in C, the tissue about it forms a considerable mass, and a second small 
cavity has formed in the middle line, apparently by the breaking down of the tissue* 
In the dorsal region (D) there was merety an unusually large accumulation of nuclei 
in the position of the canal, which, in the lumbar region, had the normal aspect (E). 
The cord presents degeneration of the right pyramidal tract (descending from the 
tumour in the pons), and of the post. med. cols, and ant. lat. ascending tract, pro- 
bably ascending from the sclerosis. 568 
SPINAL CORD. 
missure lias been formed. In Pig. 175, for instance, we have a 
central cavity, but in the commissure in front of this is a mass of 
nuclei having the usual aspect of an obliterated canal.* The cavity 
is surrounded by a zone of tissue, which in A and b sends off a fringe 
of processes, especially backwards. This tissue is increased in the 
lower part of the cervical region (c). In b, a small cavity is formed 
between the tissue and the grey matter by breaking down, and in c 
another exists in the middle line behind the growth, probably due to 
deficient closure of the original fissure, and increased by a destructive 
process. Still lower, the commissure resumes its normal appearance, 
but the collection of nuclei in the position of the canal is unusually 
large (d). In the lumbar region, the canal is patent (e). The 
degeneration of the posterior median column and of the lateral 
columns is secondary. 
We have seen that in the congenital cases we must recognise 
a process of growth of the persistent embryonal tissue, to account for 
some of the conditions met with, and a like process is suggested by 
the central mass in Pig. 105, B. Hence it is not surprising that in 
many cases the growth should attain the dimensions, and assume the 
characters, of a positive tumour. In most cases the tumour has been 
central in position, and has had the structure of a glioma. It has 
occupied a large part of the area of the cord at a certain part.f In 
the chapter on the tumours of the cord it has been pointed out that 
sarcomata also may grow from the tissue around the central canal, as 
in the case shown in Fig. 170. Hence it is not surprising that the 
condition of syringo-myelia, even if this is congenital in origin, should 
be frequently associated with definite tumours. The growths have 
often been multiple, apparently the result of a wide-spread tendency, and 
perhaps connected with a wide-spread persistence of embryonal tissue, 
of which remarkable instances are sometimes met with. In the case 
shown in Pig. 175 there was a tumour of the pons and also one of the 
cauda equina. The nature of the growths is uncertain, but they were 
probably either sarcoma or glioma. The same tendency to morbid 
growths is illustrated also by Fig. 176, which is similar in many respects 
to that just considered. In this case also there was a tumour of the 
pons and one of the cauda equina, and there was also a central 
growth in the dorsal region, occupying the greater part of the area of 
* This is the probable interpretation. At the same time it is possible that the 
nuclei have not this significance, and that it is really the central canal. It is often 
more difficult than might be imagined to say whether a cavity does or does not 
represent the central canal. The presence or absence of an epithelial lining has 
generally been taken as a criterion, but it is doubtful whether this has any signifi- 
cance. Around the whole of the original cavity the inner layer of cells is arranged 
as an epithelium, and if any part of it persists it is probable that epithelium will 
persist also. Moreover the epithelium often disappears from the wall of the dilated 
central canal itself; always where it is enlarged by breaking down of tissue. 
f As in an interesting case described and figured by Riesiuger, ‘ Virchow’s 
Archiv,' Bd. xcviii. SYKINGO-MYELIA. 
569 
the cord, to which the ascending degenerations were secondary. In a 
there is a large central cavity which is probably not the central canal, 
since, as in the last figure, 
the position of this is marked 
by the oval group of nuclei 
in the anterior part of the 
grey commissure. The zone 
of tissue which bounds it is 
narrow, but a few processes 
are given off behind. In b, 
first dorsal, this tissue forms 
a compact mass, and the pro- 
cesses are numerous and very 
similar to those in the last 
figure. In c, the commissure 
is reduced almost to normal 
conditions. In this cord we 
have also an instance of the 
fact that cavities may occur 
in other parts, very similar 
in their general characters to 
those that occur in the central 
region. In B, a large cavity 
occupies the intermediate 
grey matter and posterior 
cornu on the right side, with 
some morbid tissue bounding 
it on the medial side. In 
-c, the cavity is smaller 
Fig. 176.—Syringomyelia, from a case in which there were tumours in the dorsa 
region of the cord, the cauda equina, and the pons Varolii. A, mid-cervical region. 
A large oval cavity lies behind the grey commissure, surrounded by a narrow wall, 
chiefly composed of fine fibres, but with a wavy membrane on the inner surface. 
In front of the posterior commissure, an oval group of nuclei has the aspect of 
an obliterated central canal. A few short processes extend from the wall of the 
<avity into the posterior columns. There is secondary ascending degeneration of 
the post. med. cols., right direct pyramidal tract, and ascending antero-lateral 
tract in all the sections. B, first dorsal. Behind the posterior commissure is a 
growth consisting of small cells, round and fusiform, the latter with round nuclei. 
It contains many vessels with thickened walls. A fringe of fine processes extends 
from it into the posterior columns. An irregular cavity occupies, on the right 
side, the posterior half of the grey matter, which is reduced to a narrow layer 
around the cyst. This is lined by a delicate nucleated membrane, outside which 
is a thicker membrane, Ling in folds, the section of which is thus sinuous. Out- 
side this again is a small-celled growth similar to that behind the commissure. 
In C, a little lower, this cavity is smaller, the sinuosities of the wall greater, and 
the growth outside it more abundant. (Still lower the area was entirely occupied 
by the growth.) In the posterior commissure there is only a quantity of loose 
nucleated tissue in the situation of the growth.* 
* For the opportunity of drawing these sections I am indebted to Dr. Dreschfeld. 
A full account of the case has been published by Dr. Harris in ‘Brain/ Jan., 1886. 
The large growths were sarcomata. 570 
SPINAL COED. 
and the tissue around it is more 
abundant, but easily distinguish- 
able from the grey substance, 
while a little lower down the 
cavity disappeared and the 
tissue formed a compact rounded 
mass. The cavity is lined by a 
delicate layer of cellular mem- 
brane : outside this is a fibrous 
membrane, lying in folds which 
appear as sinuosities in the 
section. The existence of this 
membrane shows that the cavity 
is not simply formed by the 
breaking down of the tissue. 
The tissue is quite similar in 
structure to that which is behind 
the commissure in b.# 
The posterior cornu is not 
an uncommon seat of cavities, 
which may extend through the 
whole length of the horn. An 
example of this is shown in Fig. 
177. Haemorrhage had occurred 
into the cervical region of the 
cord (a), which was enlarged 
and distended with blood, so 
that the precise character of the 
cavity in this i*egion was indis- 
tinguishable ; the blood also 
filled the cavity through the 
* In connection with the tumour of 
the cauda equina in these two cases, 
it may be mentioned that the same 
coincidence has been observed in other 
instances. There was a tumour in 
that situation, for instance, in the 
case described by Itiesinger, who, 
rightly regarding the condition as 
congenital in origin, suggests that 
the tumour may be connected with the 
fact that the embryonal cord occupied 
the entire length of the canal. 
FiG. 177.—Sections of a spinal cord in which a cavity existed throughout its length. 
Haemorrhage in the cervical region was the immediate cause ot death. The extra- 
vasation had there distended the cord (A), and had burst into the cavity, which 
was filled with blood. A smaller cavity existed in the right cornu, in the upper 
dorsal region (B). In most parts the inner surface was slightly irregular, as if pro- 
duced by breaking down of the tissue, but near the position of the central canal a 
sinuous membrane existed in places, without, however, any epithelial covering. SYRINGOMYELIA. 
571 
entire length of the cord. In the upper dorsal region (b) there are 
two cavities, one in each posterior cornu, but that on the right ceased 
a little lower down, while the other extended to the lumbar region, 
as shown in the figure, reaching almost to the surface of the cord. 
The upper and inner extremity of this cavity is in the position of 
the central canal, no other trace of which exists. There is some 
abnormal tissue in the neighbourhood of the commissure, and also 
in c, where irregular tracts pass transversely from the median septum 
into the fore-part of the posterior columns. The presence of this 
tissue, and the relation to the central canal, suggest a congenital 
origin. During the reduction in size of the canal, in the deve- 
lopment of the cord, the cavity presents at one period short lateral 
processes (compare Fig. 179, a), and we can therefore understand how 
a still earlier arrest of development may lead to the persistence of a 
lateral process on one side or both, surrounded by residual embryonal 
tissue, and that the cavity should afterwards extend in this tissue or 
in the grey matter by a process of growth and disintegration, such 
as probably had occurred in Fig. 177, d. A comparison of d and e 
suggests that the two cavities were united in the middle line in the 
upper part of the cord, where the haemorrhage took place. 
In the conditions we have hitherto considered, definite limited regions 
of the cord have been involved through a considerable vertical extent. 
The changes are sometimes, however, much more diffuse in their dis- 
tribution, as is shown by the remarkable lesions represented in Fig. 
178. In this cord, which is that of an adult, we have a combination 
of the same two conditions of abnormal tissue and cavities. Scattered 
through the nerve-substance are tracts of a peculiar tissue, represented 
by the darker shading of the figure, and in many regions thus affected 
there are cavities, for the most part fissure-like, as if the cord had been 
split here and there. At first sight the appearance suggests an active 
and recent morbid process; nevertheless I think that the congenital 
origin of the condition is beyond doubt. It will be observed that the 
morbid changes, as in the other forms of syringo myelia, are chiefly in 
the posterior half of the cord; small areas of disease in the anterior 
columns, in the sections e and f, are the only exceptions. The minute 
structure of the abnormal tissue was exactly like that of the normal 
gelatinous layer beneath the pia mater. Besides the conspicuous areas 
figured, it could be traced here and there, in small tracts, through the 
whole of the posterior columns and the hinder parts of the lateral 
columns, and also in the posterior horns, in the grey matter of which 
it could be readily distinguished. The relation of the cavities to this 
substance is distinct; where they extend beyond it, this is apparently 
the result of the distension of the cavities and an actual Assuring of 
the cord, along the lines of connective tissue, by the pressure of the 
contained liquid. The medial cavity in c is doubtless due to defective 
closure of the original fissure between the posterior columns. In the 
lumbar region the nerve-fibres are absent from the front of the posterior 572 
SPINAL CORD. 
columns, where a coarse network of this residual tissue encloses 
empty spaces. 
The damage to the grey matter may entail alterations in the related 
nerves, and even, in cases of long duration, in those connected with 
the posterior roots. In the peripheral nerve-fibres of the skin and 
muscles, changes of the ordinary chronic degenerative character were 
found by Dejerine, in cases in which sensation was altered or the 
muscles wasted. 
Thus these various forms of syringo-myelia, in spite of their varia- 
tions in seat and form and general aspect, when closely studied, seem 
all to be connected with gliomatous tissue; and that the morbid state 
takes its origin in abnormal conditions during the development of the 
cord is practically certain from their seat and features. This lesson is 
clearly taught by the facts shown by the cases here illustrated. It is 
probable, therefore, that this conclusion is also true of cavities of 
similar character and position in which no gliomatous tissue can be 
recognised ; and most of the hypotheses regarding the origin of such 
cavities from processes of simple myelitis and the like have no suffi- 
cient foundation. But we are still ignorant of the mechanism by 
which the defect in the process of development is brought about. It 
has been extensively ascribed to an inflammation of the embryonal 
neuroglia at an early stage of development, but of this there is no 
real evidence. It is, moreover, no explanation to assume a primary 
intra-uterine hypei'plasia of the embryonal tissue. It is, indeed, 
possible that more than one morbid process during the early stage 
of development may cause the condition, and that closure of the 
canal below may have consequences during development which it has 
not at a later period. But it is important to recognise the fact that 
there is a gradation between the chief varieties, and that some are 
associated with developmental defects in the brain, to which they can 
only be related as the common expression of a defect in the develop- 
mental tendency of the germinal tissue; and what must be true of 
some forms is probably true of most. This may seem only to push 
the difficulty into the region of the inexplicable, but it is only placing 
the origin of the malady where we are compelled to refer the causa- 
tion of so many congenital diseases, which, after all, bear but a small 
proportion to the physiological characteristics that spring from the 
same source. 
The symptoms of the disease have followed some illness, mental 
shock or anxiety, and traumatic influences, but it is probable that in 
no case have these done more than excite the manifestations of pre- 
existing disease, or induce local changes in the morbid state. The 
possible influence of injury has certainly been over-estimated, since in 
some of the cases in which it seemed effective the malady was un- 
questionably congenital, and the traumatic influence only terminated 
its latent stage.* 
* Among the chief papers in which the subject will be found discussed are those of SYRINGO-MYELIA. 
573 
Symptoms.—The manifestations of 
syringo-inyelia depend on the secon- 
dary processes of distension and growth, 
and the damage thus produced to the 
functional elements of the cord.* 
Hence the state is sometimes dis- 
covered after death when it has given 
rise to no symptoms, and its existence 
has not been suspected during life. In 
young children, indeed, it appears never 
to cause any definite symptoms, while 
the disturbance of function is variable 
in occurrence and degree—much more 
so than in character. The central 
position of the disease entails con- 
siderable uniformity in the distri- 
bution of its local consequences, 
Schultze (see below) ; Hellich, * Arch. Boh&me 
d. Med./ 1890, iii, No. 4; Kronthal, 1 Neur. 
Centralbl./ 1888, p. 333 ; Oppenheiin, * Charite 
Annalen/ 1886, p. 409. 
* They have been fully described by Schultze, 
‘ Zeitschrift f. klin. Med./ 1888, p. 525; and 
‘ Verh. Congr. Inn. Med./ 1886 j and by Allen 
Starr, ‘Am. Journ. Med. Science/ 1888, 
vol. xev. 
Fig. 178.—Cavities in the spinal cord. A, mid- 
cervical, presenting merely some increase of 
connective tissue in the left lateral column. 
In B there are several cavities having the 
aspect of distended fissures, the largest in the 
middle line of the posterior columns and the 
right posterior cornu ; smaller ones in the 
lateral columns. Adjacent to each is a quan- 
tity of dense tissue, which had a peculiar and 
uniform structure. It consisted of a very 
fine network of fibres with minute nuclear 
bodies in the interstices. No larger cells 
were observed. Throughout the posterior and 
lateral columns this tissue could be seen, bere 
and there, thickening the neuroglia, where 
no conspicuous masses were formed. It could 
also be traced in the posterior cornu, and was 
readily distinguished from the spongy sub- 
stance by its slighter staining. The distri- 
bution of this tissue is shown in the other 
sections by the darker shading. In C, the 
fissure in the middle line is narrow. In E 
and F, the anterior part of the posterior 
columns contained a coarse network of this 
tissue, and no nerve-fibres. The central 
canal was obliterated, but the group of nuclei that mai’ked its position could be 
traced throughout the cord. 574 
SPINAL CORD. 
and hence also in the derangement of function that results 
from simple increase in the lesion either by distension or growth. 
Hence the symptoms are often such that they have considerable 
diagnostic importance, although in a minority of cases they are less 
uniform in character, probably because the disease is unsymmetrical, 
or irregular in position or extension, whether the symptoms are due 
to the distension of a cavity, or to this combined witli adjacent 
growth of tissue. It then often causes symptoms indistinguishable 
from those of a tumour of neoplastic nature. Moreover, the precise 
level at which the chief morbid process takes place, leads to a corre- 
sponding variation in the position, and therefore in the general 
aspect, of the symptoms it produces. The fact that the lesion is 
almost always greater at the cervical region causes the arms to be 
the most common seat of its manifestations, while the occasional 
invasion of the fourth ventricle by the associated growth, and the 
occurrence of coincident secondary changes in this part, explain the 
involvement of some of the cranial nerves that has been met with in 
a few instances. 
The symptoms are usually of slow development, increasing gradually 
in the course of years. Their main features are twofold, of which 
one is clearly and certainly intelligible, while the explanation of the 
other is a matter of hypothesis, although also not difficult to under- 
stand, at least in part, if the opiuions expressed in the chapter on the 
functions of the cord are correct. The two leading features are loss 
of sensibility, chiefly to pain and temperature, and muscular atrophy, 
resembling in characters that met with in the “progressive” spinal 
form. Of the two, the sensory loss is the earlier and more constant. 
The muscular atrophy is a necessary consequence of the damage to 
the anterior cornua from the compression they endure, when and 
where the central cavity or adjacent growth attains such a size as 
to damage them seriously, and they may be reduced to a mere zone 
between the cavity and the outer ring of white substance. The de- 
struction of the motor nerve-cells involves the degeneration of the 
nerves and the wasting of the muscles. The loss of sensation is 
intelligible if the path of painful impressions is by the posterior 
commissure to the aut.ero-lateral ascending tract. Although the 
fibres of this tract that lie in the periphery, and have crossed far 
below, may be expected to escape (and the sensory loss is not usuallv 
met with in the legs or lower part of the trunk), the enlargement of 
the central canal and disease in its vicinity can hardly fail to damage 
early and much the fibres that cross at the level of the chief lesion, 
and constitute the path from posterior roots not very far below. The 
course of thermal sensations is still quite unknown; the only fact we 
have—the frequency with which such sensibility and that to pain are 
involved together—points to contiguity of path, and prevents surprise 
at the special affection of this form of sensibility in syringo-myelia. 
