DISEASES OF THE EAR BY / PHILIP D. KERRISON, M.D., »•» AURAL SURGEON TO THE WILLARD PARKER HOSPITAL FOR INFECTIOUS DISEASES; JUNIOR AURAL SURGEON TO THE MANHATTAN EYE AND EAR HOSPITAL; FELLOW OF THE AMERICAN COLLEGE OF SURGEONS; MEMBER OF THE AMERICAN OTOLOGICAL SOCIETY; AMERICAN LARYNGOLOGICAI., RHINOLOGICAL AND OTOLOGICAL SOCIETY; AMERICAN ACADEMY OF OPHTHALMOLOGY AND OTO- LARYNGOLOGY; NEW YORK OTOLOGICAL SOCIETY AND NEW YORK ACADEMY OF MEDICINE / / 332 ILLUSTRATIONS IN TEXT AND 2 FULL PAGES IN COLOR Third Edition—Revised and Enlarged PHILADELPHIA fcf LONDON J. B. LIPPINCOTT COMPANY COPYRIGHT, 1913, BY J. B. LIPPINCOTT COMPANY COPYRIGHT, 1921, BY J. B. LIPPINCOTT COMPANY COPYRIGHT, 1923, BY J. B. LIPPINCOTT COMPANY PRINTED BY J. B. LIPPINCOTT COMPANV AT THE WASHINGTON SQUARE PRESS PHILADELPHIA, U.S. A. PREFACE TO THE THIRD EDITION. The purpose of successive revisions of a medical text book is naturally to make it as nearly representative, as the writer’s ability permits, of whatever is significant in recent thought or research. While the comparatively rapid exhaustion of the second edition has made any re-writing of chapters—had that been advisable—out of the question, a conscientious effort has been made to interpolate whatever of recent work has been of approved interest or value. The new matter has been carefully indexed, and it is hoped that these additions, with the bibliography relating thereto, may give to this edi- tion a greater value as a practical book of reference. The relatively recent studies and writing of Dr. A. A. Gray of Glasgow on the nature and pathology of oto-sclerosis and the wide- spread revival of Anglo-Saxon interest resulting therefrom, the developing theories as to the physiology of the so-called “otolith mechanism,” now under investigation by the Dutch School of Otologists, the renewed interest of our British collegues in the con- flicting theories of tone perception, and the obvious tendency toward a broader neurologic investigation of intracranial lesions of otitic origin give to the student and practitioner of otology much food for stimulating thought and speculation. One new chapter—on Tumors of the 8th Nerve—represents an extension of the field usually covered by text books on otology. With the constantly broadening concept of medical science as a whole, the merging or overlapping of related branches has been one of the most conspicuous tendencies of recent years. As neurology has borrowed and assimilated the results of Barany’s work on the physiology of the labyrinth, so of necessity has otology been forced at certain points to invade the domain of neurology. In a relatively recent paper, a distinguished surgeon, speaking of tumors of the acoustic nerve, brought otologists under the implied reproach of having usually failed with respect to this lesion even “to recognize the presence of a tumor at all.” Clearly, this statement, or its implications, if justified, would bring discredit upon otology. If we accept the fact that the eighth nerve, quite as much as the drum membrane or ossicles and parcel of the organ or mechanism PREFACE TO THE THIRD EDITION of hearing, it is clear that a working knowledge of this very grave lesion should not be confined to special students of oto-neurology, but should belong quite generally to the rank and file of otologists. Lack of such knowledge may lead an otherwise competent aurist into serious errors of diagnosis and treatment. The author believes that no addition to this book could be of greater interest or value to practical otologists than a chapter giving in condensed form the accepted facts as to the incidence, gross path- ology, prognosis, and particularly as to the symptomatology, of tumors of the eighth nerve. The Author June, 1923. PREFACE TO SECOND EDITION While the past few years have been marked by no startling develop- ments in otology, advances of a practical order have not been wholly want- ing. Our conception of the pathology, processes of repair and rationale of treatment of certain lesions has undergone very considerable modification. The mastoid operation of a few years ago was a bone operation pure and simple. To-day the plastic work vies in practical importance with that upon the temporal bone itself. In other words, our conception of the important role which the soft parts may play in post-operative tissue repair has led logically to a different surgical technic, which, in turn, has given us better and quicker results. To record these developments parts of this chapter have been practically rewritten. Again, the further study of the changes in the cerebrospinal fluid occurring in various diseases has conduced materially to a more correct interpretation of the men- ingeal lesions and disorders of otitic origin and has brought to light certain sources of error in diagnosis. Beyond such changes and additions as were necessary to bring these practical phases of otology in line with modern ideas, alterations in the text and arrangement of the subject matter have been avoided. Two new chapters have been added, of which the first is devoted to Barany’s theory of the cerebellar control of joint movements, with a dis- cussion of the pointing tests in their relation to vestibular and cerebellar disease. The second includes a brief account of the various types of war deafness,—deafness due to direct injury of the skull, nerve deafness due to loud explosive noises, concussion deafness due to the air displacements of near-by explosions, psychic disturbances of function, pithiatism, etc.,—phe- nomena which constitute for most of us a practically new chapter in aural disease. Direct products of military hardship and injuries, as these lesions and functional disorders undoubtedly are, their relation to certain phases of some of the commoner ear lesions is sure to provide a fruitful field for future investigation and discussion. It is hoped, therefore, that the changes and additions which distinguish this edition from the first may prove to be of distinct practical usefulness to students and practitioners of otology Philip D. Kerrison. PREFACE Probably in no branch of medicine have more notable advances been achieved during the past decade than in otology. The wholly new field of work which has been opened to us by the successful investigation of the static labyrinth; the new light upon syphilitic lesions of the labyrinth and auditory nerve resulting from the recent world-wide renewal of interest in the study of all phases of syphilis; and the investigations still in progress as to the influence of autogenous vaccines and leucocyte extracts upon certain phases of aural disease,—these and other additions to our knowledge have suggested new problems in the working out of wdiich laboratory investigations have been closely followed by practical thera- peutic results. In aural surgery our activities can no longer be confined to the narrow limits of the tympanum and mastoid process, but must include the more hazardous field of intracranial surgery and the yet more delicate and difficult work upon the auditory labyrinth itself. There is, then, some justification at the present time for yet another book,—i.e., an attempt to present the complex subject of otology in the light of recent advances. If the arrangement of the subject matter, particularly as to the pro- portionate space given to the different subjects, represents a departure from that usually followed, this has become necessary in order to bring the various subjects now pertaining to otology into a true relation with their actual and proportionate importance. For example, labyrinthine physiology, suppurative diseases of the labyrinth, and the surgery of the labyrinth, which are usually rather briefly dealt with, are here considered in three separate chapters which occupy a very considerable section of the book. Again, the suppurative lesions of the brain and meninges are accorded far more space than is usually allotted them in text-books of otology. In the Section devoted to operative surgery, the plan of illustrating each successive step of the various operations has been adopted. This, it is believed, will be of special value to students of otology living at a distance from the larger medical centres and who are therefore denied the educational advantages of large surgical clinics. With few exceptions, the illustrations throughout the book are from original drawings made under the writer’s personal supervision. PREFACE In the preparation of this manual the writer has endeavored to give greatest prominence to the practical side of otology. This has necessitated the elimination of many time-honored but discarded theories and thera- peutic measures which no longer have any bearing upon the practice of otology. In conclusion, I wish to express my thanks to Dr. J. H. Guntzer for many valuable abstracts from the literature, and to Miss Eleanor Fry, whose clever and anatomically correct drawings form so attractive and valuable a feature of this hook. I wish also to express my indebtedness to the publishers, Messrs. J. B. Lippincott Company, for many helpful sug- gestions as to the arrangement of the text. Philip D. Kerrison. CONTENTS CHAPTER I PAGE Anatomy and Physiology of the Sound Conducting Apparatus 1 The Auricle 1 Muscles of the Auricle 2 The External Auditory Meatus 3 Development of the Osseous Meatus 4 Post-natal Changes 7 The Osseous Meatus 8 The Tympanum : 9 The Inner Wall 11 The Superior Wall 12 The Anterior Wall 13 The Posterior Wall 14 The Inferior Wall. . 14 The External Wall 15 The Annulus Tympanicus 16 The Drum Membrane 16 The Ossicles 16 The Malleus 16 The Incus 18 The Stapes 18 Shrapnell’s Membrane 20 The Ossicles, Their Articulations and Relative Positions Within the Tympanum 20 The Malleus 21 Ligaments of the Malleus 21 The Incus 22 Articulations of the Malleus and Incus 22 The Incudo-stapedial Joint 23 Articulation of the Stapes with the Fenestra Ovalis 23 The Intra-tympanic Muscles 23 The Stapedius 23 The Tensor Tympani Muscle 24 The Lining Membrane of the Tympanum 24 The Pouches, or Pockets, of the Membrana Tympani 24 The Attic Spaces 26 Vascular and Nervous Supply of the Tympanum 26 Arteries 26 Veins 27 Nerves 27 The Eustachian Canal 28 The Osseous Portion of the Eustachian Tube 28 The Membrano-cartilaginous Portion of the Eustachian Tube. ... 29 Anatomical Differences Between the Eustachian Tubes of the Adult and the Infant at Term 30 Muscles of the Eustachian Tube 31 The Mastoid Process 31 The Pneumatic 32 The Diploic Mastoid 32 The Antrum 32 Physiology of Sound-conduction 34 The Pitch 34 Intensity 35 Timbre 35 CONTENTS Sound-conduction 35 Auricle and External Auditory Meatus 35 The Drum Membrane 36 The Ossicular Chain 37 The Tympanic Muscles 39 CHAPTER II Physical Examination of the Patient 41 Age, Occupation, Habit, Heredity 41 Previous History 41 History of the Present Attack 41 Objective Examination 42 Auricular Displacement 43 Palpation in Case of Postauricular CEdema 43 Palpation of the Auricle in Case of Aural Pain 44 Inspection of the Drum Membrane 44 The Source of Light 49 Technic of Objective Examination; Landmarks of the Normal Drum Membrane 50 Landmarks of the Normal Drum Membrane 53 Examination of the Eustachian Tubes 60 Valsalva’s Method of Inflation 60 Politzer’s Method of Inflation 61 Inflation Per Catheter 63 The Nose, Nasopharynx, and Throat 69 Examination of the Nose 70 The Throat 70 Posterior Rhinoscopy 71 CHAPTER III Functional Examination of the Cochlear Apparatus; Hearing Tests 73 Air Conduction and Bone Conduction of Sound 73 Normal Hearing Distances for the Watch-tick, the Acoumeter, the Conversational Voice and Whisper 74 The Watch-tick 74 Politzer’s Acoumeter 74 The Conversational Voice and Whisper ! 75 Recapitulation 76 Changes in the Tone Limits 76 Loss or Impairment of Hearing for the Lower Musical Tones 76 Loss or Impairment of Hearing for the Higher Tones of the Mus- ical Scale 77 Changes in the Period of Hearing by Bone Conduction 77 Increase 77 Diminished Hearing by Bone Conduction 79 Method of Examination 80 Watch and Acoumeter 80 Whispered and Conversational Speech 81 Determination of the Lower Tone Limit 83 Determination of the Upper Tone Limit 86 Changes in Hearing by Bone Conduction 87 Total Deafness 91 CHAPTER IV ♦ Diseases of the External Ear (Auricle; External Auditory Meatus) 97 Inflammatory Diseases of the Auricle 97 Traumatic Auricular Dermatitis 97 Treatment 97 Erysipelas of Auricle 97 Treatment . 97 CONTENTS Frost-bite 98 Treatment 98 Auricular Eczema 98 Etiology 98 Symptoms op Acute Auricular Eczema 99 Treatment 99 Chronic Eczema of the Auricle 100 Treatment 100 Auricular Perichondritis 101 Symptoms 101 Terminations 101 Treatment 101 ELematoma Auris (Othematoma) 102 Etiology 102 Symptoms 103 Terminations 103 Treatment 103 Lupus 104 Treatment 105 Lupus Tcmidus (Lupus Hypertrophicus) 105 Treatment 105 Syphilis of the Ear 105 Herpes Zoster Auricule; Herpetic Inflammation of the Genicu- late Ganglion (Hunt) 106 Malignant Disease of the Auricle; Epithelioma; Cancer of the Auricle 107 Inflammatory Diseases of the External Auditory Meatus 107 Acute Circumscribed External Otitis 107 Etiolocy 107 Symptoms 108 Physical Examination 108 Course of the Disease . 109 Prognosis Ill Treatment HI Acute Diffuse External Otitis 116 Causes . 116 Symptoms 116 Treatment 116 Otomycosis 117 Etiology 117 Symptoms H7 Treatment 117 Croupous External Otitis (Otitis Externa Crouposa) 118 Etiology 118 Symptoms 118 Treatment 118 Obstructive Conditions of the External Auditory Meatus 119 Foreign Bodies in the Meatus 119 Removal of a Foreign Body by Means of the Syringe 119 Cases Requiring the Use of Instruments 120 Removal of Cerumen from the Meatus 123 Exostoses of the Osseous Meatus; Bony Outgrowths from the Walls of the Bony Canal 125 Treatment 125 CHAPTER V Causes of Acute Tympanic Disease 126 Predisposing Causes 126 Age 126 Nasal Obstruction 126 Exciting Causes 127 Acute Rhinitis 127 CONTENTS Acute Infectious Diseases 127 External Causes 129 Occupations and Habits as Causes of Aural Disease 130 CHAPTER VI The Subjective Symptoms of Aural Disease 133 Aural Pain 133 Pain in Acute Otitis Media 133 Pain in Chronic Catarrhal Otitis Media 133 Pain in Furunculosis of the Meatus 134 Reflex Aural Pain 134 Impairment of Hearing 134 Aural Discharge 135 Discharge in Acute Otitis Media 135 Discharge in Chronic Suppurative Otitis 135 Tinnitus Aurium 136 Obstruction Sounds 136 Blood Sounds 138 Labyrinthine Sounds 140 Neurotic Sounds 141 Cerebral Sounds 143 CHAPTER VII Acute Inflammatory Diseases of the Eustachian Tube, Middle Ear, and Mastoid Process 145 Acute Tubal Catarrh; Eustachian Catarrh; Tubctympanic Conges- tion 145 Tubal Catarrh 145 Etiology : 145 Pathology 145 Symptoms /.. 146 Physical Signs 147 The Course of the Disease 148 Prognosis 149 Treatment 149 Tubal Catarrh in Children 153 Absence of Subjective Symptoms 155 Physical Examination 155 Treatment 155 Myringitis , 156 Acute Middle-ear Inflammation 157 Nomenclature: Significance of Names in Common Use 157 Otitis Media Catarrhalis Acuta; Acute Catarrhal Otitis Media.. . 158 Etiology -. 158 Anatomical Conditions in Relation to Symptoms 160 Symptoms and Signs 160 Prognosis 165 Acute Suppurative Otitis Media; Acute Purulent Otitis Media (Otitis Media Purulenta Acuta) 165 Etiology 165 Anatomical Conditions Influencing the Pathology of the Disease 165 Symptoms and Signs 166 Complications of Acute Purulent Otitis Media 170 Treatment . 171 Acute Mastoiditis 181 Etiology 181 Pathology 181 Symptoms 183 Prognosis 188 Treatment 188 CONTENTS CHAPTER VIII Chronic Middle-ear Suppuration 192 Otitis Media Purulenta Chronica 192 Etiology 192 Pathology 192 Symptoms and Signs 198 Diagnosis 200 Complications 205 Treatment 205 CHAPTER IX Chronic Non-suppurative Diseases of the Middle Ear; Otosclerosis 219 Chronic Tubal Catarrh 219 Nasal Obstruction . 221 Chronic Tubal Congestion 221 Treatment 222 Structural Narrowing of the Tube 222 Chronic Non-suppurative Tympanic Disease 223 Chronic Hypertrophic Otitis Media 223 Etiology 223 Pathology 223 Symptoms 224 Physical Signs 226 Prognosis 229 Treatment : 229 Chronic Hyperplastic Otitis Media 234 Symptoms 235 Physical Appearances of the Drum Membrane 236 Course of the Disease; Prognosis 238 Treatment 238 Otosclerosis 244 Etiology 244 Pathology 245 Symptoms and Diagnosis • 250 Otosclerosis with Involvement of the Cochlea 253 Symptoms 253 Otosclerosis Complicated by Chronic Catarrhal Otitis Media. ... 255 Treatment 255 CHAPTER X The Anatomy and Physiology of the Labyrinth 260 The Osseous Labyrinth 260 The Membranous Labyrinth 265 Physiology of Sound Perception (Cochlear Function) 274 CHAPTER XI Inflammatory and Suppurative Lesions of the Labyrinth 278 Ewald’s Experiments 278 Barany’s Experiments; The Caloric Reactions 280 Vestibular Nystagmus 281 Physiological Nystagmus 283 Rotation or Turning Experiment 283 The Symptom Complex of Vestibular Irritation: Nystagmus, Ver- tigo, Ataxia 287 Suppurative Labyrinthitis 292 Diffuse Suppurative Labyrinthitis 292 Etiology 292 Symptoms 294 Terminations; Prognosis 309 Circumscribed Suppurative Labyrinthitis 309 Symptoms 310 CONTENTS Diffuse Serous Labyrinthitis 310 Perilabyrinthitis 312 Symptoms 312 Acute Hyperemia of the labyrinth 313 Prognosis and Treatment of Diffuse Suppurative Labyrinthitis. . 313 Treatment of Circumscribed Suppurative Labyrinthitis 318 Treatment of Diffuse Serous Labyrinthitis 320 Treatment of Perilabyrinthitis 320 CHAPTER XII Symptoms of Intracranial Disease Secondary to Aural Suppuration 322 Headache 322 Vomiting 323 Temperature Changes 324 Changes in Pulse Rate 325 Unilateral Muscular Spasm as a Symptom of Cerebral Disease. 326 Unilateral Muscular Paralysis or Paresis 327 Mental Disturbances 330 Aphasia 331 Sensory Aphasia 334 Motor Aphasia 336 Motor Agraphia ...... 336 CHAPTER XIII Intracranial Lesions of Otitic Origin: Extradural Abscess; Perisinous Abscess; Septic Sinus Thrombosis or Phlebitis; Purulent Lepto- meningitis; Cerebral Abscess; Cerebellar Abscess 337 Avenues of Infection 337 Extradural Abscess; Epidural Abscess 338 Etiology 338 Symptoms 338 Prognosis 339 Perisinous Abscess and Infective Sinus Phlebitis 340 Perisinous Abscess 340 Symptoms 342 Prognosis 343 Infective Sinus Phlebitis; Suppurative Thrombophlebitis of the Sigmoid or Lateral Sinus; Sigmoid Sinus Thrombosis 343 Etiology 344 Pathology 344 Symptoms 345 Prognosis 354 Treatment 355 Abscess of the Brain 357 Etiology 357 Pathology 361 Symptoms 362 Prognosis 375 Cerebellar Abscess 375 Symptoms 375 Differential Diagnosis 379 Otitic Meningitis 382 Circumscribed Pachymeningitis 382 Leptomeningitis 382 Diffuse Purulent Leptomeningitis 383 Paths of Infection 383 Symptoms 383 Prognosis 385 Circumscribed Leptomeningitis 385 Serous Meningitis; Serous Meningoencephalitis (Korner) 387 Meningismus 389 Differential Diagnosis 389 Treatment 392 CONTENTS CHAPTER XIV Barany’s Theory of Cerebellar Centres: Normal Accuracy in Pointing with Eyes Closed; Normal Reaction Movements in Response to Ves- tibular Irritation; Loss of Pointing Accuracy And Changes in Reac- tions to Vestibular Irritation in Cerebellar Disease 394 Cerebellar Centres, Function of 394 Effect—Disease or Destruction of 394 Location of 395 Evidences of Correct Localization 395 Normal Pointing Accuracy 395 Method of Determining 395 Pointing Reactions in Response to Vestibular Disease 395 Method of Applying Tests 395 Changes in Pointing Accuracy in Cerebellar Disease 396 CHAPTER XV Surgical Operations for the Relief of Suppurative Lesions of the Middle Ear and Mastoid Process; Myringotomy; Mastoidectomy; The Radi- cal Operation; Ossiculectomy 399 Myringotomy; Incision of the Drum Membrane Paracentesis 399 Operative Dangers 400 Preparation for Operation 402 Anaesthesia 403 Technic 403 Possible Repetitions 406 Surgical Landmarks of the Mastoid Cortex 406 Mastoidectomy; The Mastoid Operation; Sometimes Called “Schwartze’s Operation” 409 Preparation of the Patient 409 Instruments 412 Position of patient on Table 412 The Initial Incision 413 The Bone Operation 414 RationalThoroughness in Obliterating the Mastoid Cells 422 The Element of Time in Mastoid Surgery 425 Postoperative Treatment 425 The “ Blood-clot Operation ” (Blake, Reik) 430 Surgical Treatment of Chronic Middle-ear Suppuration 432 Radical Mastoid Operation; Schwarzte-Stacke Operation 432 Preparation of the Patient 433 The Incision 433 Facial Paralysis 442 Zanfal-Heine Operation 443 Stacke’s Operation 444 The Korner Flap 449 The Panse Operation 450 The Siebenmann Flap 450 Postoperative Treatment 451 The Influence of the Radical Operation upon Hearing 455 The Heath Operation for Chronic Middle-ear Suppuration ... 455 Bondy’s Operation 456 Streit’s Operation * 457 . Ossiculectomy 457 Preparation 457 The Instruments 458 Operation 458 Plastic Operations for Closing a Postauricular Opening Follow- ing-the Radical Operation 459 Mosetig-Moorhof Operation 459 The Passau-Trautmann Operation 460 Author’s Operation for Preventing or Closing Postauricular Fistula Following the Radical Operation 461 CONTENTS CHAPTER XVI Labyrinthectomy; the Radical Labyrinth Operation; Surgical Drainage of the Labyrinth 463 Indications 463 Surgical Guides to the Vestibule 464 Operation 465 The Jansen Operation 465 Hinsberg’s Operation 466 Richards’s Operation 467 Neumann’s Operation 468 Comparative Advantages and Disadvantages of the Different Operations 470 Author’s Method of Reaching the Vestibule 470 Obliteration of the Vestibule for the Relief of Vertigo (Lake) 475 CHAPTER XVII Surgical Treatment of Infective Sigmoid Sinus Thrombosis 477 Sinus Operation for the Removal of an Infected Clot 479 Use of the Rongeur 481 Exploration of the Sinus 483 Resection of the Jugular Vein 485 Ligation of the Jugular Vein 488 CHAPTER XVIII Surgical Treatment of Intracranial Lesions (Continued) : Temporo- sphenoidal and Cerebellar Abscess; Otitic Meningitis 490 Surgical Treatment of Brain Abscess 490 Cerebellar Abscess 502 Meningitis 504 Serous Meningitis 504 Serous Meningo-encephalitis (Korner) 506 Purulent Leptomeningitis 506 CHAPTER XIX Facial Paralysis 508 Facial Paralysis of Otitic Origin 508 Postoperative Facial Paralysis 508 Symptoms and Physical Signs 509 Prognosis 510 Treatment 510 CHAPTER XX Congenital Abnormalities of the Auricle 514 Macrotia 514 Polyotia 514 Supernumerary Parts 514 Projecting Auricle, "Lop Ear” 516 Microtia 516 Treatment 516 Removal of Supernumerary Nodules 521 Treatment of Prominent or Projecting Ears 521 CHAPTER XXI Non-Suppurative Diseases of the Labyrinth 526 Meniere’s Disease 526 Etiology 526 Diagnosis 526 Symptoms 527 Prognosis 527 Treatment 527 CONTENTS “Vertigo ab aure l.eso” 528 Leck.emic Deafness .t 528 Symptoms ’ 529 An.emia of the Labyrinth . . 529 Treatment 530 Syphilis of the Labyrinth 530 Treatment : 532 Tuberculosis of the Ear 532 Pathology 533 Symptoms 534 Diagnosis 535 Terminations 535 Prognosis 536 Treatment 537 CHAPTER XXII Otologic Lessons of the World War. War Deafness: Deafness Due to Di- rect Labyrinthine Injury : Concussion Deafness : Psychic Deafness . Pithiatism: Simulation: Pithiatic Deafness: Diagnosis and Ra- tionale of Treatment 538 Deafness Due to Direct Cranial Injuries 539 Concussion Deafness Due to Explosions 541 Immunity of Static Labyrinth to Injury by Explosive Sounds 542 Prognosis as to Functional Improvement in Concussion Deafness 542 Chief Differential Point Between Profound Deafness Due to Direct Labyrinthine Injury and to Concussion 542 Hysterical or Psychic Deafness; Psychic Mutism 543 Pithiatism, its Etiology and Clinical Significance 543 Types of Pithiatic Deafness \ 544 Useful Diagnostic Tests 545 Rationale of Treatment 545 CHAPTER XXIII Salvarsan in the Treatment of Aural Disease. Auditory Xerve Lesions Occasionally Following Its Use 548 Cranial-nerve Lesions Following the Use of Salvarsan 549 CHAPTER XXIV Vaccine Therapy in the Treatment of Aural Disease: Autogenous Vaccines : Bactericidal Sera; Stock Vaccines 554 Preliminary Remarks 554 CHAPTER XXV Aural Disturbance Due to Dental Lesions 558 CHAPTER XXVI Deaf-mutism '. 561 Etiology 561 Morbid Anatomy 564 Treatment 565 CHAPTER XXVII Nasopharyngeal Adenoids 566 Diagnosis 566 Treatment 567 CHAPTER XXVIII Tumors of the Eighth Nerve 571 Etiology—Pathology—Mechanical Influence on Adjacent Structures 572 CONTENTS Symptoms: Gradually Developing Symptom-complex 572 Differential Diagnosis 585 Treatment: Choice of Surgical Methods 584 Diagnosis, With and Without Surgical Intervention 584 The Otologist’s Problem and Responsibilities 583 APPENDIX Aural Disease in Relation to Life Insurance 587 Artificial Aids to Hearing 588 Case Histories 589 Formula 592 Alkaline and antiseptic Solutions for Cleansing the Nasal and Nasopharyngeal Spaces 592 Oil Solutions j, 592 Astringent and Antiseptic Solutions for Direct Application to the Pharyngeal Mouth of the Eustachian Tube 593 Ointments 593 Solution for Instillation into the Ears 594 Local Anesthesia for Operation of Myringotomy 594 For the Relief of Moderate Pain 595 For the Relief of Nasopharyngeal and Tubal Congestion 595 Index 597 ILLUSTRATIONS COLOR PLATES V. Fig. 84. Lupus Hypertrophicus Auriculae 104 VI. Fig. 85. Herpetic Eruption due to Inflammation of the Geniculate Ganglion.. 106 CHARTS Chart No. 1. For Bedside Histories 572 Chart No. 2. For Office Histories 573 „G. ILLUSTRATIONS IN TEXT 1. The Auricle 2 2. Auricular Cartilage 3 3. The Auricular Muscles 3 4. Auriculo-meatal Cartilage 4 5. Petromastoid 5 6. Squamozygomatic, Outer Surface 5 7. Right Tympanic Ring 5 8. Squamozygomatic, Inner Surface 5 9. Temporal Bone ' 5 10. Infant Skull 5 11. Infant Temporal Bone 7 12. Adult Temporal Bone 7 13. Diagram: Dotted Lines Showing Influence upon Direction of Canal of Draw- ing Auricle Upward and Backward 9 14. Vertical Section through Tympanic Cavity and Bony Meatus 10 15. Inner Tympanic Wall 11 16. Tympanic Roof 12 17. Vertical Section of Temporal Bone, Showing Anterior Wall of Tympanum... 13 18. Section Showing Posterior Wall of Tympanum 14 19. Horizontal Section through Tympanum, Showing Tympanic Floor 15 20. Inner, or Tympanic, View of Drum Membrane 15 21. Ossicles, Right and Left, Only Slightly Enlarged above Actual Size 17 22. Malleus, Enlarged 17 23. Incus 17 24. Stapes 17 25. Ossicles in Articulation 17 26. Diagrammatic Picture of the Membrana Tympani and Its Attachments .... 19 27. Temporal Bone with Drum Membrane and Outer Wall of Vault Removed.. . 21 28. Tympanum of Infant Six Months Old. (Left.) 24 29. Tympanum of Infant Six Months Old. (Right.) 24 30. Transverse Section of Eustachian Tube 29 31. Temporal Bone, Outer Surface 33 32. Temporal Bone, Inner Surface 33 33. Vertical Section of Temporal Bone Passing Through Aditus ad Antrum 33 34. Section through Mastoid Process of Pneumatic Variety 33 35. Section through Mastoid Process of Diploic Type 33 36. Section through Mastoid Process of Sclerotic Variety 33 37. Tuning-fork 35 38 and 39. Head Mirrors 45 40. Head-band and Mirror 46 41. Fibre Head-band 47 42. Aural Specula 48 43. Aural Forceps 48 44. Tympanic Probe 48 45. Aural Cotton Applicator 48 ILLUSTRATIONS 46. Wall Bracket for Movable Electric Light 49 47. Forehead Lamp for Bedside Examination 50 48. Position of Physician and Patient for Aural Examination 51 49. Section through Adult Canal and Tympanum \ 52 50. Section through Canal and Tympanum of Infant at Term 52 51. Diagram Showing Direction of Auditory Canal of Adult 52 52. Diagram Showing Direction of Auditory Canal of Infant 52 53. Normal Drum Membrane 54 54. Diagram Showing Quadrants of Membrana Tensa 55 55. Semidiagrammatic Picture, Showing Relations of Ossicles in Vault and Atrium. 56 56. Bulging Drum Membrane , 57 57. Retracted Drum Membrane 57 58. Rough Pen-and-ink Diagram of the Drum Membrane 58 59. Siegel’s Otoscope 59 60. Politzer’s Inflating Apparatus 61 61. Eustachian Catheter. 62 62. Dench Inflating Apparatus 64 63. Diagnostic Tube \. 64 64. Position of Physician and Patient during Catheter Inflation 66 65. Correct Pathway of Catheter to Posterior Pharyngeal Wall 68 66. Correct Position of Catheter within Tubal Orifice 68 67. Incorrect Introduction of Catheter 68 68. Tongue Depressor (A) 68 69. Nasal Speculum (B) 68 70. Nasal Speculum (C) 68 71. Laryngeal Mirror (D) 68 72. Cotton Applicator (E) 68 73. Nasal Probe (F) 68 74. Politzer’s Acoumeter 74 75. Hartmann’s Tuning-forks 84 76. Large Tuning-fork 85 77. Kerrison’s Set of Tuning-forks 88 78. Galton Whistle 88 79. Barany’s Noise Apparatus.... 93 80. Auricular Perichondritis 102 81. Deformity Resulting from Neglect of Lesion Shown in Fig. 80 102 82. Hsematoma Auris, Resulting from Blow upon the Ear 103 83. Final Permanent Deformity Resulting from Hsematoma Auris 104 84. Lupus Hypertrophicus Auriculae 104 85. Herpetic Eruption due to Inflammation of the Geniculate Ganglion 106 86. Displacement of Left Auricle 110 87. Necrosis of Auricular Cartilage and Deformity Resulting from Extension of Infection from a Furuncle in the Canal 110 88. Furuncle Knife 113 89. Hyphomycetes, Moulds 116 90. Aural Syringe 119 91-93. Instruments for Removing Solid Substances from the Ear 121 94-96. Retracted Drum Membranes 148 97. Tubo-tympanic Congestion 149 98. Eustachian Cotton Applicator 152 99. Skull of Infant at Term 154 100. Skull of Adult 154 101-103. Acute Catarrhal Otitis Media, First, Second and Third Stages 163 104. Diagrammatic Picture of Membranous Partitions of Vault 166 105-108. Acute Purulent Otitis Media, Four Successive Stages 168 109. Incision of Membrana Tensa 174 110. Incision Indicated in Acute Purulent Otitis Media 179 111. Incision through Drum-head and Posterosuperior Canal Wall 179 112. Auricular Displacement Resulting from Postauricular Subperiosteal Abscess.. 186 113. Aural Ice-bag 189 ] 14. Leiter’s Coil 189 115. Bone Absorption Resulting from Cholesteatoma 197 116-124. Central Perforations 201 125-128. Marginal Perforations . . 203 ILLUSTRATIONS 129-131. Perforations of Shrapnell’s Membrane 203 132. Yankauer’s Eustachian Curette 209 133. Aural Polyp 210 134-137. Perforations of Long Standing 213 138. Thickening Due to Calcareous Deposits 227 139. Celluloid Bougies 231 140. Eustachian Catheter and Bougie 232 141. Eustachian Applicator 239 142. Yankauer’s Eustachian Applicator 240 143. Horizontal Section through Oval Window (Right), Dividing Stapedial Foot- plate, Vestibule, and Basal Turn of Cochlea 247 144. Horizontal Section through Stapes and Basal Turn of Cochlea 248 145. Horizontal Section through Right Oval Window 249 146. Diagrams Showing Line of Incision, and the Resulting Flap, Deflected 259 147. Bony Capsule of Labyrinth 260 148. Drawn from Metal Cast of Labyrinthine Cavity 260 149. Horizontal Section through Internal Auditory Meatus, Cochlea, and Vestibule. 