Tactile sensations are lost only in rare cases ; our ignorance of their SYKTNGO-MYELIA. 
575 
path prevents us from explaining the fact, but we know, from other 
facts of disease, that it is distinct from that for pain. Moreover, the 
occasional localisation of the morbid process in the posterior columns, 
and even cornua, may explain the involvement of all forms of sensi- 
bility, and also its occasional restriction in area, since it may be due 
to direct interference with the posterior root-fibres after they have 
entered the cord. 
In many cases the affection of sensation of pain and temperature is 
equal; in others the latter is lost to a greater degree and extent than 
the former. Its loss is often the earliest symptom, as the scars of 
burns may show. The loss to heat and cold may not correspond. 
Thermal or painful hyperaesthesia has preceded the loss, as with other 
forms of sensation when destroyed by processes that slowly damage 
the fibres, and irritate before they interrupt. Perversion of sensation 
has been noted, heat being felt as cold, and vice versa. Spontaneous 
sensations are common, doubtless from the irritation of the fibres 
in the early stage, or of their upper portions when they are inter- 
rupted—feelings of heat or cold, and in some cases pains, various in 
character, sometimes paroxysmal like neuralgia, or sharp and brief 
like those of tabes, and occasionally referred to the joints, or felt 
chiefly in some part adjacent to the seat of the other symptoms. 
Pain in the spine may be complained of, and is, perhaps, a direct 
effect of the disease. Often the malady causes no suffering. The 
loss of sensation is usually sharply limited, and the arms or upper 
half of the trunk is its common seat. It is usually found in the 
same part as the muscular wasting, but is more extensive, especially 
below the seat of atrophy. Thus, when the muscles of the shoulders 
and upper arms only are wasted, the sensory loss may be in the 
forearms and hands. This we should expect from the fact that the 
crossing of the sensory path is some distance above its entrance into 
the cord, while the motor roots arise from nerve-cells mostly near 
their level of exit. Exceptions may be due to the affection of the 
root-fibres, as explained above. Further, the fact that the distension 
and damage always extend through a considerable vertical extent of 
the cord makes the relation of the two sets of symptoms more exten- 
sive and less regular than if the disease were limited to a small region. 
The “ muscular sense ” is said to have been generally normal when 
tested. Occasionally there has been unsteadiness on standing with 
the eyes closed. 
The motor symptoms usually come on after the sensory loss, long 
after in slight cases, and consist in muscular weakness and wasting 
in the upper limbs ; while, if the legs suffer, it is generally from simple 
spastic paralysis, such as would result from, and is no doubt due to, 
compression of the pyramidal tracts by the disease in the upper part 
of the cord. It is rarely complete. The unsteadiness of move- 
ment, above mentioned, we may connect with the tendency of the 
lesion to involve the posterior columns, and so probably to inter- 576 
SPINAL CORD. 
fere with the path from the muscles to the cerebellum. Rarely 
there is atrophy of the legs similar to that of the arms, and in such 
cases the disease extends into the lumbar enlargement. Reflex action 
in the legs varies according to their state; it may be normal or in- 
creased ; the knee-jerks are often augmented, with rectus- and foot- 
clonus, or, in the cases last mentioned, mvotatic irritability may be 
lost—very rarely on one side only. A curious tremor of the limbs 
has been noted in some cases. 
The muscular atrophy in the arms begins in, and affects most, 
certain parts, according to the position of the chief damage to the 
grey matter of the cord. It may be in the hand and region of the 
ulnar nerve, or in the muscles supplied by the musculo-spiral and 
radial nerves, or in the shoulder and upper arm muscles.* It is a 
slow wasting, with gradual lowering of the electrical irritability, as in 
progressive muscular atrophy, although, as in that disease, some 
groups of muscles may present indications of the reaction of degene- 
ration in the early stage of their affection. Fibrillation is common. 
As the wasting and weakness increase in the part first affected, they 
spread to others, to the rest of the limb, and to the adjacent parts of 
the trunk. Weakness of the trunk muscles often leads to lateral 
curvature of the spine; and the convexity, owing to posture, is usually 
to the left. The occurrence of similar symptoms in the legs is ex- 
tremely rare. Both sides usually suffer together; a unilateral affec- 
tion has indeed been observed, but is altogether exceptional. The 
sphincters may. escape or be involved. 
Trophic disturbances in the extremities affected with sensory 
loss are not uncommon. The skin may become thin and glossy, or 
thick and horny. Acute changes may occur, eczema, herpes, or bullae ; 
whitlows ; deep, obstinate ulceration, and even gangrene. More fre- 
quent, however, is simple vaso-motor disturbance, coldness andlividitv 
of the extremities, or redness with swelling and heat, and sometimes 
a tough oedema, which may be local like a tumour, and afterwards 
pass away. The nails share the trophic changes in the hands, be- 
coming grooved, fissured, and cracked; they may even drop off. The 
secretion of sweat is lessened in the part, as was well marked in one 
unilateral case.f The action of pilocarpine has been found to be 
delayed, although ultimately increased iGrrasset). The bones may 
become thickened or brittle, and joint changes, like those of*tabes, 
sometimes occur. 
It is rare for the symptoms to extend into the region of the cranial 
nerves, although in occasional cases various disturbances of function 
* Blocq thinks that spastic paraplegia is chiefly met with in the cases in which 
the atrophy begins in the region of the ulnar nerve, and tabetic symptoms in the 
legs when it begins in the radial area; but the data for the generalisation need to be 
more extensive. 
f Allen Starr, ‘Am. Journ. Med. Sc.,’ May, 188S; Rumpf, ‘ Neur. Cent.,’ 18S9, 
p. 257. SYRINGO-MYELIA. 
577 
have occurred, presumably due to the extension of the changes into 
the medulla and pons, and chiefly met with when there is upward 
extension of the associated growth, already mentioned. Thus there 
have been paralysis of one vocal cord, the tongue, and of the face, 
difficulty in swallowing, disorder of respiration and of the heart’s 
action. The organs of the special senses usually escape, with the 
exception of the eyes, in which certain disorders may occur, probably 
due to disease of the path of the sympathetic in the cord, or to that 
of the fourth ventricle. Thus the pupils are often unequal, the 
smaller being on the side of the more severe cord symptoms, on 
which the fibres for the radiatiug muscle of the iris are likely to be 
damaged. Narrowing of the palpebral fissure and slight ptosis have 
been also noted. Nystagmus is not rare.* 
The course of syringo-mvelia is, as a rule, slow, and measured by 
years, although an apparent exception is presented by the cases in' 
which it is associated with spreading overgrowth of the adjacent 
gliomatous tissue, or acute destructive processes occur in this and. 
spread to its vicinity. In such cases a considerable development of 
the disease may be attained before symptoms are produced, and these 
may rapidly reach a considerable degree, and cause death in a few 
months or even less. In most cases death is the result of exhaustion,, 
of the impairment of the functions of the medulla, or, more com- 
monly, of some complication—bedsores, cystitis, and the like. 
Diagnosis.—The resemblance of the disease to more common 
maladies led to its confusion with them during life, until th& 
careful observations of the last few years have established features by 
which its existence can often be at least surmised. The most im- 
portant characteristic is the combination of muscular atrophy with 
still earlier sensory loss, involving temperature and pain far more 
than tactile sensibility. But the occasional implication of all forms 
of sensation must be kept in mind, and also the fact that in slight 
and slow or anomalous cases, the sensory symptoms may long pre- 
dominate, and for a time exist alone. The position of these sym- 
ptoms (in the arms), and their frequent combination with spastic 
palsy in the legs, is a further characteristic—not, however, une- 
quivocal. 
Cervical pachymeningitis causes symptoms which, in general 
character and in distribution, alike in the arms and the legs, 
very closely resemble those of syringo-myelia; but the affection 
runs a more rapid course, the anaesthesia involves all forms of 
sensibility, and has not a greater but a less extent than the muscular 
wasting ; the two correspond more closely in their seat; pain is a 
far more prominent symptom, and the reaction of degeneration is 
common in the wasting muscles. Tumours of the spinal cord only 
cause symptoms of like character, and especially of similar symmetry. 
* Contraction of the fields of vision, especially for colours, lias been observed, but 
ts not easy to explain (Dejerine and Turland). 
VOL. I. 578 
SPINAL COED. 
when they are central in situation, and the diagnosis may then be 
very difficult and even impossible. But the resemblance is often 
more than superficial, for such growths generally arise from residual 
gliomatous tissue, and are such as are frequently associated with 
syringo-myelia. It is chiefly from the more rapid development of 
symptoms, and their more speedy extension, that such a growth can 
be suspected ; and only the presence of slighter chronic preceding 
symptoms of the character above described would justify the expecta- 
tion that a cavity is associated with the growth. 
Progressive muscular atrophy is sufficiently distinguished by the 
absence of impairment of sensation, and in peripheral neuritis the 
pains, mode of onset, and degenerative reaction in the muscles should 
preclude any danger of mistake. In “ Morvan’s disease,” to be pre- 
sently described, the symptoms may bear a close resemblance to 
those of syringo-myelia, and it is possible that they are due in part 
to a similar condition of the spinal cord. As a rule, however, the 
early loss of tactile sensibility, and the greater prominence of trophic 
disturbance in the tissues, especially the painless whitlows, enable 
the diagnosis to be made. There is only one acute affection of the 
cord that enters into the diagnostic problem, and that is spinal 
haemorrhage. It has been mentioned in the account of this condition 
that the haemorrhage is sometimes into a pre-existing cavity—as in 
the case shown in Fig. 177. The presence of a cavity into which the 
blood has been effused may be suspected if the haemorrhage has been 
preceded bv any symptoms suggestive of syringo-myelia, inquiry for 
which should always be made; or if a rapid extension occurs through 
a considerable vertical extent of the cord, distinctly abolishing its 
central functions. 
The malady, however, varies much in seat and characters, as is 
evident from even a cursory glance at the illustrations given above; 
the symptoms, of necessity, vary with the lesion. The diagnosis may 
be difficult and even impossible in such cases, especially in the early 
stages and slighter forms, when irritation and pain predominate, and 
even neuralgia may be simulated. It may be necessary to wait, for 
time to show the course of the symptoms. . Their progressive increase, 
in spite of variations, should always be taken into account; it fre- 
quently is the first feature that suggests the nature of such a disease, 
contrasting, as it does, with the tendency of inflammatory affections 
to arrest and improvement. A peculiar difficulty is presented by the 
cases, not few, in which the first symptoms follow some influence— 
an illness, a blow, or even mental disturbance—that seems to be their 
cause, and suggests disease of very different nature. Often, then also, 
it is only by waiting and watching that a right opinion can be formed. 
When bulbar symptoms come on rapidly, the nature of the case can 
only be inferred from previous spinal symptoms. 
The Prognosis and Treatment of syringo-myelia are subjects on 
which, unfortunately, its nature permits little to be said. If its ANALGIC PARANITKJM. 
579 
existence can be recognised, the malady is generally advanced, and its 
observed rate of progress is the only ground on which a forecast can 
be based. When the central functions of the cord are considerably 
impaired, and the symptoms are steadily increasing, it is rare for life 
to be prolonged for more than one or two years, and the subacute 
onset of considerable paralysis may herald a course that leads to 
death in a few months. On the other hand, a stationary condition 
may last for many years. Treatment can do nothing for the morbid 
state, nor is it likely that the progress of spinal surgery can afford 
the means of relief. The severity of some of the individual symptoms 
may, however, be lessened by appropriate measures ; especially trophic 
changes may be diminished by care and early treatment, bedsores 
may be prevented, cystitis guarded against, and if any acute para- 
lysis occurs, the possibility of some recovery may suggest the main- 
tenance of the irritability of the muscles by electricity, which cannot 
be expected to influence the slower atrophy. Pain may need the 
customary sedatives; but early pain, especially with the hypersesthesia 
that depends on the intensification of the nerve-impulses at the irritated 
part, may be much lessened by the diminution of these by cocaine, 
used as in tabes. Sudden pain in the spine may indicate commencing 
haemorrhage, and should lead to the adoption of the posture and other 
measures appropriate to that grave affection. 
Analgic Panaritium ; Morvan’s Disease. 
By the term Morvan’s Disease is generally known an affection that 
was called Panaritium Analgicum, or “ Painless Whitlows,” by the 
physician of Brittany, Morvan, who, in 1883, first described it.* 
Observations on it afie still few,f but, judging from two fatal cases,X it 
appears to consirt in a combination of a condition of syringo-myelia, 
or of the associated gliomatosis, with a peripheral neuritis in the extre- 
mities. The symptoms make the constancy of the neuritis probable ; 
we must wait to learn how far the morbid state of the cord is constant, 
and whether the changes in the nerves take origin in developmental 
conditions. It is quite possible that they may share the condition of 
arrested development, entailing a liability to later morbid changes, 
especially in view of the analogous conditions observed in the case 
mentioned on p. 469.§ At the same time, it is possible that the 
* ‘ Gaz. Hebd.,’ 1883, Nos. 35—44. 
t The chief writings are those of Louazel, * La Maladie de Morvan,’ Paris, 1890; 
Joffroy and Achard, ‘Arch, de Med. Exp.,’ 1890; Charcot, ‘Prog. Med.,’ 1890, 
Nos. 11 and 12 ; Hackel, ‘ Miinch. med. Wochenschr.,’ 1889. 
J Gomhault, quoted by Charcot; Joffroy and Achard, * Arch, de Med. exp.,’ 1891. 
§ In a case recorded by Jolly (‘ Charite Ann./ xvi, 1891) there was also a con- 
genital anomaly of the fingers, a web of skin between the third and fourth fingers 
of each hand. 580 
SPINAL CORD. 
symptoms of this affection may be due to local neuritis of various- 
nature, and we must be cautious in inferring from them that the 
pathological state is the same in origin in all cases. In some instances 
the malady has been apparently set up by an injury. The affection 
has been met with in both sexes, but more frequently in males, and 
has generally commenced during the first half of adult life, between 
twenty and forty. When local injury has [(receded the symptoms it 
has sometimes been at a considerable interval (Hiickel), and it has 
been unilateral when the latter have been bilateral, so that its relation 
to them is uncertain. 
The characteristic symptoms are in the upper extremities; only in 
rare cases do the feet suffer at a late period. Neuralgic pains may 
occur first, but the definite symptoms consist of weakness and 
muscular wasting in the hands and forearms, loss of all forms of 
sensation, and especially a peculiar trophic change—whitlows on the 
fingers, with recurring deep ulcerations in various parts of the digits ; 
those near the extremity of the fingers may only heal with the loss of 
some of the terminal phalanges. The loss of sensibility involves all 
forms, and usually precedes the occurrence of the whitlows, so that 
these are painless—a peculiarity which constitutes the most salient 
feature of the disease, and suggested, in the first instance, its special 
character. Occasionally the trophic disturbance precedes the anaes- 
thesia, and the whitlows and ulcers are then painful. The latter are 
deep, and often resemble the perforating ulcers of tabes; cracks iu 
the skin accompany them, and the nails shrivel and split. Vaso- 
motor derangements, lividity and pallor, often precede and accompany 
the disturbance of nutrition. The progress of the affection is very 
slow, and extends over many years; one hand is usually affected 
some time before the other. The electrical irritability of the nerves 
of the part has been found normal in the early stage, and slowly vanish- 
ing as the malady progressed. Although the trophic changes are 
limited, as a rule, to the hands, and the muscular wasting does not 
extend above the forearms, the loss of sensation is occasionally more 
extensive, involving the whole arms, parts of the trunk, and even the 
face. An affection of the shoulder-joint has been observed.* The 
feet are occasionally, though rarely, the seat of aniesthetic ulceration ; 
the legs have also been found weak, with excessive knee-jerk and 
foot-clonus (Hiickel). 
In the autopsy that was made by Gombault neuritis was found 
in both arms, and also a diffuse overgrowth of connective tissue in 
the posterior part of the grey matter of the cord and the posterior 
columns. This growth involved also the coats of the vessels, which 
were in places so thickened as to obliterate their cavity. Neuritis 
has also been invariably found in the extremities of the fingers when 
these have dropped off. 
The features of the malady are so peculiar that, if they are known. 
* Morvan, ‘ Gaz. Hebl./ 18s7, No. 34. SPINA BIFIDA. 
581 
the nature of a case cannot well be mistaken. Anaesthetic leprosy 
presents the closest resemblance, but in this the peculiar ulcerations 
are absent, and pigmentary alterations occur in the skin; while in 
Raynaud’s disease there is not the peculiar loss of sensibility, nor an 
equal tendency to whitlows, and vaso-motor disturbance is a more 
conspicuous feature. In the peculiar malady known as “ sclero- 
dactyla” (a form of scleroderma that affects the fingers and face), 
there is no loss of sensibility or tendency to destruction of the finger 
ends. Simple syringo-myelia is distinguished by the common absence 
of the whitlows, by the subordination, in time and degree, of the 
trophic changes to the other symptoms, and by the common 
preservation of tactile sensibility. But the distinction is probably 
not an absolute one. In Morvan’s disease there is peripheral neuritis 
as well as syringo-myelia, and to this is due its special features, 
and especially the early and intense trophic disturbance.* 
Spina Bifida. 
Spina Bifida, or split spine, depends on a defect in the closure of 
the vertebral arches, which usually leads to the protrusion of the 
membranes as a sac, forming an external tumour, into which the lower 
part of the spinal cord often extends, normal or variously altered in 
conformation, sometimes even reduced to a neural lining of part of the 
wall. Rarely, there is no external prominence—a form known as 
“ spina bifida occulta.”f The condition is most common in the lumbar 
region of the spine; sometimes is present at more than one place, very 
rarely in the whole length of the vertebral column. It is met with 
in about one child out of every thousand born (Chaussier). The 
disease is one of chiefly surgical interest, and therefore only an outline 
of the more important facts is here given. The spinal cord, whether 
normal or not, generally reaches lower than usual in the vertebral 
canal, as it does at the early period of development, when the morbid 
state is produced,—becoming adherent at its lower extremity and 
remaining so. In many cases the central canal of the cord is enlarged 
above, and the lower part of the cord may also be similarly distended. 
The precise condition presents many variations, which can be, in part 
at least, understood by what is known of the process of development, a 
subject that has been very ably discussed by Bland Sutton. The 
essential element in spina bifida, the defect in the vertebral arches, 
* The absence of any fundamental difference between this malady and syringo- 
myelia has been pointed out by Bernhardt (‘ Verh. Vereins inn. Med./ Berlin, 
January 19th, 1891) and Jolly (loc. cit.). But the additional element of neuritis 
must not be ignored. 
f The best accounts of spina bifida are in the “ Report of the Committee of the 
Clinical Society” (‘ Transactions/ 1885), and Bland Sutton’s “ Lectures on Evolution 
in Pathology ” (‘ Lancet/ February 25th, 1888). Spina bifida occulta is described by 
the same writer in the * Lancet/ February 25tli, 1887. 582 
SPINAL COED. 
depends on a deficiency in that ingrowth of the mesoblast from each 
side which should enclose the embryonal spinal cord, and form bone, 
after the superficial epiblastic layers have united to form the epidermis. 
A similar ingrowth of mesoblast forms the corium, muscle, &c. This 
apparently takes place in excess in spina bifida occulta, and leads to 
a curious condition, usually present—an excessive growth of hair over 
and about the affected part, which is generally the lumbo-sacral region. 
On the other hand, in many cases in which there is a tumour, this 
superficial mesoblastic ingrowth seems to be deficient, as well as that 
for the vertebral arches, so that, at the upper part of the tumour, there 
is an area in which there is no proper skin, but a peculiar shiny 
membrane destitute of hair. It is probably this superficial mesoblastic 
deficiency that permits the protrusion, and formation of an external 
tumour. 
In spina bifida occulta the defect in the arches can be felt on pal- 
pation, either in the lumbar or sacral region, and the spinal cord 
extends lower than normal, as in the ordinary form. The latter, in 
which there is an external tumour, presents three chief varieties, 
according as the sac contains only the spinal membranes (meningocele), 
the spinal cord as well as the membranes (meningo-myelocele), or the 
latter distended by enlargement of the central cavity (syringo- 
myelocele). These are the chief classes ; they do not, indeed, exhaust 
the rarer forms, but to take full cognizance of these would entail a 
very complex list of varieties.* 
Of the several forms, that without an external tumour has been 
least frequently met with, although it is probable that a knowledge of 
the significance of the growth of hair in the lumbar region would lead 
to the detection of this state in many cases in which it is now 
undiscovered. Putting this form aside, simple meningocele and 
* Several other varieties are enumerated by Bland Sutton (loc. cit.). 
Fig. 179.—Spina bifida: sections of a spinal cord, from a case the symptoms and 
history of which I was unable to ascertain. In A, cervical retrion, the only abnor- 
mality is a large cruciform central canal and an unusually thick grey commissure. 
This continues through the dorsal region, at the lowest part of which there is a 
great change. In B, the canal is larger, and the necks of the posterior horns (and 
posterior vesicular columns) are united by much commissural tissue ; in this, many 
vertical fibres could be seen, and others running from before backwards in the 
middle line. In C, an extension of the canal backwards has taken place, and it is 
bounded by a sinuous membrane: the outer part of the grey substance is atro- 
phied. In D, the cavity has extended into each posterior horn almost up to the 
surface of the cord, in part by a breaking down of tissue, because the membrane 
limiting the enlarged canal remains undestroyed. In E, still at the junction 
of the dorsal and lumbar regions, the cavity has receded from the left horn. In 
F, the division of the cord has taken place, not in the direction of the cavity in 
the horn (which is filled up), but in the middle line, at or close to the median 
septum. In G, a wider separation of the posterior columns has taken place, and a 
cavity has formed on the right side, which extends into the horn, and almost cuts 
off the posterior column. In H, the cord is spread out and formed part of the wall 
of the sac. The posterior nerve-roots (p r) mark the position at which the 
posterior horn comes to the surface. The grey matter is in many parts atrophied 
and translucent, and, in H, contains many large vessels. The septal lobulation on 
the surface of the cord is greater than normal. SPINA BIFIDA 
583 
Fio. 179. 584 
SPINAL CORD. 
syringomyelocele are both rare; the common form is meningo- 
myelocele, in which the cord, altered or intact, extends within the sac. 
The Clinical Society’s Committee found that this was the condition in 
62 per cent, of the cases in which there was an external tumour. The 
lower part of the spinal cord is generally adherent to the posterior 
wall of the sac, where its traction often causes a depression on the 
surface, always at the membranous area, which, as already mentioned, 
is generally to be observed in the upper portion. The cord may again 
become free, and extend downwards in the cavity, or it may be 
flattened, expanded, and lost in the wall, of which its tissue really 
forms an inner layer. In this layer there is no distinction of grey and 
white substance. In either case, the lower nerves arise in the wall, and 
pass, first in this, and then forwards, across the cavity, to their fora- 
mina of exit. The arachnoid always extends into the sac, and the 
fluid is that contained within the subarachnoid space; sometimes 
there is an external opening from which the fluid flows. 
As a rule, the central canal of the cord is not continuous with the 
sac; and it may be closed, even in the condition of syringomyelocele, in 
which the canal is dilated. In other cases the canal opens into the 
cavity, sometimes by only a small aperture, even when the lower part of 
the cord expands into the wall, and the nerves course along the wall 
in a layer continuous with the arachnoid and superficial to the 
membrane that represents the cord-tissue from which they arise. 
As stated, ordinary syringo-myelia may exist in the upper part of the 
cord. The extension of the cord in the wall of the sac probably 
indicates a developmental defect similar to that of the bony canal; 
in the lumbar region the primitive canal has failed to close, so that 
the cord is open posteriorly, and the two posterior columns may even 
be far apart, or the cord may even be applied, in the form of a thick 
or thin lamina, to the wall of the sac. 
An instructive although rare example of the involvement of the 
cord in the developmental effect is shown in Fig. 179, which illus- 
trates also the manner in which the latter may involve in some degree 
the whole cord. In the cervical region the grey commissure is 
unusually large, and the canal is cruciform, a shape which it presents 
at one period of development, and which is here persistent. This 
condition obtains throughout the dorsal region until, in the lower 
part, the tissue behind the commissure is so abundant as to unite the 
necks of the posterior horns. Below this, the canal enlarges into a 
condition of syringo-myelia, surrounded by the abnormal tissue which, 
as we have seen, is commonly associated with such enlargement; the 
canal is limited, moreover, by the sinuous membrane that is so often 
met with (see p. 567). The cavity extends also into the posterior 
horns, clearly by a process of disintegration, since in d the membrane 
lining the enlarged canal persists, and marks the limit of the canal and 
the extent of the simple disintegration. The progressive separation of 
the posterior columns is shown in f, g, and n. In the lowest part SPINA BIFIDA. 
585 
of the cord, the development of the posterior columns has been appa- 
rently hindered, as will be observed if a be compared with f. In the 
former there are also some fissures in the grey substance, formed 
apparently by disintegration. The grey substance of the cord is con- 
spicuously wasted in the lumbar region, thin and translucent. 
In rare cases there has been no proper development of the cord. 
It was represented by a mere ncrve-like string in a child, who also had 
hydrocephalus, but lived five weeks. Another child of the same parents 
had a similar condition.* 
Symptoms.—If the cord is intact, symptoms may be absent. In 
the cases in which there is an external opening, and a constant escape 
of cerebro-spinal fluid, the child usually dies in a few weeks. In 
other cases the defective development of the lower part of the cord, 
or its distension in syringo-myelocele, is manifested by an absence of 
function, amounting to complete paraplegia in severe cases, which 
also seldom live. Some cases, however, survive, with paralysis and 
wasting of the legs, and often absence of power over the sphincters. 
In slighter forms the paralysis and wasting have been partial, either 
existing from the first, or supervening at some later period, probably 
from the occurrence of damage to the nerve-roots or cord-tissue by in- 
creased tension, or by inflammation; of the latter abundant traces 
may be found after death, and various external influences may readily 
set it up. Some children, whose legs have appeared natural, have never 
been able to stand ; possibly the defect in the posterior columns has 
given rise to a sort of congenital tabes. Even in the slighter forms, 
including spina bifida occulta, paralysis and atrophy have come on 
after some years, and even after adult life has been reached. Indeed, 
in the unsuspected forms without a tumour, there may be special 
danger of injury to the unprotected structures, and damage to the 
nerve-roots. The muscular paralysis and atrophy have been usually 
below the knees, and the muscles least prone to suffer are thetibiales 
antici. Hence talipes varus tends to occur. These muscles may 
alone persist, probably from the higher position of origin of their 
nerves (Remak). Another peculiarity of these cases is the tendency 
to perforating ulcer in the feet, which has several times neces- 
sitated amputation. Chronic changes in the tarsal and metatarsal 
bones have also been met with, somewhat like those of tabetic 
arthropathy. + The ulcers suggest neuritis, which was found in one 
case ; and, in this and others, the arteries have presented thickening of 
the muscular coat, even leading to their closure. These symptoms 
may be greater on, or confined to, one side, and on this the knee-jerk 
has been lessened.X These points of resemblance to tabes may also be 
* S. Wolfe, * Phil. Rep./ June 2nd, 1883. 
f In one case Sutton found the compact tissue very scanty, and the bones filled 
with semi-fluid fat; a deep ulcer reached a carious spot. 
X Details of cases by Fischer, v. Recklinghausen, Brunna, and others, are quoted 
by Bland Sutton (loc. cit.). See also Delafosse, ‘These de Paris/ 1874; Remak, 
* Berlin, kl. VVochenschrift/ 1885. 586 
SPINAL COED. 
due to the greater degree of exposure to damage of the posterior roots, 
as well as to neuritis, perhaps descending. 
The treatment of spina bifida is purely surgical. That of the con- 
sequences just described is the same as for similar states in other 
diseases. 
TRAUMATIC LESIONS OF THE SPINAL CORD. 
Injuries to the cord fall within the province of the surgeon, but 
some account of them is needed because the subjects often afterwards 
come under medical observation, and because the cases present every 
gradation to the maladies that have been described in the preceding 
pages. 
Causes.—In fractures and dislocations of the spine, the cord gene- 
rally suffers compression or laceration, as already described in the 
chapter on injuries of the vertebral column. The cord may also be 
directly wounded by stabs and gunshot injuries, in which it may be 
divided completely or partially. Such injuries furnish a considerable 
proportion of the cases of unilateral lesion of the cord. In gunshot 
wounds the cord more often suffers from displaced fragments of bone 
than from the ball itself. 
Far more common than direct injury is damage to the cord by con- 
cussion of the spine, either local or general. Gunshot wounds occa- 
sionally furnish examples of local coucussion ; a bullet may strike the 
spinal column and lodge iu its vicinity, with the effect of causing 
immediate paraplegia, as complete as if the cord were divided, and yet 
it may be fouud that the spinal column has not been injured, and the 
cord is merely softened at the spot. Other causes of concussion are 
the fall of heavy bodies on the back, such as a beam of timber or a 
sack of corn, a blow on the back from some blunt weapon, a fall 
upon the back, either on a flat surface or on some projecting object. 
Less frequently the cord suffers from a general concussion of the 
body, in which the spinal column is not specially involved. The 
cervical region is occasionally damaged in falls on the head. Railway 
accidents are frequent causes of concussion of the spinal cord; the 
back may be struck with violence when the body is thrown from one 
side of the carriage to the other. Another common cause is a fall 
from a horse upon the back, or a fall downstairs, in which the spinal 
column is bumped against the edges of the steps. A violent bending 
of the spine may also injure the cord directly, especially in the more 
mobile cervical portion, where the region of the fourth and fifth 
vertebrae is especially apt thus to suffer (Thorburn).* The jar of the 
spine caused by a jump from a height may even be effective. Occa- 
sionally effects, very similar to those which are produced by a blow on 
* * Brain/ January, 1837. 587 
TRAUMATIC LESIONS. 
the spine, are caused by a sudden contraction of the spinal muscles in 
some violent effort, a “ rick of the back,” as it is popularly termed. 
It is possible that, in such cases, the primary damage is sometimes to 
the vertebral ligaments and articulations, and that the cord suffers 
secondarily. The symptoms may only come on a few hours after the 
injury in such cases, as if effused blood compressed the cord, or the 
tension upon it and slight damage set up a graver inflammation. 
Thus a soldier, in a drunken quarrel, was extended by four comrades, 
two pulling on his feet and two on his arms, while a fifth sat on his 
back. No immediate effect followed, but the next morning there was 
complete paralysis of both arms and legs, which very slowly passed 
away. 
Pathology.—The anatomical lesions in cases in which the vertebral 
column is not injured vary much in different cases. Haemorrhage is 
often found, sometimes outside the dura mater, sometimes on the 
inner surface of the membrane, in the pia mater, in the substance of 
the cord itself, very rarely into the central canal.* Occasionally the 
substance of the cord has been found lacerated when the vertebral 
column has not been injured. In many cases there is local softening, 
commonly yellow in tint, sometimes mingled with red, often involving 
the whole thickness of the cord, and occasionally extending, as central 
softening, through a considerable vertical extent. Under the micro- 
scope, the usual products of inflammation are seen, sometimes with 
heematoidin crystals. Such softening may occur rapidly in severe 
local concussion, and be found complete a few weeks, or even a few 
days, after the injury.f On the other hand, in some cases of complete 
paralysis, no lesion of the cord has been found, either with the naked 
eye or the microscope, a few days after the injury J In other instances, 
in which the cord is examined some weeks or months after the accident, 
the signs of chronic myelitis are found, in scattered foci or more 
diffuse tracts, in the white columns or grey substance. The nerve- 
fibres are wasted, and the connective-tissue elements are increased in 
quantity, and, in the early stages, there may be a leucocytal infiltration 
about the vessels, dilatation of the capillaries, and minute extravasa- 
tions, although none may have been visible to the naked eye. In the 
anterior cornua the motor nerve-cells may be damaged, sometimes 
swollen and vacuolated, or shrunken, and the anterior root-fibres may 
be degenerated. The grey matter is especially apt to suffer when the 
enlargements are injured; in the dorsal region the change may be 
confined to the white columns. Ill-defined cavities may exist in 
* As in a case reported by Chucan and Wickham, ‘ Prog. Med.,’ 1887. Probably 
it is only when the canal is previously dilated that this occurs, as it may, without 
serious injury to the nerve-tissue. 
f Edmunds, ‘ Brain,5 vol. vii, p. 103; Obersteiner, ‘ Wien. med. Jahrb.,’ Bd. iii, 
1879; Lochner, * Bayer. Aerztlicli. Int.-bl.,5 1857, No. 42; Fromuller, ‘ Memorabilien,' 
1870, No. 12. In the last, described further on, softening was found thirty-two 
hours after the injury. 
J Fischer, * Deut. Zeitschr. f. Chirurg.,5 1883, Bd. xix. 588 
SPINAL CORD. 
old cases, where the nerve-elements have perished. The usual 
ascending and descending degenerations may be found above and 
below the most damaged parts. Occasionally there are indications of 
meningitis, diffuse or disseminated, and sometimes confined to the 
dura mater. 
Symptoms.—The effects, immediate and remote, of injuries of the 
spinal cord extend over almost the whole range of symptoms of cord- 
disease, and their variations in character and course are almost infinite. 