261 150. Horizontal Sections through Modiolus from Base to Apex 262 151. Vertical Section through Tympanum, Vestibule, and Internal Auditory Meatus 263 152. Labyrinthine Vestibule, with Roof Removed 264 153. Relative Positions of Three Semicircular Canals 265 154. Membranous Labyrinth 266 155. Diagrammatic Section of Ampullar End of Horizontal Semicircular Canal Showing Position of Crista Acustica 267 156. Structures Common to the Crist* Acustic* and Macul* Acustic* 268 157. Diagrammatic Cross-section of Cochlear Canal 269 158. Organ of Corti 271 159. Inner and Outer Rods of Corti 271 160. Semicircular Canals of Pigeon 278 161. Diagrammatic Picture of Inner Tympanic Wall 281 162-166. Types of Vestibular Nystagmus 282 167. Revolving Chair: Patient and Physician in Position for Rotation Test 284 168-169. Author’s Scheme for Remembering Semicircular Canal Planes 285 170-172. Author’s Scheme for Remembering Exact Relative Positions of the Three Canals 286 173. Diagrammatic Picture of a Horizontal Section of Skull, Passing through Horizontal Semicircular Canals 287 174-177. Diagrams Showing Falling Directions in Relation to Vestibular Nystagmus 290 178. Diagrams Showing Different Forms of Rotation Nystagmus 291 179. Barany’s Fixator and Self-retaining Basin 301 180. Horizontal Section of Skull Passing through both Horizontal Semicircular Canals. Nystagmus During Rotation to Right 302 181. Nystagmus During Rotation to Left 302 182. After-nystagmus (i.e., Immediately Following Rotation to Right), Both Laby- rinths being Sound 302 183. After-nystagmus (i.e., Immediately Following Rotation to Left), Both Laby- rinths being Sound 302 184. After-nystagmus (i.e., Immediately Following Rotation to Right), Right Mem- branous Canal having been Destroyed by Disease 302 185. After-nystagmus (i.e., Immediately Following Rotation to Left), Right Mem- branous Canal having been Destroyed by Disease 302 186. Diagrammatic Picture of a Transverse Section of the Brain 329 187. Chart Showing Important Aphasia Centres 332 188. Otitic Pathways’of Pus to Brain or Meninges (Diagrammatic) 337 189. Semi-diagrammatic Picture Showing Section of Sigmoid Sinus and Separation of Dural Layers 341 190. Showing Perisinous Abscess 341 191. Showing Possible Pathways of Infection 341 192. Venous Channels of the Brain 356 193. Invasion of Brain through Tympanic Vault 362 194. Vertical Cross Section of Brain Showing Influence of Transmitted Pressure from Temporosphenoidal Abscess upon Motor Area Above (Diagrammatic) 869 195. Vertical Cross Section of Brain, Showing a Large Temporosphenoidal Abscess (Diagrammatic) 370 ILLUSTRATIONS 195a Vertical Cross Section of Brain, Showing Small Abscess Involving Internal Capsule (Diagrammatic) 370 196. Inferior Surface of Encephalon 398 197. Incision Indicated in a Suppurative Lesion Confined to the Atrium 399 198. Incision Indicated in a Suppurative Lesion Involving the Tympanic Vault 399 199. Incision Supplementing Inadequate Perforation 399 200. Incision Occasionally Indicated in Chronic Suppurative Otitis Media for the Evacuation of Pus Retained in the Vault 399 201. Vertical Section through External Auditory Canal and Tympanic Cavity 401 202. Diagram Showing Technical Error Likely to Result from an Incision made from Above Downward 401 203. Diagram Showing Double Movement (i.e., Downward and Inward) Required in Incising the Membrane from Above Downward 401 204. Dangerous Accident (Stapedial Dislocation) which May Result from an Inci- sion from Above Downward 402 205. Incision of Drum Membrane from Below Upward, the Correct Method 402 206. Correct Method of Holding Myringotome 404 207. Surgical Landmarks of Mastoid Cortex 407 208. Level of Safety in Opening Mastoid 408 209. Area Shaved for Mastoid Operation 409 210. Instruments Called for in any Surgical Operation 408 211. Self-retaining Retractors 409 212. Langenbeck’s Periosteal Elevator 409 213. Large Grooved Chisel, or Gouge (A) 408 214. Whiting’s Gouge (B) 408 215. Whiting’s Gouge (C) 408 216. Jansen’s Chisel (D) 408 217. Jansen’s Chisel (E) 408 218. Mastoid Mallet (F) 408 219. Mastoid Rongeurs 409 220. Mastoid Curettes 410 221. Richards’s Mastoid Curettes 411 222. Wooden Head-rest, or Block, for Use in Mastoid Surgery 412 223. Initial Incisions for Exposing the Mastoid Cortex 413 224. Mastoid Cortex Adequately Exposed for Operation 415 225. Position of Gouge in Removing Mastoid Cortex 416 226. Representing the Extent and Outline of the Initial Opening Usually Made with the Mallet and Gouge 416 227. Illustrating the Use of the Rongeur in Removing the Mastoid Cortex 417 228. Diagram Showing the Use of the Bent Probe in Locating the Aditus 418 229. Lines Representing Surgical Guides to a Very Small Antrum 419 230. Vertical Section through the Aditus 420 231. Mastoid Excavation Completed, Showing Extensive Development of Zygo- matic Cells 421 232. Line of Section Extending through Mastoid Process and Petrous Portion of the Temporal Bone 422 233. Pneumatic Spaces Extending from Mastoid Process to Apex of Petrous Bone... 423 234. Continuous Chains of Pneumatic Spaces Extending from Mastoid to Petrous Portion of the Bone 423 235. Iodoform Gauze Plugs for Control of Hemorrhage in Case of Accidental Open- ing of Sinus 425 236. Operation of Mastoidectomy Completed 427 237. Mastoid Bandage 427 238. Postauricular Incision for the Radical Operation 433 239-240. First Stages of Radical Operation 434 241. Jansen’s Chisel 435 242. Radical Operation 436 243. Radical Operation, after Removal of “Bridge” formed by Posterosuperior Canal Wall 437 244. Radical Operation, after Lower Half of Posterior Canal Wall has been Reduced so as to Appear as a Direct Continuation of the Facial Ridge . 438 245. Tympanic Floor 439 246. Ring Curette .. 440 ILLUSTRATIONS 247. Tympanic Structures Usually Exposed in Radical Operation ... 441 248. Stacke’s Operation 444 249. Stacke’s Protector 445 250. Kerrison’s Tympanic Rongeur 446 251-254. Diagrams Illustrating Plastic Operations Forming Part of Radical Operation 448 255. Narrow-bladed Knife Required in the Plastic Work of the Radical Operation .. 449 256. Instruments Essential in the Operation of Ossiculectomy 45 ) 257. Incision Lines in Ossiculectomy 458 258-261. Mosetig-Moorhof Operation, Four Successive Steps 459 262-265. Successive Steps of the Passau-Trautmann Operation 460 266-268. Author’s Operation for Preventing or Closing Postauricular Opening Fol- lowing Radical Operation 462 269. Section through Tympanum, Aquseductus Fallopii, and Ampullar Ends of Hori- zontal and Anterior Vertical Canals 463 270. Hinsberg’s Labyrinthine Operation 466 271. So-called “Solid Angle” 467 272. Vertical Section through Aditus and Vertical Portion of Facial Canal 468 273. Surgical Guides to Vestibule (Neumann’s Operation) 469 274. Radical Operation Preliminary to Opening Labyrinth 471 275. Excavation Preliminary to Uncovering Vestibule 472 276. Author’s Curette 472 277. Vestibule with Roof Removed 472 278. Horizontal Section through Cochlea 474 279. Bone Operation Preliminary to Exposure of Sigmoid Sinus 480 280. Position of Chisel in Uncovering the Sigmoid sinus 480 281-282. Rongeurs 481 283. Exposure of Sinus Wall Preliminary to Its Exploration 482 284. Position of Gauze Plugs for Controlling Hemorrhage when Sinus is Opened.... 483 285. Line of Incision for Jugular Resection 486 286. Internal Jugular Vein 487 287. Relations of Brain to Temporal Bone 490 288. Incision for Exposing Squama, Preliminary to an Exploratory Operation for Brain Abscess 493 289. Dural Exposure Preliminary to Exploration of the Brain for Suspected Tem- porosphenoidal Abscess 495 290. Narrow-bladed Knife for Exploring the Brain 496 291-292. Drawings Made from a Section of the Brain, Showing Schematically the Advantages of Exploring the Brain through Separate Incisions of the Dura as Compared with Exploratory Punctures in Different Directions through a Single Dural Incision 497 293. Whiting’s Encephaloscope 500 294. Gauze Wmk for Use in Brain Abscess 501 295. Chart Showing Directions and Depths of Exploratory Punctures of Cerebellum 503 296. Exposure of Dura Covering Cerebellum 504 297. Exposure of Dura Covering Cerebellum 505 298. Exposure of Facial and Hypoglossal Nerves 512 299. Lateral Implantation of Facial Segment into Hypoglossal Trunk 512 301. Anastomosis of Facial and Hypoglossal Nerves 513 301-303. Three Common Types of Macrotia 515 304. Supernumerary Cartilaginous Nodules 515 305. Supernumerary Nodules 515 305. Projecting Auricle; “Lop Ear” 516 307-308. Mierotia 517 309-311. Usual Method of Reducing an Abnormally Large Auricle 519 312-315. Operation for Reducing Abnormally Wide Auricle 520 316-318. Operation for the Correction of Moderate Projection 522 319-323. Ituttin’s Operation for Projecting Auricles 523 324-328. Duel’s Operation for Projecting Ears 524 329. Radiogram Showing Abscess at Roots of Two Incisor Teeth 559 330. Radiogram: Roots of a Bicuspid Tooth Projecting into Antrum of Highmore. . . 559 331. Radiogram Showing Imperfect (Partial) Eruption of Wisdom Tooth 559 332-333. Radiograms: Unerupted and Abnormally Placed Teeth 559 334. Area of Tumor Showing (X 80) Characteristic Architecture of the Fibrous Areas , 574 335-336. Characteristic Architecture of Fibrous and Recticular Areas 574 DISEASES OF THE EAR CHAPTER I. ANATOMY AND PHYSIOLOGY OF THE SOUND-CONDUCTING APPARATUS. Anatomically, the ear may lie divided into three parts,—viz., the outer ear (auricle and external auditory meatus), the middle ear (tym- panum and structures contained therein), and the inner ear, or labyrinth. Physiologically, the organ of hearing must be regarded as consisting of two distinct mechanisms,—viz. (1) a sound-conducting apparatus, having to do solely with the conduction, or transmission, of sound waves; and (2) a perceptive mechanism, an organ specialized for the reception and analysis of sound waves, and their appreciation as sound. From the view-point of the otologist, the latter is much the more prac- tical and useful division, suggesting at once the necessary separation of all aural disorders into two main groups,—viz. (1) those which originate in, or involve chiefly, the labyrinth or end-organs of the auditory nerve (labyrin- thine diseases); and (2) those depending upon pathological changes in some portion of the conducting mechanism (diseases of the conducting apparatus). The conducting apparatus is composed of the following structures: the auricle and external auditory meatus; the drum membrane, and ossicu- lar chain with the muscles and ligaments attached thereto; the tympanic cavity in which the ossicles are suspended, and the Eustachian tube. The perceptive apparatus includes: the auditory nerve, its nuclei of origin, trunk, association fibres, cortical nuclei, its terminal fibres in the cochlea, and the membranous cochlea itself. The Auricle, or Pinna (Fig. 1).=—The auricle is an irregularly ovoid structure which might well Vie described as an outer terminal expansion of the cartilaginous meatus. It is roughly convex posteriorly, concave anteriorly. It consists chiefly of a thin cartilaginous plate, covered by perichondrium, to which the integument is closely adherent. The lower dependent portion, containing no cartilage, is composed of connective tissue containing some fat cells, and is called the lobule, or lobe of the ear (Fig. 1, 10). The free margin of the cartilaginous plate is curled toward the anterior surface of the auricle, forming a narrow ridge which is called the helix (1). The helix begins in front just above the orifice of the meatus, and ends-behind at a point which marks the beginning of the posterior border of the lobule. Separated from the helix by a narrow curvilinear de- pression (the fossa of the helix, 2), and parallel with its posterior portion, is another elevation, known as the antihelix (4). The antihelix divides above into two arms, or crura, which inclose a triangular depression, the 1 2 ANATOMY AND PHYSIOLOGY fossa of the antihelix (3). The antihelix terminates below in a prominence directed forward and upward, called the antitragus (8). Opposite this, but directed backward and somewhat overlapping the orifice of the meatus, is another projecting lamella of cartilage, the tragus (7). The tragus and antitragus are separated below by a deep notch, the incisura intertragica (9). These structures—viz., the antihelix above and behind, the anti- tragus and incisura intertragica below, and the tragus in front—form the boundaries of a deep central depression, the concha (5). In the anterior part of the floor of this concavity is the orifice of the external auditory canal (6). -Helix (1) “Fossa of the helix (l) “Fossa of the antihelix (3) -Antihelix (*) “Concha (5) of external auditory meatus (6) -Tragus (?) -Antitragus (5) -Incisura intertragica (9) •Lobule of the ear (10 Fig. 1.—The auricle. The auricle varies greatly in size and shape, and also in the angle which its posterior surface forms with the side of the skull. Its cartilagi- nous frame consists of a single plate of reticulated cartilage, the various folds of which assist in the formation of the elevations and depressions described above (Fig. 2)-. Muscles of the Auricle.—These consist of two sets,—viz. (A) those which arise from the side of the head and are inserted into some portion of the auricle, their contraction serving to move the auricle as a whole; and (B) those which have both origin and insertion upon the auricle itself, their contraction serving to change its form or shape. (A) The muscles arising from the side of the head are three in number, —viz., the attrahens aurem, or auricularis anterior; the attolens aurem, or auricularis superior, and the retrahens aurem, or auricularis posterior. While man in the process of evolution has lost the voluntary control of these muscles, there are some partial exceptions to this rule, certain indi- viduals being able to move the ear in one or more directions (see Fig. 3), MUSCLES OF AUEICLE 3 (B) The second group of muscles—those having no attachment other than to the auricle itself—are six in number. Four of these—the helicis major, helicis minor, tragicus, and antitragicus—are attached to the an- terior, concave surface of the auricle, the other two—the transversus Helix Fossa of the helix Fossa of the antihelix Antihelix Crista helicis Concha Tragus - .Antitragus Fig. 2.—Auricular cartilage (from dissection by the author). auriculae and obliquus auris—being confined to its posterior surface. With the exception of the transversus auriculae and the obliquus auris, the form and distribution of all these muscles are clearly shown in the accompanying illustration (Fig. 3). Auricularis superior (attolens aurem) Auricularis anterior (attrahens aurem) Helicis major Helicis minor Tragicua- Auricularis posterior (retrahens aurem) Fig. 3.—The auricular muscles. Antitragicus The External Auditory Meatus.—The external canal in the adult consists of two parts,—(1) a membrano-cartilaginous tube, and (2) an inner bony tube, to which the former is joined. 4 ANATOMY AND PHYSIOLOGY The membrano-cartilaginous canal (Fig. 4) is an inward tubular exten- sion of the auricle. Its external orifice is just behind the tragus in the anterior part of the floor of the concha. Its cartilaginous walls are deficient in the upper and posterior part of the canal, this deficiency being supplied by firm connective tissue which is continuous internally with the periosteal lining of the bony meatus. The cartilaginous frame of the meatus con- sists of an irregularly tongue-shaped plate of cartilage, curved longitu- dinally into a tortuous trough, which gives form to the outer half of the external canal. Its outer side, or base, which is continuous with the cartilaginous concha, is curved into an incomplete ring, deficient above and behind, which represents the orifice of the cartilaginous meatus. From this point its mar- gins gradually converge to form the narrow strip of cartilage the inner end of which is firmly at- tached to the rough outer extremity of the bony meatus. At the outer end of the canal, then, the anterior wall, floor, and part of the posterior wall are formed of cartilage; but as it extends inward, the cartilaginous plate becomes nar- rower until at its junction with the osseous meatus only the floor is formed of cartilage. The cartilaginous canal is rendered less rigid by two—sometimes three—fissures, passing through its anterior wall. These fissures, more or less vertical in direction, and transverse to the long axis of the canal, are called the fissures of San- torini. They render the canal more pliable and lessen the amount of trauma in certain surgical operations requiring great displacement of the auricle. The general direction of the membrano-cartilaginous canal is inward and somewhat upward and backward. Development of the Osseous Meatus.—The external auditory canal presents marked differences in the adult and the infant at term. In order to obtain a clear view of the anatomy of the conducting apparatus, it is neces- sary to refer briefly to the development of the temporal bone, and trace cer- tain changes which it undergoes between birth and the middle of the fourth year, when it attains essentially the adult type. At birth the temporal bone is separable into three distinct parts,—the petromastoid, the squamo- zygomatic, and the tympanic. A fourth part, the styloid process, is carti- laginous at birth, and forms no part of the organ of hearing (see Plate I). In the primordial, or cartilaginous, skeleton there is but one repre- sentative of the future temporal bone,—viz., the so-called cartilaginous ear-capsule, which encloses the otic vesicle and its outgrowths (cochlea and semicircular canals), and therefore constitutes the essential part of the organ of hearing. This is later converted by numerous centres of ossification (Hertwig-Mark) into the os petrosum, or petromastoid. On the outer surface of the os petrosum (Plate I, 5) is an irregular depression Fig. 4.—Auriculo-meatal carti- lage, showing narrow strip of car- tilage entering into the formation of the membrano - cartilaginous meatus. DEVELOPMENT OF OSSEOUS MEATUS 5 Plate I. Fig. 5.—Petromastoid: o, antrum; b, tegmen tympani; c, tympanic vault; d, incus; e, tympanic floor. Fig. 6. — Squamozygomatic, outer surface: a, superior plate; b, Rivinian notch; c, inferior plate. Fig. 7.—Right tympanic ring, outer surface. Fig. 9.—Temporal bone: a, squa- mozygomatic; b, tympanic ring; c, petromastoid bone, posterior half; d, inner tympanic wall; e, Rivinian notch. This figure shows the rela- tively enormous size of the infant tympanic cavity which is practically of the same size as in the adult. Fig. 8. — Squamozygomatic, inner surface: o, inner horizontal plate (which forms part of the floor and the mid-cranial fossa); b, Rivinian notch. Fio. 10.—Infant skull, showing oblique position of the tympanic ring and drum membrane. 6 ANATOMY AND PHYSIOLOGY or concavity, which represents the cavity of the middle ear,—its bounda- ries constituting the inner wall, floor, roof, and also parts of the anterior and posterior walls of the tympanum. The tympanic cavity is completed by the squama and tympanic ring, which, with the drum membrane, form what in the adult becomes the outer tympanic wall. The tympanic ring and squamozygomatic portion of the temporal bone have no developmental relation to the cartilaginous cranium, being developed, each from a single centre of ossification (Heisler), from the connective tissue of its enveloping membrane. The tympanic ring (Plate I, 7) at birth is a small, somewhat flattened ring of bone, which is deficient in its upper and anterior eighth. Its inner concave margin presents a groove (sulcus tympanicus) for the attachment of the tympanic mem- brane, or membrana tensa. The tympanic ring is applied against the outer surface of the os petrosum, shutting in the lower and outer part of the infant middle-ear cavity. Firm osseous union occurs during the first year of life. The squamozygomatic (Plate I, 6) in the new-born infant is a flat plate of bone which externally is divided into two surfaces by the small zygomatic process. Above the zygoma is the shell-like lamina of bone which forms part of the outer wall of the mid-cranial fossa. Below the zygoma, the squama is formed of two plates, an outer and an inner. The outer plate, passing downward and somewhat inward from the level of the zygoma, forms the outer wall of the tympanic vault. Its lower border is concave, and, by articulation with the two extremities of the tympanic ring, completes the bony circle surrounding the drum membrane. The bony ring thus formed is of irregular outline. That part of it formed by the lower margin of the outer plate of the squama is ungrooved and does not give attachment to the membrana tensa, or drum membrane proper. It represents the arc of a small circle, and is known as the Rivinian segment (Plate I, 9, e). The tense membrane (membrana propria) is attached only to the grooved concave margin of the tympanic process and between its upper margin and the lower margin of the squama is a space known as the Rivinian notch (9, e). This space in the living subject is closed by the membrana flaccida, or Shrapnell’s membrane, to be described later. The inner, or horizontal, plate of the squama bends inward at about the level of the zygoma, and, by articulation with the tegmen tympani, enters into the formation of the floor of the middle fossa of the skull (8, a). The articulations of the bones which unite to form the infant temporal bone are clearly indicated by the illustrations of Plate I. Fig. 9 shows the temporal bone of an infant a few weeks old. It does not, however, cor- rectly indicate its position when in articulation with the other bones of the cranium. This is better shown by Fig. 10, in which the drum membrane is shown foreshortened by its very oblique position. In fact, so nearly do the tympanic ring and drum membrane approach the horizontal plane at birth that they seem to constitute the inferior, rather than the outer, wall of the tympanic cavity at this stage of tympanic development. The external auditory canal and drum membrane of the infant at term present the following differences from the adult type: (1) There is no bony DEVELOPMENT OF AUDITORY CANAL 7 meatus; the drum membrane is, therefore, not protected by its position at the fundus of a bony canal, but lies in the same plane as the outer inferior surface of the skull. Its position more nearly approaches the horizontal plane than in the adult. (2) The entire external canal is mem- brano-cartilaginous; its direction is outward and upward, so that the drum membrane and the roof of the meatus are nearly in the same plane. The floor of the canal is in contact with the roof. These facts have a practical bearing upon the examination of the ears of infants, it being necessary by downward traction of the lobe to draw the inferior wall away from the roof, and change the direction of the canal so that the drum membrane may be brought into view. Post-natal Changes.—Shortly after birth the following changes are inaugurated: By deposition of new bone upon the outer surface of the tympanic process or ring, this bone is converted into a bony trough, which forms the anterior wall, floor, and greater part of the posterior wall of the bony canal. That the conversion of the tympanic ring into a partial canal is effected solely by deposition of new bone upon its outer surface is evidenced by the position of the sulcus tympanicus, which remains un- changed,—i.e., at the inner margin of the canal. Coincidently with these changes in the tympanic ring, the roof of the osseous meatus is formed by Fig. 11.—Infant temporal bone. Fig. 12.—Adult temporal bone the following changes in the squama: The outer plate is gradually bent inward at the level of the zygoma, thus forming an angle with the superior, parietal plate and finally in the adult bone assuming a position nearly, but not quite, horizontal. That the superior wall of the bony meatus results largely from this bending of the outer plate of the squama, rather than from massed deposition of bone at any particular point, is shown by the changed relation of the posterior root of the zygoma, which at birth is 5 to 6 mm. above the upper margin of the tympanic orifice, and in the adult marks the upper boundary of the bony meatus (Figs. 11 and 12, a). 8 ANATOMY AND PHYSIOLOGY These changes progress with remarkable rapidity, so that early in the second year of life the drum membrane is located at the fundus of a short, incomplete, but well-defined canal. Coincident with the development of the bony canal, changes quite as marked are taking place in the membrano- cartilaginous meatus. As the tympanic ring is built out into a bony trough, the anterior wall, floor, and posterior wall of the membranous meatus are drawn downward and outward, becoming adherent as a mem- brano-cutaneous lining to the walls of the osseous canal. The floor of the membranous meatus is, therefore, no longer in contact with the roof. At the end of the first year, the interior of the meatus in its natural position no longer presents the appearance of a transverse slit as at birth, but of a tube with a well-defined lumen. The Osseous Meatus.—In the adult the bony canal presents fairly constant characteristics. Its four walls—i.e., the superior, anterior, infe- rior, and posterior—differ in structure, conformation, and length. The superior wall, or roof, is formed of the outer plate of the squama, its direction from without being inward and slightly downward. The an- terior wall and floor are formed of very dense bone, and developed wholly from the tympanic ring. They are markedly convex in the direction of the long axis of the canal. The greatest convexity of both the anterior wall and floor is found at a point nearer the inner than the outer extremity of the canal. This is the narrowest part of the bony meatus and is called the isthmus. Beyond the isthmus, the floor dips strongly downward to the point of attachment of the inferior margin of the drum membrane, forming a depression, or sulcus, in which foreign bodies if small may be hidden from view. The posterior wall is composed in part of the dense tympanic plate, and partly of the premastoid plate from the outer lamella of the squama. A consideration of the relative length of the different walls of the canal helps one to appreciate the oblique position of the drum membrane. The anterior wall is longer and projects 5 or 6 mm. further inward than the posterior wall, and the floor projects further inward by 5 or 6 mm. than the roof. As the inner, terminal margins of these walls merge into the elliptical frame or groove which supports the drum membrane, it is obvious that the latter occupies a plane which forms an obtuse angle with the superior and posterior walls, and an acute angle with the anterior wall and floor. The drum membrane is, therefore, not placed vertically or at right angles to the long axis of the canal, its outer surface looking outward, downward, and forward. Politzer gives the average length of the four walls of the bony canal as follows: superior wall, 14 mm.; inferior wall, 16 mm.; posterior wall, 15-16 mm.; and anterior wall 17-18 mm. Some years ago the author made careful measurements of a series of bones with a view of determin- ing the length of the postero-superior canal wall,—i.e., taken from the annulus tjunpanicus internally to the spine of Henle externally,—and found variations between 12 and 18 mm., the average being 14.5 mm. Obviously the length of the bony canal is subject to very considerable LENGTH OF AUDITORY CANAL 9 variations in different individuals. Cross section of the outer third of the bony meatus shows it to be of rather circular form, whereas internally— i.e., beyond the isthmus—it becomes elliptical. The external auditory canal as a whole presents great variations in different individuals. Some are wide and sufficiently straight to allow easy inspection of the drum mem- brane, while others are narrow and present curves necessitating con- siderable manipulation in order to bring the lower half of the drum membrane into view. The length varies from 1 to 134 inches, 134 inches being about the average. Of this the bony canal forms rather less than half. The membrano-carti- laginous portion is somewhat curled upon its long axis, and is rather wider in its central portion than at its orifice in the concha or at its junction with the bony meatus. The long axes of the two portions of the canal are not in the same straight line, the membrano-carti- laginous part being directed inward and slightly upward and backward, and the osseous canal inward and slightly downward and forward. It is often necessary, therefore, in order thoroughly to inspect the drum membrane, to draw the auricle upward and backward, thus bringing the two portions of the canal into the same straight line and the lower portion of the membrana tympani into view. The integument lining the auditory canal is continuous externally with that of the concha, and internally with that covering the outer sur- face of the drum membrane. The skin covering the drum membrane and canal seems to grow eccentrically from a point at the centre of the mem- brana tympani, light substances—e.g., small disks of paper—attached to any part of the drum membrane being found to travel first to its periphery and thence along the wall of the canal to the concha. The integument is much thicker in the membrano-cartilaginous than in the bony meatus. In the membranous canal it is from 1 to 134 mm- m thickness, and contains hair-follicles, sebaceous glands, and numerous ceruminous glands. The latter are arranged thickly in the posterior Avail and floor. The ducts of the ceruminous glands may open either directly into the auditory canal or into the hair-follicles. The Tympanum.—The tympanum (tympanic or middle-ear cavity) is the name applied to the bony space which contains the ossicular chain. Fig. 13.—Diagram: dotted lines showing influ- ence upon direction of canal of drawing auricle upward and backward. 10 ANATOMY ANI) PHYSIOLOGY Its outer wall is composed largely of the drum membrane, and but for this structure it would be open to the outside air by way of the external audi- tory canal. It does communicate with the nasopharynx by means of the Eustachian tube. The roof of the tympanum lies on a plane considerably higher than the roof of the bony meatus, and its floor lies below the level of the floor of the bony canal. This fact has led to its being considered as composed of three parts,—namely: (1) The vault (attic, epitympanic space), or that portion of the tym- panic cavity lying above the level of the short process of the malleus. (2) The atrium, or that portion of the middle-ear cavity the upper and lower boundaries of which are horizontal lines, or planes, passing through the upper and lower margins of the membrana tensa. (3) The hypotympanic space, or that part lying below the level of the floor of the bony canal (Fig. 14). Fig. 14.—Vertical section through tympanic cavity and bony meatus. Above line A-B, tympanic vault. Between lines A-B and C-D, atrium. Below line C-D, hypotympanic space. The tympanum, or middle ear, viewed as a whole, is an irregularly wedge-shaped cavity, lying for the most part between the outer surface of the petrous bone and the drum membrane. Its greatest diameter is the vertical; its smallest is from without inward,—i.e., from the drum mem- brane to the inner tympanic wall. Its roof corresponds in position with the floor of the middle cerebral fossa; its floor is in relation with the jugular fossa which lodges the bulb of the jugular vein. The roof is much wider— from without inward—than the floor, which measures but 2 to 3 mm. The gradual convergence from above downward of the outer and inner ANATOMY’ OF TYMPANUM 11 walls brings the cavity of the tympanum somewhat into the form of a wedge, the edge of which—directed downward and inward—corresponds with the tympanic floor. The tympanic cavity presents six walls, which call for careful study. The Inner Wall (Fig. 15).—The inner wall of the tympanum is formed by the outer surface of the petrous bone. It presents the following important landmarks: At a variable distance above the mid-point between the roof and floor is a well-marked ridge running from before backward (Fig. 15, a), and forming a natural boundary line between the inner wall of the vault and the inner wall of the atrium. This is formed by the outer wall of the Fallopian canal, which lodges the facial nerve. Just below the posterior half of the facial ridge is an oval depression, the fossa ovalis, at the bottom of which the oval window (Fig. 15, b) is plainly visible. The long diameter of the oval window is horizontal. It leads inward and Facial ridge (a) Oval window (6) Incomplete canal for tensor tympani muscle (/) Prominence of horizontal semicircular canal (c) Orifice of Eustachian canal (e) Round window (d) Fia. 15.—Inner tympanic wall (drum membrane and outer bony wall of tympanic vault removed). somewhat backward into the central cavity of the bony labyrinth (vesti- bule). In the living subject it is closed by the foot-plate of the stapes. Below the oval window the inner wall bulges into the cavity of the atrium, forming a rounded eminence, convex from above downward, called the promontory. This prominence is formed by part of the first turn of the cochlea. In form it resembles roughly the lateral half of a cone divided longitudinally from apex to base, the apex being directed forward and the base backward. Immediately behind the promontory, and belowr anti some- what behind the oval window, is another depression, the niche of the round window (15, d). From this niche a somewhat circular orifice, the fenestra rotunda, leads forward and inward into that portion of the spiral tube of the cochlea known as the scala tympani. The round window is closed by 12 ANATOMY AND PHYSIOLOGY a delicate membrane which has received the name membrana tympani secundaria (Scarpa). Again comparing the promontory to a divided cone, we find that the apex is lost near the junction of the inner and anterior walls, or rather where the anterior wall merges into.the funnel-shaped orifice of the Eustachian tube (e). Just above the Eustachian tube is the canal for the tensor tympani muscle. That portion of the tensor tympani canal presenting upon the inner wall of the tympanum is usually incom- plete (15, /). It passes obliquely upward and backward above the prom- ontory to a point in front of the anterior end of the oval window. Here it terminates in a thin lamella of bone, curled somewhat outward (processus cochleariformis), around which the tendon of the tensor tympani turns to pass outward and downward to its attachment to the hammer handle. Passing now to the vault, we find just above and parallel with the posterior end of the facial ridge a linear elevation of the inner wall. This elevation marks the position of the external or horizontal semicircular canal. It occurs not as a distinct ridge, but simply as a longitudinal bulging of the inner wall at this point (15, c). It is characterized chiefly by the smooth and ivory-like density of the bone in this situation. The Superior Wall (Fig. 16).