It is therefore neither practicable nor necessary to do more, in this 
jilace, than to describe their general characters. According to the 
difference in course, we may divide them into three classes. (1) 
Those in which the injury causes immediate and severe paralysis, 
due to instant damage to the spinal cord, the consequence of its 
laceration, compression, or concussion. (2) Those in which there are 
at first either no symptoms or only trifling disturbance of function, 
but in which grave symptoms come on a few days or weeks after the 
injury. (3) Those in which there are no early symptoms, or only 
slight and transient disturbance, but at the end of one or several 
months, symptoms gradually come on, often such as indicate disease 
of some definite system of structure of the cord, degenerative in 
nature. 
(1) The first class, in which the injury causes instant and considerable 
disturbance of function, includes the cases in which the cord is directly 
injured, and also some in which there is no visible sign of damage if 
the patient dies within a few days. In the former class there is 
often a manifest lesion of the spine, and the cases are, at least at first, 
purely surgical in their practical relations. In the latter, the 
mechanical influence has apparently abolished the function of the 
nerve-elements. If such patients live longer, either quick recovery 
ensues, or local softening from disintegration of the fibres that are 
most damaged. It is an interesting fact that concussion may thus 
derange function. The absolute integrity of structure on early micro- 
scopical examination shows that the result is not due to any minute 
vascular lesion. The effect has been compared by Reynolds, not 
inaptly, to the demagnetisation of iron by a blow. Doubtless the 
influence is exerted on the molecular nutrition of the nerve-elements, 
and the possibility of recovery, or the subsequent structural disinte- 
gration, depends upon the degree of nutritional damage.* 
The symptoms, in these cases of severe and immediate effect, are 
generally those of complete impairment of function. When the injury 
is direct and partial, such as a liemisection by an incised wound, or a 
partial bruise of the cord by a spiculum of bone being driven against 
it (as in the case mentioned at p. 197), the effect may be a partial 
(e. g. one-sided) derangement of function ; but in most other cases 
* These conclusions have been recently formulated more definitely, but without 
essential extension, by Sclimaus, partly from experiments on rabbits (‘ Munch, med. 
Wochensch./ 1890). TRAUMATIC LESIONS. 
589 
there is abolition of all tbe conducting functions at tlie level of the 
injury. There is complete paraplegia, motor and sensory, with loss 
of power over the sphincters. The symptoms are thus those of a 
total transverse lesion at the affected level (see p. 226). When the 
cervical region is injured, the arms are necessarily affected according 
to its seat. Such cases often illustrate very clearly the relation of 
arm-function to the cord.* The fibres for the sympathetic are often 
implicated, especially those for the iris, causing inequality of the pupils. 
Reflex action below, abolished at fh’st by shock, usually soon returns 
and becomes excessive, but remains absent if the lumbar enlargement 
is damaged, or is invaded by haemorrhage; it may be again lost by 
the downward extension of secondary inflammation, which is equally 
effective when partial (in the posterior columns or grey matter) as 
when total, and is more difficult to detect in the former case.f Loss 
of consciousness is occasionally produced by an injury which does not 
directly involve the head, as in the case mentioned on p. 590; 
vomiting is very common at the outset. The cases of direct injury 
often run a severe and rapid course; and when the secondary inflam- 
mation spreads downwards, or the lower part of the cordis injured (as 
is frequently the case), the tendency to trophic changes in the skin, 
and to the occurrence of cystitis and pyelo-nephritis, is very great. 
(Edema of vaso-motor origin, and effus on into joints, may be pre- 
sent in the early stage. If the cord has been directly injured in its 
whole thickness, survival beyond a fortnight is rare. When it is 
damaged indirectly, with secondary softening—in what may be termed 
concussion myelitis—death occurs less rapidly, but many patients die 
at the end of four or six weeks, while in those who survive the first 
two months slow recovery often occurs. Even in such cases, death 
sometimes occurs very quickly, but it is possible that there is then a 
laceration of the cord. A man, whose case has been recorded by 
Fromiiller, was struck on the back, at the level of the third dorsal, bv 
a heavy beam, and had loss of motion and sensation up to the level 
of the nipples. The palsy of the muscles of respiration increased, 
and he died from asphyxia at the end of thirty-two hours. At the 
spot struck the cord was reduced to a pulp for cm., without any 
haemorrhage. 
The following case illustrates the occasional loss of consciousness, 
* See especially Thorburn, ‘Brain,’ January, 1887. 
f This is the explanation of most cases of injury above the lumbar enlargement, 
with permanent loss of myotatic irritability, or of all reflex action, as in those 
described by Bowlby (f Lancet/ 1890, i, 1071). Such descending inflammation must 
not be confused with the descending degeneration in the pyramidal tracts which 
entails myotatic excess. The very rare exceptions mentioned on p. 229, in which 
such loss exists with no lesion to explain it, may be associated with the fact that 
myotatic irritability is sometimes lost in cases of cerebellar tumour. But the fact 
that superficial reflex action in the legs is never lost unless the lower part of the cord 
is diseased, is one of the most certain in pathology. Proof of such descending in- 
flammation is given in the chapter on tumours (p. 552, note). 590 
SPINAL CORD. 
when there is no evidence of any cerebral lesion. A heavy weight 
fell upon a man’s back; he was unconscious for two days, and 
at the end of that time the legs were completely paralysed, and con- 
tinued so for three months, with retention of urine. Then, improve- 
ment commenced, in the left leg before the right, and in the latter 
some spasm developed. At the end of six months, he could walk 
across the room on crutches. Improvement continued, but at the end 
of two years his condition became stationary, and when I saw him, 
six years after the accident, he could only walk half a mile; the right 
leg was still weak in all parts, and a foot-clonus was present in each 
leg, greater in the right than in the left. 
In cases in which the lowest part of the back receives the force 
of the blow, as when a severe fall ends in the sitting posture, and the 
sacral region is struck, the nerves of the cauda equina seem often to 
be specially damaged, and the posterior roots in greater degree than the 
anterior. The effect is to cause loss of sensibility in the legs, varying 
in extent and seat according to the part injured, in some instances 
specially great about the anus, in others extending over almost the 
whole of the legs, in others again it is chiefly in the sciatic area: all 
forms of sensation are usually involved. It is generally accompanied 
by some muscular paralysis and rapid atrophy, with the reaction 
of degeneration, especially in the muscles below the knees. Rarely 
no muscular paralysis exists; but there is loss of power over the 
sphincters in most cases. Reflex action is lost, and trophic changes 
are readily produced, both on the feet and over the sacrum. The 
sensory loss is often permanent; the injury to the nerve-roots being 
apparently too severe to permit recovery. As the case just mentioned 
shows, when the earlier effects of the injury are survived and im- 
provement sets in, it is remarkable how long this may continue, and 
how considerable a degree of recovery may be ultimately attained, it 
may be in the course of three or four years. 
(2) In cases of the second class initial symptoms are absent or slight. 
After the accident the sufferer may not imagine himself injured, and 
may be able to walk some distance without inconvenience. In other 
instances there is tingling in the legs, or in all the limbs, immediately 
after the concussion, sometimes with some weakness of the limbs, 
more often with a feeling of stiffness. In the course of a few days 
graver symptoms come on, usually attended with spinal pain and 
tenderness, sometimes with some stiffness of the back, and often with 
pyrexia. Tingling in the limbs increases or develops, and is accom- 
panied by weakness, which often goes on to complete paralysis in the 
course of one to four weeks. The symptoms vary in their character 
and distribution, according to the position of the morbid process and 
its extent. In some cases, in which the dorsal region is most affected, 
the symptoms are those of simple paraplegia, usually with spasm, and 
sometimes with early contraction of the muscles. In other cases, in 
which the grey matter of the enlargements suffers, there is scattered TRAUMATIC LESIONS. 
591 
• muscular atrophy in the limbs, often with indications of the degene- 
rative reaction. Tremor in the limbs is conspicuous in some in- 
stances. A girdle-pain in the trunk, or sense of constriction in the 
limbs, is very common. The sphincters generally suffer, and the ten- 
dency to trophic changes is usually strong. The character and course 
of the symptoms is that of a subacute myelitis, and the meagre facts 
of morbid anatomy lea re little doubt that this is the common lesion. 
Thus a lady was severely shaken in a railway collision. She seemed, 
immediately after the accident, to have suffered no injury, but in a 
few days paraplegia developed, and from its consequences she died six 
weeks after the accident. Throughout the dorsal region of the cord 
I found indications of subacute myelitis, chiefly in the white columns, 
varying in its extent in different regions, but in most parts con- 
siderable in the pyramidal tracts.* Complete motor and sensory palsy, 
up to the level of the umbilicus, developed in the course of a week, 
after a fall downstairs in which the back struck successive steps, 
although the patient was able to walk immediately afterwards. The 
symptoms in these cases are sometimes unilateral. A man, driving 
under a low archway, leaned back to save his head, and his spine was 
pressed suddenly against the sharp edge of the seat-back. He felt 
but little immediate effect, but in the course of two or three days, 
complete motor palsy of the left leg came on, accompanied by hyperses- 
thesia, but without any loss of sensation either in that leg or in the 
other. Power slowly returned at the end of three months, and was 
in time perfect. In some cases of this kind the symptoms are due 
not to direct damage to the cord, but to its compression by inflam- 
matory products outside it, the result of injury to the vertebral column. 
A clergyman was thrown from his horse, and there was immediately 
sufficient weakness of the legs to prevent him from walking; this 
subsequently increased, so that at the end of a fortnight the right 
leg was completely paralysed, while the left retained considerable 
power. There was a girdle-pain at the level of the umbilicus, and a 
bedsore formed, but he slowly improved, and regained the power of 
standing at the end of eight months. Such symptoms may come on 
weeks after the concussion, especially when the effects of this are so 
slight as to be disregarded, and the patient leads his usual life. 
When the damage involves the grey matter, the extent of the 
muscular wasting varies greatly. It seldom affects both arms and 
legs, but it is usually irregular in distribution, sometimes wide-spread, 
sometimes limited. Thus a young man fell from a horse and pitched 
on the head. He was stunned, and on recovering consciousness about 
two hours later, felt “pins and needles” in both hands and pain in 
the back, followed by swelling of the neck and difficulty in moving it. 
* Iii the face of such a case as this, it is superfluous to discuss the question raised 
by some writers whether or not the cord can suffer concussion. Moreover, it is 
certain that such an effect as was extreme in this case, may and must often occur in 
slighter degree. 592 
SPINAL CORD. 
The tingling ceased, but was followed by a sense of oppression about 
the shoulders, and persistent pain in the cervical region of the spine. 
When I saw him, two months later, there was some weakness of the 
right arm and wasting of the two outer interossei, and of that part of 
the long extensor which acts on the two outer fingers, with loss of 
faradic and preservation of voltaic irritability. 
Sensory symptoms are prominent in some cases of this class. 
Besides the pain in the spine, to be presently mentioned, pains are 
often felt in the legs, various in character; still more frequent are 
spontaneous sensations of tingling, “ pins and needles,” and the 
feelings of defective sensibility described as “numbness.” Various 
forms of hyperaestliesia are also common, with or without such sub- 
jective sensations. This may exist in any part, in the soles, feet, 
thighs, or not infrequently about the genitals. In the latter region, 
and about the anus, a sense of coldness is often complained of. In 
these regions there may be a distinct defect of sensibility, but this 
is slighter and less frequent than in the cases of the first class. Some 
degree of anaesthesia to touch may be associated with increased 
sensitiveness to stronger impressions. These sensory disorders may 
exist alone or be accompanied by motor weakness. Slight unsteadiness 
or definite inco-ordination is present in some cases, usually resembling 
that met with in ataxic paraplegia. 
Incases which survive the acute stage thei'e is usually slow improve- 
ment, which is often ultimately very great. In many cases recovery 
is incomplete, but improvement goes on for years, as it does in the 
eases of considerable damage to the cord already mentioned ; the 
ultimate degree attained is commonly much greater than in cases of 
corresponding character and severity due to other causes than injury. 
Some permanent symptoms are left, chiefly when the initial derange- 
ment of function has been severe, and has lasted for some time. 
(3) In the cases of the third class, chronic symptoms slowly follow an 
injury at an interval usually of some months, and the cases have the 
aspect less of a traumatic lesion of the cord than of a primary cord 
disease, the relation of which to the injury is rather an inference from 
the sequence, coupled with the absence of other causes, than an ob- 
trusive fact, as in the cases of the first and second clasps. The sym- 
ptoms are usually those of a definite system disease of the cord, less 
frequently those of a disseminated chronic myelitis of irregular dis- 
tribution, still more rarely those of chronic focal myelitis. Primary 
spastic paraplegia, ataxic paraplegia, locomotor ataxy, and pro- 
gressive muscular atrophy are the diseases which most frequently 
thus result. The fact that an injury is occasionally the cause of these 
maladies has been already mentioned in the account of their etiology, 
and the symptoms of such cases so far resemble those that are due to 
other causes that it is not necessary here to add anything to their 
history as already given.* We must assume that the shock to the 
* A case may, however, be mentioned in which typical tabes followed slowly a TRAUMATIC LESIONS. 
503 
nerve-elements causes a slow perversion of nutrition, which is only 
manifested by disturbance of function when it has gradually attained 
a certain degree. Occasionally, other causes co-operate, capable of 
producing degeneration. Previous syphilis, or neurotic inheritance, 
can sometimes be traced, and it is a reasonable assumption that the 
predisposition thus arising may assist in rendering the traumatic 
influence efficient, or in augmenting its effects. Intermediate cases 
connect this class with the last, cases in which we must assume, from 
indications of chronic inflammation, that definite injury was produced 
at one or more spots. An instance of this, and also of focal myelitis, 
was presented by a man with permanent spastic paraplegia and an 
intense girdle-pain at the level of the umbilicus. These symptoms 
commenced three months after a jump from a table, and slight 
unsteadiness, with pains in the legs, connected the jump and the 
paralysis. 
The several consequences of injury, which we have considered as oc- 
curring in separate form, are not only connected by intermediate cases, 
but are also sometimes distinctly combined. Thus an actual and imme- 
diate lesion of the cord may be associated with an early and severe 
increase in the symptoms from the development of subacute myelitis 
in other parts. The traumatic inflammation, at the spot damaged, often 
attains an intense degree,and runs a severe course, in consequence of the 
influence which may give rise to such inflammation apart from a positive 
lesion ; and, in both cases, the damage to the cord may be perpetuated 
by a degenerative tendency. It is very common, for instance, for an 
injury to the cord, in those who have had syphilis, to cause acute 
symptoms which subside, but not perfectly; and the residual disturb- 
ance of function may persist, and even increase in the course of years, 
in consequence of the influence of the previous syphilis in rendering the 
nerve-elements prone to degenerate. Again, it has been pointed out 
that the gouty diathesis is an unquestionable cause of myelitis, and often 
of the grave relapsing and spreading disseminated variety. A concus- 
sion of the cord, which causes only slight symptoms, may excite the 
occurrence of this form of myelitis in persons thus predisposed ; the 
symptoms of the later inflammation may come on months after the 
injury (the effects of which have generally not quite passed away), 
and are sometimes excited by some over-exertion, or slight fresh con- 
cussion, which would have had no effect on a healthy individual. I have 
known the symptoms of insular sclerosis, cerebral and spinal, to 
quickly follow traumatic paraplegia. 
One other symptom remains to be considered, which is common to 
all forms of traumatic lesion of the cord, and is often severe and per- 
sistent when other symptoms are slight,—spinal pain. It may con- 
tinue for years after other symptoms have ceased, and probably 
depends on a neuralgic state of the nerves of the membranes, or of 
fall on the back, recorded by Barbour (‘Journ. of Neivous and Mental Diseases,’ 
March, 1891, Case IV). 
VOL. I. 594 
SPINAL CORD. 
those of the vertebral column ; often, probably, the pain depends on 
the nerves of the joints and ligaments of the spine. It is essentially 
a traumatic spinal neuralgia. The pain may be felt at one or more 
spots ; when severe, it often extends through a considerable length of 
the spine, and sometimes passes up to the occiput. It is occasionally 
referred to the sacrum, and may there have the character of a sense of 
weight or more vague discomfort. The pain is associated with tender- 
ness of the spine, usually deep-seated, chiefly developed at the injured 
part, but sometimes present also at other spots. It may gradually 
assume the features of a true neuralgia, may occur in paroxysms, and 
be induced by mental and other influences which do not act directly 
on the spine, as well as by exertion, posture, and other agencies that 
may immediately influence the affected structures. This condition is 
often called “ spinal irritation.” 