—The roof of the tympanum is of surgical interest chiefly from the fact that its upper surface forms part of Floor of mid-cranial fossa" -Roof of tympanum Antrum- 'Tympanic vault Posterior wall of bony meatus*1 SBony external auditory meatus Fig. 16.—Tympanic roof. the floor of the middle cerebral fossa. It is of varying thickness in differ- ent bones, is often exceedingly thin, and occasionally exhibits defects of continuity (apertures), in which case the cavity of the middle ear is sepa- rated from the middle fossa of the skull only by loose connective tissue. The plate of bone forming the roof is a direct continuation of that covering the superior surface of the petrous bone. Externally it is united to the ANATOMY OF TYMPANUM 13 inner horizontal plate of the squama, forming the petrosquamosal suture, which is plainly visible in infancy and occasionally persists in adult life. A statement repeated in several text-books is to the effect that the inner horizontal plate of the squama enters into the formation of the tympanic roof. This statement is not correct. In any temporal bone in which the petrosquamosal suture can be recognized, it will be found that, if we make a vertical perforation downward through this suture, the instrument will appear below in the bony meatus and not in the tympanic cavity. The roof of the tympanum is formed, therefore, wholly by the superior plate of the os petrosum. The Anterior Wall (Fig. 17).—The upper and lower limits of the ante- rior wall of the tympanum are not clearly defined. Superiorly it merges by a gentle curve into the roof, and below it presents no angle of junction or natural landmark separating it from the tympanic floor. Internally and externally its limits are clearly defined by the inner and outer walls. It presents two prominent landmarks,—namely, the mouth of the Eusta- chian tube and the canal for the tensor tympani muscle. Two or three Canal for tensor tympani 'muscle (c) Processus- cochleariformis (6) Orifice of Eustachian canal (a) Fig. 17. Vertical section of temporal bone, showing anterior wall of tympanum. mm. above the level of the tympanic floor is the tympanic orifice of the Eustachian tube (Fig. 17, a). The length of this bony canal averages about 12 mm. Its direction from the tympanum is forward, inward, and downward. Just above the Eustachian orifice is the beginning of the tympanic portion of the canal for the tensor tympani muscle (c), which has already been described in connection with the inner tympanic wall. This canal begins at the base of the skull in the anterior part of the petrous bone. In its passage through the petrous bone it lies just above and internal to ANATOMY AND PHYSIOLOGY 14 the Eustachian canal, from which it is separated by a thin lamella of bone. The lower portion of the anterior tympanic wall is in relation to the canal for the internal carotid artery. In this situation the bony plate separating the middle-ear cavity from the artery is in some bones exceedingly thin. The Posterior Wall (Fig. 18).—The posterior wall presents two portions which must be examined separately, — namely, the posterior wall of the vault and the posterior wall of the atrium. The posterior wall of the vault presents centrally a large, irregularly triangular opening the base of which is directed upward and the apex downward. This tri- angular opening is known as the aditus ad antrum, and marks the divid- ing line between the tympanic vault and the so-called mastoid antrum. Ampulla of horizontal semicircular canal Labyrinthine vestibule' _ Posterior wall of vault, “showing aditus ad antrum Internal auditory meatus- Posterior wall of "bony meatus Tympanic floor* 'Posterior wall of atrium Fio. 18.—Section showing posterior wall of tympanum. The antrum in reality is nothing more than a posterior prolongation of the vault. The posterior wall of the atrium is narrow from within out, its greater diameter being the vertical. Its chief landmark is a small pyra- midal process (processus pyramidalis) which projects forward into the atrium a little above the mid-point between the round and oval windows. It incloses a canal which contains the stapedius muscle, and presents at its apex a small opening through which the stapedius emerges to pass forward to its attachment to the neck of the stapes. The Inferior Wall (Fig. 19).—The floor of the tympanum is a nar- row space inclosed between the lower segment of the annulus tympanicus externally and the inner wall of the hypotympanic space internally. Viewed from above downward, it appears as a narrow depression, 5 to 7 mm. long and 2 to 3 mm. wide, containing more or less cancellous or di- ploic tissue. This diploic tissue throws into clear relief the hard, compact bone of the floor of the osseous canal, which forms its outer boundary. The floor of the tympanum is in relation anteriorly with the canal for the internal carotid artery, posteriorly with the jugular fossa. The bony plates separating the hypotympanic space from the artery in front and ANATOMY OF TYMPANUM 15 the bulb of the jugular vein behind are sometimes exceedingly thin. More- over, cases have been observed in which, as a congenital defect or as a result Floor of middle ear Floor of bony meatus Fig. 19.—Horizontal section through tympanum, showing tympanic floor. of necrosis, defects in the tympanic floor have allowed one or the other of these vessels to protrude into the lower part of the tympanic cavity,—a fact which, though exceedingly rare, should be borne in mind in carrying out any surgical measures in this region. The External Wall.—It now remains to be explained how this irregular but perfect little cavity is closed externally. The outer wall is Tympanic vault Marginal bony portion of m outer wall of tympanum, 'formed by original tym- panic ring Fig. 20.—Inner, or tympanic, view of drum membrane formed chiefly by the membrana tympani; but, since the middle ear ex- tends in all directions somewhat beyond the limits of the drum membrane, 16 ANATOMY AND PHYSIOLOGY there is a peripheral frame of bone which must be accounted for as part of the outer wall. This in the atrium and hypotympanic space consists of the inner surface of the tympanic ring. In the vault the outer wall is formed of the thickened inner edge of the outer inferior plate of the squama. This presents usually a fairly compact surface of bone (Fig. 20). The Annulus Tympanicus.—The inner margin of the bony meatus forms an irregular ring (annulus tympanicus), to which the drum mem- brane is attached. Owing to inequalities in the lengths of the different walls,—the floor and anterior wall being longer and extending further inward than the roof and the posterior wall,—this ring is irregularly ovoid or elliptical in shape, the long axis of the ellipse being from above down- ward and forward. These peculiarities also explain the oblique position of the drum membrane, which is not at right angles to the long axis of the bony meatus but forms decidedly obtuse angles with its roof and posterior wall. The Drum Membrane.—The membrana tympani is the strong lamina of fibrous tissue which forms the outer boundary of the middle ear. It is covered externally by integument continuous with that lining the ex- ternal auditory canal, internally by mucous membrane continuous with that covering the tympanic walls. Centrally it is drawn inward by the lower end of the hammer handle, to which it is attached, so that its outer surface is concave. It is attached peripherally to the concave margin of the annulus tympanicus, so that it necessarily assumes the oblique posi- tion of that bony ring, its outer surface looking outward and also strongly downward and forward. So intimately is it connected with certain parts of the malleus that it is impossible to give any practical description of the drum membrane without assuming some knowledge of the anatomical peculiarities of that little bone. We shall pause, therefore, in order to describe briefly the ossicular chain. The Ossicles.—The auditory ossicles are a system of little articulated bones, three in number, which connect the drum membrane with the labyrinth. The malleus, placed externally, is directly connected with the drum membrane; the stapes, the smallest of the three, presents a flat- tened bean-shaped surface which fits into and closes the oval window; and the incus, or middle bone, articulates externally with the malleus and internally with the stapes, thus forming a chain of movable levers which responds easily to the slightest movements of the drum membrane and transmits all sonorous impressions through the oval window to the laby- rinth and end-organs of the auditory nerve. The malleus, or hammer (Plate II, 22), is the only one of the ossicles which is in direct contact with the drum membrane, and is therefore the only one which can invariably be seen through the auditory canal. The head (22, A) is the upper, rounded portion which articulates with the body of the incus. It is smooth in all its aspects except the posterior, which presents an irregular surface for articulation with a rough depression on the anterior surface of the incus. It terminates below in a constricted THE AUDITORY OSSICLES 17 Plate II. Fig. 21.—Ossioles, right and left, only slightly enlarged above actual size. Fig. 22.—Malleus, enlarged; A, head; B, articular process; C, cog-process; D, neck; E, hammer handle; F, umbo, G, short process. Fig. 23.—Incus; A, body; B, short process; C, long arm; D, cog-process. Fig. 24.—Stapes; A, head; B, neck; C,C, crura; D, foot-plate. Fig. 25.—Ossicles in articulation; A, cog-processes in apposition; B, incudo-stapedial joint; C foot-plate. 18 ANATOMY AND PHYSIOLOGY portion, the neck (22, D). Passing downward and backward from the neck is a narrow shaft of bone called the hammer handle, or manubrium mallei (E). The handle presents two rather sharp edges,—an external edge attached to the drum membrane, and an inner edge directed toward the inner tympanic wall. These two edges are separated by two compara- tively broad surfaces which are directed forward and backward respectively. At its lower extremity the hammer handle broadens into a somewhat flattened surface of bone called the umbo (F). At the beginning of the external margin of the hammer handle, or rather at its junction with the neck, is a short, pointed process of bone, directed outward and somewhat forward and upward, the short process (G). This also is in contact with the drum membrane, which it pushes before it into the cavity of the audi- tory canal. As viewed by reflected light through the auditory meatus, it appears as a small, whitish glistening projection in the upper anterior quadrant of the membrana tympani, and constitutes one of the most constant and useful landmarks. From the anterior surface of the neck, a slender spiculum of bone passes forward and slightly downward, its an- terior extremity lodging in the Glaserian fissure (see mallei in small figures, Plate II, 21). This is the long process of the malleus, or processus foli- anus. It is always present at birth, but is usually absorbed later in life. Its position is identical with that of the anterior ligament of the malleus, which usually surrounds it. The incus (Plate II, 23) is the central link of the ossicular chain. It consists of a body and two processes. The body (23, A) with the short process (B) forms an irregular cone, flattened from without inward, and presenting on its anterior surface, or base, a rough depression for articula- tion with the head of the malleus. Posteriorly the body terminates :n a somewhat pointed extremity, the short process of the incus (23, B). Ex- tending downward from the anterior inferior corner of the body, and almost at right angles with its long axis, is a slender shaft of bone, the long arm (23, C). When the ossicles are in normal position, this process extends downward and backward, and is almost parallel with the manubrium mallei. Its lower extremity hooks sharply inward, and terminates in a rounded surface for articulation with the head of the stapes. This is known as the lenticular process. The stapes (Plate II, 24) is the smallest and—functionally at least— the most important of the three ossicles. It resembles almost perfectly a stirrup in form, and consists of a head (A), neck (B), two crura (C), and a bean-shaped plate of bone, the foot-plate (D), which fits into and closes the oval window. The foot-plate varies somewhat in size and shape in differ- ent individuals to conform to variations in the size and shape of the oval window. The arms, or crura, arise from either end of the outer surface of the foot-plate, and gradually converge to meet in a small button-shaped process, the head. Between the head and the point of junction of the two crura is a circular constriction, the neck. Upon the outer surface of the head is a very slight depression, or facet, which receives the lenticular THE MEMBRANA TYMPANI 19 process of the incus. When the foot-plate is in its normal position within the oval window, the whole ossicle is somewhat depressed within the oval niche, the head extending but slightly into the cavity of the atrium. We are now in a better position to study the structural peculiarities of the membrana tympani, which the accompanying diagram may help to make clear. As stated in a foregoing paragraph, the drum membrane is composed of three layers,—an external cuticular, a middle fibrous, and an internal layer of mucous membrane. The outer, cuticular layer is easily separated from the underlying fibrous membrane, as is frequently shown by its early exfoliation when the drum membrane is the seat of an acute inflam- mation. The internal, mucous layer, on the other hand, is so closely adherent as to be practically inseparable. The drum membrane as a whole is divisible into two parts,—(1) the tense membrane, or membrana propria; and (2) the flaccid membrane, or Shrapnell’s membrane. The membrana tensa forms the outer wall of the atrium. It is attached peripherally to the sulcus tympanicus, or that portion of the annulus tympanicus which represents the original auditory process, or tympanic ring. Toward the upper and anterior pole of the drum membrane is seen in the living subject a small knob-like projection. This is the short process of the malleus (Fig. 26, D). Extending downward and backward from Posterior attachment stria of Prussak (A) Shrapnell’s membrane, inclosing the Rivinian notch, also spoken of as Prussak’s space (B) 'Rivinian segment (O Posterior extremity of_ tympanic ring (B) Anterior extremity of tympanic ring (£) Posterior fold of membrana_ tympani (K) Anterior attachment stria ’of Prussak (A) ’Short process (D) Radiating fibres (J) - ■Hammer handle (E) ■ Umbo (F) Annulus tympanicus (f) - ■Radiating fibres (0) Circular fibres (H) - Fia. 26.—Diagrammatic picture of the membrana tympani and its attachments. the short process to the centre of the drum membrane is a line showing the position of the hammer handle (26, E), the lower terminal expansion of which is known as the limbo (F). The middle fibrous layer of the drum membrane is confined to the membrana tensa. It is composed of two layers,—an outer layer of radiating fibres (G, J), and an inner layer of circular fibres (H). The outer, radiating fibres are attached centrally to 20 ANATOMY AND PHYSIOLOGY the umbo and to some extent also to the lower half of the hammer handle, from which central attachment they radiate toward the periphery of the membrane. They are therefore more closely arranged at the centre, and for this reason appear thicker and more numerous here than at the peri- phery. The inner circular fibres are arranged in concentric circles about the umbo. They are very sparsely distributed toward the centre of the membrane, but are much more numerous in the outer circles. In the upper part of the membrane they cross the radiating fibres in considerable numbers. The circular fibres are said to collect at the periphery and, together with certain cartilage-cells and tough connective-tissue fibres, aid in forming the thickened peripheral margin (annulus tendinosus) which is inserted into the tympanic ring. The membrana propria (M. tensa) is inserted into the tympanic groove throughout the entire extent of the original tympanic ring. Between the anterior and posterior extremities of the tympanic ring (spina tympanica major and spina tympanica minor), the upper margin of the membrana tensa has no bony attachment except to the short process of the malleus. In the living subject this upper margin is sometimes indicated by two delicate lines radiating from the short process, one leading forward to the spina tympanica major and the other leading upward and backward to the spina tympanica minor. These two lines (A, A) are known as the attachment striae of Prussak. Between Prussak’s striae below and the Rivinian segment above, is a small, somewhat fan-shaped space known as the Rivinian notch (B). This space is inclosed by the membrana flaccida (Shrapnell’s membrane), next to be described. Below the posterior stria of Prussak, and more horizontal in direction, is a prominent fold of the drum membrane, always easily discernible, known as the 'posterior fold (K). It passes backward from the short process to the tympanic ring. Shrapnell’s Membrane.—The Rivinian space, or notch, is closed by a membrane which is thinner and less tense than the membrana tensa; hence the name, membrana flaccida. It consists’ chiefly of an outer cuta- neous layer continuous with the integument covering the membrana tensa and the roof of the bony meatus, and an inner layer of mucous membrane continuous with that lining the tympanic cavity. Between these there are a few interlacing fibres of delicate connective tissue, but there is no distinct layer of fibrous tissue. It is in reality a very small membrane which is sometimes difficult to outline in the living subject: that is to say, there sometimes seems to be no demonstrable space between the striae of Prussak and the inner margin of the roof of the bony meatus (incisura Rivini). Shrapnell’s membrane forms part of the outer wall of the vault, and measures, according to Politzer, \l/o, mm. vertically and 2 mm. transversely,—i.e., from before backward. The Ossicles, their Articulations and Relative Positions within the Tympanum (Fig. 27). — Before going further it is essential that the student should have a clear understanding of the position within the middle ear of the different parts of the ossicular chain. THE OSSICULAR CHAIN 21 The ossicles are lodged partly in the vault and partly in the atrium. In the vault are found the head of the malleus and the body of the incus. The remaining parts of the ossicular chain—i.e., the short process and handle of the malleus, the long arm of the incus, and the stapes—are located within the atrium. The Malleus.—The head of the malleus is lodged in the anterior part of the vault. Posteriorly it presents a rough surface for articulation with the incus. The neck of the malleus is on a level slightly below the inner margin of the roof of the bony meatus. Just below the outer ante- Short process of incus Head of malleus Posterior ligament of malleus’ B Anterior ligament of malleus Incudo-stapedial articulation Umbo Short process of malleus Fiq. 27.—Temporal bone with drum membrane and outer wall of vault removed, showing relative position and ligaments of the ossicles. rior surface of the neck, the short process projects into the cavity, or lumen, of the bony canal, pushing the drum membrane before it. An imaginary horizontal line tangent to the upper surface of the short process (Fig. 27, AB) marks the boundary line between the atrium and vault. Extending downward and backward from the short process is the hammer handle, or manubrium mallei. Its sharp external margin is connected with the drum membrane by means of a thin interposed layer of cartilage. Ligaments of the Malleus.—The head of the malleus is attached to the under surface of the tegmen tympani by a thin suspensory ligament. From the anterior surface of the neck and from the long process (pro- cessus folianus) a short, thick, fibrous band, the anterior ligament, passes forward to the spina tympanica major and Glaserian fissure, to which it is attached. It surrounds the long process which is commonly ab- sorbed in later life. The posterior ligament seems really to be a posterior fasciculus of the lateral ligament. It extends backward from the pos- terior surface of the neck to be attached to the outer wall of the vault. These two ligaments,—the anterior and posterior,—though not quite in the same straight line, are sometimes spoken of as the rotary axis band of the 22 ANATOMY AND PHYSIOLOGY malleus. They prevent lateral displacement of the malleus, and account for the constancy of the short process as a landmark of the drum mem- brane: the short process may change its position—i.e., revolve—as the malleus rotates about its axis band, but its location remains practically unchanged. The external ligament (ligamentum laterale) is attached to the outer surface of the neck above the short process, and spreads out, fan-shaped, to be attached to the outer bony wall of the vault. The Incus.—The body of the incus occupies the posterior half of the vault. Its posterior conical extremity, the short process, is lodged in a small depression, or facet (fossa incudis), in the posterior wall of the vault just below the aditus, or opening into the antrum. Both the fossa incudis and the articular surface of the short process are covered with thin layers of cartilage. The joint is held together by a strong cap- sular ligament and also by bands of fibrous tissue springing from the periosteum of the adjacent bone surfaces. Like the malleus, the incus is supplied with a suspensory ligament connecting its superior surface with the tympanic roof (Bruhl)1. The anterior surface of the incus articulates with the head of the malleus. Articulation of the Malleus and Incus (Plate II, 25).—In describ- ing this joint it is necessary to allude once more to certain points in the anatomy of the bones. The posterior surface of the head of the malleus presents an irregularly oblong and spiral depression, or groove, extending from above downward and inward to the neck. The lower end of this groove is bounded externally by a projecting point of bone which exerts inward pressure upon a somewhat similar point of bone on the incus. This is called the cog, or tooth-process, of the malleus (Plate II, 22, C). On the anterior surface of the body of the incus is a spiral ridge which conforms to, and is received into, the spiral groove of the malleus. Internal to the lower end of the incudal ridge is a triangular projection of bone (23, D), which is spoken of as the cog, or tooth-process, of the incus. When the bones are in normal articulation, the tooth-process of the malleus is in contact with that of the incus (Plate II, 25). The result of this mech- anism is that when the malleus rotates inward,—i.e., when the hammer handle moves inward,—the incus is made to execute a similar inward rotation; when, however, the malleus is forcibly rotated outward,—as in sudden forcible condensation of the air in the tympanum, sneezing, Val- salva inflation etc.,—the cog, or tooth-process, of the malleus separates from that of the incus and the joint opens, so that excessive outward ex- cursions of the hammer handle are not necessarily accompanied by corre- sponding excursions of the long arm of the incus. By this provision, the stapes is guarded against the influence of extensive outward movements of the drum membrane which might otherwise result in dislocation of the 1 Bruhl states that there are distinct suspensory ligaments connecting both the malleus and incus with the tympanic roof. As there is a difference of opinion, however, as to the usual presence of a suspensory ligament of the incus, such a ligament is not included in Fig. 27, the author himself never having seen it. THE OSSICULAK CHAIN 23 stapes from the oval window. The opposed articular surfaces of the mal- leus and incus are lined with cartilage. The joint is provided with a strong capsular ligament and is further strengthened by strong fibrous bands. The long arm of the incus passes downward and backward into the cavity of the atrium. It is behind and more or less parallel with the ham- mer handle, but is not in contact with the drum membrane. It is shorter than the hammer handle, usually terminating about the mid-point of the latter, or even at a higher level. The Incudo-stapedial Joint is in the upper and posterior part of the atrium (see Fig. 27, and Plate II, 25). The rounded lenticular process of the incus and also the depression on the head of the stapes are covered with hyaline cartilage, and are held together by a capsular ligament. Articulation of the Stapes with the Fenestra Ovalis.—The margins of the oval window and the edges of the foot-plate of the stapes are covered with a thin layer of cartilage, which is said also to line the vestibular surface of the latter. These surfaces are held together by an annular ligament consisting of elastic and connective fibres derived from the periosteum of the inner margins of the fenestra and passing to the foot- plate of the stapes. The annular ligament is much wider in front than behind. So far as the writer knows, the ossicular chain is the only system of movable joints in the body the movements of which are not under the control of voluntary muscles. Aside from their minute size, the articular structures of these joints are the same in kind as are found in connection with the larger bones elsewhere. The movements of the ossicles, however, are initiated and maintained altogether by forces originating outside the body,—i.e., aerial vibrations set in motion by some vibrating body. The ossicular ligaments seem, therefore, to play a particularly important role, for they not only hold the joint surfaces in proper apposition, but serve to limit the activity of each ossicle to that particular form of motion to execute which is apparently its sole function. The Intra=tympanic Muscles. — The stapedius (Fig. 28) is a small muscle, about 5 or 6 millimetres long, the belly of which is enclosed in the bony canal of the eminentia pyramidalis. This canal is buried in the premastoid plate, lying in front of and parallel with the descending portion of the facial canal. Its upper extremity curves forward and appears upon the posterior wall of the tympanum as a very small bony prominence known as the eminentia 'pyramidalis (Fig. 28), the apex of which is just behind the oval window. The muscle arises from the walls of this canal, its fibres converging above into a tendon which emerges through a small orifice in its apex. From this point it passes forward to be attached to the head of the stapes and lenticular process of the incus. The canal of the pyramidal eminence communicates by a small orifice with the facial canal behind it, and through this a small branch of the facial nerve passes to supply the stapedius muscle. 24 ANATOMY AND PHYSIOLOGY The Tensor Tympani Muscle (Fig. 29)—This muscle is from 18 to 20 millimetres long. It arises chiefly from the walls of an incomplete bony canal lying just above the osseous portion of the Eustachian tube, from the superior wall of the cartilaginous part of the Eustachian canal, and also by a few fibres from the inferior surface of the petrous bone. Its Stapedius muscle Oval window Hammer handle' Eminentia pyramidalis Pyramidal emi- nence and sta- pedius muscle Tensor tjt "pani mutt Round window Round window Fig. 28.—Tympanum of infant six months old. (Left.) Fig. 29.—Tympanum of infant six months old. (Right. tendon passes backward and upward across the inner wall of the tympanum, and emerges from its bony canal in front of the anterior end of the oval window. Here it curves around the processus cochleariformis and passes outward to be attached to the upper part of the handle of the malleus (Fig. 29). It is supplied by the fifth nerve. The Lining Membrane of the Tympanum. — The mucous mem- brane lining the tympanic cavity is directly continuous through the Eu- stachian tube with that of the nasopharynx. Histologically it varies in character in different parts of the tympanum. Over the promontory it is of the cuboidal variety, while on the anterior half of the floor, and in the vicinity of the tympanic orifice of the Eustachian tube, it consists of cili- ated cylindrical cells (Politzer, Gruber). In the vault the cells are of the squamous variety, this type being continued into the aditus and antrum and persisting throughout the lining membrane of the mastoid cells. Beneath the epithelial, or mucous, layer are two layers of closely related connective-tissue fibres, the deeper of which is in contact with the osseous walls of the tympanum and constitutes their periosteal lining. The peri- osteal layer is very richly supplied with blood-vessels. Within the atrium the mucoperiosteal lining is for the most part smooth and very closely applied to the tympanic walls. In the vault, on the other hand, the mucosa is thrown into folds and reduplications, some of which hang down from the tegmen tympani and cover the bodies of the malleus and incus. The Pouches, or Pockets, of the Membrana Tympani.—There are three fairly constant and partially closed spaces (pockets, pouches) in relation to the drum membrane, which now must be described. The THE POCKETS OF THE DRUM MEMBRANE 25 first is a small space lying between the neck of the malleus internally and Shrapnell’s membrane externally. It is bounded above by the external ligament of the malleus, internally by the neck of the malleus, below by the superior surface of the short process, and externally by the membrana flaccida. It is called Prussak’s space, its location being indicated upon the outer surface of the drum membrane by the boundary lines of the Rivinian notch (Fig. 2G, B). Prussak’s space is said to communicate, by a small aperture in the external ligament of the malleus (its roof), with the attic, or vault. Stretching from before backward across the upper part of the cavity of the atrium, and passing between the handle of the malleus and the long arm of the incus, is a reduplication of mucous membrane which, by its attachment to the posterior surface of the neck and upper half of the hammer handle, is divided into two parts,—the anterior and posterior folds. The posterior fold is attached anteriorly to the neck and upper half of the handle of the malleus, and above and behind to the postero- superior margin of the drum membrane. Its dependent, free margin covers the chorda tympani nerve as it passes upward and forward toward the Glaserian fissure. Between this fold and the inner surface of the drum membrane is a pocket, or space, opening downward, which is known as the posterior pouch of the membrana tympani. The anterior fold is smaller, and extends from the neck and handle of the malleus to the antero-superior margin of the drum membrane. Between it and the inner surface of the drum-head is another, smaller space,—also opening downward, —the anterior pouch of the drum membrane. Prussak’s space is said to communicate with the posterior pouch behind, but has no communication with the anterior pouch. Both pockets of the drum membrane—i.e., the anterior and posterior—open below into the cavity of the atrium. With regard to the exact histological relations of the membranes enter- ing into the formation of these pouches, somewhat different views have been held. Von Troltsch, who first described the anterior and posterior pockets, regarded the membrane as a true reduplication of the membrana tympani, —this view being based upon his observation of certain fibres which he believed to be identical in structure with those of the fibrous lamina of the drum membrane. Politzer appears to regard them as reduplications of the inner, or mucous, layer of the drum membrane. Gruber in his investi- gations failed to find any fibres characteristic of the membrana propria, and regards the reduplications in question simply as folds of mucous membrane depending from the tympanic roof. The three spaces above described are all situated below the level of the external ligament of the malleus which forms the roof of Prussak’s space. Above this level the attic is itself divided into compartments more or less completely separated from each other by folds of mucous membrane. These spaces, while less constant in their arrangement than the pockets of the membrana tympani, must nevertheless be held in mind 26 ANATOMY AND PHYSIOLOGY on account of their possible influence upon the course of a suppurative process within the vault. The Attic Spaces.