The cause of traumatic lesions of the cord often acts also on the 
brain. A cerebral lesion may occur from the violence which affects 
the cord; the cerebral symptoms then coexist with those of the 
spinal lesion, and may mask the latter during the early stage. More 
common, however, is functional disturbance of the brain, the result 
partly, perhaps, of the physical concussion, but chiefly of the mental 
shock which a serious accident necessarily causes. The resulting 
condition is favorable to the development and persistence of sub- 
jective sensory symptoms. Attention, maintained by concern, has a 
powerful intensifying influence on all forms of nerve-pain, and 
certainly aids in keeping up the pain in the back, and even the 
tenderness which follows injuries to the spine. So marked is the in- 
fluence of “nervousness” on the subjective symptoms, that it has 
been even maintained that in a large number of cases of concussion of 
the spine the symptoms are of hysterical origin * Well-marked sym- 
ptoms of hysteria are sometimes manifested by these patients. But, on 
the other hand, it is necessary to avoid the danger of over-estimating 
the effect of mental influence, and of regarding, as entirely due to this, 
symptoms which are real, and are merely intensified by attention. The 
danger is especially great in cases of railway injuries, concerning which 
an unbiassed judgment is not easy to secure, and in which, when ob- 
jective symptoms are absent, it is easy to minimise suffering, and 
attribute too much to the mental condition. Tbe sinister influence of 
litigation on tbe intellect may be traced very widely.f I believe that 
it is rare for symptoms to be purely mental. It is often asserted by 
those employed for railway companies that subjective symptoms 
quickly subside when the suffei'ei-’s “ claims ” are settled, but it should 
be remembered that mental anxiety is a potent cause of diseases of 
* J. J. Putnam, ‘ Boston Med. and Surgical Journal/ 1883, Sept. 6th. 
f Not many years ago it was customary for the “experts ” who gave evidence on 
behalf of railway companies to deny that the spinal cord could be injured if the legs 
were unwasted. Although the opinion dare not now be exp.essed, its significance is 
not without analogies at the present day. TRAUMATIC LESIONS. 
595 
the nervous system, and must be strongly opposed to recovery from 
geuuine disordei's. The occurrence of improvement when suspense is 
at an end, is thus no proof in itself of the nature of the case, and its 
significance has been unquestionably over-estimated; moreover, in a 
great many individuals whom I have had an opportunity of observing 
long after they had received their “ damages ” (as the expression 
curiously runs) this subsidence had not occurred, and even the “ sove- 
reign balm ” of substantial compensation has appeared to do very little 
for the relief of the sufferer. 
These opinions have been formed from a study of cases other than 
those that involve litigation, in which no elements existed to bias the 
judgment, and from a comparison of these with many “ railway ” cases 
observed apart from forensic proceedings. Those who desire to learn 
what can be said on the subject of “ railway spines,” as they have come 
to be termed, when viewed from the opposite sides, will find abundant 
material for consideration in the writings of Erichsen (‘ On Concussion 
of the Spine,’ London, 1875) and Clevenger (‘ Spinal Concussion, or 
Erichsen’s Disease,’ Philadelphia, 1889) on the one side, and of Page 
(‘ Injuries of the Spine and Spinal Cord,’ London, 2nd ed., 1885) on the 
other. Scattered papers by J. J. Putnam, Walton, Spitzka, Buzzard, 
and others, more or less instructive, will be found epitomised in 
Clevenger’s work, where indeed is collected the pith of almost all that 
has been written on the subject. 
Diagnosis.—The chief points in the diagnosis of traumatic lesions 
to the cord have been already incidentally considered. Immediate 
symptoms may be due to laceration, haemorrhage, or to simple con- 
cussion, and the diagnosis between these is not always possible at 
first. If there are immediate symptoms of a partial lesion, these 
indicate direct injury, while the rapid subsidence of the disturbance 
of function renders simple concussion probable, and excludes any 
considerable direct injury. The later development of paralysis in- 
dicates myelitis, unless there is evidence of considerable irritation of 
the nerve-roots at a certain level, which suggests inflammation outside 
the cord, and perhaps even outside the dura mater. The greatest 
diagnostic difficulty is presented by the cases just mentioned, in which 
the symptoms are subjective, and anxious attention has been long 
given to the local discomfort. The chief elements in the diagnosis 
of these cases have been, however, already indicated. It is important 
to search for, and to give due weight to, any symptoms beyond the 
simple spinal pain. Slight “tingling” or “creeping” sensations may 
be of cerebral and “ functional ” origin, but a persistent sensation of 
“ pins and needles ” rarely is of that nature. A definite sense of con- 
striction is also strongly suggestive of organic disease, and so is a 
well-marked difference in the power of the muscles on the two sides. 
The latter is of least significance if the excess is slight, general, and 
on the right side—of much greater significance if the diminution is 
partial, and affects only certain groups of muscles, such as the flexors 596 
SPINAL COLD. 
of the liip and knee, or the peronei. Any impairment of power over 
the bladder or rectum is of great diagnostic importance ; loss of sexual 
power, on the other hand, is of little value, since this function is 
readily depressed by mental anxiety and preoccupation. A slight 
change in reflex action is most significant when it is partial. A foot- 
clonus, or rectus-clonus, is strong presumptive evidence of organic 
mischief. A slight excess of the knee jerk is of little value ; although 
it probably always indicates some changes in the nutrition of the 
spinal cord, it does not indicate structural disease. In all it 
should be remembered that the absence of any common symptom is 
of far slighter significance, as evidence of integrity of the cord, than 
is the presence of that symptom as evidence of disease. It may seem 
superfluous to insist on a consideration so elementary, but it is still 
possible, as experience proves, for a medical witness to assert in a 
court of law that a claimant’s spinal cord cannot have been injured 
because some symptom is absent, the presence of which would be 
important. 
Prognosis.—Immediately after an accident a cautious prognosis 
should be given, even if the symptoms are slight, on account of the 
possibility that grave disturbance may develop in the course of a few 
days. In developed cases, the prognosis must in general be guided 
by the same considerations as those which determine our estimation of 
the probable course of symptoms of similar character and severity 
due to spontaneous myelitis. To this there are, however, two general 
exceptions. First, the danger of death, if any exists, is greater in trau- 
matic cases than in others, as long as the symptoms are increasing. 
Secondly, if there is no danger to life, or such danger has passed, the 
prospect of improvement is distinctly greater than in a case of similar 
features but of non-traumatic origin. If the symptoms are slight or 
moderate in degree, approximate recovery may be anticipated, although 
slight symptoms often endure for a very long time. Indeed, in 
many cases, recovery, although approximate, is not perfect. The 
patient is never quite as strong, never becomes quite as capable 
of exertion, as before the injury. A cautious prognosis should also 
be given whenever there is the late and gradual onset or increase of 
symptoms that suggests a degenerative process. Such degeneration 
presents far less tendency to arrest or subsidence than do the earlier 
lesions. As a rule, the sooner symptoms occur, the better is the pros- 
pect of ultimate improvement or recovery, provided they are not so 
severe as to be incompatible with life. 
Treatment.—The early treatment of these cases, and much of the 
later treatment of those in which the spinal column is injured, is 
purely surgical. The points of medical character alone need special 
mention, and many of these have been anticipated in the pre- 
ceding pages. In all cases in which spinal symptoms are present 
immediately after an injury, however slight those symptoms may be, 
absolute rest should be insisted on for some days or weeks, according TRAUMATIC LESIONS. 
597 
to the severity of the early symptoms. This is necessary on account 
of the secondary inflammation, which, as we have seen, so often occurs. 
The treatment of developed symptoms must be conducted on the same 
general principles as in cases of myelitis; the details need not be 
here repeated. If there is muscular wasting, it is important that the 
nutrition of the muscles should be maintained by electrical stimula- 
tion, since a very considerable amount of ultimate recovery may be 
anticipated, and it is important to heap the muscular tissue as far 
as possible in a condition to respond to the nerve-power when this 
returns. If there is reason to believe that there is inflammation of 
the membranes, or inflammatory effusion outside the cord, com- 
pressing it, mercury may be given, but this condition is probably 
much more rare than might be anticipated. The influence of 
mercury on inflammation of the substance of the cord is doubtful. 
The chief element in treatment is patiently to permit time to do its 
work, and the tissues to slowly regain such integrity of structure and 
function as is possible; meanwhile preserving the patient from all 
influences likely to interfere with the process or to set up other mischief, 
such as cystitis or bedsores, which would entail fresh danger. There 
is, however, one therapeutic measure that is of unquestionable value 
in the treatment of the later stages, especially of the cases in which 
the recurring symptoms suggest a relapsing myelitis as the sequel of 
injury ; and that is the repeated application of a mild “ actual cautery ’ 
on each side of the spine opposite the affected region. Several 
applications should be made, with or without an ansestlisetic. It is 
not desirable to lessen the pain by cocaine, because this is likely to inter- 
fere with the influence of the proceeding, the beneficial character of 
which is undoubted.* The degenerative sequelae of injuries to the 
cord need the same treatment as the similar degenerations that occur 
apart from traumatic influences. Whenever there is evidence of dis- 
placement of the bones, or reason to suspect that the cord is compressed 
by fractured fragments, or even by products of secondary inflammation 
outside it, the propriety of trephining the spine needs to be considered. 
The problem is chiefly surgical, but the fact that it will probably not 
be necessary to open the dura mater increases the desirability of 
giving the patient this chance of relief. If needed, the sooner the 
measure is adopted, when improvement has ceased, the better. 
The treatment of the neuralgic condition of spinal pain and tender- 
ness, which so often succeeds injury, is frequently difficult. Counter- 
irritation is often useful, either by the actual cautery, blisters, iodine, 
or repated sinapisms. Of sedatives, Indian hemp is most effective, 
next to morphia, which should be used as seldom as possible. Hypo- 
dermic injections of cocaine may be tried. When all active mischief 
is over, and the pain has become purely neuralgic, it is often neces- 
sary to encourage the patient to neglect it in some degree, and to 
* For first directing my attention to the fact, and the evidence supporting it in 
these ea-es, I am indebted to Dr. John Anderson. 598 
SPINAL CORD. 
exert himself in spite of it, while avoiding whatever increases it in 
considerable degree and for a considerable time. At the same time, 
extreme care should be observed by all persons who possess the 
constitutional states above mentioned, predisposing them to myelitis, 
&c. This is especially necessary when any symptoms persist, and 
often difficult to secure, except by uncompromising insistence, in those 
who have been accustomed t,o a. life of active exertion. 
FUNCTIONAL AND NUTRITIONAL DISEASES. 
Functional Diseases. 
Very little is lrnown, though much is heard, of functional diseases 
of the spinal coid. It is, indeed, open to doubt whether there are any 
morbid states which can accurately be thus designated; as was 
pointed out in the introduction, most morbid states thus described 
are either due to disturbance of cerebral functions, or are the result 
of changes in the nutrition of the elements of the cord. The 
deranged function may be an expression of altered nutrition, as it is 
of altered structure, but such cases can only be termed “ functional ” 
by a loose misuse of words. We have an example of the transference 
of our conceptions of functional derangements from the brain ta 
the cord, in the fact that hysterical paraplegia is often regarded as a 
functional affection of the cord because the symptoms have the same 
distribution as those of organic diseases of the cord; but a little 
consideration will show that, in a case of purely hysterical paraplegia, 
the morbid functional condition is cerebral; the brain-centres which 
act on the legs are at fault, but the condition of the functions of the 
cord itself may be absolutely normal. The spinal motor centres are 
in a state of inactivity because the related cerebral centres are inactive, 
but this is no more a diseased condition of the cord than is its corre- 
sponding functional state during physiological rest. Hysterical 
paraplegia will be described, with other palsies of like origin, in the 
chapter on hysteria—a malady for which the term “ functional ” is 
often employed in various ways, as a convenient euphemism. 
At the same time, it must be remembered that there is no sharp 
line of demarcation between functional derangement and nutritional 
changes. As already mentioned, no functional state can exist 
without leaving behind it some corresponding change in the finer 
molecular nutrition of the structures; and if functional derangement 
of lower structures results from that of higher cerebral centres, and 
is maintained for long, the change in nutrition that results may be 
considerable, and may be so definite as to persist even after its cause- 
lias ceased to act. Moreover the general enfeeblement of defective 5oa 
FUNCTIONAL DISEASES. 
nutrition of the nerve-elements is a potent cause of this functional 
disturbance, and at once facilitates and augments such effects. The 
process may be observed in many cases not only of hysteria, but 
also of other derangements of the cerebral functions, and it is seen 
also, in lower centres, as an effect of pam. 
Isolated disturbance of functional centres in the cord does, however, 
sometimes occur. It is seen in the conditions of inhibition which are 
designated ‘‘reflex paralysis.” Such palsies were once thought to be 
common and persistent, but it has been proved that many, and it is 
probable that all, cases of considerable and prolonged palsy, formerly 
thought to be of reflex origin, are due to organic disease, either 
primary in the cord or secondary to an ascending inflammation of 
nerves. But transient paralysis sometimes occurs, which cannot be 
otherwise explained than as an inhibition of a spinal centre, due to 
peripheral irritation. Such, for instance, is the curious inability to 
pass urine which sometimes follows an operation on the anus,—the 
division of a fistula, for instance, or the removal of haemorrhoids. 
The inability may continue absolute for several days. Transient 
weakness of one arm is said sometimes to follow an operation for 
empyema (Lepine), but the fact that the weakness may be attended 
by choreoid movements in both arm and leg of one side (Weil) 
makes it probable that the influence is exerted on a cerebral rather 
than on a spinal centre. Considerable paraplegia was thought to be 
sometimes a reflex effect of disease of the bladder, or of a calculus or 
other organic disease in the kidney, but it is probable that such cases 
are always of organic nature. Ascending neuritis, reaching the cord, 
has also been proved to be the cause of lasting symptoms in many 
cases supposed to be of reflex origin. In one important class of cases 
in which functional disturbance of the cord is purely secondary to a 
morbid state of the brain, organic or not, as has been already mentioned, 
the expression in the limbs of all deranged functions of the brain is 
through the spinal cord; but such disturbance of the cord is purely 
secondary, and ceases when the cerebral centres resume their normal 
state; or, if it is continued longer, this is merely for a brief space of 
time, until the disturbed structures can regain their normal state. 
Thus, in idiopathic epilepsy, the convulsion is produced through the 
agency of the spinal structures, and their over-action may leave them 
so exhausted that the reflex functions are for a short time abolished. 
But such conditions cannot be regarded as coming into the category 
of functional disease of the cord. 
The nearest approach to such disease is presented by certain forms 
of spasmodic disorder, such as transient fixed spasm, catalepsy, and 
certain forms of tonic spasm, which depend proximately on spinal 
centres ; and by some varieties of neuralgic and other painful affec- 
tions or dvssesthesise, in which the sensory elements of the cord are 
deranged in action. But we can seldom feel sure that the symptoms 
in the former class are dependent on a primary derangement of the 600 
SPINAL CORD. 
cord j more often they are clearly secondary to disturbance of cerebral 
centres, -which may indeed coexist, and the cases are better described 
among the general functional affections of the nervous system ; while 
those of the second class have features and alliances which make 
it more convenient to describe them among the forms of neuralgia. 
In another series of cases, derangement of the motor functions of 
the spinal cord is secondary to pain, generally that which has such 
a seat that it is increased by movement; sometimes pain that is not 
related to movement, but is so intense as to act, by mere severity, on 
related structures. It may be in the spine itself, in the trunk, or in 
the limbs. Over-action of the motor centres and spasm may be the 
result, or the centres may be inhibited, causing a pseudo-paralysis, 
which may be real, but often blends with a voluntary indisposition to 
move the parts, lest pain be produced. Spasm is generally brief, and 
the reflex result of some sudden pain, as is often seen in the case of 
the “lightning pains” of tabes. When more prolonged contracture 
results, as in cases in which hysterical contracture follows some 
painful affection of a limb, the co-operation of cerebral centres cannot 
be excluded. The inhibitory influence is strikingly seen in the 
immobility of one half of the thorax in pleurodynia; and in brachial 
neuritis, the effect may render it impossible to say whether or not 
there is real motor weakness. Some forms of spasm may perhaps be 
due to primary disorder of the spinal centres, such as the peculiar 
cramp in the hands, coming on during sleep, that is described in 
vol. ii as “nocturnal tetany,” aud the startings of the limbs on going 
to sleep; but, for the most part, these spasmodic affections are either 
secondary to morbid states of the cerebral motor centres, or form part 
of diseases of Avider range in connection with which they are described. 
Other cases which may be regai’ded as functional are those in 
which symptoms, commonly subjective in character, result from 
some morbid blood-state. The conditions which most frequently 
have this effect are gout and diabetes. Occasionally there is defi- 
nite failure of poAver, lasting for a feAV days or weeks, without 
objective symptoms, and passing away. But the most common 
symptoms from this cause are sensory and subjective,—feelings 
of tingling and formication in the legs, dull aching, and sometimes 
actual pain; this is usually transient, but occasionally continues for 
some days or Aveeks, various in position, but, in gouty cases, often felt 
in the heels. Such symptoms due to morbid blood-states occur chiefiv 
during the second half of life. Those of gouty origin, like other 
symptoms of the same class, are especially common in persons wbo 
inherit a tendency to gout, but have not suffered from attacks of 
definite arthritis. 
In the diagnosis of functional disorders, the first element is the ex- 
clusidn of any sign of positive disease, and the second is the discovery 
of some morbid state capable of giving rise to the functional derange- 
ment, or of associated symptoms unequivocally functional in character. 601 
NUTRITIONAL DISEASES. 
The first of these is that of primary and paramount importance, 
which, alike in practice and reasoning, should precede the others. The 
various points involved in the diagnosis of hysterical affections are 
■described in the chapter on that disease in vol. ii; one only need be 
mentioned here—the importance which attaches to the state of myo- 
tatic irritability in the legs, and the great difficulty in ascertaining it 
presented by many of these cases. Permanent excess shows that 
there is more than functional derangement; although it does not 
exclude the latter, it indicates changes in nutrition, and will be re- 
turned to presently. The cases in which the knee-jerk is apparently 
absent present a special difficulty. It is never really absent in func- 
tional disorder (except when the centres are exhausted by violent 
convulsion), any more than it is in health. Failure to obtain it is 
due to the inability of the patient to relax the muscles, which may 
render attempt after attempt futile, until, in some fortunate moment, 
relaxation is secured and a characteristic jerk is obtained. The ex- 
pedients that facilitate the attempt have been already mentioned (p. 
15), and the subject has been sufficiently discussed in the account of 
the diagnosis of tabes. 
The treatment of functional disorders is that of the morbid states 
to which they are due, or of which they form part, and does not need 
special description. That of the symptoms due to toxic influences is 
necessarily the removal of the condition which causes them, but they 
may be to some extent relieved by sedatives, of which bromide of 
potassium, cocaine, Indian hemp, cimicifuga, and small (7 or 10 gr.) 
doses of chloralamide are the most effective. 
Nutritional Diseases. 
Among the cases often classed as functional diseases of the spinal 
cord are some in which objective symptoms of deranged function, 
slight in degree but definite in character, persist for months, years, or 
for life. They commence chiefly in those in the early and middle period 
of adult life, and are more common in women than in men. Such 
symptoms are inability to walk more than a short distance without 
fatigue, impaired nutrition of the legs, slight increase of myotatic 
irritability, often associated with pain in the back, aching in the legs 
(sometimes amounting to actual pain), and various spontaneous sensa- 
tions of tingling, “ pins and needles,” formication, and the like. There 
is often aching in the legs at night, especially when the patient lies on 
the back, and hence probably due to passive accumulation of blood in 
the spinal vessels. Such symptoms occur especially in those of neurotic 
disposition, who often present other signs of the nervous weakness that 
it is now fashionable to term “neurasthenia.” In many cases, if the 
history of such symptoms is traced, they will be found to date from 
some definite exciting cause, from an attack of acute illness, such as 602 
SPINAL OOKD. 
typhoid fever or acute rheumatism, from pregnancy, a fall, over, 
exertion, and the like, or to have come on during a period of general 
or nerve weakness, anaemia, anxiety, &c. Enfeeblement of the 
nervous system often results, and the impaired nutrition of the 
cord may be only part of a similar general state. A slight increase in 
myotatic irritability is exceedingly common, enough to permit the 
knee-jerk to be obtained by tapping the depressed patella; but there 
is rarely a distinct clonus,—at most only two or three jerks, quickly 
ceasing. We cannot conceive that symptoms so pjersistent can 
depend on any mere functional derangement; it is probable that they 
depend upon changes in the finer nutrition of the nerve-elements, 
too slight to be detected by the microscope, but causing a corresponding 
and persistent alteration of function. We have seen that the termi- 
nation of the upper segment of the motor path is probably that 
structure of the cord which has least nutritional stability, and is 
therefore most susceptible of nutritional derangement. Its degenera- 
tion is the apparent cause of persistent excess of myotatic irritability, 
and hence we can understand the frequency with which there is such 
an excess in these cases. There are probably gradations between such 
conditions and actual structural disease, in which minute examination 
reveals visible alteration; and there are certainly gradations between 
the symptoms above described, and those in which the derangement 
of function is so considerable and special that the case must be 
regarded as one in which actual disease exists, of one or other of the 
types described in the preceding pages. We have already had occa- 
sion to consider these nutritional changes as probably underlying the 
condition of arthritic muscular atrophy, and we have seen that the 
alterations in spinal nutrition in that disease are apparently the result 
of the impressions on the peripheral nerves. In women, such a con- 
dition is often associated with uterine or ovarian pain, and with sacral 
pain apparently of uterine origin. It is possible that the condition 
we have been considering is sometimes secondary to such uterine pain, 
which acts in a manner somewhat analogous to that in which joint 
inflammation acts, and that this is the explanation of many of the 
cases in which a reflex disturbance of the functions of the cord has 
been supposed to be of uterine origin. The condition is also often 
associated with spinal pain and tenderness, which may have a similar 
influence. 
In the diagnosis of these nutritional affections of the spinal cord, 
it is important to remember that they maybe closely simulated by analo- 
gous changes in the peripheral nerves, constituting the slighter degrees 
and forms of polyneuritis. The chief points in the distinction have been 
described in the account of that disease. It is in the parenchymatous 
forms, and especially in the sensory varieties, that the danger of con- 
fusion is apt to arise. Symmetry in the distribution of the subjective 
sensations, or positive anaesthesia, and their localisation in the ex- 
tremities, are the most important features of neuritic change. NUTRITIONAL DISEASES. 
603 
Connected with this distinction is another, of not less importance. 
Nutritional changes, equally with the simpler functional derangement, 
may be the result and expression of the action of some toxic blood- 
state, and all that has been said in connection with mere alteration in 
function applies also to the class now under consideration. Toxic 
influences cannot, indeed, act for long without leading to changes in 
nutrition, which may speedily attain a degree that amounts to visible 
structural disease. A search for such an agency should never be 
neglected in any case in which the symptoms have not followed an 
adequate cause, and do not form part of a general state of the same 
nature. But it must be remembered that the peripheral nerves are, 
as a rule, more susceptible to toxic influences than is the spinal cord, 
and this fact gives additional weight to any indications that it is from 
these that the symptoms proceed. Lastly, symptoms suggestive of 
mere changes in the finer nutrition of the nerve-elements are 
frequently the earliest indications of organic disease of one or 
another of the types already described, and in all recent and pro- 
gressive cases, their general chai’acter and aspect must be carefully 
considered and compared with the known features of the various 
organic diseases. 
The cases with such slight but persistent symptoms as have been 
just described, vary much in their features, and may present all sorts 
of slight symptoms, in the utmost diversity of degree and combina- 
tion. To consider them in detail would be to describe an indefinite 
series of individual cases, no two of which are identical. The precise 
degree and manner in which the nerve-elements suffer may, it is 
evident, be almost infinitely various. Their corresponding manifesta- 
tions present features, combinations, and gradations, that entirely 
baffle an attempt to designate them, or even to perceive definite tjpes 
about which they can be grouped. These are some of the cases of 
disease which exemplify the failure of types in practical work, 
the error involved in the attempt to give names, and the paramount 
importance, in the process of diagnosis, of considering what morbid 
condition the symptoms indicate, and of dealing with each case as a 
new problem, sui generis, whether or not it is ultimately found to be 
one of a familiar series. This method, moreover, conducts tho 
practitioner at once to the morbid processes that need treatment, 
and should determine the character of his efforts to alter that which 
is at fault. 
It is unfortunately not common for the indications of nutritional 
disturbance of the cord, when they have been long established, to pass 
away altogether, although some degree of improvement can often be 
secured; and in many cases, especially in those of brief duration, 
approximate restoration to a normal state may take place. 
The treatment necessarily varies according to the precise con- 
dition that exists, and the causes on which it depends. The removal 
of these as far as possible, and of any influence likely to depress the 604 
SPINAL CORD. 
nervous system, must be the first consideration. It should be remem- 
bered that no part of the nervous system is unaffected by mental 
depression, and that impairment of the general health may render im- 
possible recovery from local disease. From these general principles, 
the details of the treatment of individual cases, too various to be here 
described, may readily be deduced. Therapeutic measures that are 
thus reasoned out and determined on by the indications of the special 
case are far more likely to be successful than those that are simply taken 
from a description of treatment. The only points that need special 
mention are, first, the importance of securing mental tranquillity by 
producing the conviction, when possible, that no grave disease exists 
or is impending, and with it the disregard of those slighter sensations 
of discomfort that become more aggressive and disabling the more they 
are noticed. At the same time, it is important that the patient should 
avoid all over-exertion, all risk of falls or chills, and should be espe- 
cially careful in regard to sexual intercourse, which often has a peculiar 
effect in augmenting the symptoms; and in the unmarried, perfect 
chastity should be enjoined. Often, indeed, in the case of men, the 
mental preoccupation causes an apparent failure of sexual desire, which 
itself is a source of concern—generally groundless. Reassurance on 
this point frequently helps to secure the desired mental state. Equally 
important is it to disabuse the sufferer’s mind of the idea that seminal 
loss is weakening—an error widely prevalent; the truth being that any 
depressing influence comes only from the associated nervous action. But 
it is important to lessen undue frequency of nocturnal emissions, and 
for this nothing is so effective as Milton’s remedy, large doses of the 
tinct. ferri perchlor. (rqxx or xxx) three times a day, coupled with 
the avoidance of lying on the back. 
The relief of disabling pain, by the measures described in the 
chapter on neuralgia, and by the treatment of any local morbid state, is 
indispensable. Rest from work, the improvement of the general health, 
and the administration of nervine tonics, such as arsenic, phosphorus, 
quinine, strychnia, and the like, are the chief other points in treatment. 
A course of massage, or of gentle faradisation of the muscles, is also 
often useful. INDEX. 
A 
Abdominal reflex, 14 
Abductor minimi digiti, 45 
— pollicis, 37, 45 
Abscess of spinal cord, 332 
Accessory haemato-myelia, 392 
Action, antei’gic, 7 
— reflex, 13 
— synergic, of muscles, 7 
Acute anterior polio-myelitis, 351 
— ascending paralysis, 327, 380 
— atrophic paralysis, 351 
— myelitis, 299 
Adductor brevis, 40 
— longus, 40 
— maguus, 40 
— pollicis, 37 
Adductors of thigh, 40, 193 
A5>thesiometer, 9 
Albinism and pseudo-hypertrophic para- 
lysis, 507 
Alcoholic ataxia, 125 
— meningitis, chronic, 280 
— neuritis, 110 
— pseudo-tabes, 110, 125, 400 
Alimentary canal, nerve-centres for, 208 
Allocheiria, 9, 405 
— in tabes, 405 
Amyloid bodies, 304, 468 
Amyotrophic lateral sclerosis, 471, 494 
Anaemia of spinal cord, 296 
Anaesthesia, 8, 10 
— dolorosa, 99,154, 217, 343 
Analgesia, 10 
Anastomotic artery, 188 
Anatomical diagnosis in cord disease, 211 
Anatomy of spinal cord, 162 
Aneurism, erosion of vertebrae by, 262 
Angioglioma, 544 
Angiosarcoma, 544 
Angular curvature, 244 
Ankle-clonus, 17 
Annular myelitis, chronic, 33 
— sclerosis, 338 
Anode, 56 
Antergic contraction, 7 
Anterior central artery, 188 
— column, 164 
— cornua, anatomy of, 167 
— crural nerve, diseases of, 94 
— ground-fibres, 184 
— median arteries, 188 
fissure, 164 
— polio-mvelitis, 351 
— pyramidal tracts, 170, 172 
— radicular arteries, 189 
— root-fibres, 170, 186 
— spinal artery, 188 
— — vein, 189 
Antero-lateral column, 164 
— tract, ascending, 170, 183 
degeneration in tabes, 421 
— function of, 195 
Arachnitis, 265 
Argyll-Robertson pupil, 407 
Arm, diseases of nerves of, 79 
Arteries of spinal cord, 188, 189 
Arthritic muscular atrophy, 498 
Arthritis in ataxic paraplegia, 456 
— vertebral, 263 
Articulation in ataxic paraplegia, 455 
Articulations of spine, diseases of, 263 
Ascending neuritis, 64 
— paralysis, acute, 380 
Ataxic paraplegia, 403, 453 
— — and general paralysis, 456 
and meningitis, 288 GOG 
INDEX, 
Ataxy, hereditary (Friedreich), 461 
in multiple neuritis, 125 
in tabes, 401 
— of movement, 7 
Atrophic spinal paralysis, acute, 351 
subacute and chronic, 378 
Atrophy, atonic muscular, 479 
— muscular, from over-use, 502 
— progressive muscular, 471 
— of auditory nerve, 409 
— of optic nerve, 408 
B 
Bending of spine, violent, 586, 591 
Beri-beri, 151 
Biceps muscle, 33 
— cruris, 40 
Bladder, centre for, 207 
— condition of, in pseudo-hypertrophic 
paralysis, 513 
— ulceration of, in myelitis, 318 
Blood-supply of cord, 187 
Bones iu infantile palsy, 360 
— in syringo-myelia, 577 
— nutrition of, 206 
Brachialis anticus muscle, 33 
Brachial neuritis, 97 
— plexus, diseases of, 79 
Brain-sand, 544 
Bronchial crises, 414 
Burdach’s column, 163, 181 
C 
Caisson disease, 387 
Calf muscles, centres for, 194 
Caput cornu posterioris, 169 
Carcinoma of cord, 513 
Caries of spine, disease of cord in, 243 
symptoms of, 245 
syphilitic, 261 
— — and tumour, 259 
Cauda equina, tumour of, 546, 547, 552, 
555, 557, 558 
Causes, general, of cord disease, 234 
Cautery, actual, in traumatic lesions, 597 
Cavities in cord, 562 
Cells of anterior horn, 167 
Central canal, 185, 564 
Cerebellar tract, direct, 170 
Cerebro-spinal motor segment, 176 
Ce'-vical enlargement, localisation in, 192 
— muscles, centres for, 192 
Cervical vertebrae, fracture of, 212 
Charcot’s joint disease, 411 
Cbeyne-Stokes breathing, 275 
Chlorotic paraplegia, 298 
Chronic atrophic paralysis, 378 
— meningitis, 279 
— myelitis, 333 
— polio-myelitis, 471 
— spinal muscular atrophy, 471 
Circulation in cord, 188, 189 
Circumflex nerve, disease of, 83 
Clarke’s column, 169 
— — in tabes, 422 
Clasp-knife rigidity, 222, 443 
Classification of cord diseases, 231 
— of nervous diseases, 1, 2 
Claw-like hand, 36, 89, 478, 531 
Clonus, foot, 17, 210 
— spurious, 451 
Coarse disease, 1 
Column of Burdach, 163, 181 
— of Clarke, 189 
— of Goll, 163 
— of Gowers, 170, 183, 195, 421 
— of Tvirck, 173 
— posterior, 178 
— postero-external, 163, 181 
— postero-median, 163, 170 
Combination of symptoms iu cord disease, 
226 
Comma-shaped degeneration, 181 
Commissural artery, 188 
Commissures of cord, 184 
Compression, effects of, on nerves, 63 
myelitis, 245 
— of cord, 345 
Concussion myelitis, 586 
— of cord, 595 
Conduction in cord, 190, 194 
Congenital paramvotone, 540 
— spastic paraplegia, 411 
Conjunctival reflex, 15 
Contraction, fibrillary, 5, 479 
— idio-muscular, 5 
— in pseudo-hyrpertrophic paralysis, 512 
— muscular, in cord diseases, 512 
Contracture, 214 
— in primary spastic paraplegia, 444 
Contralateral muscle, 27 
Convulsions in cord disease, 226 
Co-ordination of movement, 13, 203, 408 
Cord, abscess of, 332 
— blood-supply of, 187 INDEX 
G07 
Cord, degeneration of, 396 
— embolism of, 333 
— inflammation of, 299 
— in idiopathic muscular atrophy, 528 
— in peripheral neuritis, 134, 142 
— in pseudo-hypertrophic paralysis, 517 
— symptoms in compression, 345 
Corpora amvlacea, 304, 468 
Counter-irritation in cord disease, 289 
Cramp, 5 
— effect of, on nerves, 11 
Crema>teric reflex, 14, 193 
Crises in tabes, 413, 414 
Crossed pyramidal tracts, 170 
Cross-legged progression, 4, 46 
Crureus muscle, 40 
Crutch palsy, 85 
Cuneate nucleus, 181 
Curvature, angular, 244 
— in Friedreich’s disease, 464 
— in Idiopathic muscular atrophy, 525 
— in infantile paralysis, 363 
— in pseudo-hypertrophic paralysis, 512 
Cutaneous reflexes, 14 
Cysticerci of cord, 544 
Cysts in cord tumours, 549 
D 
Deafness in tabes, 409 
Deep reflexes, 15 
Deformities from infantile palsy, 360 
Degeneration, comma-shaped, of cord, 181 
— fatty, of muscle, 484 
— granular, 484 
— reaction of, in muscle, 25, 54 
— — in sensory nerves, 405 
— secondary, of nerves, 47, 48 
Degenerations of cord, 396 
— — ascending, 171, 178 
— — descending, 171, 176 
— vitreous, of muscle, 53, 484 
Degenerative neuritis, 64 
— reaction, 25, 54 
— tendency, inherited, 533, 579 
Deiter’s cells, 164, 307, 339 
Delay of sensation in tabes, 405 
Deltoid muscle and centre, 29, 83, 192 
Descending antero-lateral tract, 178 
— degenerations, 173 
Deuteropathic lateral sclerosis, 472, 494 
Development of cord, 563 
Diabetes, functional disease from, 600 
Diagnosis, pathological, 231 
Diaphragm, action of, 27 
— centre for, 192 
— paralysis of, 78, 145, 477, 525 
Diffuse myelitis, 321, 336 
Diphtheria and cord disease, 235 
Diphtheritic neuritis, 110, 112, 115 
Direct cerebellar tract, 170, 181 
— pyramidal tract, 170, 172 
Dislocation of spine, 238 
Disseminated myelitis, 288, 309, 321 
— neuritis, 65 
— sclerosis, 232, 417 
Divers’ paralysis, 3S7 
Dorsal reflex, 15 
— region, tumours of, 544 
— vertebrae, fracture of, 243 
Dura mater, haematoma of, 279 
— — tumours of, 543 
Dynamometer, 6 
Dysaesthesia, 10 
Dyslexia, 297 
Dystrophy, muscular, 503 
E 
Echinococci, 543 
Elbow extensors, centre for, 193 
— flexors, centre for, 192 
Electrical irritability, 24 
— reaction in progressive muscular 
atrophy, 479 
Electricity in tabes, 439 
Embolism of cord, 333 
Embryonal tissue and syringo-myelia, 564, 
565, 568 
and tumours, 547, 568 
in nerves in Friedreich’s disease, 469 
persistence of, 563 
Emphysema, subcutaneous, in myelitis 
318 
Empyema, paralysis from, 599 
Enchoudroma of cord, 543 
Endemic neuritis, 112, 150 
Epigastric reflex, 15 
Epilepsy in pseudo-hypertrophic paralysis, 
519 
Erb’s paralysis, 91, 163, 193 
Erosion of spine by aneurism, 262 
Essential paralysis of children, 351 
Excentric pain, 218 
Exophthalmos in pseudo-hypertrophic 
paralysis, 524 
Exostoses, vertebral, 260 
Exposure in cord disease, 234 608 
INDES. 