—The head of the malleus and body of the incus divide the attic into two chambers, an inner and an outer chamber. This partition is often completed by a fold of mucous membrane (the malleo- incudal fold) passing from the tympanic roof to the upper surfaces of the malleus and incus. This vertical fold incloses between its layers the sus- pensory ligaments of the malleus and incus, and extends from the anterior ligament of the malleus in front to the aditus ad antrum behind. The outer chamber of the attic is bounded internally by the bodies of the ossicles and the malleo-incudal fold, and externally by the outer bony wall of the vault. The outer chamber is subdivided by a horizontal fold of mucous membrane into an upper and a lower attic space. This horizontal fold is attached to the head of the malleus and body of the incus internally and to the osseous outer wall of the attic externally, and extends from the anterior ligament of the malleus in front to the short process of the incus and cella incudis behind. The lower attic space is bounded below by the ligamentum laterale mallei, which separates it from Prussak’s space. The upper attic space opens behind into the aditus ad antrum (Brtihl). The membranous partitions between these spaces, while usually present, probably present many variations from those above described. They are said to contain many small apertures through which fluid may pass from one enclosure to another. This subdivision of the attic into compartments adds very materially to the gravity of a sup- purative process within the vault. It explains the surgical inadequacy of merely puncturing the drum membrane (paracentesis), and the importance of making a free incision through Shrapnell’s membrane and the soft tissues immediately behind it in all cases of acute purulent inflammation involving the vault. Vascular and Nervous Supply of the Tympanum.—Arteries.—The arterial supply of the middle ear is derived from the external and internal carotid arteries. From the external carotid are derived: (1) the tympanic branches of the ascending pharyngeal artery. This vessel gives off several small branches which enter the Eustachian tube, supplying the tubal muscles and mucous membrane. One or more of these enter the tympanum, pass upward over the promontory, and anastomose with the tympanic branches of the middle meningeal artery. (2) The tympanic bra?iches of the middle meningeal artery. After entering the skull the middle meningeal gives off a branch (the petrosal) which enters the hiatus canalis Fallopii, anastomosing with the stylomastoid, and also several small branches which enter the tym- panum through the petrosquamosal suture. These latter supply the roof and part of the inner wall of the tympanum. (3) The tympanic branch of the internal maxillary enters the tympanum through the Glaserian fissure, supplying the mucous membrane of the anterior wall and drum membrane and anastomosing with the tympanic branches of the internal carotid TYMPANIC BLOOD-VESSELS 27 artery. (4) The stylomastoid artery (branch of the posterior auricular) anastomoses within the facial canal with the petrosal branch of the middle meningeal artery. It gives off several tympanic branches which enter the tympanum through small orifices in its posterior wall. It also sends a branch to the canal which terminates in the eminentia pyramidalis, sup- plying the stapedius muscle (Zuckerkandl). From the Internal Carotid Artery.—The tympanic branch of the internal carotid enters the tympanum through an aperture in the carotid canal and anastomoses with the tympanic branches of the internal maxillary and stylomastoid arteries. Veins.—The veins which remove the blood from the tympanic cavity correspond somewhat to the tympanic arteries. They leave the tympanum by various routes,—i.e., (a) through the petrosquamosal suture, or minute foramina remaining after its obliteration, emptying into the veins of the dura mater; (b) through small foramina in the carotid canal, empty- ing into the carotid plexus; (c) by way of the Glaserian fissure, join- ing the veins about the temporomaxillary joint. There are also a large number of small veins which perforate the drum membrane at its periphery to join those of the external auditory meatus. Engorgement of these latter is the cause of the characteristic peripheral redness of the drum membrane, so often seen in tubotympanic congestion, or when the venous return flow has been impeded by continuous pressure upon the walls of the meatus, as by a speculum too large or retained in posi- tion too long. Nerves.—The nervous supply of the middle ear is derived chiefly from the glossopharyngeal, the sympathetic, and the trifacial. The tympanic branch of the glossopharyngeal (Jacobson’s nerve) is derived from its petrous ganglion, which is situated on the inferior part of the petrous portion of the temporal bone. It enters the tympanum through a small foramen in the tympanic floor, and, passing upward upon the promontory, divides into branches which are distributed to the round and oval windows and to the mucous membrane of the middle ear and the Eustachian tube. It also gives off branches of communication which lie in grooves upon the promontory and pass in different directions to their anastomotic connec- tions. This division of the tympanic (Jacobson’s) nerve into branches of distribution, together with its association with other nerves, constitutes the tympanic plexus. Its branches of communication are three in number. One of these passes downward and forward to unite with the tympanic branches of the sympathetic. A second communicating branch passes upward and forward to join the large superficial petrosal nerve. A third, receiving a small branch from the otic ganglion, passes upward in the substance of the petrous bone as the small superficial petrosal nerve. It receives in passing a filament from the ganglionic enlargement of the facial nerve. The Sympathetic.—The tympanic branches of the sympathetic (nervi carotici-tympanici) are derived from the carotid plexus. They enter the 28 ANATOMY AND PHYSIOLOGY tympanum through small openings in the carotid canal, and there unite with filaments of the communicating branches of Jacobson’s nerve, aiding in the formation of the tympanic plexus. The Trifacial.—This nerve contributes to the nerve supply of the middle ear chiefly through the otic ganglion, which supplies two small branches, one to the membrano-cartilaginous Eustachian tube and the other to the tensor tympani muscle. The stapedius muscle is supplied by a branch of the facial, the tensor tympani by a small branch from the otic ganglion. The chorda tympani nerve traverses the tympanum without supplying it. It leaves the facial canal a little above the stylomastoid foramen, and passes obliquely upward and forward through a canal in the premastoid plate to enter the tympanum. It passes forward through the upper part of the atrium,—between the hammer handle and the long arm of the incus,—and leaves the tympanum at the Glaserian fissure through a canal known as the iter chordae anterius. In its passage across the tym- panum it is covered by the fold of mucous membrane which enters into the formation of the posterior pocket of the drum membrane. The Eustachian Canal.—The Eustachian tube connects the cavity of the tympanum with that of the nasopharynx, and forms a very impor- tant part of the sound-conducting apparatus. Structurally it is some- what analogous to the external auditory meatus in that it consists of two parts,—(1) an osseous and (2) a membrano-cartilaginous portion. Its length in the adult varies from 31 to 38 mm. (about 1J4 to inches), of which about one-third is bony and two-thirds fibrocartilaginous. The two portions of the tube are not quite in the same straight line, their point of junction forming an obtuse angle, opening downward. The general direction of the canal from the tympanum to the nasopharynx is forward, inward, and downward,—so that its pharyngeal orifice is anterior to, and on a lower level than, the tympanic orifice. The tube is somewhat ex- panded at either end, the vertical diameter of the tympanic orifice being from 3 to 4 mm., while that of the pharyngeal orifice is 5 to 8 mm. The narrowest part of the tube is where the bony and cartilaginous portions join (the isthmus), at which point the calibre of the bony tube is not more than V/i to 2 mm. There are, however, parts of the membrano-cartilagi- nous tube in which the calibre is made even less than this by approxima- tion of the anterior and posterior walls. The osseous portion of the Eustachian tube extends from the anterior wall of the tympanum forward, inward, and downward through the upper and outer portion of the os petrosum. It is in immediate rela- tion above with the canal for the tensor tympani muscle, this being roofed over by a continuation of the tegmen tympani. Internally it is separated by a thin plate of bone from the canal for the internal carotid artery. From its tympanic orifice the calibre of the tube becomes gradually smaller, reaching its minimum diameter at its anterior, or inner, extremity, which EUSTACHIAN TUBE 29 presents somewhat roughened edges for the attachment of the cartilagi- nous portion of the canal. The membiiano-cartilaginous portion of the Eustachian tube is attached to the base of the skull, and at the isthmus rests in the groove between the inferior border of the greater wing of the sphenoid and the petrous portion of the temporal bone. It commences at the anterior inner end of the bony canal, and from this point extends forward, inward, and downward to its orifice in the lateral wall of the nasopharynx. Its cartilaginous frame is not complete,—only its posterior wall, roof; and upper part of the anterior wall being cartilaginous, the remainder being completed by fibrous tissue (Fig. 30). Its posterior (median) wall is formed by a plate of fibrocartilage which becomes wider as it extends for- ward and inward, its pharyngeal margin causing a somewhat vertical projection upon the lateral wall of the nasopharynx. This projection, or Cartilaginous plate of anterior, or lateral, wall Cartilage of roof Tensor palati muscle Posterior, or median, cartilaginous plate Anterior, membranous wall- Floor of membranous canal Fia. 30.—Transverse section of Eustachian tube (after Schwalbe, reduced). ridge, forms the posterior wall of the pharyngeal mouth of the tube, and the anterior wall of the fossa of Rosenmuller. The upper margin of the cartilage of the posterior wall curls forward and then downward, being thus continuous with the roof and cartilaginous plate of the anterior wall. The narrow groove between the anterior and posterior plates forms the roof of the canal. The anterior (external) cartilaginous plate is narrow and forms only one-fifth of the anterior wall of the tube. Below this the anterior wall and floor are formed by a dense fibrous membrane (tunica propria) which is richly supplied with blood-vessels. The fibrous layer is continuous with the perichondrial lining of the cartilaginous portion of the tube (Rudinger). The mucous membrane lining the Eustachian tube is of the ciliated cylindrical variety. In the pharyngeal end of the canal it is thicker and more loosely applied, and upon the anterior (membranous) wall it forms several longitudinal folds which admit of a certain degree of expansion of the tube without stretching the mucosa. Much has been written, and many varying views advanced, as to the 30 ANATOMY AND PHYSIOLOGY patency of the Eustachian tube when the palatal muscles are at rest. Since post-mortem conditions, as shown by cross-sections of the tube, can not be relied upon as determining the condition of the parts in the living subject, it seems safest to confine one’s statements to demonstrable facts. In all parts of the membrano-cartilaginous tube its vertical diam- eter far exceeds the lateral, which in most situations is obliterated by the contact of opposing surfaces. Owing to the absence of a complete car- tilaginous frame, the anterior (membranous) wall is in contact with the posterior wall. In the upper part of the tube, however, the narrow car- tilaginous plate which forms part of the anterior wall should tend to pre- serve the patency of this part of its lumen. It is this upper portion of the lumen of the membrano-cartilaginous tube which represents the direct continuation of the bony canal. It is probable that in health the lumen of the osseous canal is always patent; and that its anterior extremity, acting as a support, aids in maintaining the patency of the contiguous portion of the membrano-cartilaginous tube. The patency of the pharyngeal end of the tube is also, in all probability, maintained by its better cartilaginous support in this situation. Between these two terminal portions of the fibrocartilaginous tube, it seems probable that its anterior and posterior walls are for the most part in contact except when acted upon by the palatal muscles. Anatomical Differences Between the Eustachian Tubes of the Adult and the Infant at Term.—In the new-born infant the Eusta- chian canal presents the following marked variations from the adult type: (1) It is very much shorter, measuring not more than 14 or 15 mm.2 (33 to 38 mm. in the adult). (2) The tympanic orifice and the calibre of the bony tube are quite as large as in the adult. The whole canal is, therefore, in proportion to its length much wider. (3) The two portions of the tube (i.e., the membranous and the bony) are more nearly in the same straight line, so that there is no demonstrable angle at their point of junction. (4) The whole tube is nearly horizontal in direction, so that, while the pharyn- geal orifice in the adult is on a lower level by 12 to 14 mm. than the tym- panic orifice,3 it is on the same plane as the latter in the infant at term. (5) The pharyngeal mouth of the tube in the infant at term is on the same level as the hard palate,—i.e., just behind the choanae,—whereas in the adult it is not less than 10 mm. above the hard palate. 2 The statement found in many text-books, that the Eustachian canal of the infant at birth is 18 to 20 mm. long, is not correct. Remembering that the infant tube is nearly or quite horizontal in direction, examination of the base of the skull of an infant at term seems to demonstrate clearly that the length of the entire tube can not at this period exceed 14 or at most 15 mm. 3 The statement of Politzer (Diseases of the Ear, p. 38), repeated by Briihl (Atlas of Otology, p. 37), that the tympanic orifice is in the adult on a level about 2.5 cm. higher than the pharyngeal orifice, is obviously incorrect, since, with Politzer’s esti- mated length of 34 to 36 mm., this difference in the level of its two extremities would bring the direction of the canal into a plane much nearer the vertical than it is known to occupy. MUSCLES OF THE EUSTACHIAN TUBE 31 The above anatomical differences, while undergoing fairly rapid modi- fication with the growth of the child, may be accepted as characteristic of the tubal type in infancy as compared with the adult type. Muscles of the Eustachian Tube.—When at rest, the Eustachian canal is supposed to be practically a closed tube. At frequent intervals, however, it is made to dilate in response to the action of two muscles, which must, therefore, be briefly described. The levator palati arises from the anterior part of the under surface of the petrous bone, and passes obliquely downward and inward along the outer wall of the nasopharynx to be attached to the posterior sur- face of the soft palate. In its course toward its palatal attachment, some of its fibres are attached to the floor of the membranous canal. Its contraction serves to elevate the soft palate and to dilate the Eusta- chian tube by elevating its floor. The levator palati is supplied by the great superficial petrosal nerve (from the superior maxillary branch of the 5th). The tensor palati muscle consists of two portions, which are some- times spoken of as the vertical and horizontal portions- respectively. The vertical portion arises from the scaphoid fossa at the base of the pterygoid plate, from the spine of the sphenoid, and from the anterior membranous wall of the Eustachian canal. These fibres unite to form a broad, thin muscle, which passes downward and slightly forward to the hamular process of the internal pterygoid plate. The muscle then winds around the hamular process and passes inward (horizontal portion), to be attached to the anterior surface of the soft palate. Its contraction elevates the soft palate and dilates the Eustachian tube by drawing its anterior wall down- ward and forward and thus away from the posterior wall. This muscle is supplied by the otic ganglion. There is still another small muscle, the salpingo-pharyngeus, the con- traction of which influences the calibre of the tube. It arises from the tubal prominence, or pharyngeal end of the posterior cartilaginous plate of the tube, and passes backward to be inserted into the posterior pharyn- geal wall. The Mastoid Process (Plate III).—The mastoid process is the large conical protuberance of bone which projects downward behind and below the bony meatus. It is bounded above by the tegmen antri, which sep- arates it from the middle cerebral fossa. The interior of the upper part of the mastoid process communicates with the tympanic vault, which lies immediately in front. Below this it is separated by the dense bony plate of the posterior canal wall from the osseous meatus. Interiorly it projects downward below the level of the floor of the meatus, terminating in the conical process known as the tip (Fig. 31, 6). The outer surface is convex (31, a) and more or less roughened for the attachment of muscles. The inner surface of that portion of the mastoid lying above the floor of the meatus forms part of the posterior cerebral fossa. It presents the deep groove (32, a) which lodges the descending portion of the lateral sinus. 32 ANATOMY AND PHYSIOLOGY The position of this groove in its relation to the tympanum varies greatly in different skulls. It is one of the most important surgical relations of the tympanum, and will be considered more fully in a later chapter deal- ing with the surgical anatomy of the temporal bone. The inner surface of the tip—that portion of the mastoid which projects downward below the base of the skull—forms the outer boundary of a groove, running from before backward, for the attachment of the posterior belly of the digastric muscle (31, c). The mastoid process consists of an outer shell, or cortex, of dense compact bone, inclosing a central chamber, which may be subdivided into pneumatic spaces or filled with diploic tissue. Accordingly two types are recognized, viz.: (1) The pneumatic (Fig. 34), in which the interior is subdivided into distinct spaces, which are lined with mucous membrane, and may be of very considerable size. In this variety there is invariably a large cell at the tip, in which pus is apt to collect during the course of a suppurative mastoiditis. (2) The diploic mastoid (Fig. 35).—In this variety, instead of dis- tinct, pneumatic spaces, we find the interior of the mastoid filled with cancellous tissue, somewhat resembling that which occupies the space between the inner and outer plates of the cranial bones. In the dried bone this tissue appears as if composed of very small, thin-walled osseous cells. In the living subject, as seen during an operation upon the mastoid, it consists of a vascular, spongy tissue offering only moderate resistance to the rongeur or curette. Even in bones of this type there is usually present a single large cell at the tip. Between the two varieties above described, there are many bones which present the characteristics of each,—i.e., pneumatic spaces and diploic tissue occupying different parts of the same bone. Still another type of bone has been described as the sclerotic mastoid. In this variety there may be throughout the greater part of the mastoid process complete absence both of pneumatic spaces and of diploic tiss.ue, their place being occupied by fairly compact bone. This solidification sometimes occurs as a pathological change resulting from chronic middle- ear suppuration of long standing. There are undoubtedly cases, however, in which the mastoid is practically filled with a solid mass, in spite of the fact that the tympanum may present no evidences of having been the seat of disease. The accompanying illustration (Fig. 36) was made from ia specimen prepared by the author. That there had been no prolonged suppurative process within the tympanum was shown by the condition of the ossicles and drum membrane, which were intact and normal. The Antrum.—There is one space, usually of considerable size, which is always present,—viz., the so-called mastoid antrum. This is the large space situated in the upper and anterior part of the mastoid process imme- diately behind the tympanic vault. There can be no doubt that this space forms part of the tympanic cavity. Its roof is directly continuous with THE MASTOID PROCESS 33 Plate III. Fig. 31.—Temporal bone, outer surface; a, mas- toid process; b, tip of mastoid; c, groove for posterior belly of digastric muscle. Fig. 32.—Temporal bone, inner surface; a, groove for sigmoid sinus,— i.e., descending part of lateral; b, tip of mastoid; c, internal auditory meatus. Fig. 33.;—Vertical section of temporal bone passing through aditus ad antrum; a, aditus, leading forward into tympanic vault. Flo. 34.—Section through mastoid proc- ess of pneumatic variety, showing typical pneumatic spaces or cells. Fig. 35. — Section through mastoid process of diploic type ; a, antrum. Fig. 36. — Section through mastoid process of sclerotic variety. 34 ANATOMY AND PHYSIOLOGY that of the vault, from which it is differentiated only by the triangular constriction known as the aditus ad antrum (33, a). The antrum is fully developed in the new-born,—i.e., before even a rudimentary mastoid can be demonstrated. Later it is surrounded and appropriated by the devel- oping mastoid process. In this brief description of the mastoid process, the author has deemed it best to deal only with those general characteristics a knowledge of which is absolutely essential to the intelligent study and appreciation of the commoner acute middle-ear lesions. He has endeavored to emphasize the fact that the antrum is not to be considered separately as one of the mastoid cells, but rather as the posterior end of the tympanic vault. This method of describing it enables the student more easily to remember its exact position and its surgical significance. It has the further advantage of being, from the stand-point of its development, the only correct view; for even in fetal life—i.e., long before even a rudimentary mastoid is present—the antrum is an easily demonstrable cavity. Physiology of Sound-Conduction. It is impossible to consider the process of sound-conduction without having in mind both the physics of sound and the physics and physiology of the conducting mechanism. With special students of otology, more or less familiarity with the physics of sound may be assumed. For the busy medical practitioner, however, it may not be amiss to recall briefly certain elementary, though perhaps forgotten, facts upon which our knowledge of the physiology of sound-conduction is based. Sound is a form of motion produced by some vibrating body. A sound- wave is a series or chain of alternate condensations and rarefactions in the surrounding air, by which the vibratory movements of the sounding body are conveyed to the drum membrane. When these vibrations occur singly or follow each other irregularly, the resulting sound is discordant and is spoken of as a noise. When the vibrations recur rhythmically or at regular intervals, and with sufficient rapidity, a musical tone results. The pitch, or relative position of sound in the musical scale, depends upon the rapidity with which the vibrations follow one another, the pitch being raised as the number of vibrations per second is increased. The human ear normally appreciates musical tones between two extremes of vibration rapidity, the lower tone limit being eighteen vibrations per second, and the upper tone limit somewhere between 32,500 and 50,000 vibrations per second. Vibrations recurring rhythmically at a rate of less than eighteen per second may be heard as separate impulses, but are not heard as a continuous musical tone. Taking any note in the musical scale,—e.g., C-2, 32 double vibrations,—by doubling the number of vibra- tions we may produce a tone one octave higher. Thus 32, 64, 128, and 256 double vibrations per second represent C tones one octave apart. Pitch, then, is determined solely by the number of vibrations per second. PHYSICS OF SOUND 35 Intensity.—The intensity with which a sound-wave impresses the per- ceptive mechanism depends upon its amplitude of vibration. Taking for example a tuning-fork such as is represented by Fig. 37. a double vibra- tion includes the passage of the prong from a to b, its recoil to c, and its return to a, its position of rest. The line b-c represents what is called the amplitude of vibra- tion. Supposing this to represent its vibration when set in motion by a moderate tap, a more vigorous blow will result in more extensive movements, the amplitude of vibration being greater and the intensity of the sound being correspondingly increased. This is in accordance with the physical law which declares that the intensity of sound is proportional to the square of the amplitude. Timbre.—There is a third property of musical sound, that peculiar quality by which we are able to distinguish tones of the same pitch as produced by different musi- cal instruments; e.g., the C tone of the piano, of the violin, and of the human voice. For an explanation of this quality of sound, and of the harmonics or overtones to which it is due, the reader is referred to any of the standard works on physics. Sound-Conduction.—The Auricle and External Audi- tory Meatus.—To most of the lower animals the auricle is undoubtedly of great value in aiding them to concen- trate their auditory effort at will upon some particular sound by turning the auricles in the direction from which it comes. In man, on the other hand, the auricle has lost much of its importance as a part of the conducting apparatus since the auricular muscles have lost the property of voluntary contraction,—in other words, since man has lost the power of moving the auricles at will. That he still retains an intuitive appreciation of their function is shown by the impulse which leads the hard- of-hearing instinctively to draw the ear forward toward the source of sound and to augment its concavity by that of the hollow of the hand. While it is now recog- nized that fairly good hearing is not inconsistent with complete loss of the external ear, it can not from this be assumed that the auricle is without influence upon the auditory function. Politzer has called attention tc the fact that by filling the concha with wax, even though the orifice of the external auditory canal be left open, we reduce considerably the acuteness of audition; whereas obliteration of the other auricular depressions—e.g., the fossa of the helix, fossa of the antihelix, etc.—does not influence the hearing appreciably. The concha, therefore, must be regarded as in man the most important part of the auricle, its Fig. 37.—Timing-fork. 36 ANATOMY AND PHYSIOLOGY function being to receive and carry forward the sound-waves to the inner surface of the tragus, by which they are deflected into the external auditory meatus. The external auditory canal presents curves and variations in calibre in different parts, which undoubtedly have to do with the proper focusing of sound-waves upon the membrana tympani. These anatomical pecularities, however,—provided that its lumen is not completely occluded, —seem to be less essential to perfect hearing than almost any part of the conducting apparatus. Individuals with abnormally narrow auditory canals seem often to hear equally as well as others with canals of normal calibre. The author has seen several cases in which the bony meatus was very considerably narrowed in one or more of its diameters by exostoses from one or other of its walls, in which no appreciable impairment of hearing could be demonstrated. Another phenomenon with which every aurist is familiar is the excellent hearing power frequently exhibited by individuals whose auditory canals are apparently filled with cerumen, exfoliated epithelium, or other foreign substances. Whether in such cases the obstructing mass vibrates in unison with the sound-waves from without and thus transmits them to the column of air between it and the drum membrane, or the sound-waves are projected through some space between the foreign body and one of the canal walls, may be a debatable question. The latter hypothesis seems the more plausible. Sound- waves, then, are collected in the concha, whence they are deflected by the inner surface of the tragus into the external auditory canal, by which in turn they are conveyed to the outer surface of the membrana tympani. The Drum Membrane.—In the membrana tensa we have an ideal medium for the transmission of sound-waves to the ossicular chain. It is a tense, inelastic, fibrous membrane, drawn inward at the centre by its attachment to the lower half and extremity of the hammer handle, and presenting, therefore, a somewhat funnel-shaped concavity toward the meatus. From the central depression at the umbo to its peripheral attach- ment, the membrane is slightly bowed or curved in the direction of the meatus. This outward curvature of the normal membrane is not without influence upon its value as part of the conduction mechanism, Helmholtz having established by experiments the greater resonance of curved mem- branes as compared with flat ones. If the drum membrane were highly- elastic it would respond easily to sound-waves, but would hold these and other vibrations due to harmonics, 'or overtones, after the original stimulus had spent itself; and these after- tones would interfere with the proper transmission of sound-waves immedi- ately following. But the membrana tensa is a comparatively unyielding and inelastic structure, responding readily to all forms of sonorous stimuli, but returning rapidly to a condition of rest as soon as it ceases to be acted upon by sound-waves from without. As with all stretched membranes and sonorous bodies generally, the membrana tensa has a fundamental THE FUNCTION OF THE MEMBRANA TYMPANI 37 note of its own. By this is meant that the drum membrane, if set in motion by a light tap, or any force momentarily bending it, must execute a series of to-and-fro movements, or vibrations, before it can return to a condition of rest; and that these movements will be rhythmic in character and will take the form of sonorous vibrations having a constant rate of rapidity per second; in other words, they would if sufficiently extensive and pro- longed produce a musical tone of constant pitch, its fundamental tone. One disadvantage of a loud fundamental note in the drum membrane would be the confusion which would inevitably result if it were acted upon by sound-waves having the same number of vibrations per second. It must be remembered that the drum membrane is capable not only of responding to all kinds of sonorous impressions, but of transmitting several sound-waves simultaneously. One can readily appreciate, there- fore, that a fundamental tone of any part of the conducting mechanism which would respond loudly even to overtones of the same pitch might cause great disturbance of function. Against this result, the handle of the malleus acts as a control mechanism, the effect of its attachment to the drum membrane being somewhat analogous to the pressure of a finger against the prong of a vibrating tuning-fork,—i.e., the vibra- tions due to the fundamental tone of the drum membrane are immedi- ately overcome by the inertia of the attached ossicular chain, leaving the membrana tensa free to receive and transmit new sound-waves from without. The Ossicular Chain.