Extensor quadriceps, 40 
Extensors, nerve-centres for, 193 
— of ankle, 41 
— of elbow, 193 
— of fingers, 34 
— of foot, 41 
— of knee, 40, 193 
— of thumb, 36 
— of wrist, 33 
External meningitis, 266 
— ophthalmoplegia, 408 
— popliteal nerve, disease of, 95 
Extra-dural tumours of cord, 544 
Extra-meningeal haemorrhage, 290 
Eyeballs, reflex fixation of, 481 
— trophic changes in, 23 
Eye symptoms in tabes, 407 
F 
Face in idiopathic muscular atrophy, 524 
Facial nerves in leprous neuritis, 160 
— type of muscular atrophy, 521 
False neuroma, 72 
Family tendency to ataxy, 462 
Faradism, 24 
— in infantile palsy, 375 
Fatty degeneration of muscle, 484 
Fibres, regeneration of, in cord, 312 
Fibrillation of muscle, 479 
Fifth nerve, degeneration of, in tabes, 424 
Fingers, extensors of, 34, 193 
— flexors of, 34, 193 
Fissures in cord, 562 
Fla foot, 43 
Flexors of elbow, 192 
— of fingers, 34, 193 
— of foot, 43 
— of knee, 40, 193 
— of wrist, 33, 193 
— long, of fingers, 45 
— short, of fingers, 45 
— long, of thumb, 37 
— short, of thumb, 37 
— short, of little fingers, 45 
— nerve-centres for, 193 
Foot-muscles, 41, 43 
— nerve-centres for, 194 
Foot-clonus, 17 
— nerve-centre for, 210 
Forearm, muscles moving the, 32 
Fracture of spine, 238 
Fractures, spontaneous, of hone, 411 
Friedreich’s disease, 461 
Front-tap contraction, IS 
Functional disease, 1, 234, 598 
Functions of cord, 189 
— mutual relations of, 209 
G 
Gait in Friedreich’s ataxy, 463 
— in spastic paraplegia, 444 
— in pseudo-liypertrophy, 507, 510, 511 
— in tabes, 402 
Gastric crises, 413 
Gastrocnemius, 41 
Gelatinous grey substance, 169 
Gemelli muscles, 39 
General causation of cord disease, 234 
— paralysis and ataxic paraplegia, 45(> 
and tabes, 417 
Girdle-pain, 219, 316, 591 
Glia-cells, 104 
Glioma of cord, 544 
Gliomatosis, 566 
Glossy skin, 23, 61, 63 
Gluteal muscles, 193 
— reflex, 14 
Gluteus maximus, 38 
— medius, 39 
— minimus, 39 
Glycosuria'in tabes, 418 
Goll’s column, 163 
Gout and cord disease, 600 
— and myelitis, 303, 593 
Gracilis muscle, 40 
Granular degeneration of muscles, 484 
Grey commissure, 185 
— substance, 165 
degeneration of, 420 
of Rolando, 169 
Ground-fibres, 170 
Growths in spinal column, 256 
Gunshot wounds of spine, 586 
H 
Hsematoma of dura mater, 279, 283 
Haemato-myelia, 390 
Hsematorrhachis, 290 
Haemorrhage into cavities of cord, 392* 
578 
— into central canal, 587 
— into cord, 276, 327, 390, 587 
— into spinal membranes, 290, 587 
— and meningitis, 276 
Haemorrhagic myelitis, 304, 315, 321 INDEX. 
609 
Hand, muscles moving the, 33 
nerve-centres for, 193 
— in idiopathic muscular atrophy, 543 
— in progressive muscular atrophy, 478 
— in pseudo-hypertrophic paralysis, 509 
Heart action in cervical cord disease, 224 
in tabes, 224 
— disease in tabes, 418 
Hemiatrophy of tongue, 409 
Hemiparaglegia, 229 
Hereditary ataxy, 461 
Hip-joint, muscles moving the, 38 
nerve-centres for, 93, 193 
Hydatid disease of cord, 543 
of spine, 262 
Hydromyelia, 562 
Hydrorrhacliis interna, 562 
Hyperaemia of cord, 298 
Hyperaesthesia, 10 
— in cord disease, 217 
Hyperalgesia, 10 
— in cord disease, 217 
Hyperpyrexia in cord disease, 226 
Hypertrophic pachymeningitis, 283, 572 
Hypertrophy, muscular, 516, 528, 534 
Hysterical paraplegia, 594 
I 
Idio-muscular contraction, 5 
Idiopathic muscular atrophy, 503, 521 
Iliacus muscle, 40 193, 
Incontinence of urine, 225, 317 
overflow, 225, 317 
reflex, 225, 317 
Inco-ordination of movement, 7, 215 
— mechanism of, 428 
Infantile paralysis, 351 
regression in, 363 
Inflammation of cord, 299 
— of membranes, 265 
— of nerves, 64 
Infra-spinatus muscle, 30 
in pseudo-hypertrophic palsy, 5C8 
Injuries to spine, 234 
Injury to nerves, 54 
Intermediate grey substance, 166 
— group of cells, 168 
— process, 168 
— septal artery, 188 
— septum of cord, 178 
Intermedio-lateral tract, 1C8 
Internal meningitis, 269 
Internal meningitis, chronic, 279 
— popliteal nerve, 95 
Intercostals in progressive muscular 
atrophy, 477 
Interossei of foot, 45 
— of hand, 35 
Interstitial neuritis, 64 
Intra-meningeal haemorrhage, 290 
Intra-spinal tumours, 542 
Irritability, electrical, of nerve and muscle, 
94 
— faradic and voltaic, 24, 54 
Irritative degeneration of pyramidal fibres, 
223 
Irritation, spinal, 594 
J 
Jaw-jerk, 445 
Joints in infantile palsy, 360 
— in tabes, 411 
— nutrition of, 206 
Juvenile muscular atrophy, 521 
K 
Kak-k<j, 151 
Kathode, 56 
Kidney disease in ataxic paraplegia, 456 
in tabes, 416 
Knee, extensors of, 40, 193 
— flexors of, 40, 193 
— muscles moving the, 40 
Knee-jerk, 15 
— centre for, 202, 210 
— in diphtheria, 433 
— in Friedreich’s disease, 463 
— in idiopathic muscular atrophy, 525 
— in leprous neuritis, 159 
— in pseudo-hypertrophic palsy, 513 
— in tabes, 401 
— latent period of, 19 
— loss of, 221, 229, 401, 513, 525, 552 
— return of, in tabes, 415 
L 
Laceration of cord, 586, 588 
Landry’s paralysis, 327, 380 
Laryngeal crises, 414, 416 
Lateral arteries of cord, 1S9 
— column, 164 
— curvature, symptoms of, 263 (see 
Lordosis) 
VOL. T. 610 
INDEX, 
Lateral horn, 166 
— limiting layer, 170, 172, 182 
— sclerosis, primary, 440 
— tracts, 170, 172 
Latliyrism, 442 
Latissimus dorsi in pseudo-hypertrophy, 
518, 523 
Leg, disease of nerves of, 93 
Leprous neuritis, 72, 157 
Lepto-meningitis, 265 
— chronic, 279 
Levator anguli scapulae, 29 
Lightning pains, 403 
Lipoma of cord, 543 
Lipomatous muscular atrophy, 505 
Lissauer’s tract, 183, 187, 420 
Localisation of function in cord, 191 
Locomotor ataxy, 397 (see Tabes) 
Lordosis in Friedreich’s disease, 464 
— in idiopathic muscular atrophy, 525 
— in progressive muscular atrophy, 478 
— in pseudo-hypertrophic muscular 
atrophy, 512 
Lower limbs, muscles of, 38. 
Lumbar enlargement, localisation in, 193 
— plexus, diseases of, 93 
— region, tumours of, 544 
Lumbricales of foot, 45 
— of hand, 35 
M 
Main-en-grille, 36, 89, 478, 531 
Mechanical appliances in palsy, 397 
Median nerve, disease of, 37 
Membranes of cord, diseases of, 265 
— — tumours of, 543, 544, 553 
Meningeal haemorrhage and meningitis, 
276 
Meningitic streak, 275, 552 
Meningitis, spinal, 265 
— — external, 266 
internal, 269 
acute, 270 
chronic, 279 
Meningocele, 582 
Meningo-myelitis, 270, 341 
— myelocele, 582 
Mental distress in cord disease, 234 
Metameres, 162 
Middle form of reaction, 26, 348 
Mixed reaction, 26, 368 
Morvan’s disease, 579 
Morvan’s disease and Raynaud’s disease, 
581 
neuritis in, 580 
sensibility in, 580 
Motion, disturbance of, 4 
Motor over-action, 213 
— path, 176 
— points for ann, 31, 32 
for leg, 41, 42 
— segments, upper and lower, 176 
disease of, 212 
— symptoms, 4 
in cord disease, 212 
in tabes, 402 
Movement, co-ordination of, 203 
— defect of, of muscular origin, 5 
— direction of, 7 
— inco-ordination of, 7, 214 
— spontaneous, 7, 403 
Multiple neuritis, 64, 108 
— neuroma, 74, 544 
— tumours of cord, 555, 557 
of nerve-roots, 556 
and tabes, 556 
Muscle-reflex action, 15 
— centres, 201 
Muscles, action and paralysis of, 26 
— antergic, action of, 7 
— fatty degeneration of, 484 
— vitreous, 53, 484 
— in peripheral neuritis, 134 
— moving foot, 41 
— — forearm, 32 
— — band, 33 
— — liip-joiut, 38 
knee, 40 
shoulder-joint and scapula, 27 
toes, 45 
— nutrition of, 205 
— nutritive changes in, 53 
— of lower limbs, 38 
— of thumb, 35 
-- peripheral guidance of, 8 
— reflex action, 15 
— sensory nerves of, 20 
— synergic action of, 7 
— thenar, 37 
Muscular anaesthesia in tabes, 406 
— atrophy, chronic spinal, 416 
— — facial type, 521 
from over-use, 402 
idiopathic, 503 
in lead, 295, 474 INDEX 
611 
Muscular atrophy in tabes, 417 
— — peroneal type, 482, 505, 509. 525 
— contraction, paradoxical, 21 
— hypertrophy, 516, 528, 534 
— sense, 12 
— sensibility, 11 
— — test for, 13 
Musculo-cutaneous nerve, 84 
— spiral, 81 
Myelitis, acute, 299 
— and gout, 303, 593 
— and injury, 590 
— central, 321 
— chronic, 333 
— — annular, 338 
— diffuse, 336 
— disseminated, 288,309, 321 
— focal, 321 
*— haemorrhagic, 304, 315, 321 
— parenchymatous, 322 
— sclerotic, 341 
— transverse, 321 
Myolipoma of cord, 517. 544 
Myopathic atrophy, 503 
— face, 524 
Myosis, spinal, 407 
Myotatic contractions, 21 
— irritability, 14, 199 
in artlir tic atrophy, 500 
Myotonia congenita, 536 
Myxomata of cord, 544, 548 
N 
Nails in syringo-myelia, 576 
Nephralgic crises, 314 
Nerve, anterior crural, 94 
— circumflex, 83 
— fibres, functions of, 47 
— inflammation, 64 
— injury and degeneration, 54 
— lesions, 48, 62 
— median, 87 
— musculo-cutaneous, 84 
— musculo-spiral, 84 
— obturator, 94 
— plantar, 95 
— posterior thoracic, 82 
— popliteal, 95 
— sciatic, 93 
— superior gluteal, 94 
•— supra-scapular, 83 
•— ulnar, 88 
Nerve-roots, cervical, 80 
— dorsal, 80 
— lumbar, 93 
Nerve-stretching in tabes, 439 
Nerves, compression of, 63 
— diseases of, 46 
— inflammation of, 64 
— irritation of, in caries, 244 
— lesions of, 48, 62 
— of arm, combined palsies of, 89 
— of lower limb, 93 
—• of upper limb, 79 
— physiology of, 47 
— regeneration of, 52 
— secondary degeneration of, 49, 50, 51 
— special, diseases of, 77 
Nervi nervorum, 47 
Nervousness, 594 
Neurasthenia, 601 
Neuritis, 64, 82 
— adventitial, 65, 109 
— after acute diseases, 114 
— alcoholic, 117 
— and atrophic paralysis, 380 
— atheromatous, 118 
— brachial, 97 
— cachectic, 112, 117 
— cancei'ous, 67 
— chronic, 67 
— classification of, 110 
— diabetic, 116 
— diagnosis, 69 
— diffuse, 65 
— endemic, 112, 150 
— focal or disseminated, 65 
— in leprosy, 72, 157 
— in leucocythaemia, 67 
— in Morvan’s disease, 579 
—■ in peroneal atrophy, 532 
—• lipomatous, 65 
— malarial, 114, 151 
—- migrans, 64, 90 
— multiple, 64, 108 
course, 127 
complications, 129 
diagnosis, 139 
—. — pathological anatomy, 130 
pathology, 135 
prognosis, 144 
— — symptoms, 119 
treatment, 147 
—■ near bedsores, 65 
— optic, in ataxic paraplegia, 455 612 
INDEX, 
Neuritis, optic, in chlorosis, 298 
multiple neuritis, 130, 455 
myelitis, 318 
tabes, 401 
— parenchymatous 64, 109 
— peripheral, 109 
— prognosis in, 69 
— radicular, 97, 257 
— rheumatic, 112, 116 
— senile, 117 
— septicaemic, 114 
— syphilitic, 67, 113 
— toxaemic, 111 
— toxic, 111 
— treatment, 70 
Neuroglia, development of, 563 
— structure of, 164 
Neurokeratin, 165 
Neuroma, 72, 544 
— amyelinic, 72 
— false, 72 
— multiple, 74, 544 
— myelinic, 72 
— plexiform, 73 
— of nerve-roots, 544 
Neuropathic disposition in cord disease, 
234 
Neuro-tabes, 113, 141, 432 
Nucleus cuneatus, 181 
— gracilis, 180 
— post-pyramidal, 178, 180 
Nutrition, changes in, 22 
— influence of, on cord, 205 
Nutritional disease of cord, 234, 598, 601 
— diseases, 1 
Nutritive changes in muscles, 53 
Nystagmus in ataxy, 455 
— in Friedreich’s disease, 463 
— in multiple neuritis, 123 
— in progressive muscular atrophy, 481 
— in spastic paraplegia, 445 
— in syringo-myelia, 577 
O 
Obturator internus, 39 
(Edema, vaso-motor, 553 
Onset, modes of, in cord disease, 236 
Operation for tumour, 561 
Ophthalmoplegia, 408 
Opponens pollicis, 37 
Optic atrophy, 408, 424 
— — in ataxic paraplegia, 455 
Optic neuritis in chlorosis, 298 
in myelitis, 318 
Overflow incontinence, 225, 317 
Over-use, muscular atrophy from, 502 
Organic diseases of cord, 1, 234 
P 
Pachymeningitis, 140, 265, 495 
— cervical hypertrophic, 286, 557 
— — syringo-myelia, 577 
— chronic, 279 
— external, 266 
— internal haemorrhagic, 2S3 
Pain, after injury, 593 
— conduction of, in cord, 198 
— in cord diseases, 218 
tumours, 550 
— reflex, 21 
— sensibility to, 10 
in syringo-myelia, 574 
Pains, excentric radiating, 218 
Palsy, Erb’s type of, 363 
— infantile, 351 
Paradoxical muscular contraction, 21 
Parsesthesia, 10 
Paralysis and paresis, 6 
— acute ascending, 380 
— from lessened pressure, 387 
— infantile, 351 
— of muscles, 26 
Paramyotone, ataxic, 541 
— congenital, 540 
Paraplegia, 211 
— ataxic, 453 
and meningitis, 283 
— chlorotic, 298 
— dolorosa, 257 
— simple senile, 470 
— spastic primary, 440 
Parasitic tumours of cord, 544 
Parenchymatous myelitis, 322 
— neuritis, 64, 109 
Pathological diagnosis in cord disease, 231 
Pathology and etiology of cord disease, 
231 
Pectineus muscle, 40 
Pectoralis major, 30 
Pellagra, 442, 460 
Perimeningitis, 266 
Peripachymeningitis, 266 
Peripheral arteries of cord, 188 
— nerves in tabes, 424 INDEX. 