—According to the commonly accepted theory, sound-waves striking upon the membrana tympani are by it communi- cated to the ossicular chain, by which in turn they are transmitted through the foot-plate of the stapes to the labyrinthine fluids. Each excursion in either direction of the stapes is accompanied by a corresponding movement, or displacement, of the fluid in the vestibule, and in this way fluid waves are inaugurated which finally impress the terminal filaments of the audi- tory nerve. For the exercise of these passive movements, the drum mem- brane and ossicles constitute a perfectly adapted mechanism. The ossicles form a system of finely adjusted and sensitive levers which respond in- stantly to the slightest movements of the drum membrane. The handle of the malleus being the only part of the ossicular chain directly attached to the membrana tympani, it is through this process that the movements of the drum-head are transmitted to the ossicles. The handle of the malleus is longer than the long arm of the incus; so that, according to the laws governing leverage, with each inward excursion of the hammer handle, the long arm of the incus moves inward, carrying with it the stapes through a shorter distance but with greater force. This provision has a particularly important bearing upon the transmission of the lower musical tones, which are produced by vibrations of large amplitude but relatively little force. The funnel-shaped concavity of the drum membrane and its outward curve from centre to periphery have also an important bearing upon the 38 ANATOMY AND PHYSIOLOGY function of the conducting mechanism,—such a membrane, according to Helmholtz, transmitting low vibrations of smaller force than would a flat membrane. Apparently, therefore, the ossicular chain is most essential in transmitting the lower tones of the musical scale,—tones produced by vibrations of large amplitude but little force, which the ossicular levers convert into vibrations of smaller amplitude but of greater force. The higher tones, on the other hand, are produced by sonorous vibrations of smaller amplitude, but whose relatively greater force is capable of inaugu- rating a fluid wave within the labyrinth without augmentation of force through the leverage system of the ossicular chain. With this theorem in mind, we should be at no loss to explain the impairment of hearing for the lower tones of the musical scale which invariably attends any severe lesion of the conducting mechanism. The relative movements of the different ossicles have been investigated by Helmholtz, Politzer, and others. According to their experiments, the maximum excursion of the hammer handle (at umbo) which can be in- duced by condensation and rarefaction of the air in the external auditory canal is % mm., the maximum movement of the stapes being Yu to Y\% mm. These measurements throw light on the influence of leverage on the ossicu- lar movements, and furnish additional proof that the ossicles move sepa- rately and individually as parts of a movable chain, and never in unison as parts of a rigidly bound whole. It must be understood, however, that the measurements given represent only the excursions which may be experimentally induced, Riemann having proved by mathematical calcu- lations that the largest excursion of the stapes possible in response to sound- waves would be smaller than the eye could appreciate. Another view, which has been entertained, as to a possible pathway for sound-waves is that they may reach the labyrinth by way of the round window. Thus, Politzer4 states that “the vibrations of the drum membrane are transmitted to the labyrinth partly through the ossicles by means of the foot-plate of the stapes, ajid partly through the air in the tympanic cavity to the membrane of the fenestra rotunda.” The writer can not conceive how in a healthy ear it is possible for the membrane of the round window to take so direct a part in the transmission of sound-waves. To accept such a view, it would be necessary to assume that, with each in- ward movement of the membrana tympani, the membrane of the round window is also forced inward by condensation or displacement of the air in the tympanic cavity, an untenable hypothesis. The membrane of the round window moves inward toward the lumen of the scala tympani only during the period of rarefaction of sound-waves,—i.e., during the period in which the stapes moves outward. In other words, its function seems purely one of compensation for the movements of the stapes, thus preserv- ing the stability of intralabyrinthine pressure. 4 Diseases of the Ear, last English edition, p. 57. ROLE OF THE TYMPANIC MUSCLES 39 The Tympanic Muscles.—The function of the tensor tympani and stapedius muscles has been the subject of a great deal of controversy. Contraction of the tensor tympani, drawing the hammer handle and drum membrane inward, renders the latter more tense. Contraction of the stapedius draws the head of the stapes backward and the anterior end of the foot-plate of the stapes somewhat outward into the niche of the oval window. Acting together, the two muscles oppose each other, one drawing the ossicles inward, the other tending to draw the stapes out- ward. In this way it is believed that they may constitute a sort of con- trol mechanism, guarding the labyrinth, on the one hand, from the effect of loud or explosive noises which might drive the stapes violently in- ward, and, on the other, neutralizing the effect of sudden and forcible condensation of the air within the tympanum which might cause ex- cessive excursions of the hammer handle and drum membrane in the other direction. Another theory is that which was proposed by Mach as long ago as 1863. According to this view, the muscles act as an accommodation appa- ratus, varying and regulating the tension of the conducting mechanism according to the requirements of different sound-waves, and also enabling the individual by an effort of will to select and follow certain sounds. This view, with some modifications, has received the support of most later observers. Henson, in 1876, showed by experiments upon living ani- mals that the tensor tympani muscle not only contracts in response to sound-waves, but executes a distinct contraction foi each particular sound; and further that its contractions were stronger for high tones than for the lower tones of the musical scale. Giving these facts greater significance were the later experiments of Poliak, which proved that after removal or destruction of the cochlea in living animals the tensor tympani no longer contracts except in response to electrical stimulation. While absolute proof as to their function is beyond our reach, this view—viz., that different sound-waves require variations in the tension of the sound-conducting mechanism for their perfect transmission, and that such variations are controlled and regulated by the tympanic muscles—is in harmony with laboratory investigations, and furnishes the only hypothesis which seems adequately to explain these perfect little muscles. A question which is still the subject of occasional discussion, and apparently with little prospect of definite solution, is whether sound-waves are in any degree conducted through the ossicles and labyrinthine fluids by molecular motion, or altogether through vibration of these structures en masse. The fact that the higher musical tones are in many cases well perceived in spite of advanced obstructive lesions in the conductive mech- anism, is by some regarded as pointing to a possible transmission of these sounds by molecular processes, rather than by mass movements of the ossicular chain. In this regard the following expression of belief by the 40 ANATOMY AND PHYSIOLOGY late Professor Bezold5 of Munich is of interest: “I share the conviction . . . that not molecular movements, but mass movements of the con- ducting chain, together with the labyrinthine water column, transmit the sound-waves from the air; ... I am, moreover, on the side of those 'physiologists who regard bone conduction as osteotympanic. In other words, in conduction through bone, the excitation of the auditory nerve takes place exclusively with the aid of the sound-conducting appa- ratus, vibrating with the bone.” This view, while not final, probably expresses the belief of a majority of otologists and physiologists to-day. 5 Archives of Otology, vol. xxxv, No. 3, p. 217. CHAPTER II. PHYSICAL EXAMINATION OF THE PATIENT. Under this heading should be included a short but comprehensive history of the case; and this should include not only all essential data as to the present attack, but also an account of any previous conditions or disorders which may throw light on the aural disease. Age, Occupation, Habit, Heredity.—Age has a particularly impor- tant bearing upon aural disease and should always be taken into account. The patient’s occupation and habit or mode of life—e.g., environment, excessive addiction to alcohol or tobacco, habitual overwork, dissipation, etc.—should be kept in mind as having a possible bearing upon the aural affection. The question of heredity is apt to be considered chiefly in connection with adult patients suffering from impaired hearing. It might be taken into far more useful account in our dealing with the children of the deaf or hard-of-hearing, with whom especial effort should be made to correct any conditions predisposing to aural disease. Previous History.—This should include a record of (A) any consti- tutional disease, inherited or acquired,—e.g., syphilis or tuberculosis. (B) Diatheses, of which gout and rheumatism are the most impor- tant. That rheumatism is the indirect cause of many cases of etiolog- ically obscure aural disease there can be no doubt; and there are some observers (Buck, O. Wolf, Von Urcherman) who believe that acute rheu- matism is not infrequently manifested as a primary lesion within the tympanum. (C) The acute infectious diseases, either in childhood or in later life. At least 8 per cent, of all cases of scarlet fever, diphtheria, and measles develop some form of middle-ear inflammation. Particularly are many cases of chronic suppurative otitis media traceable to such lesions early in life. (D) Previous attacks of acute otitis media. There are many children whose histories are completely negative as to infectious diseases who have, however, experienced two or more attacks of acute tympanic inflammation. Recurring attacks of aural pain and discharge, for which no exciting cause can be assigned, should always suggest the possibility of some abnormal condition within the nasopharynx. Certainly such a history should make one more guarded in one’s prognosis until the nasopharyngeal lesion, whatever it may be, has been corrected. History of the Present Attack.—This should begin with a statement of the disease to which the aural disorder was secondary, or with the exciting cause. In order to fix as nearly as possible the date of the onset, we should begin with the initial symptom—pain, deafness, tinnitus—and the date on which it was first experienced by the patient. In acute cases, next to the initial symptom, it is important to learn if possible the time which has elapsed between the onset of the attack and the appearance of 41 42 EXAMINATION OF THE PATIENT the aural discharge, provided this be present. The importance of this lies in the fact that in acute tympanic disease the prognosis is, as a rule, more favorable in those cases in which spontaneous rupture of the drum mem- brane follows quickly upon the initial symptom than in cases in which it is delayed several days or a week. Further than this but little can usually be learned beyond what the physician’s examination will bring to light,— unless, of course, the patient has been under the care of a trained observer. It is, of course, well in the case of a seriously ill patient to inquire as to whether rigors, profuse sweating, or sudden and pronounced alterations of temperature have been noticed ; but the statements of the family or attend- ants in regard to such symptoms are rarely to be relied upon. In other words, the physician is usually obliged to await the results of his own observation on these points. In cases of chronic aural disease the history may extend over a period of months or as many as ten or twenty years. Obviously such cases require a more thorough weighing of individual symptoms, their sequence, and relative severity or prominence in different stages of the disease. To epitomize: The main points of interest in the history of a patient suffering from tympanic disease group themselves about the following facts: (1) The primary disease to which the otitis was secondary, or the exciting cause. (2) The date and character of the onset. (3) In acute cases, the date and character of the discharge. (4) The presence or absence of symptoms of constitutional disturb- ance,—nausea, vomiting, rigors, septic temperature, etc. (5) In chronic cases, the sequence of the various symptoms, and their relative severity in different stages of the disease. (6) The course of the disease as shown by subsidence or persistence, increase or diminution of symptoms. From what has been written, it may seem that the writer has proposed a somewhat voluminous history. This, however, is not necessary, it being quite possible to include all that is of practical importance within a comparatively small space. To facilitate this, some form of printed his- tory blank is almost essential. The writer has found two forms of history cards useful,—i.e., one for office histories, used mostly in cases of chronic aural disease (e.g., deafness, etc.), and a more abridged form for “bed- side histories,” which are of great convenience in cases of acute tympanic or mastoid disease. Copies of these two forms will be found in a final chapter or appendix. Objective Examination. — Before attempting to inspect the drum membrane by reflected light, much may be learned by a careful observ- ance of the patient. One may often determine at a glance whether the patient breathes normally—i.e., through the nose—or is a typical or partial mouth-breather. Habitual mouth-breathing in children is usually due to the presence of adenoids. This obstacle to normal breathing is, however, INSPECTION OF PATIENT 43 by no means invariably announced by the typically dull and vacant ex- pression so often described in the earlier text-books. The child is often of extremely healthy appearance. He may breathe quite normally during the day or when perfectly quiet, but with noticeable difficulty at night when the recumbent position favors nasopharyngeal congestion, or when engaged in any active physical exercise. While, therefore, we may often determine the presence of adenoids at a glance, our ability to do so can not be relied upon. Mouth-breathing in adults is less frequent, and usu- ally, therefore, more noticeable than in children. Whatever the patient’s age, habitual mouth-breathing should be noted as likely to throw light not only upon the etiology, but also upon the prognosis and treatment of the aural disease. In talking to a patient with advanced catarrhal deafness, one intui- tively gauges the degree of deafness by one’s difficulty in making him hear or by the evident difficulty on his part; also which is the deafer ear, by observing which ear is turned toward the speaker. By observing the patient’s expression and the intentness with which he scans the face of the person talking, one not infrequently discovers a capacity for lip- reading of which the patient himself may be only partly conscious. By such practical observations one may obtain very useful information as to the degree of deafness for which relief is sought. Auricular Displacement.—Of great importance, because of their possible surgical significance, are changes in the position of the auricle due to inflammatory processes in or about the ear. Note if the two auri- cles are identical in the angles which they form with the sides of head. While slight differences in this respect may represent simply an anatomical variation, marked differences are much more likely to be the result of an inflammatory condition in the ear or temporal bone of one or the other side. Marked projection outward and forward, or outward and downward, of one auricle beyond the position occupied by the opposite ear, points usually to an inflammatory process either in the mastoid cells (acute mastoiditis) or in the posterior wall of the fibrocartilaginous meatus (furunculosis). This outward displacement of the auricle is due either to a subperiosteal abscess or to oedema of the structures behind the ear,— i.e., those covering the mastoid process. The postauricular sulcus—linear depression between the auricle and side of the head—may therefore be obliterated. Such postauricular swelling, with outward displacement of the auricle, points in young children almost invariably to a suppurative inflammation involving the mastoid cells. In the adult, on the other hand, they may mean mastoid inflammation, with resulting subperiosteal ab- scess, but far more frequently are the result of an extension of inflammation from a furuncle in the ■posterior wall of the fibrocartilaginous meatus. Palpation in Case of Postauricular (Edema.—With oedema be- hind the auricle much may be learned as to the original focus of infection by careful palpation. Gradually exerted, but firm, pressure at a point upon the mastoid process just behind the auricular attachment, but so 44 EXAMINATION OF THE PATIENT directed as not to disturb the auricle, will elicit deep-seated bone tender- ness only if the mastoid process is the seat of an acute inflammatory process. If the mastoid is not involved, little or no pain will result from pressure so directed. On the other hand, pressure at exactly the same point, but directed slightly forward so as to move the auricle, will cause the patient to wince or cry with pain, even though the mastoid is perfectly healthy, if the fibrocartilaginous meatus be the seat of an acute inflam- mation. This latter phenomenon is, of course, explained by the fact that any movement of the auricle along the line of its attachment to the side of the head is necessarily communicated to the cartilaginous framework of the external auditory canal. It is a differential point of very consider- able diagnostic importance, and will be referred to again in a later chapter. Palpation of the Auricle in Case of Aural Pain.—Whenever ear pain is complained of, it is well to determine, if possible before any attempt is made to examine the drum membrane by reflected light, whether this pain is in any part due to an inflammation of the external canal. Except in infants and very young children, in whom the anatomical relation be- tween the drum membrane and external meatus is exceedingly close, manip- ulation of the auricle causes absolutely no pain when the inflammation is confined to the middle ear. On the other hand, very slight movements of the auricle are extremely painful even in the initial stages of a furuncle in the meatus. By pressing one’s finger firmly against the cheek immedi- ately above and in front of the auricle, and bringing it downward along the anterior attachment so as to press the tragus inward, one will elicit tenderness in every case in which the anterior wall of the meatus is the seat of an acute inflammation. If no pain results from this procedure, the auricle should be moved in different directions,—upward, backward, downward, and forward. These movements will change the position of the different walls of the meatus, and if no pain is experienced one may with confidence exclude the fibrocartilaginous canal as the seat of an acute inflammation. If we have properly cultivated our powers of observation, we have now with the expenditure of but a few moments of time possessed our- selves of certain facts bearing upon the patient’s condition. We have made a practical estimate of the degree of functional impairment (deaf- ness) by his difficulty in interpreting the conversational voice, have noted his capacity for lip-reading and the probable influence of this in supple- menting his power of audition, and have probably determined which is the deafer ear. If his disease is acute, we have either located the inflammation in the auricle or external auditory canal, or have excluded that part of the conducting mechanism as without bearing upon the aural disorder. The next step in the examination is the inspection of the drum membrane. For this purpose, the following mechanical aids are essential: (a) some form of artificial light, (b) a forehead mirror for focusing the light upon the membrana tympani, and (c) a properly constructed aural specu- lum. These appliances are found in the instrument houses in a variety THE FOREHEAD MIRROR 45 of designs. While some of them are excellent in every respect, others are so far from correct in design and structure as to be practically without value in aural work. It is important, therefore, that a brief statement be made as to the essential points which these instruments should possess. The Forehead Mirror.—In selecting a mirror for otological work, the points to be looked to are its size, the size of its central orifice, the position of the ball by which it is attached to the head-band, and, most important of all, its focal distance. Within certain limits, the size is a matter of personal preference, some instrument dealers showing them in various sizes from 2/ to 4 inches in diameter. In the writer’s experience, a mirror 3 inches in diameter has represented the most satisfactory size. This Fig 38.—Head minor. Fig. 39.—Head mirror. throws a stronger light than those of smaller size, and, on the other hand, is lighter and less clumsy than larger ones. A 3K-inch mirror, however, if its attachment to the head-band is properly adjusted, can be used very satisfactorily and is the choice of many aurists. The central orifice should be not less than one-quarter of an inch in diameter, a smaller aperture entailing a certain amount of unnecessary eye-strain. The writer’s per- sonal preference is for a central orifice one-half inch in diameter, as shown in Tig. 38. This is particularly advantageous in tympanic surgery and in the post-operative treatment of mastoid wounds, a smaller aperture being apt to necessitate more frequent readjustments of the mirror, a serious inconvenience when one wishes to avoid touching anything not absolutely sterile. The ball by which the mirror is connected with the head-band should be attached to the peripheral edge (Fig. 38), rather than to its 46 EXAMINATION OF THE PATIENT posterior surface as shown by Fig. 39. The advantage of the peripheral attachment is that it allows a wider range of movement and also enables one to bring the central orifice nearer the eye. Undoubtedly the most important point to be investigated in select- ing a mirror for aural work is the focal distance. By this is meant the distance between the concave reflecting surface of the mirror and its principal focus, or that point in front of it at which the reflected rays con- verge to give the greatest brilliancy of illumination. It can be readily understood that a focal distance which would be quite satisfactory in examining the pharynx might be altogether unsuitable to the inspection of Fig. 40.—Head-band and mirror. so small a field as is afforded by the membrana tympani. Thus, a focal distance of 18 inches may afford a clear definition of the structures of the throat and pharynx, but would be altogether too great for the examination of structures so small as the minute landmarks of the drum membrane. For examining the ear, the focal distance should be not greater than 10 or 12 inches. This may be easily tested by holding the mirror with its reflecting surface about twelve inches from the flame of a candle, lamp, or gas jet, and noting the distance at which the outline of the flame is most clearly shown upon any flat surface,—e.g., a book-cover or the palm of the hand. This is also the point at which the convergent rays meet to give the most brilliant illumination. THE MIRROR AND HEAD-BAND 47 The Head-band.—Of this but little need be said beyond the mention of certain points to be avoided. A head-band of an}r elastic material is unsuitable, because it allows a degree of motion which is precisely what one wishes to avoid. The flexible band should be made, therefore, of leather or of very stout silk ribbon at least an inch wide. The attachment of the mirror to the forehead piece should be effected by means of a double ball- and-socket joint, as shown by Fig. 40. A single joint does not allow of placing the mirror in the position which gives the least eye-strain and the clearest vision. Fig. 41 represents a stiff fibre head-band which the writer has found very satisfactory in practical use. If properly fitted to the head, it is comfortable, and easily removed and put on. It has also the additional Fig. 41.—Fibre head-band. advantage over the ordinary head-band that it is more easily put on by an attendant or nurse during a surgical dressing, and usually falls automatically into its proper position on the head. To epitomize: If one were obliged to depend upon ordering a mirror and head-band by mail, one would do well to include the following speci- fications: Diameter of mirror 3 to 3K inches; diameter of central orifice not less than one-quarter of an inch; attachment ball to be on the periph- eral edge of the mirror; focal distance 10 or 12 inches; head-band to be of stout unyielding material, and attachment mechanism to be provided with a double ball-and-socket joint. A mirror fulfilling these require- ments should prove quite satisfactory in otological work. 48 EXAMINATION OE THE PATIENT Fig. 42—Aural specula. Fig. 43.—Aural forceps. Fig. 44.—Tympanic probe. Fig. 45.—Aural cotton applicator. AURAL SPECULA 49 Aural Specula (Fig. 42).—The accompanying illustrations represent some of the specula which are offered for sale, and with any of which the ear may be satisfactorily inspected by a competent aurist. In making one’s choice one should bear in mind the mechanical results which the speculum is intended to facilitate. What one needs is not a long and nar- row funnel which can be introduced deeply into the external auditory canal, but rather a short tube for introduction into the orifice of the fibro- cartilaginous meatus. Any unnecessary length of the tubular end of the speculum is a hindrance to inspection and the facile use of instruments. The outer expanded portion of the speculum serves a double pur- pose,—viz. (1) that of a handle by which it is held in place and manipulated, and (2) that of a receptacle for collecting the light from one’s mirror and throwing it into the auditory canal. Any superfluous length of this portion of the speculum simply adds to the difficulties of inspection and local treatment of the ear. As a teacher of practical otology, the author has been interested in ob- taining whatever speculum would best aid the medical student in acquiring quickly and easily a certain degree of facility in ex- amining the ear. He knows of no more practical or satisfactory speculum than that shown in Fig. 42, B, known as the Boucheron speculum. They are made in sets of four sizes. Three other instruments es- sential in aural examination are shown in the accompanying illus- trations (Figs. 43, 44, and 45). The Source of Light.—Excellent light for otological work can be obtained from the flame of an oil lamp or gas jet, or from an electric bulb connected with the ordinary street current. Whatever the source may be, the light itself must be connected with some form of movable bracket which can be moved both in the vertical and horizontal planes (Fig. 46). The electric light is now quite generally used in the cities, and, when properly installed, gives a satisfactory and suitable form of illumination. Electric Forehead Lamp for Bedside Examinations.—Before leaving this subject, mention should be made of the lamp and pocket battery Fia. 46.—Wall bracket for movable electric light. 50 EXAMINATION OF THE PATIENT shown in Fig. 47. This little apparatus, which dispenses altogether with the mirror, has become an indispensable adjunct to one’s equipment for bedside examinations. The battery is supplied wflth six dry cells, which, unfortunately, must be renewed every four or five weeks. This, however, is a trifling disadvantage compared with the difficulties of inspection by other methods of illumination in private houses. Technic of Objective Examination; Landmarks of the Normal Drum Membrane.—Obviously our examination must be without value unless wre have first prepared ourselves to recognize the physical charac- teristics of the normal ear. The student of otology will put his time to poor advantage unless his growth in technical skill and his knowledge of special anatomy are advanced simultaneously. The writer will, therefore, refer frequently to the anatomy of the parts under ex- amination. As with all kinds of work requiring technical skill, each in- dividual will inevitably in some degree develop his owrn method and technic. There are, however, certain points which the beginner will do well to bear in mind and adhere to strictly. Position of Physician and Pa- tient.—For aural examination it is much better that the physician should be seated to one side of the patient (Fig. 48), rather than directly in front of him with knees parted. This brings his eye within easy visual range of the ear to be examined and is the most comfortable position both for him and for his patient. To examine the opposite ear, it is easy to reverse this position either by revolving his own or the patient’s chair, or by rising and assuming the same position on the other side of the patient. Management of the Light.—The light should be about on the same horizontal plane as the patient’s ear, and so placed that the rays from it to the mirror and from the mirror to the ear shall be as nearly as possible parallel; i.e., they should form as acute an angle as possible. If the focal bistance of the mirror were exactly 10 inches, it would be better to bring doth the light and the ear under examination within that distance of the mirror. Usually, however, the focal distance is rather more than 12 inches, so that the best illumination is obtained by placing the light be- Fig. 47.—Forehead lamp for bedside examination. INSPECTION OF EAR 51 Fig. 48.—Position of physician and patient for aural examination. 52 EXAMINATION OF THE PATIENT hind and to one side of the patient’s head, making the distance between the light and the mirror at least 18 inches. Fig. 49.—Section through adult canal and tympanum. Ftg. 50.—Section through canal and tympa- num of infant at term. Fig. 51.—Diagram showing direction of audi- tory canal of adult. Dotted lines showing changed direction of canal by traction upward. Fig. 52.—Diagram showing direc- tion of auditory canal of infant. Dotted line showing influence of traction downward upon calibre of canal. Use of the Mirror.—In inspecting so small a structure as the drum membrane by reflected light, one must necessarily use but one eye,—i.e. the eye behind the central orifice of the mirror. Both eyes, however, should be kept open, the habit, common to many beginners, of closing LANDMARKS OF THE NORMAL DEEM MEMBRANE 53 the opposite eye, causing a certain amount of unnecessary eye-strain, The mirror should be adjusted with the central orifice opposite the eye nearest the source of light. That is to say, if the light is placed to the patient’s left side, the mirror should be worn over the physician’s right eye, and vice versa. As inspection of the ear frequently occupies several minutes, and tympanic operations much longer, it is important that the physician’s body, head, and neck should be in a comfortable position The light should, therefore, be thrown upon the ear and readjustments made altogether by movements and manipulations of the mirror,—the effort, common with beginners, to direct or adjust it by movements of the head usually resulting in very strained and uncomfortable positions of the neck. Having the light properly focused upon the ear, the student should devote some little time to holding it there steadily, inspecting carefully meanwhile the auricle and particularly the size and condition of the orifice of the meatus. He will make no satisfactory headway in the use of the speculum until he has the light under perfect control. Speculum Examination.—Before practising the use of the speculum, the student may refresh his memory of the anatomical differences between the external auditory meatus in the infant and that of the adult by ref- erence to the accompanying illustrations (49, 50, 51, 52). With adults it is often necessary to draw the pinna upward and backward in order to straighten the canal and bring the drum membrane into view. In the case of infants, on the other hand, one must usually draw the auricle somewhat downward and outward, in order to separate the floor of the canal from the roof and increase the angle between the drum membrane and the axis of the canal. As to the size of the speculum best suited to any particular case, one should select the largest that will enter the meatus easily and without force. Nothing is accomplished beyond discomfort to the patient by the attempt to use too large a speculum. The speculum is gently introduced into the meatus and carried beyond the hairs which occasionally obstruct its lumen near its external orifice. We may then examine the different walls of the meatus for signs of acute or chronic inflammation, and for the presence or absence of obstructing substances,—e.g., masses of ceru- men, foreign bodies, pus, serum, etc. The latter being absent, or having been removed, we may go on to the examination of the fundus of the canal,—i.e., the drum membrane (Fig. 53). Landmarks of the Normal Drum Membrane.—For the purposes of the present study, let us assume that we are to inspect a perfectly normal and healthy drum membrane. Letting the eye follow the roof or posterior wall to the fundus of the canal, one readily recognizes the membrane by the abrupt structural and color changes which distinguish it from the surrounding walls of the meatus. As seen by reflected light, it presents the appearance of a tense membrane stretched across the lumen of the inner extremity of the canal. It varies from bluish white to ivory white in color, having a peculiar sheen, or lustre, which is one of its most con- stant physical characteristics in health. While the color varies somewhat 54 EXAMINATION OF THE PATIENT within physiological limits in different individuals, loss of lustre invariably denotes either structural changes due to chronic disease, necrosis of the surface layer of epithelial cells resulting from acute myringitis, or the deposition of some foreign substance—e.g., mould (aspergilli), dried secre- tion, or powder blown into the canal—upon the drum membrane. The peripheral attachment to the tympanic ring (annulus tympanicus) is clearly outlined, showing the contour of the drum membrane to be irreg- ularly ovoid (Fig. 53). Toward the upper pole of the membrane, and nearer the anterior than the posterior margin, may be seen a small, projecting, glistening point, whiter than the surrounding structures,—usually described as of pin- head size, but in reality much smaller. Its appearance exactly portrays the actual condition,—that of a minute portion of the drum membrane pushed outward and forward into the lumen of the meatus by the small, projecting process of bone behind it,—the short process of the malleus (Fig. 53, c). This little structure, it will be remembered, lies almost in Fig. 53.—Normal drum membrane. the line of attachment of the anterior and posterior ligaments, or axis band, of the malleus, by which it is held firmly in position. It is the most constant landmark of the membrana tympani. It is found always in the upper and anterior part of the membrane, and is sometimes situated so far forward as to be apparently in contact with the annulus tympanicus. Scanning now the surface of the membrane, we discover the second landmark in a more or less prominent line running directly from the short process downward and backward toward the centre of the membrane. This is the manubrium mallei, or handle of the malleus (d). The hammer handle and short process are directly continuous one with the other. Hence each is the guide to the other. Thus, if the hammer handle is first located, by tracing it upward and forward we arrive at the short process; locating first the processus brevis, we trace the hammer handle by its invariable direction downward and backward from the short pro- cess toward the centre of the membrane. Until we have located one or the other of these landmarks, we can never be positive as to what part of the drum membrane we have in view,—nor in cases of middle-ear disease can we always determine with certainty whether it is the drum membrane. THE NORMAL DRUM MEMBRANE 55 Looking now at the lower and anterior part of the drum membrane, we see a brilliantly shining triangular spot, the apex of which is located at the umbo, the opposite base being in the neighborhood of the lower and anterior arc of the tympanic ring. Its direction, therefore, from apex to base is downward and forward (e). This is spoken of as the cone of light, or light reflex, the latter term being not only descriptive but ex- planatory. It is due not to any structural change at this point, but simply to the fact that the tense membrane, drawn inward by the lower end of the hammer handle, falls normally throughout this triangular space into a plane perpendicular to the direction of the rays of light from the mirror, and, as this stream of light and the line of vision are coincident, the trian- gular light reflex results. Naturally, when the position of the drum mem- brane is changed in either direction,—i.e., is either bulging or retracted,— the cone of light is either altered or lost. Alterations or absence of this landmark are, therefore, indicative of displacement, but not necessarily of any structural change in the membrana tympani. Looking once more to the upper part of the drum membrane, we see passing almost horizontally backward from the short process a line or fold which is known as the 'posterior fold of the drum membrane (6). It is almost identical in position with the posterior ligament of the malleus which lies behind it. A shorter fold—so short ir many cases as to be undemonstrable—runs for- ward from the short process to the anterior peri- pheral attachment of the drum membrane (b') It is called the anterior fold of the membram tympani. Above these folds we may sometime* make out two very fine lines, running from the short process forward and upward, and upwarc and backward respectively (a, a'). These lines are known as the attachment strice of Prussak They pass from the short process of the malleus to the extremities of the original tympanic pro- cess or ring. Above these lines, and between them and that ungrooved part of the bony frame of the drum membrane which is formed by the outer plate of the squama, is a small space known as Prussak’s space.1 It is identical in position with the Rivinian notch and is inclosed by Shrapnell’s membrane. Quadrants of the Drum Membrane (Fig. 54). — For convenience of description, the drum membrane is divided into four quadrants. If we imagine a vertical line passing directly downward from the umbo to the inferior margin, the drum membrane will be divided by this line and the hammer handle into two parts, an anterior and a posterior segment. Now, suppose another line, horizontal in direction, to pass through the umbo, Fig. 54.—Diagram showing quad- rants of membrana tensa. 1 Prussak’s space is so called because it marks upon the drum membrane the posi- tion of a small space within the middle ear called by the same name. (See description on page 25.) 56 EXAMINATION OF THE PATIENT and the drum membrane is divided into four quadrants,—viz., the pos- terosuperior (A), the posteroinferior (B), the anteroinferior (C), and the anterosuperior (D).^ The student or physician intending to practise otology, either as a specialty or in connection with other branches of medicine, should make himself thoroughly familiar, by examination of many ears, with the physical picture of the drum membrane as above drawn. At the same time he should bear in mind that what he sees is only part of the outer wall of the middle-ear cavity. Unless, therefore, he can supplement this picture by another, seen through the mind’s eye, of the structures behind the drum membrane, his examination is robbed of half its usefulness. He should know the position and relations of the different parts of the ossicular chain so thoroughly as to be unable to look at the drum membrane without subconsciously calling to mind the relations of the deeper structures within. In recalling these relations the student will perhaps be aided by reference to Fig. 55. In the vault are located the head of the malleus and body of the incus, the former an- teriorly and the latter posteriorly. In the atrium are found the short process and handle of the malleus, the long arm of the incus, and the whole of the stapes. Locating more exactly the parts of the ossicles in the atrium, we find in the antero- superior quadrant the short process of the malleus; in the posterosu- perior quadrant, the incudostapedial joint. Separating the anterosupe- rior from the posterosuperior quad- rant is the handle of the malleus. Behind the posteroinferior quadrant of the drum-head is the niche of the round window. The import- ance of fixing these points clearly and permanently in mind must be apparent. Of the four quadrants of the drum membrane the posterosuperior is the one which most insistently claims our attention in tympanic disease. In acute or chronic tubal catarrh retraction of this part of the drum membrane, by pressing upon the long arm of the incus, interferes in some degree with the movements of the incudostapedial joint, with consequent impairment of hearing. In hyperplastic or sclerotic processes involving the tympanum, the newly formed connective tissue in this region may reduce the mobility of the stapes and bring about very serious loss of function. In acute suppurative otitis media, also, the posterior segment of the drum membrane is commonly most noticeably involved. It is in this region that incisions of the membrana tympani are Fig. 55. — Semidiagrammatic picture, showing relations of ossicles in vault and atrium. Line A-B represents dividing line between atrium and vault. DISPLACEMENT OF DRUM MEMBRANE 57 usually indicated. Obviously this operation, often so lightly undertaken and so imperfectly executed, is not without danger in unskilful hands. Having familiarized ourselves with its physical characteristics in health, we should now scrutinize each drum membrane examined for changes in color, position, or structure. Color.—To the practised eye even slight changes in color are not dif- ficult to recognize. Very considerable experience may, however, be re- quired to enable one to determine whether moderate redness is the result of temporary congestion or is due to a subacute inflammatory process with- in the tympanum. The interpretation of the commoner color changes will be spoken of in a later chapter dealing with the acute middle-ear diseases. Position.—While extreme displacement of the drum membrane in either direction is easily noted, slight changes from the normal, position are quite difficult for the beginner to determine. Displacement outward, or bulg- ing, is usually accompanied by signs of acute inflammation, and is com- paratively easy to determine. The line of attachment of the hammer handle may be rendered indistinct or be completely lost to view as a result Fig. 56.—Bulging drum membrane. Fig. 57.—Retracted drum membrane. of inflammatory thickening or infiltration of the drum membrane. The bulging portion of the drum membrane balloons outward into the lumen of the canal and appears nearer the examiner’s eye, as it really is, than the peripheral portions (Fig. 56). Displacement of the drum membrane inward, or retraction, is com- monly unaccompanied by any of the signs of acute inflammation. The membrana tensa, carrying with it the hammer handle, is moved inward toward the promontory. The drum membrane, in being drawn or forced inward, folds itself about, or tends to form angles with, the structures to which it is attached. Hence the short process, the foreshortened hammer handle, the anterior and posterior folds, and in some cases the annulus tympanicus may appear unduly prominent (Fig. 57). While extreme retraction is easily made out even by the beginner, it requires consider- able practice and experience to determine slight departures from the normal in this direction. The characteristic signs of moderate retraction will be described under tubal catarrh. Structural Changes.—Changes in structure may take the form of uni- 58 EXAMINATION OF THE PATIENT form or localized thickening, of moderate or extreme atrophy of the drum membrane, of cicatrices due to old perforations, or of actual loss of con- tinuity,—i.e., perforations,—which may vary in size from a small pin- head orifice to practical destruction of the membrana tensa. Localized thickening of the drum membrane is shown usually by areas of opacity. Such opaque spots are not infrequently seen in the drum membranes oi individuals whose hearing is not noticeably impaired, and are supposed in some cases to be due to calcareous deposits representing one of the tissue changes resulting from the rheumatic, or uric acid, diathesis. Atrophy, either general or localized, is shown in some cases by abnormal thinness and transparency of the membrana tensa. In others the atrophic area appears opaque and thicker than the rest of the membrane. The latter condition represents an increase in connective tissue at the expense of the fibrous layer of the drum membrane. In such a case the atrophy is revealed only by the abnormal relaxation, or loss of tension, in the areas involved, as shown by Siegel’s pneumatic otoscope to be described presently. Perforations of the drum membrane are best observed by mapping out as nearly as possible the limits of the membrane by its peripheral attachment to the annulus tympanicus, and then looking closely for any loss of continuity in its surface within this space. As the line of demarcation between the roof of the meatus and Shrapnell’s membrane is sometimes obliterated by inflam- matory thickening or infiltration at this point, it is well to begin by letting one’s glance travel inward over the roof of the canal and follow the drum membrane down- ward to its inferior margin. When the margins of a per- foration are clearly defined and there is an appreciable space between the membrane and the inner tympanic wall, the form and extent of the perforation are easily determined. On the other hand, with a swollen tympanic mucosa in contact with a small and ill-defined perforation, its detection may present great difficulties to the beginner. A perforation having been made out, its exact position should next be observed, and this can be determined positively only by noting its relation to either the short process or handle of the malleus. For example, a perforation behind the hammer handle must be in the posterosuperior quadrant. The student will do well to acquire early the habit of drawing diagrams of the drum membrane and noting thereon the morbid changes observed. The accompanying diagram (Fig. 58), made with a few strokes of the pen, indicates more clearly the exact size, form, and location of the perforation than could any amount of descriptive written matter. Variations in Tension.—Conditions which cannot be determined by inspection alone are general loss of tension, relaxation of certain portions of the membrane, adhesions between the membrane and the inner tym- panic wall, fixation of the hammer handle to the promontory, etc. To investigate these conditions one must depend upon some apparatus which, while leaving the drum membrane in clear view, produces alternate con- Fig. 58.—Rough pen-and-ink dia- gram of the drum membrane. VARIATIONS IN TENSION 59 densation and rarefaction of the air in the external auditory meatus. The Siegel otoscope (Fig. 59) admirably fulfils this need. It consists essentially of a speculum (a), the expanded end of which is closed by a thin plate of glass through which the movements of the drum-head may be observed. Communicating with its interior by an aperture in the side of the speculum is a short rubber tube (6) the other end of which is connected with a Delstanche pump or, better, with a rubber bulb (c). With the small end of the speculum moistened and introduced into the auditory canal, the interior of the speculum and of the auditory meatus form practically an air-tight compartment. When the bulb is compressed, the air in the external auditory canal is condensed and the drum-head is forced inward; when pressure upon the bulb is Fig. 59.—Siegel’s otoscope. released, the air in the meatus is rarefied and the drum membrane is sucked outward into the canal. Using the Delstanche pump, we produce the same mechanical results by moving the piston alternately toward and from the drum membrane. Under these manipulations the normal drum- head moves fairly evenly, the posterior segment on account of its larger surface moving rather more than the anterior. In these movements the hammer handle participates, though its excursions are less extensive and more difficult to follow with the eye than those of the posterior segment of the drum membrane. Obviously the use of this instrument is advisable and of value only in chronic disease of the tympanum. It is equally clear that the move- ments of the diseased drum membrane might differ greatly from those characteristic of health, and might throw very considerable light upon the lesion with which the physician has to deal. Thus, a generally relaxed 60 EXAMINATION OF THE PATIENT drum membrane would execute exaggerated movements both in the an- terior and posterior segments, these movement having relatively small influence upon the hammer handle. Atrophy or loss of tension, localized in certain portions of the drum membrane, would be evidenced by the ballooning of these sections, independently of the rest of the membrane, outward into the meatus. Adhesions of the drum membrane to the prom- ontory or to any structures within the tympanum would be clearly dem- onstrated by its fixation at those points. Examination of the Eustachian Tubes.—In all cases of chronic aural disease the condition of the Eustachian tubes must be determined be- fore a correct diagnosis can be made. Inflation of the tympanum, which throws light both on the patency of the tubes and the condition of the middle ear, is therefore an essential part of the aural examination in a large class of cases. There are three recognized methods of inflation,— viz. (1) Valsalva’s method, (2) Politzer’s method, and (3) inflation by means of the Eustachian catheter. Valsalva’s method of inflation has a very limited field of useful- ness. It is performed when the patient, with lips tightly closed and nostrils occluded by compression of the nose, attempts forcible expiration. By this procedure the air in the nasopharynx is condensed and finds its way under pressure through the Eustachian canals to the middle-ear cavities. This normally requires little effort, but naturally calls for greater force if the calibre of the tubes is reduced, or if the pharyngeal orifice of either tube is occluded by localized swelling or congestion in that region. It is a measure of which little use is made in otology. Patients, however, often intuitively acquire the habit of inflating the ears in this way as a means of relieving the discomfort arising from tubal catarrh, and when this is made known to us we may safely conclude that the function of the Eusta- chian tubes is disturbed. We may also in such cases draw conclusions as to which tube is the more occluded by requiring the patient to repeat the act and to note which ear is first inflated,—the ear last inflated cor- responding, of course, to the more obstructed tube. If this ear is also the one in which the subjective symptoms are most marked, we have already some data upon which to base an opinion. Personally the author makes use of the Valsalva method of inflation in the diagnosis of one condition only, —viz., cases in which one may suspect the existence of a small perforation in the drum membrane which can not be determined definitely by inspec- tion alone. In such a case if the patient be required to force air into the tympanum while the drum membrane is kept under view, a drop of fluid— serum or pus—will appear at the point of the perforation, or a more or less shrill whistle will result from the passage of through the small opening in the membrane. If the drum membrane balloons outward into the lumen of the meatus without the appearance of cither of these phenom- ena, it may be confidently assumed that no perforation exists. This, in the writer’s opinion, is the one condition in which the Valsalva method is of real diagnostic value. That is to say, there is no other condition in POLITZER’S METHOD OF INFLATION 61 which all that may be learned from Valsalva inflation may not be better obtained in some other way. It is a measure which may easily become a habit with the patient to the detriment of the ear, and its general or frequent use is to be advised against. Politzer’s method of inflation resembles that of Valsalva in that both depend upon condensation of the air in the nasopharynx. Since this procedure was first proposed, the universal recognition of its value and its general adoption by otologists of all countries have resulted in some slight modifications in the instruments employed. Politzer’s inflating apparatus (Fig. 60) consists of a compressible, soft rubber air-bag communicating at one end with a piece of rubber tub- ing the end of which fits over a hard rubber tubular nozzle, or nose-piece. Fig. 60.—Politzer’s inflating apparatus. The air-bag is provided with a valve by means of which, after the contained air has been expelled, a fresh supply is taken in without the necessity of removing the nozzle from the patient’s nose. Technic.—The patient and physician are seated opposite each other. The former is given a glass of water and told to take a sip of it into his mouth and to swallow it at a signal from the physician. With his left hand the physician now inserts the nozzle of the inflating apparatus into the patient’s nostril corresponding to the ear he wishes to examine, at the same time closing the nasal passages by pressure upon both alae nasi. The air-bag meanwhile is held ready for use in the physician’s right hand. The patient is now told to swallow and, synchronously with this act on his part, the air-bag is quickly and forcibly compressed. The act of deglu- tition brings the soft palate into contact with the posterior wall of the pharynx and effectually closes the nasopharynx. The air in the naso- 62 EXAMINATION OF THE PATIENT pharynx is at the same time condensed by the influx of additional air from the inflating bag, and forces its way through the Eustachian tubes into the tympanic cavities. By reason of the valvular opening in the air-bag, inflation by this method may be repeated several times without removing the end-piece from the patient’s nose. A modification of Politzer’s method is by requir- ing the patient, instead of swallowing water, to repeat some word ending in K,—thus, hock, hock, hock, etc.,—the lingering enunciation of this guttural as a terminal sound serving to hold the soft palate in contact with the pos- terior pharyngeal wall and thus shut off the nasopharynx from the laryngopharynx below. The first method, however, has the advantage that the act of swallowing not only closes the nasopharynx but also serves to separate the anterior from the posterior wall of the membrano-cartilaginous tube, and thus facili- tates the freer passage of air to the tympanum. Another method is by requiring the patient, after the tip of the inflating apparatus has been properly adjusted, to close the lips tightly and forcibly balloon out the cheeks. This, of course, does not close the nasopharynx, but serves to condense the air in the entire respiratory tract. Obviously the pressure of additional air from the air-bag would tend to force the patency of the tubes. It seems to be a combination of the Valsalva and Politzer methods. It is very useful in dealing with cer- tain children who will not co-operate with the physician in carrying out the method as proposed by Politzer. Politzer’s method of inflation has a wide field of usefulness. As a diagnostic measure its posi- tion is distinctly secondary to inflation by cathe- ter. It must be used, however, in certain classes of cases, among which are the following: (1) Young children, who will rarely submit to catheterization. (2) Very nervous adults who in some cases (rare) will not submit to the use of the catheter at the first sitting. (3) Adult patients in whom nasal abnormalities or occlusions contra- indicate or render impossible the use of the catheter (rare). Fig. 61.—-Eustachian catheter (silver). INFLATION BY CATHETER 63 Inflation per Catheter.—In the writer’s opinion the catheter offers by far the most satisfactory and reliable method of examination in the great majority of cases. Its full usefulness, however, requires a degree of technical skill and experience in interpreting the sounds heard through the otoscope, which can be acquired only after long practice. The student of practical otology can not, therefore, too carefully or persistently practise its use. If at the end of a year’s practice in a busy clinic he has acquired considerable skill in catheterization, he will assuredly be yet more skilful at the end of a second year. By skill is meant not merely the ability to find the tubal orifice, but to accomplish this with the least mechanical irritation of the nasal and pharyngeal mucosa, and therefore with minimum injury and discomfort to the patient. As it is absolutely essential that the necessary instruments be of right material and design, a few words may well be devoted to them here. The Catheter.—The accompanying figure (Fig. 61) clearly illustrates the correct size and form. The expanded outer end (a) receives the tip or end-piece of the inflating apparatus. The small end (b) must be smooth, —i.e., without sharp edges which might injure the nasal or tubal mucosa. The curve near the end enables the physician, after it has passed into the cavity of the nasopharynx, by rotating the catheter, to bring the beak into the Eustachian orifice. While the curve indicated in the illustration is the one best suited to a majority of cases, it obviously must be changed somewhat to meet the anatomical requirements of certain pharynges. The catheter should therefore be made of malleable silver to allow of such changes as may be required. The ring (c) is of use as a guide by which in a case presenting anatomical difficulties the surgeon may know in what direction the beak is pointing. As to length, the writer uses and prefers a catheter of 5% inches. It should not exceed 6 inches. Any unnecessary length—i.e., which leaves more of the catheter outside of the nose than is necessary for its manipulation—simply interferes with its proper control and adds to the patient’s discomfort. A catheter longer than 6 inches has never in the writer’s experience been found necessary. The catheters come in three sizes, or calibres, of which the illustration represents the intermediate, and the one indicated in the great majority of cases. The largest is practically never used by the wrriter. The smallest is necessary in some cases.2 The Dench inflating apparatus (Fig. 62) is undoubtedly the best so far devised for catheter inflation. Between the air-bag (a) and the tip (c) which fits into the outer end of the catheter, is a hard-rubber bottle (6). This bottle enables one to employ medicated vapors in the treatment of the tubal and tympanic mucosa. When the stopper is in the position 2 Catheters of hard rubber, described in some text-books, are to be condemned, if for no other reason, because they can not be thoroughly sterilized. Catheters of hard “German silver” offer the decided disadvantage that they can not be bent. Catheters with bulbous ends do not admit of as fine adjustment as those of smaller terminal calibre, but may offer distinct advantages as practice instruments for beginners. 64 EXAMINATION OF THE PATIENT shown in the illustration (d-e), air expelled from the air-bag does not pass through the bottle and is therefore not influenced by its contents; but when the stopper is turned so as to occupy the position indicated by the line f-g, the air must pass through the bottle before reaching the catheter and is in this way impregnated with any volatile drugs—e.g., alcohol, Fig. 62.—Dench inflating apparatus. solutions of menthol, camphor, iodine, etc.—therein contained. The rubber tubing prevents the movements of the air-bag from being commu- nicated to the catheter. The valvular opening into the air-bag enables the physician to repeat the act of inflation any number of times without moving the catheter. The Otoscope or Diagnostic Tube (Fig. 63). — This is simply a piece of rubber tubing, about 30 inches long, into each end of which is fitted a small hollow ear-piece somewhat similar to, but smaller than, the ear-tips Fig. 63.—Diagnostic tube. of the ordinary stethoscope. Usually one is of white bone and the other of hard black rubber. This enables one to distinguish them,—an obvious advantage in a busy clinic, where the aurist may be pardoned for wishing to reserve one end for himself, leaving to his patients the exclusive use of the other. Inserting one end into his own ear and the other into that of his patient, he can during inflation obtain fairly accurate information as DIAGNOSTIC VALUE OF OTOSCOPE 65 to the condition of the tube and tympanum by the auscultatory signs obtained through the otoscope. With a normal tube and tympanum, he will hear during inflation a rather low, blowing sound giving somewhat the impression of a sound originating in his own ear. While usually low, the pitch will of course vary somewhat with variations in the calibre of different tubes. Of abnormal conditions which may be made known to us by the oto- scope, may be mentioned the following: (a) Absolute occlusion of the tube as shown by absence of all sound of air entering the tympanum. Obviously this sign is without value unless the physician has sufficient technical skill to feel sure that his catheter is properly placed. (b) Patent but abnormally narrow tube, shown by clear sound of unusu- ally high pitch. (c) Abnormally wide tube, made known by very low-pitched, rough sound and the absence of any resistance to the compression of the air- bulb. (d) Presence of excessive mucus or other fluid secretion within the tube, shown by small, intermittent rales, finally ceasing as the moisture is dis- tributed or blown into the nasopharynx by the return air current. (e) Presence of fluid in atrium, shown by more or less constant, bub- bling rales, giving the impression of air passing through fluid,—the actual physical condition. (f) Abnormal relaxation of the drum membrane, as shown by certain characteristic sounds due to the flapping outward of the drum membrane during compression of the air-bag, and its recoil as the air pressure subsides. (g) Small perforations of the drum membrane, made known by whistling, squeaking, or singing sounds due to vibration of the edges of the perforation. (h) Large perforations in, or absence of, the drum membrane, made known by the sensation of air blowing against the physician’s drum membrane. It is quite useless to attempt to describe more minutely than as given above the various sounds and signs obtained through the otoscope during inflation. With practice and careful study of cases, these sounds will soon rank among the most valuable guides as to the conditions present. Technic.—The physician is seated directly opposite his patient, with the ends of the diagnostic tube adjusted in his own and the ear to be inflated (Fig. 64). The patient is directed to hold the head with chin slightly depressed, to keep the mouth closed, to continue breathing quietly through the nose, and to resist the impulse to jerk or move the head back- ward and out of the physician’s reach. He is asked to hold the bottle of the inflating apparatus, this arrangement leaving the air-bag in convenient reach of the physician’s hand. To be in proper relation to the mouth of the tube, the catheter must reach the nasopharynx by way of the inferior meatus of the nostril corresponding to the ear to be inflated (Figs. 65 and EXAMINATION OF THE PATIENT 66 Fig. 64.