613 
Peroneal type of atrophy, 482, 505, 509, 
525, 530 
— — combined with idiopathic, 534 
Peroneus longus muscle, 43 
— brevis muscle, 45 
Phrenic nerve, diseases of, 77 
Phthisis and peripheral neuritis, 135 
Plantar nerves, diseases of, 95 
reflex, 14 
Plaster-of-Paris jacket in Pott’s disease, 
254 
Plexiform neuroma, 73 
Polio-myelitis, 342, 351 
— chronic and subacute, 342, 378 
Polymsthesia, 9, 405 
Polyneuritis, 108 
— septica;mic, 114 
— tubercular, 113 
Popliteal nerves, diseases of, 95 
Popliteus muscle, 41 
Posterior central artery, 188 
— column, function of, 178 
— cornual artery, 188 
— ground fibres, 170 
— intermediate septum, 163 
— medial artery, 188 
— median column, function of, 217 
septum, 163 
— nerve-roots in tabes, 423 
— pyramid of medulla, 180 
— radicular artery, 188 
— root-fibres, 170, 186 
zone, 163, 181 
— sclerosis, 178, 398 
— spinal vein, 189 
— thoracic nerve, 82 
— vesicular tract, 169 
Postero-external column, 163, 178, 181 
— median column, 163,170, 178 
Post-pyramidal nucleus, 178, 180 
Posture, adaptation to, 202 
— loss of sense of, 12, 217, 406 
Pott’s disease, 245 
Power, measurement of, 6 
Pressure, sense of, 9 
Pressure-myelitis, 345 
Priapism, 221 
Primary hsematomyelia, 390 
— lateral sclerosis, 440 
and general paralysis, 447 
— — and hysteria, 451 
— — infantile, 445 
— multiple neuritis, 64, 111 
Primary spastic paraplegia, 440 
infantile, 445 
Primitive canal of cord, 563 
Progressive muscular atrophy, 471 
and tabes, 417 
Pronators, S3 
— nerve-centres for, 193 
Pseudo-hypertrophic paralysis, 5, 505 
mode of rising in, 511 
— — varieties of, 514 
— -neuroma, 72 
— -paralysis, 600 
— -tabes, 125, 141 
Psoas muscle, 40, 193 
Ptosis in tabes, 408 
Pupil in cord disease, 224 
Pyramidal fibres, 172, 173 
mode of ending in cord, 175 
— tracts in progressive muscular atrophy, 
488 
Pyrexia in cord disease, 225 
Pyriformis muscle, 39 
Q- 
Quadratus femoris muscle, 39 
Quadriceps, 40 
— centre for, 193 
Qualitative changes in irritability, 56 
Quantitative changes in irritability, 56 
R. 
Rachialgia, 218 
Radiating pains, 218 
Radicular neuritis, 97, 287 
Railway spine, 595 
Reaction of degeneration, 25, 54 
in infantile palsy, 358 
— — mixed form, 26, 348 
Rectal crises, 413 
Rectum, centre for, 206 
Rectus femoris, 40 
Red softening of cord, 304 
Reflex action, 13, 199, 219 
cutaneous, 14 
in nerve injury, 61 
muscular, 15 
two kinds of, in cord, 199 
— arc, 14, 201 
— centre, 14, 201 
— paralysis, 599 
— spasm, 222 614 
INDEX 
Sensibility, tactile, 8 
— — modifications of, 9 
— to paiD, 10 
— to temperature, 10 
Sensory conduction in cord, 194 
— symptoms, 8 
— — in cord diseases, 21G 
— — in nerve lesions, 60 
in tabes, 403 
Septicaemia in cord diseases, 235 
Septicsemic polyneuritis, 114 
Serratus magnus, 29 
— — nerve to, 82 
Sexual functions, centre for, 192 
— power in nutritional disease, 604 
in tabes, 406 
— — in traumatic lesions, 596 
Simple idiopathic muscular atrophy, 23, 
503, 521 
Skin glossy, 23 
— nutrition of, 22, 206 
— representation in cord, 197 
Sleep palsies, 81 
Softening of cord, 233, 304 
— — red, 304 
white, 304 
— — yellow, 301 
Soleus muscle, 42 
Spasm, 5 
— in cord disease, 213 
— in progressive muscular atrophy, 480 
— reflex, 222 
Spastic paraplegia, congenital, 441 
— — primary, 440 
Sphincter ani, centre for, 206 
Sphincters in tabes, 410 
— paralysis of, 224 
Spider cells, 164, 307, 339 
Spina bifida, 581 
deformities in, 585 
trophic changes in, 585 
occuita, 581 
Spinal column, growths in, 256 
— cord, anaemia of, 296 
anatomy of, 162 
blood supply of, 187 
— — compression of, 345 
— — functions of, 189 
— — hyperaemia of, 298 
inflammation of, 299 
softening of, 304 
— — structure of, 163 
symptoms of disease of, 211 
Reflexes, deep, 15 
— superficial, 14 
latent period of, 20 
Regeneration of fibres in cord, 312 
— of nerves, 52 
Regressive period in infantile palsy, 363 
Representation of movements in cord, 
191 
Reticular formation, lateral, 165 
posterior, 165 
Rheumatic neuritis, 112, 116 
Rheumatism of dorsal muscles, 277 
Rhomboids, 28 
Rigidity, clasp knife, 222, 443 
— in cord diseases, 213 
— in progressive muscular atrophy, 480 
Romberg’s symptom, 402 
Root-fibres, course of, 185 
— symptoms in compression, 348 
— zone, 563 
S. 
Sacral plexus, diseases of, 93, 94 
Sarcoma, 544 
Sartorius muscle, 40 
Scapular muscles, 27 
Sciatica, 93, 101 
Sciatic nerve, disease of, 93, 95 
Sclerodactyla, 581 
Sclerosis, annular, 338 
— focal, 341 
— in chronic muscular atrophy, 488 
— insular, 232 
— lateral, 440 
Sclerotic myelitis, 341 
Secondary ataxy, 349 
— degeneration of cord, 171 
— — ascending, 171, 178 
— — descending, 171, 176 
of nerves, 47, 48 
— tabes, 401 
Semimembranosus, 40 
Semitendinosus, 40 
Sensation, localisation of, 8 
— rhythmical recurrence, 405 
Sensations, spontaneous, 219 
Sense, muscular, 11, 12, 13 
— of pain, 10 
— tactile, 8, 9 
— temperature, 10 
Sensibility, modes of testing, 8—11 
— muscular, 11, 13 INDEX 
C15 
Spinal curvature in idiopathic atrophy, 525 
— — infantile palsy, 363 
progressive muscular atrophy, 478 
pseudo-hypertrophy, 512 
— epilepsy, 222 
— hemiplegia, 229 
— irritation, 594 
— membranes, 162 
— meningeal haemorrhage, 290 
— meningitis, 265 
— muscular atrophy, 471 
— pain, 593 
— paralysis, acute atrophic, 351 
— — subacute, chronic, 378 
Spine, caries of, 243 
— concussion of, 586 
— diseases of articulations of, 263 
— dislocation of, 238 
— fracture, 239 
— gunshot wounds of, 586 
— injuries of, 233 
— syphilitic diseases of, 261 
— tumours of, 256 
Spino-muscular motor segment, 176 
Spongy grey substance, 166 
— zone, 170 
Spontaneous movements, 7 ; in tabes, 403 
— sensations, 219 
Sterno-mastoid, 27 
Stretching nerves in tabes, 439 
Structural diseases, 2, 234 
Strychnia in muscular atrophy, 497 
Subscapularis, 30 
Supinator brevis, 33 
— longus, 33 
Supinators, 193 
— in idiopathic atrophy, 523 
Supra-scapular nerve, 83 
Supra-spinatus, 30 
Suspension in tabes, 439 
Symptoms, combination of, 236 
in cord disease, 226 
— motor, 4, 216 
— sensory, 8, 216 
— mode of investigation, 4 
Synergic contraction, 7 
Syphilis and spinal degenerations, 235 
— and injury to cord, 593 
— and tabes, 399 
Syphilitic caries, 261 
— diseases of cord, 235 
— meningitis, 287 
Syphilomata of cord, 547, 548 
Syringomyelia, 562 
— and cervical pachymeningitis, 577 
— and hemorrhage, 578 
— and injuries, 572 
— and leprous neuritis, 161 
— and meningitis, 288 
— and progressive muscular atrophy, 578 
— and tumours, 547, 549, 565, 574 
— motor symptoms in, 575 
— muscular atrophy in, 574 
— pain-sense in, 574 
— sweating in, 576 
— temperature-sense in, 574 
Syrin go-myelocele, 582 
System diseases, 211, 232, 234, 396 
T 
Tabes dorsalis, 397 
and diphtheritic paralysis, 433 
and general paralysis, 417 
and neuritis, 400 
and syphilis, 426 
— — and tumours of nerve-roots, 556 
eye symptoms in, 407 
heart disease in, 418 
motor symptoms in, 402 
pathological anatomy, 418 
— — pathology of, 425 
reflex symptoms, 406 
secondary, 401 
sensory symptoms, 403 
sphincters in, 410 
— — trophic and vaso-motor symptoms 
in, 410 
visceral symptoms in, 413 
Tabetic foot, 413 
— multiple neuritis, 400 
— neuralgia, 432 
— ptosis, 408 
! Taclie spiuale, 275, 552 
Tactile sensibility, 8, 9 
Talipes calcaneus, 43 
— valgus, 45 
— varus, 44 
— in infantile palsy, 361 
— in pseudo-hypertrophy, 512 
Temperature-sense, path of, 198 
— — in syringo-myelia, 574 
Tendon-reflex, so-called, 14, 15, 17 
Tensor vaginae femoris, 40 
Teres major, 31 
— minor, 30 616 
INDEX 
Tetanoid rigidity, 480 
Tetanus and meningitis, 276 
Tetany, nocturnal, 600 
Thenar muscles, 37 
— — centre for, 193 
Thigh, adductors of, 40 
— rotators, 38, 39, 40 
Thomsen’s disease, 536 
— — and pseudo-hypertrophy, 514 
Thrilling sensations, 10 
Thumb muscles, 35, 37,193 
Tibialis anticus, 43 
— posticus, 45 
Tingling sensations, 10 
Toes, muscles, moving, 45 
Tone, muscular, 5, 21 
Tonic atrophy of muscles, 480, 493 
Touch, sensibility to, 8 
Tract, autero-lateral, ascending, 170 
— antero-lateral, descending, 178 
— comma-shaped, 181 
— direct cerebellar, 170, 181 
— Lissauer’s, 183, 187, 420 
Tracts, pyramidal, 172, 173 
Transverse lesions of cord, 226 
— — knee-jerk in, 229 
— myelitis, 321 
Trapezius, 27 
Traumatic lesions of cord, 586 
— spinal neuralgia, 594 
Triceps, 32; paralysis of, 85 
Trophic changes in myelitis, 318 
in tabes, 410 
— disorders, 22, 61, 222 
in concussion, 589 
— nerves, 22 
Tubercula dolorosa, 73 
Tubercular meningitis, 273, 554 
— polyneuritis, 113 
— tumours of cord, 544, 560 
Tumours of cord, 542, 554 
— — and hysteria, 558 
— — and membranes, 550, 553 
surgical treatment of, 561 
— of spine, 256; and caries, 259 
U. 
Ulcer, perforating, 410 
Ulnar nerve, disease of, 88 
Unilateral lesions of cord, 229 
Upper arm type of palsy, 3G3 
— limb muscles, 27; nerves, 79 
Urethral crises, 414 
Uterine disease and cord disease, 602 
— functions, centres fox*, 208 
V. 
Vacuolation of cells, 306 
Vagus in peripheral neuritis, 145 
Vascular thickening in tabes, 422 
Vaso-motor centres, 209 
— disorders, 61, 222 
in tabes, 410 
Vasti muscles, 40 
Veins of cord, 189 
Vertebrae, erosion of, 262 
— fracture of, 239, 240 
Vertebral arthritis, 263 
— column, disease of, 238 
— exostoses, 260 
Vesical crises, 414 
— control, 206 
Visceral disturbance, 224 
— pains in tabes, 404 
— symptoms in tabes, 413 
Vitreous degeneration, 53, 484 
Vocal cords in tabes, 409 . 
Voltaic irritability in infantile palsy, 375 
Voltaism in diagnosis, 25 
W. 
Wallerian degeneration, 49 
Wasting palsy, 471 
Westphal’s symptom, 407 
White commissure of cord, 184 
— softening, 304 
—. substauce, 170 
Y. 
Yellow softening, 304 
Z. 
Zygomatic muscles in idiopathic atrophy, 
524, 528 
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P. BLAKISTON, SON & CO., Publishers, 
1012 Walnut Street, Philadelphia. 
The Prices of all Books are Net. Published Annually for 45 Years. 
The Physician s Visiting List 
(LINDSAY & BLAKISTON’S.) 
Special Improved Edition for 1896. 
In order to improve and simplify this Visiting List we have done away with the two 
styles hitherto known as the “ 25 and 50 Patients plain.” We have allowed more space 
for writing the names, and added to the special memoranda page a column for the 
‘‘Amount” of the weekly visits and a column for the “Ledger Page.” To do this with- 
out increasing the bulk or the price, we have condensed the reading matter in the front 
of the book and rearranged and simplified the memoranda pages, etc., at the back. 
The Lists for 75 Patients and 100 Patients will also have special memoranda page as 
above, and hereafter will come in two volumes only, dated January to June, and July to 
December. While this makes a book better suited to the pocket, the chief advantage is 
that it does away with the risk of losing the accounts of a whole year should the book 
be mislaid. 
Before making these changes we have personally consulted a number of physicians 
who have used the book for many years, and have taken into consideration many sugges- 
tions made in letters from all parts of the country. 
CONTENTS. 
PRELIMINARY MATTER.—Calendar, 1896-1897—Table of Signs, to be used in keeping records— 
The Metric or French Decimal System of Weights and Measures—Table for Converting Apothecaries’ 
Weights and Measures into Grams—Dose Table, giving the doses of official and unofficial drugs in both 
the English and Metric Systems—Asphyxia and Apnea—Complete Table for Calculating the Period of 
Utero-Gestation—Comparison of Thermometers. 
VISITING LIST.—Ruled and dated pages for 25,50, 75, and 100 patients per day or week, with blank page 
opposite each on which is an amount column, column for ledger page, and space for special memoranda. 
SPECIAL RECORDS for Obstetric Engagements, Deaths, Births, etc., with special pages for Addresses 
of Patients, Nurses, etc., Accounts Due, Cash Account, and General Memoranda. 
SIZES AND PRICES. 
REGULAR EDITION, as Described Above. 
BOUND IN STRONG LEATHER COVERS, WITH POCKET AND PENCIL. 
* 
For 25 Patients weekly, with Special Memoranda Page, $100 
50 “ “ “ “ “ 1 25 
50 “ “ “ “ “ 2 vols. 
r January to June 
L July to December 
...... 2 00 
75 “ “ “ “ “ 2 vols. 
January to June 
July to December 
January to June 
July to December 
2 00 
IOO “ “ “ “ “ 2 vols. 
2 25 
PERPETUAL EDITION, without Dates. 
No. i. Containing space for over 1300 names, with blank page opposite each Visiting List page. 
Bound in Red Leather cover, with Pocket and Pencil, 25 
No. 2. Same as No. 1. Containing space for 2600 names, with blank page opposite, 1 5° 
MONTHLY EDITION, withoilt Dates. 
No. 1. Bound, Seal leather, without Flap or Pencil, gilt edges, 75 
No. 2. Bound, Seal leather, with Tucks, Pencil, etc., gilt edges, 1 00 
©gp* All these prices are net. No discount can be allowed retail purchasers. 
Circular and satnple pages upon application. 
P. BLAKISTON, SON & CO., Publishers, Philadelphia.