—Position of physician and patient during catheter inflation TECHNIC OF CATHETER INFLATION 67 66). At the start the catheter is held between the thumb and forefinger of the right hand, the tip of the inflating apparatus being held between the third and little fingers of the same hand, ready for introduction into the outer expanded end of the catheter as soon as the latter shall have been placed in proper position. Holding the catheter at first almost in the vertical position, with the curved end pointing forward, the tip is intro- duced into the inferior meatus of the nostril corresponding to the ear to be inflated. In order to insure against its entering the middle meatus, it is now quickly elevated from the vertical into the horizontal position as it enters the nostril, the tip being kept in light contact with the nasal floor, and is carried directly backward until it is felt in very light contact with the posterior pharyngeal wall. It is next rotated outward toward the ear until the guide ring points in a direction about midway between the hori- zontal and vertical planes. It is then withdrawn slightly until its beak is arrested by the anterior wall of the fossa of Rosenmuller, which, it will be remembered, corresponds in position with the posterior wall of the Eustachian orifice. Over this elevation it is now lightly drawn, the cathe- ter being then rotated further outward and upward until the guide ring points somewhat upward, describing an angle of 30 or 35 degrees with the horizontal plane. This should bring its extremity into its proper position in the pharyngeal mouth of the tube. The outer end of the catheter is now transferred to the left hand and the tip of the inflating tube carefully inserted.3 The right hand is thus free to grasp the air-bag, and the difficult part of the procedure is accomplished. The sounds heard through the otoscope now furnish additional information as to the exact position of the catheter within the Eustachian orifice, and enable one to make such slight readj ustments as are necessary to give the best inflation. Other methods of placing the catheter have been described,—as, for instance, (1) by passing the catheter as before, through the inferior meatus until its beak touches the posterior wall of the pharynx, rotating it toward the opposite ear, withdrawing it until its curved end is engaged by the posterior margin of the nasal septum, then rotating it downward and outward in the opposite direction until its beak enters the Eustachian orifice; (2) passing the catheter backward with beak resting on the nasal floor, noting when the beak sinks into the nasopharynx and then rotating it directly into the orifice of the tube to be inflated. These are distinctly less reliable than the method first described, which is the one which should be practised by the student of practical otology. By so doing he will surely in time acquire a facility which will enable him to dispense with 3 Some aurists prefer and advise that the tip of the inflating apparatus should be securely inserted into the outer end of the catheter before the latter is introduced into the patient’s nose. This prevents the discomfort which might arise during its adjust- ment after the catheter is in position. In the writer’s experience a more delicate manip- ulation of the catheter has seemed possible by the method above advised. A little practice will enable one to make the connection between the catheter and the inflating apparatus without discomfort to the patient. 68 EXAMINATION OE THE PATIENT some of the steps described. Thus, the practised aurist learns to ignore the fossa of Rosenmuller as a guide, and intuitively withdraws the catheter to the right position opposite the mouth of the tube. The student, however, will do well to follow literally the steps here described, which alone will lead to the degree of technical skill which robs this procedure of its discomfort to the patient. Fig. 65.—Correct pathway of catheter to posterior pharyngeal wall. Fig. 66.—Correct position of catheter within tubal orifice. Fig. 67.—Incorrect introduction of catheter,— i.e., through middle meatus. There are one or two points mention of which may be of use to the beginner. He should learn at the start to recognize surely the sound which comes to him through the otoscope when the end of the catheter is not in the mouth of the tube but in the fossa of Rosenmuller. This sound is loud, rough, does not have the character produced by air passing through an open tube, and does not sound as if originating in or near the physician’s own ear. Unless this sound is definitely recognized, the stu- dent may waste considerable time in the mistaken belief that he is prac- Plate IV. Fig. 68.—Tongue depressor (A). Fig. 70.—Nasal speculum (C). Fig. 72.—Cotton applicator (E). Fig. 69.—Nasal speculum (B). Fig. 71.—Laryngeal mirror (D). Fig. 73.—Nasal probe (F). SURGICAL EMPHYSEMA 69 tising inflation while in reality his catheter may never have entered the Eustachian orifice. When properly placed, the catheter is held in position by slight pressure of the outer end against the nasal septum, this tending to throw the other end, or beak, in the opposite direction and further into the Eustachian orifice. If now the patient complains or shows signs of pain, learn from him whether the pain is referred to the nose or the throat. If in the nose, slight shifting of the position of the catheter here or easing of the pressure will usually relieve the discomfort. If, however, the pain is referred to the throat, it is due often to rotation of the catheter too far in one or the other direction. A little care in correcting these minor errors of technic will render this a bearable, if never a pleasant, experience to the patient. Surgical Emphysema.—There is one accident which must be mentioned as a possible result of careless catheter inflation,—viz., traumatic emphy- sema. It occurs when air from the inflating apparatus is propelled through some false passage into the tissues surrounding the membrano-cartilaginous tube. It probably always indicates either an abrasion of the tubal mucosa, or an incorrect position of the catheter, as a result of which air is forced through the mucous membrane into the tissues beneath. The accident usually gives rise to very sharp and sudden pain, which is, therefore, an indication that the inflation should be immediately discontinued. The diagnosis is confirmed when palpation of the tubal region—i.e., between the tip of the mastoid and the angle of the jaw and downward along the anterior border of the sternomastoid—is accompanied by distinct crepitus. While painful and often alarming to the patient, the condition is not dan- gerous, the air being usually absorbed within from 24 to 48 hours. The patient should, therefore, be assured that the symptoms will disappear spontaneously within a day or two. If treatment is called for, very gentle massage may help to expel the air from the tissues. The Nose, Nasopharynx, and Throat. — The relation of the ear to the nose and nasopharynx is so intimate, and the diseases of the two regions are so interdependent, that one must assume for the special stu- dent of otology some preliminary or collateral study of rhinology and laryngology. No examination of the ear is complete until one has care- fully inspected the nose and nasopharynx. The author will speak very briefly of this region, dealing only with what he believes to be absolutely essential to a complete aural examination. A forehead mirror with focal distance of from 12 to 15 inches gives very satisfactory illumination. In addition to the mirror, the instruments necessary in an examination of the nose and pharynx are a tongue depressor (Fig. 68), a nasal speculum (Figs. 69, 70), a postnasal mirror (Fig. 71), cotton applicators (Fig. 72), and a nasal probe (Fig. 73). One saves time by observing some regular order in one’s examination, and the author prefers to examine first the nasal cavities, then the posterior wall of the pharynx and the faucial tonsils, and last the nasopharynx, or postnasal space. 70 EXAMINATION OF THE PATIENT Examination of the Nose.—From the view-point of the anrist the examination of the nose is chiefly for the purpose of determining any condition within the nasal cavities which may predispose to, or directly excite, nasopharyngeal congestion and catarrh of the Eustachian tubes. The conditions to be looked for are: (1) Abnormalities of the nasal septum,—e.g. (a) deflections to one or the other side. This may be very slight or so marked as completely to occlude one nostril. It may be limited to the anterior cartilaginous portion, or include the posterior or osseous part of the septum, involving the vertical plates of both the vomer and ethmoid, (b) Localized septal ridges or spurs, which again may be confined to the cartilaginous part (ecchondroses) or to the posterior bony portion (exostoses), or the ridge may include both, running from before backward and upward along the line of junction of the vomer to the cartilage in front and to the ethmoid plate behind. (2) Hypertrophy of the turbi- nated bodies. By anterior rhinoscopy one can usually see only the anterior half of these structures. If one or both inferior turbinates are noticeably enlarged, we should determine by palpation whether the increase in size is due to an actual hyperplasia—i.e., depositions of new connective tissue— or to engorgement of the turbinal vessels. In the former case the turbinal body offers considerable resistance to compression by means of the nasal probe, and its size is only moderately reduced by the application of adren- alin or cocaine. When the enlargement is due to vascular engorgement, the turbinate pits deeply on pressure but quickly regains its former size as soon as the compressing probe is removed, and it shrinks enormously under the influence of the suprarenal preparations. The middle turbinates are not quite so easily inspected. When the septum is deflected to one or the other side, it may be quite impossible to see the middle turbinate on the side to which the septum is bent, without first shrinking the corresponding inferior turbinal body. Usually, however, by means of a proper speculum and by tilting the patient’s head somewhat backward, both middle turbinates may be brought into view. Whenever either of these bodies are noticeably enlarged, the corresponding nasal cavity should be thoroughly exsanguinated by means of adrenalin chloride. This aids in determining to what extent, if any, the enlargement is due to simple congestion. The nasal cavity should now be carefully inspected for nasal polypi and for a possible escape of pus from the middle meatus, —i.e., from beneath the middle turbinate. Either of these conditions might point to disease involving either the frontal sinus or the anterior ethmoid cells, or both. The Throat.—In examining the throat, one should endeavor to train one’s eye to observe quickly, prolonged use of the tongue-depressor caus- ing discomfort, reflex pharyngeal irritation, and often retching. This may render subsequent examination of the postnasal space unsatisfactory or impossible. The tongue-depressor should be introduced into the mouth only so far as is necessary to press upon the most elevated and arched portion of the dorsum of the tongue,—pressure too far back causing re- POSTERIOR RHINOSCOPY 71 flex irritation and “gagging,” or retching. With the tongue depressed, one should note quickly first the size of the faucial tonsils,—i.e., whether they are of normal size or hypertrophied. As to the standard by which the size is to be judged, so distinguished an authority as Bosworth is of the opinion that whenever the tonsil is demonstrable by inspection, it should be regarded as representing an abnormal growth. The more com- monly accepted view is that any projection of the tonsil toward the median line so as to encroach, however slightly, upon the cavity of the pharynx is abnormal, and represents hypertrophy. It must be remembered that tonsils but slightly enlarged while the patient is in his usual health may be subject to great increase in size under the influence of any nasopharyngeal congestion or inflammation,—e.g., a common “cold.” Moderate hyper- trophy of the tonsils in adults may, however, be absolutely without in- fluence upon the ears. In young children, on the other hand, any consid- erable enlargement of the faucial tonsils is almost invariably associated with the presence of pharyngeal adenoids. Tonsillar hypertrophy has, therefore, a very decided bearing upon the condition of the ears in childhood. On the posterior pharyngeal wall one should note the presence or absence of the following conditions,—viz.: (a) Dilatation of the superficial veins, a condition which in adults very frequently results from nasal obstruction and the irritation due to mouth-breathing during sleep, (b) The so-called granular pharynx, characterized by the presence of granula- tions upon the pharyngeal wall. They are usually most noticeable along the median line of the pharynx just behind and below the uvula. This condition in children almost invariably indicates the presence of naso- pharyngeal adenoids, (c) The presence of dried or tenacious secretion adhering to the pharyngeal wall. With this is frequently seen a more or less glazed condition of the pharyngeal mucosa, a condition characteristic of atrophic rhinopharyngitis, (d) The physical signs of acute pharyngitis. Posterior Rhinoscopy.—The examination of the postnasal space by means of the small rhinoscopic mirror forms an important part of the examination of adult patients suffering from aural disease. It consists of depressing the tongue by means of a tongue-depressor, and inserting a small mirror backward over the tongue, under and behind the soft palate, so that by reflected light one may obtain a clear view of the roof of the pharynx, the posterior margin of the nasal septum, the posterior ends of the middle and inferior turbinal bodies, the fossae of Rosenmuller, and the pharyngeal orifices of the Eustachian tubes. Here, even more than in examining the posterior pharyngeal wall and faucial tonsils, it is important to acquire the habit of quick but accurate observation. Of possible abnor- malities bearing upon an existing aural disorder, one should look especially for the following conditions,—viz.: (A) Hypertrophied lymphoid tissue upon the roof of the nasopharynx. An adenoid growth in this region, if of considerable size and located well forward, will inevitably cut off from view the upper part of the nasal septum. If the whole of the posterior 72 EXAMINATION OF THE PATIENT margin of the septum can be seen, and the roof of the pharynx arches evenly above this without noticeable obstructing mass, the cause of an existing nasal or aural disorder must be looked for elsewhere. (B) Lym- phoid hypertrophy in the fossce of Rosenmuller. In some cases—and par- ticularly where previous operations for the removal of adenoids have been performed—the pharyngeal roof may be practically clear yet con- siderable masses of adenoid tissue are found behind the Eustachian ori- fices in the fossae of Rosenmuller. This condition is particularly likely to induce morbid changes in the middle ear, leading to permanent impair- ment of hearing. (C) Hypertrophy of the posterior ends of the inferior turhinal bodies. This condition is nearly always dependent upon some other lesion in the anterior nares. (D) Congestion, or swelling, of the tissues about the Eustachian tubes. This is often quite noticeably present during acute tubal catarrh, and is usually dependent upon some coexisting nasal or nasopharyngeal lesion. Any of the above conditions would necessarily have some bearing upon an aural disorder. Their presence or absence is best determined in adult patients by posterior rhinoscopy. With young children, on the other hand, the use of the postnasal mirror is in most cases impossible, and we are obliged to depend upon digital examination. The technic of examin- ing the postnasal space by reflected light has been so fully described in most text-books on diseases of the throat and nose, that its repetition here hardly seems necessary.4 Inspection of this part of the respiratory tract forms, however, a very important part of every aural examination in adults, and should be carefully practised by every aurist who would do thorough and effective work. Obviously there are many cases—including all cases of non-suppura- tive aural disease—in which the examination would be altogether unsatis- factory without careful testing of the patient’s hearing power. This, however, is a subject of such importance in otology that it seems better to consider it in a separate chapter. 4 A clear and satisfactory statement of the technic of this procedure and the diffi- culties it may present will be found in Coakley’s “Manual of Diseases of the Nose and Throat.” CHAPTER III. FUNCTIONAL EXAMINATION OF THE COCHLEAR APPARATUS; HEARING TESTS. To the average practitioner of medicine the functional examination of the ears is an unknown art. If he has kept his medical knowledge intact as he received it from the medical school, he should be in a position to make a practical differentiation between the commoner nerve lesions. But if his patient suffers from impaired hearing, he can not by his own efforts determine whether this functional loss is due to an attack of acute tubal catarrh or to a lesion involving the labyrinth or auditory nerve. Nor is it an easy matter for him to gain from otological literature or text- books a practical working knowledge of the more important hearing tests, their rationale and the proper ‘method of applying them. The author wishes, therefore, if possible, to present the essentials of this important subject in a form more easily available both by the busy physician and by the overworked medical student. Before can draw any practical conclusions from a functional exam- ination, we must have in mind some normal standard of hearing with which to compare results. It will be remembered that the normal ear appreciates musical tones between two extremes of pitch,—the tone pro- duced by a sonorous body executing 18 double vibrations per second rep- resenting approximately the lower limit of normal hearing, and 41,000 double vibrations per second representing the upper tone limit.1 Air Conduction and Bone Conduction of Sound.—Sound is brought to the organ of hearing in two ways,—(1) by air conduction, as when the vibrating body is at a variable distance from the ear, the sound waves being transmitted through the medium of the surrounding air; and (2) by bone conduction, as when the vibrating body is in contact with the skull, the sound waves being propagated through the solid medium of the cranial bones. Rinne demonstrated in 1855 that the human ear in health appre- ciates a given musical sound—e.g., that produced by the C tuning-fork (128 d. v.)—twice as long by air conduction as by bone conduction. This fact may be demonstrated in the following way: the fork having been thrown into maximum vibration, place the end of its handle in contact 1 There can be no doubt that slight variations both as to the upper and lower tone limits may occur in different normal individuals. These variations possibly explain in part the different conclusions of different observers. Thus, Bezold, as a result of his examination of a large number of normal ears, placed the lower limit at 12 double vibrations per second. Helmholtz gave 32,500 double vibrations per second as the upper limit of possible tone perception. Politzer places it at 40,000 double vibrations, and Bezold at 41,000 double vibrations per second. 41,000 double vibrations correspond to the sound produced by the Edelmann-Galton whistle shortened to 0.5 and this may be accepted as the upper tone limit for the human ear. 73 74 FUNCTIONAL EXAMINATION. COCHLEAR APPARATUS with any portion of that side of the skull corresponding to the ear to be examined. The sound will be conveyed to the ear by means of the cranial bones. Request the person upon whom this test is made to indicate by raising his hand the exact moment, as nearly as he can determine it, at which the tone is lost to him. Now remove the fork from the skull and, without setting it in fresh vibration, bring the ends of the still vibrating prongs opposite the auditory canal of the ear to be examined. The tone will be again distinctly heard, and will continue to be appreciated during a period about equal to that during which it was heard through the cranial bones. In other words, it is heard by air conduction about twice as long as by bone conduction. This approximately l-to-2 ratio between bone conduc- tion and air conduction is one of the most constant functional characteristics of the normal ear, and is changed only in certain forms of aural disease. Normal Hearing Distances for the Watch=tick, the Acoumeter, the Conversational Voice and Whisper.—The experience of many observers in making a large number of hearing tests in persons with normal ears has established certain hearing distances for particular sounds as representing approximately the normal standard. The Watch-tick. — This is a popular hearing test with the laity and medical profession alike. Nat urally this sound varies considerably in intensity with the size, form, thick- ness of covers, etc., of different watches. Taking, however, a man’s watch of average size, its tick will be heard by the normal ear of a young adult—say, of twenty to thirty-five years—at a distance of 40 to 50 inches. This hearing distance is sub- ject to considerable variations within physiological limits, 30 inches not necessarily implying impaired hear- ing, and 60 inches falling within the hearing range of some individuals. As age advances, the hearing distance for the watch is gradually dimin- ished, and in old age—-i.e., after sixty years—may be completely lost in individuals who, nevertheless, retain sufficient hearing power for the ordinary purposes of life. It is not always a reliable test of the usefulness of the organ, many persons whose hearing for the watch- tick is much below par having apparently no difficulty in interpreting the voice sounds in conversation. Politzer’s Acoumeter.—This very useful little instrument is so clearly shown by Fig. 74 that a detailed description is hardly necessary. The horizontal metal bar (a) is immovably attached to the upright column Fig. 74.—Politzer’s acoumeter. THE CONVERSATIONAL VOICE AND WHISPER 75 of hard rubber. The upper rod, or hammer, is movable so that when the short end (6) is depressed, the hammer is raised, and when the short lever is released, the hammer falls of its own weight, and, therefore, always with the same force, upon the metal bar. It produces a clicking sound somewhat similar to the watch-tick, but very much louder. The different parts are of prescribed size and length, so that different instruments are supposed to produce approximately the same intensity of sound. The results of many tests have established 45 to 50 feet as about the normal hearing distance for the acoumeter. The Conversational Voice and Whisper.—This is the final test of the patient’s hearing power as a means of communicating with the world of practical affairs. It is, therefore, the test in which he is most vitally interested. In making this test, the physician and patient stand at opposite ends of the room, the ear to be examined being turned toward the physician. The opposite ear is closed by a finger pressed firmly into the meatus. Standing thus sideways toward the physician, the patient can not see his lips, and the element of lip-reading is eliminated. The physician now repeats the words or numbers which he wishes to employ, the patient having been instructed to repeat them after him. If the patient can not hear, or hesitates or calls the words incorrectly, the physician at once moves nearer and repeats the experiment, using different words, but those having as nearly as possible the same sound values. The dis- tance between patient and physician is thus reduced until one is reached at which the words are repeated promptly and correctly. This is esti- mated in feet and carefully noted upon the test card. Owing to the difficulty in commanding always the same tone and intensity of voice, we are accustomed to test also with whispered words. In whispered speech, tone or pitch variations are practically eliminated, and it is much easier to cultivate a uniform intensity. Thus, one may employ a very low whisper, which can barely be heard by the normal ear at a few feet from the ear, or a very loud whisper, as when one partially fills one’s lungs and speaks the words without voice as forcibly as possible. Between the low and the forced whisper, a moderate whisper may be employed, which with a little practice may be made nearly, if not quite, of uniform intensity. Words spoken in the forced whisper can be heard by the normal ear at a greater distance than the same words spoken in a moderately low conversational voice, and the moderate whisper of one who has practised its use can probably be heard by the perfect organ of hearing at about the same distance as the moderately low speaking voice. Considerable time and effort have been expended by many distinguished students of otology in an attempt to determine the normal hearing dis- tance both for the conversational voice and for whispered speech. Owing to variations in pitch, timbre, volume, etc., in the voices of different individuals, and also to possible differences in clearness of enunciation, such questions can not be determined exactly. Making allowance for such voice variations, however, it may be said, probably with approximate 76 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS accuracy, that the average conversational voice will be comprehended by the normal ear in a perfectly quiet room or hall at a distance of from 60 to 70 feet, and that the whisper of moderate force will be heard at about the same distance. Recapitulation.—Defining briefly the functionally normal ear, we may say that an ear which hears the watch tick at a distance of 35 to 50 inches, and the acoumeter 40 to 50 feet; which hears and correctly inter- prets the conversational voice and the whisper of moderate force at a dis- tance of 60 to 70 feet; which appreciates musical tones ranging between 18 double vibrations and 41,000 double vibrations per second; and which hears a vibrating tuning-fork of 128 double vibrations, C, twice as long by air conduction as by bone conduction, is normal so far as its function is concerned. Before taking up in regular order the various tests by which we en- deavor to determine the site of an aural lesion, I wish to speak briefly of certain functional changes which occur quite regularly in advanced tym- panic disease, and of others which are equally characteristic of the deafness caused by labyrinthine or auditory nerve lesions. These functional changes are few in number; but once they are accepted as typifying the two main divisions of aural disease (i.e., tympanic and labyrinthine), it will be seen that the various functional tests are for the most part but convenient methods of establishing the presence or absence of changes the significance of which we already know. Changes in the Tone Limits.—Loss or Impairment of Hearing for the Lower Musical Tones.—It is a fact well known to otologists that lesions confined to the sound-conducting apparatus are almost invariably accompanied by some loss of hearing for the lower tones of the musical scale while the perception of high musical tones may be in no way inter- fered with. A very simple experiment will enable us to demonstrate this phenomenon as characteristic of tympanic disease. Ask a person with normal hearing to close both ears with a finger placed in each meatus. Now bring a vibrating tuning-fork of low pitch—e.g., of 26, 32, 36, 40, 43, or 48 double vibrations—in front of the auricle. Its sound will not be heard. Repeat this experiment with the C-1 fork (64 d. v.) and its tone can not be excluded, while forks of still higher pitch—e.g., c1 (256 d. v.)—are heard quite loudly in spite of any effort to close the external auditory canals. This loss of hearing for the lower musical tones occurs in stenosis of the Eustachian tubes, in chronic catarrhal otitis media, or as a result of occlusion of the external auditory meatus. In other words, lesions involv- ing any part of the sound-conducting mechanism interfere with the per- ception of low musical tones, the hearing for the high notes being affected comparatively little thereby. This phenomenon may seem a little more comprehensible if we bear in mind that very low musical tones represent long sound waves with slow vibrations of relatively great amplitude, whereas tones of high pitch are produced by short sound waves with rapid vibrations of very small amplitude. It is conceivable that mechanical INCREASED HEARING BY BONE CONDUCTION 77 obstacles to the movements of the ossicular chain would interfere first with the slower and greater excursions necessary to the transmission of the lower tones, and only in very advanced stages of ossicular fixation with the very rapid but slight excursions required to transmit the high musical tones. In elevation of the lower tone limit, or impaired audition for the lower musical tones, then, we have the first functional change which is characteristic of disease of the sound-conducting mechanism. Loss or Impairment of Hearing for the Higher Tones of the Musical Scale.—While not necessarily or invariably present, diminution or loss of hearing for the extreme upper tones of the musical scale occurs with sufficient regularity in diseases of the labyrinth or auditory nerve to justify a diagnosis of labyrinthine involvement in a majority of cases. This is rather difficult to understand, since it would at first seem that morbid processes within the labyrinth would be likely to involve any of the cochlear structures. It is known, however, that that portion of the basilar membrane which has to do with the perception of the higher musi- cal sounds is situated in the lower part of the cochlea,—i.e., in that part which is in most immediate relation to the foot-plate of the stapes and the membrane of the round window. It is believed-that in most labyrinthine disorders (i.e., other than congenital deafness or deaf-mutism) this part of the cochlea and membrana basilaris is most frequently involved, and that the perception of the high tones is thereby interfered with. However this may be, it is a fact which clinical experience has abundantly confirmed, that with acquired lesions of the inner ear some loss of hearing for the upper end of the musical scale is almost invariably present. The author has repeatedly made functional tests in patients to whom half the notes of the Galton whistle were totally inaudible, whose lower limit was only moderately changed. Here, then, in lowering of the upper tone limit we have a counter functional change which points quite strongly to disease of the labyrinth, and we are prepared for our first step toward a differential diagnosis. Changes in the Period of Hearing by Bone Conduction. — In- crease.—To Schwabach is due the credit of having definitely established the fact—already partially demonstrated by Rinn6—that in disease of the sound-conducting apparatus the period of hearing by bone conduc- tion is distinctly prolonged. This may be easily demonstrated by the following simple experiment: holding a vibrating tuning-fork in contact with the skull of a person of normal hearing, ask him to indicate by a motion of his hand the moment at which the tone is no longer perceived. Now, without removing the fork from the skull, require him to close both ears by a finger placed in each external auditory meatus. The sound of the still vibrating fork will again be distinctly heard. In other words, we have created the mechanical equivalent of an obstructive lesion of the con- ducting apparatus with the result that bone conduction is increased. The explanation of the increase in hearing by bone conduction in tympanic disease proper is not altogether clear. Bezold believed that in 78 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS bone conduction the sound is not transmitted directly through the cranial bones to the structures of the cochlea, but is conducted through bone to the drum membrane, or at least to the foot-plate of the stapes, and is transmitted thence to the labyrinth; in other words, that it is distinctly an osteo-tyrnpanic conduction. In explanation of the increased bone con- duction regularly resulting from tympanic disease, he advanced the fol- lowing hypotheses: (1) That normally the whole conducting chain— drum membrane, ossicles, and annular ligament connecting the foot-plate of the stapes to the rim of the oval window—is in a state of perfectly mobile equilibrium. (2) That any abnormal or pathological condition within the tympanum, either by changing the position of the stapes 6r inducing inflammatory changes in the region of the oval window, places the fibres of the ligamentum annulare in some degree on the stretch. (3) That stretching of the annular ligament interferes with the transmission of sound waves reaching the ear by air conduction, but distinctly favors the propagation of sound waves through the cranial bones to the foot-plate of the stapes. According to this theory it is also obvious that ankylosis of the stapes due to hyperplasia of connective tissue about the oval window should also tend to increase and prolong hearing by bone conduction. This theory, while not wholly convincing, is as satisfactory as any yet advanced so far as the writer knows. It does not, however, satisfactorily explain the increased hearing by bone conduction which occurs when the ear is closed by a finger placed lightly in the auditory meatus. This phe- nomenon, in the author’s opinion, is better explained as follows: In hear- ing by bone conduction part of the force of the vibrations thus transmitted is expended upon the column of air in the auditory meatus and thus con- veyed outward and dispersed through the medium of the surrounding atmosphere. When, however, a finger is inserted into the orifice of the meatus, this canal is converted into a closed cavity, and constitutes a resonance chamber in which the sonorous vibrations are collected and thrown back upon the drum membrane to augment those transmitted directly from the cranial bones to the annular ligament and foot-plate of the stapes. That the increased perception of sound is brought about by the walls of this artificially closed cavity acting as resonators, and not by compression of the contained air, is shown by the fact that the sound is heard loudest when the finger tip is placed lightly in the meatus, and is reduced when the finger is forced deeply into the canal so as to produce condensation of the inclosed air. The phenomenon in its causation is somewhat analogous to the increased noise which we have all experienced in a railroad train during its passage through a tunnel. Leaving the question of its causation out of consideration, it is an established clinical fact that lesions of the conducting mechanism, not complicated by labyrinthine disease, are almost invariably accompanied by a prolonged period of hearing by bone conduction. The test for this phenomenon is as follows: Supposing the physician’s ears and hearing to be normal, he holds the handle of a vibrating tuning-fork in contact with DIMINISHED HEARING BY BONE CONDUCTION 79 his own mastoid process. As soon as he loses its sound the fork is trans- ferred, without renewing its vibration, to the mastoid of the patient. If he then perceives its tone, it may be assumed that his bone conduction is abnormally prolonged. Increased audition by bone conduction is the second and, in the author’s opinion, the most important functional sign of disease of the conducting apparatus. Diminished Hearing by Bone Conduction.—That the influence of labyrinthine or auditory nerve lesions upon hearing by bone conduction should differ from that exerted by tympanic disease hardly requires ex- planation. The labyrinth and auditory nerve with the cortical brain centres constitute the perceptive mechanism proper. When the hearing is impaired as a result of disease in any of these structures, it follows logically that the hearing power is diminished by all the normal pathways of sound transmission. Hearing is, therefore, reduced by bone conduction and air conduction alike. The test for this functional change is exactly the reverse of that by which we detect increase in bone conduction. The vibrating tuning-fork is first held in contact with the patient’s mastoid process cor- responding to the ear to be examined. When he indicates that its tone is no longer heard, the fork is transferred to the mastoid of the physician, —provided that his ears are functionally normal. If its tone is now dis- tinctly heard by him, the patient’s hearing by bone conduction is assumed to be less than normal. Loss or diminution of hearing by bone conduction is characteristic of all forms of labyrinthine or auditory nerve disease. We have, then, certain functional changes which show simply impair- ment of hearing, and which are met with in diseases affecting either the perceptive or the sound-conducting apparatus. Chief among these are (1) impaired audition for the watch or acoumeter, and (2) impaired hear- ing for the conversational voice and whisper. These changes do not materially aid us in locating the site of the lesion. Of differential changes—i.e., of functional changes characteristic of tympanic disease on the one hand, or of labyrinthine or nerve disease on the other—there are four which outrank all others in importance—viz.: Functional changes characteristic of disease of the conducting appa- ratus: (1) Elevation of the low7er tone limit, or loss of hearing for the lower tones of the musical scale. (2) Increased, or prolonged, audition by bone conduction. Functional changes characteristic of labyrinthine disease: (1) Reduc- tion of the upper tone limit, or loss of hearing for the higher musical tones. (2) Diminution or loss of hearing by bone conduction. The writer believes that these changes in the tone limits and in the perception of sound as conveyed through the cranial bones, constitute the basic facts to be determined by our functional examination, and that the various differential tests are but convenient methods of demonstrating their presence or of determining their extent. There are many functional irregularities shown by different individ- uals suffering from chronic deafness,—e.g., disproportionate loss of hear- 80 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS ing for certain sounds, as of the conversational voice as compared with the watch and acoumeter, or vice versa; disproportionate impairment for certain words or consonants, etc. In spite of much careful study of such changes by O. Wolf, Bezold, and others, they have not yet been sufficiently worked out to be of great practical value, either in locating the lesion or as an indication of the line of treatment to be pursued. We shall now take up briefly the method of applying the various tests. Method of Examination. — Watch and Acoumeter. — In testing with a watch or acoumeter, the ear not under examination is closed by pressing a finger firmly into the orifice of the meatus. The watch is held for a moment close to the ear to be examined to familiarize it with the character of the sound. It is then removed four or five feet from the ear, and brought gradually nearer until its sound is heard, the distance in inches being noted. The experiment is now repeated once or twice for corroboration, the patient closing his eyes so that his imagination will not be stimulated by his knowledge of the position of the watch. The dis- tance thus finally reached is carefully noted upon the test card. It has been found that the watch-tick can be heard farther if the watch is first held close to the ear and the distance gradually increased than if the reverse method be employed,—i.e., holding the watch outside of the hearing range and gradually approximating it to the ear.2 The latter method is more reliable, since the imagination is brought less into play. If the watch sound can not be heard even when held within an inch of the ear, it should be placed in contact with the auricle, and the result, according to whether its sound can or can not be heard, should be thus noted upon the test card,—“heard only on contact,” or “not heard on contact.” In cases in which the watch is heard only on contact, or but a few inches from the ear, it is better to discard this test altogether and depend upon the acoumeter. One reason for this is the fact that such patients often make more or less pronounced functional gains for other sounds with relatively little change for the watch-tick; and again, the patient may so concentrate his attention upon his hearing for this particular sound as to become depressed or even neurasthenic because his functional gain as shown by this test does not seem sufficiently marked. With chronic aural disease as with other physical disorders it is desirable that the patient’s attention should not be focused upon his symptoms. In cases of slight impairment of hearing, however, the watch-tick affords a most useful test. The acoumeter is employed in exactly the same way as the watch except that one begins the test at a greater distance from the patient,—i.e., standing at the opposite end of the room. The result is noted upon the test card either in inches or feet, according to the degree of deafness. 2 This phenomenon is explained by the fact that the individual’s power of auditory concentration and accommodation enables him to follow a sound once heard to a dis- tance greater than that at which it is first perceived when the sounding body is gradually moved toward the ear. SOUND VALUES OF DIFFERENT CONSONANTS 81 Whispered and Conversational Speech.—The patient’s hearing power for whispered and spoken words or numbers furnishes us with a quick and convenient method of determining functional impairment or loss. We can not employ this test intelligently, however, without some preliminary study of sound values,—i.e., of the varying carrying power of the different letters, alone and in combination. Sound Values in Conversational Speech.—There are certain general facts which experience quickly impresses upon those coming in frequent contact with the partially deaf. We soon learn, for example, that the vowel sounds are heard farther and with greater distinctness than the consonants. A person with advanced catarrhal deafness may, therefore, hear the vowel sounds with comparative ease after the hearing for many of the consonants has become difficult, or possible only when they are spoken in loud tones. This fact explains the frequently repeated statement of the hard-of-hearing: “I hear your voice, but can not understand what you say.” It also explains the not uncommon experience, in testing the hearing of such a patient for spoken words, that he repeats not the word we have employed, but one having the same vowel sounds: thus, we call the word “faster,” and he says “master,” guessing at the initial consonant. Further than this, we find that certain consonants are heard better than others; that in testing with whispered numbers, those beginning with s— e.g., 67 or 76—may in some cases be heard easily at 20 or 30 feet, while numbers beginning with f or th—e.g., 53 or 35—are heard only with dif- ficulty at one-third of that distance. Or conditions may be reversed. Obviously the subject of sound values is one of considerable importance in practical otology. Of the vowels a, e, and i are heard farther than o and u. While it has long been known that the vowels each possess a distinct tone or pitch (Helmholtz), it remained for Oskar Wolf3 to prove that the consonants also possess each its own tone. By this is meant that each consonant, spoken without voice (i.e., whispered) gives rise to a certain number of rhythmic vibrations per second, which determines its particular tone. This fact throws some light on the difficulties of the hard-of-hearing in interpreting conversational speech. For if the patient’s ear has lost the power of responding readily to the tone inherent in a certain consonant, he will hear this consonant poorly or not at all. If in such a case the con- sonant in question is spoken in a tone of voice falling within the patient’s range of tone perception, he will hear the voice but will not distinguish the consonant sound. Hence his confusion in following the trend of conversation. The tones (pitch) inherent in the different letters are distributed rather widely over the musical scale. The letters 1, m, n, and r are in the lower half of the musical scale, while the self-tones of the sibilants, s and sh, belong to the upper half of the scale. Bezold found that deaf-mutes who 3 Sprache und Ohr, akustiseh-physiologische und pathologische Studien, 1871. 82 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS possessed “islands” of tone perception which included the self-tones of the principal consonants, could be taught by means of the ear to speak; but that deaf-mutes having “islands” of tone perception which did not include the self-tones of the consonants, could not be taught through the ear. The various elements of speech differ very considerably in the dis- tances at which they can be heard by the normal ear. The s and sh sounds, for example, carry farthest and can be heard three times as far as f, v, t, th, d, and k. Again, f, v, t, d, and k are heard farther than b or p. While it is not important that the aurist should know the exact hearing dis- tance for each consonant, it is quite essential that he should know and bear in mind that certain sounds are heard more easily than others. Thus, in the whisper test, the normal ear will be able to hear the words “sense” and “shine” farther than the words “pepper” and “five.” When, however, the hearing is impaired by disease, the relative auditory acuteness for different sounds may be changed. An approximate analysis of the relative loss of hearing for the different elements of speech may be made in the following way: Standing at a distance from the patient well beyond his range of hearing for the whisper, we begin our test with words or numbers spoken in a rather low whisper. It will be found that while most of the selected words are quite beyond his power of audition, certain words or numbers will be caught and repeated promptly and correctly. These words and the distance at which they are heard should be noted. We now move a few feet nearer the patient and repeat the test, when certain other sound values for this particular patient may be demonstrated, which also should be noted on the history card. The next step is to reduce the distance to a point where the patient can hear and repeat all words promptly and correctly. This distance must, of course, be recorded as representing his hearing distance for the moderately low whisper. We now7 possess rather definite data. Confining ourselves, for example, to the use of numbers, our results may read somewdiat as follows: Right Ear: Moderately low whisper,—6 feet (i.e., distance at which all numbers are heard). N-sounds,—e.g., 19, 9, 99,—9 feet. S-sounds,—e.g., 16, 67, 76,—12 feet. Such functional reactions are by no means uncommon in chronic aural disease. With such a record, one wrould not be likely to fall into exag- gerated or erroneous conclusions as to a functional improvement when none had occurred. In other words, the haphazard use of words in test- ing is apt to lead to confusion, leaving the question of functional gain or loss in doubt. So distinguished an authority as the late Professor Bezold4 advised 4 Text-book of Otology, p. 72. DETERMINATION OF LOWER TONE LIMIT 83 that we make use exclusively of numbers in our functional tests, express- ing his belief that we can obtain with numbers all the data that might be gained by testing also with words. My own actual experience has led me to a quite different conclusion in regard to this particular point. If in testing, either with conversational voice or whisper, we employ only num- bers, the patient quickly learns to associate certain sounds as the examiner utters them with the corresponding numbers, even though his actual hear- ing of them has not improved. His improvement is, therefore, more appar- ent than real. The writer believes that one should use words as well as numbers, the alternation of the one with the other furnishing the very best criterion of the patient’s hearing power for conversational speech. The conversational voice is also a useful means of determining the degree of impairment, but is of little value as a test for purposes of comparison. In cases of very advanced deafness, however, even the forced whisper may be unavailable, in which case it becomes necessary to use the voice, speak- ing in a very loud and moderately high tone. In such cases one must depend upon other tests to demonstrate slight changes either in the way of functional gain or loss. Before leaving this subject, a word should be said as to the disparity between the estimated normal hearing distance for speech and whisper and the dimensions of the average testing room at the physician’s command. We must remember that the sole purpose of functional testing is to deter- mine the degree and character of the impairment. The aurist whose testing room is but 30 feet long soon learns to moderate the intensity of his whisper or voice in accordance with the space at his command, and his results are practically as reliable as they would be in a larger room or hall. Determination of the Lower Tone Limit (Figs. 75 and 76).—For this purpose a set of tuning-forks is essential. Hartmann’s set, consisting of five forks, supplies a convenient means of roughly estimating the lower tone limit in cases of very advanced catarrhal deafness. These forks represent C-tones one octave apart,—i.e., 128, 256, 512, 1024, and 2048 double vibrations per second. But since the lowest fork of this series— i.e., 128 d. v.—is about three octaves higher than the lowest tone perceived by the normal ear, a lower fork is required in cases of slight or moderate impairment of function. The large clamped fork (Fig. 76) is capable of executing either 26 or 64 double vibrations per second. With the clamps or weights attached to its prongs, it vibrates 26 times per second; and with the weights removed, 64 times per second. With this fork supple- menting the Hartmann set, we can determine positively whether the lower tone limit is appreciably elevated. While 26 d. v. does not represent accu- rately the lower limit of normal tone perception, this fork is the lowest employed in many aural clinics, it being assumed that if the patient clearly perceives its tone, his hearing for the lower musical notes can not be greatly reduced. In testing the patient’s hearing for the lower musical tones, he should be required to close the ear not under examination. Using first the low, 84 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS clamped fork (26 d. v.), it is set in vigorous vibration and held near the external auditory meatus. If its tone is distinctly heard, it is assumed that his lower tone limit is normal, or nearly so; if heard but faintly and for a moment or two only, one may infer that the lower tone limit is elevated, and that the hearing for still lower tones—e.g., 18, 20, 21, and 24 d. v.—is lost. If not heard at all, the clamps should be removed from the fork, 128 d.v. 256 d.v. 512 d.v. 1024 d.v. 2048 d.v. Fig. 75.—Hartmann’s tuning-forks. and the hearing tested for the next higher tone of this series of forks,—i.e., C-1, or 64 d.v. per second. If this also is inaudible to the patient, the hear- ing is tested with successively higher forks—e.g., 128, 256, 512 d. v., etc.— until one is reached which the patient can distinctly hear. This tone, or vibration rate, is then recorded upon the test card as the lower tone limit, —i.e., as nearly as it can be determined by this incomplete set of forks. In using so large and heavy a fork as that producing 26 vibrations per second, the patient may feel the vibrations yet not hear its tone, and this DETERMINATION OF LOWER TONE LIMIT 85 sensation he may mistake for tone per- ception. He must be made, therefore, to differentiate between the sensation due to the impact of the aerial move- ments upon the ear, and the per- ception of these movements as a continuous musical tone, or hum. If there be difficulty in making this difference clear to the patient, he may be required to describe the charac- ter of the sound, to state whether it is of high or low pitch, etc. If one ear only is involved, a comparison of the impression received by the opposite ear will usually remove any doubt as to whether the tone is heard by the diseased organ. Another possible source of error in the use of tuning- forks is the occurrence of overtones. In testing with unclamped forks,—e.g., that producing 64 d. v.,—one usually hears immediately after it is set in vibration not only its fundamental tone (C-1), but also certain higher tones, or harmonics, and these may be the only sounds heard by the patient. This, of course, might lead the examiner to very erroneous conclu- sions. One may easily eliminate over- tones, however, by exerting moment- ary pressure with the thumb upon one of the prongs at a point as near as pos- sible to the handle or shaft. It is im- portant that this point be kept in mind. With the limited set of forks above described, it is obviously impossible to determine the lower tone limit exactly. They enable us, however, in the great majority of cases to arrive at correct conclusions as to the character of the lesion so far as we are able to deter- mine it from changes in the lower tone limit. For exact notation of the functional changes resulting from treat- ment, on the other hand, there is obvious advantage in the possession Fig. 76.—Large tuning-fork. 86 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS of a set of forks by which the lower tone limit may be exactly deter- mined. For example, a patient may not be able to hear 128 d. v. (c), but may hear 256 d. v. (c'). Testing with the Hartmann set, we are obliged to note 256 d. v. as the lowest tone heard by the patient. But there are six full tones between 128 d. v. and 256 d. v. The lower tone limit may, therefore, be 144, 160,171, 192, 213, 240, or 256 double vibrations per second. If now, after treatment, the patient can hear 128 d. v., it makes a great deal of difference whether his lower tone limit previously had been 144 d. v. (d) or 256 d. v. (c'), for in the one case he would have gained a single note, and in the other his tone range would have been extended by an entire octave. Bezold’s Tuning-forks.—Undoubtedly the most complete set of instru- ments for detecting gaps in the range of musical tone perception is that of Bezold and Edelmann of Munich. This set consists of ten large forks provided with clamps by which the tone of each fork may be varied, four smaller unclamped forks, two organ-pipes, and a modified Galton whistle. These forks are heavy, somewhat cumbersome, rather expen- sive, and are not made in this country. They can be ordered, how- ever, through any reliable firm of instrument dealers, and enable one thoroughly to test the patient’s hearing throughout the entire range of normal tone perception. They were designed especially for detecting tone gaps or islands of hearing in partial deaf-mutes, for which purpose they are undoubtedly the most complete and perfect instruments made. For measuring the degree of functional impairment in the hard-of-hearing, on the other hand, the full set is certainly not required. For determining exactly the lower tone limit, the author in his private work makes use of a set of tuning-forks which were made for him accord- ing to his own specifications (Fig. 77). The prongs of these forks are of uniform width and thickness, the variations in pitch being regulated by gradations in their length. Without clamps they produce every full note from C-2 (32 d. v.) to c2 (512 d. v.), and by weighting forks C-2, D-2, and E-2 notes corresponding to 16, 18, and 20 d.v. are obtained. These forks have proved most satisfactory and useful in the writer’s practice. Impaired hearing for the lower musical tones points to a tympanic lesion, and the loss of hearing for successively higher tones marks, as a rule, the progress of the disease. Determination of the Upper Tone Limit (Fig. 78).—Diminution, or lowering, of the upper tone limit is most easily determined by the Galton whistle. This is practically a closed organ-pipe provided with an ob- turator, by moving which the tube may be lengthened or shortened at will. As the tube, or pipe, is shortened, the length of the sound wave is short- ened and the vibration rate is increased. On the outer surface of the tube is a numbered scale,—0, 1, 2, 3, etc.,—provided with a mechanism by which changes in the length of the tube are indicated. By certain mathe- matical calculations these numbers and fractions thereof may be converted into the corresponding numbers of vibrations per second. This, however, ALTERATIONS IN BONE CONDUCTION 87 is not essential to practical diagnosis, the numbers themselves soon be- coming associated in the aurist’s mind with the normal in tone perception and certain degrees of departure therefrom. In testing with the Galton whistle, the instrument is held near the ear to be examined, the opposite ear being closed by a finger in the meatus. Air is propelled through the tube by compression of the rubber bulb attached to it. The patient will be likely to distinguish two sounds,—i.e., a puffing or blowing sound as of escaping air, and a clear whistle. He should be required to indicate the point at which a clear whistle is heard. With the improved Bezold-Edelmann whistle, a clear note is heard with the marker at 0.5. Shortening the tube further than this, no clear whistle is heard. On the other hand, when the tube must be lengthened beyond 0.5 in order to obtain a note audible to the patient, it becomes evident that his upper range of tone perception is lowered. Some diminution of hearing for the extreme upper tones of the musical scale is physiological in old age, and may occur in certain disorders of the general nervous system. Generally speaking, however, any appre- ciable diminution of hearing for the upper musical tones in a person not over fifty years of age points either to a labyrinthine or nerve lesion, or to some aural disorder in which the labyrinth is secondarily involved. An ingenious mechanism, which, if it could be made generally available, would add greatly to the accuracy and scientific value of our hearing tests, is the so-called tone-range audiometer devised by Dr. Lee Wallace Dean and Mr. C. C. Bunch, of the State University of Iowa.5 Roughly speaking, this instrument consists of an electrically driven toothed wheel, the cogs of which come successively in contact with a magnet, the tone being produced by the rhythmic opening and breaking of the circuit. It is said to produce an approximately pure musical tone, the intensity of which can be controlled, and the pitch of which can be rapidly or slowly elevated or lowered between the tonal limits of 30 and 10,000 double vibrations. The advantages of such an instrument over tuning forks in the detection of gaps in tone perception are obvious. As with every notable advance in diagnostic method and accuracy, it is probable that this mechanism in the hands of its distinguished inventor will add to our scientific knowledge of disease by establishing shades of functional difference between certain closely related lesions,—shades of difference not definitely determinable by the older methods. Changes in Hearing by Bone Conduction.—There are two methods of determining changes in the duration of hearing by bone conduction, one of which has already been mentioned. Assuming the examiner’s ears to be functionally normal, the handle of a vibrating tuning-fork of 128 d.v. (c) is held in contact with his own mastoid process, and transferred as soon as its tone is no longer heard to that of the patient corresponding to the ear to be examined. If its tone is distinctly heard by him, it is inferred that bone conduction is increased; and if we count the number of seconds during which it is heard by the patient and find this to be, say, 10 seconds, we may record 5 Dean and Bunch: Audiometer: Laryngoscope, August, 1919. 88 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS this result upon our test card as follows: “B. C., fork 128 d. v., increased ( + 10 seconds).” If the sound of the vibrating fork thus transferred from the physician’s to the patient’s mastoid is not heard by the latter, we may assume at least that bone conduction is not increased. The reverse experi- ment is now tried,—i.e., the vibrating fork is held first against the patient’s mastoid and transferred, when its tone becomes inaudible, to that of the examiner. If its tone is now audible to the physician, we know that the patient’s hearing by bone conduction is diminished; and the degree of dimi- nution will be determined by the length of time during which it is heard by the physician. Supposing this to be 10 seconds, the result may be noted thus: “B. C., fork 128 d. v., diminished (-10 seconds).” If the patient’s duration of hearing is neither more nor less than that of the examiner, his bone conduction is charted “normal.” The method of examination just described is convenient and quite re- liable so long as the examiner’s ears, and particularly his hearing by bone conduction, conform to the normal standard. So soon, however, as his hearing becomes impaired, it is obvious that he will no longer be able to make correct deductions from a comparison of the patient’s hearing with his own. If we wish to reduce this test to an absolutely correct basis, it is necessary that we should know the normal duration of hearing by bone con- duction for certain forks, and determine whether the patient’s hearing con- forms to this standard. The corresponding forks of different sets vary, however, in the intensity of sound produced and in the period during which they can be heard. It is necessary, therefore, that the aurist should deter- mine for himself the normal sound duration for his particular forks to be used in this test. This can be done with approximate accuracy by testing them {i.e., determining in seconds their sound duration) upon a certain num- ber of supposedly normal ears, which also show a normal standard as gauged by other tests,—e.g., watch, acoumeter, whisper, Rinne, etc. And as two forks—i.e., the 128 d. v. and 256 d. v. forks of the Hartmann set—will suffice for all tests of bone conduction, it is not a difficult matter to determine their normal period of sound transmission through the cranial bones. In testing by this method, the fork should be struck forcibly, to obtain its maxi- mum vibration, and the handle at once placed in contact with the mastoid process of the ear under examination. The number of seconds during wrhich its sound is heard by the patient should be counted by means of a stop watch. Supposing, for example, that we are using a fork the normal duration of which has been found to be 20 seconds, it is an easy matter to determine by how many seconds the patient’s hearing by bone conduction is either in- creased or diminished. This method of testing bone conduction is given as the only one open to the physician who is himself the victim of advanced aural disease. With fairly normal ears, however, the first method is much quicker, infinitely more convenient, and yields sufficiently accurate results. Impairment or absolute loss of hearing by bone conduction in one ear is sometimes difficult to determine, from the fact that the sound may be trans- mitted through the cranial bones to the opposite ear. Usually, however, Fig. 77.—Kerrison’s set of tuning-forks. The number opposite each fork corresponds to the number of double vibrations which that par- ticular fork (in producing its fundamental tone) executes. The number opposite forks C-2, D-2, and E-2indicate the number of double vibrations which these forks execute when the clamps are removed. With the clamps adjusted and moved to different positions upon the prongs, much lower tones—i.e., tones corresponding to 14, 16, 18, 20, 22, 24, and 26 double vibrations per second—can be produced Fig. 78.—Galton whistle. SCHWABACH’S TEST: RINNE’S TEST 89 one can obtain sufficiently positive data to enable one to draw correct con- clusions as to the character of the lesion. Having tested the patient’s hearing both as to the tone limits and as to changes in bone conduction, we are in a position to form a fairly definite opinion as to the site of the lesion. In the writer’s opinion, further tests, while of undoubted value, are for the most part corroborative. That is to say, with elevation of the lower tone limit and increased bone conduction, the hearing for the upper tones remaining normal, the inference is definitely in favor of disease confined to the conducting apparatus. If, on the other hand, the upper tone limit is lowered, the lower limit but little changed, and hearing by bone conduction is decidedly diminished, we are not likely to prove in error in concluding that the labyrinth or nerve is chiefly at fault. Schwabach’s Test.—Schwabach attempted to determine the periods in seconds during which tuning-forks of different pitch are heard through the cranial bones by the normal ear. He proved that there is an absolute in- crease in bone conduction in diseases of the conducting apparatus. His test, therefore, proposed the determination of the patient’s duration of hear- ing by bone conduction of a large number of forks, and their comparison with the normal standards therefor. This test adds little to the knowledge obtained from the simpler experiment by which increase or diminution of bone conduction is determined. Its results are corroborative. Rinne’s Test.—Rinne’s experiments proved two things,—viz.: (1) that the normal ear hears a vibrating tuning-fork twice as long by air conduction as through the cranial bones, and (2) that in tympanic disease this ratio be- tween air conduction and bone conduction may be absolutely reversed. The c fork (128 d. v.) and the c' fork (256 d. v.) of the Hartmann set are appro- priate for this test. For young adults the c' fork is preferable, but with pa- tients past middle life, in whom hearing by bone conduction is physiologically reduced, the c fork (128 d. v.) gives more reliable data. Rinne’s test is ap- plied in the following way: the fork is set in vigorous (maximum) vibration and the handle at once placed in contact with the mastoid corresponding to the ear to be examined. As soon as the patient indicated that its tone is no longer heard, the fork is removed from contact with the cranium and the ends of the still vibrating prongs are brought near to and opposite the orifice of the meatus. If now he again hears its tone and continues to hear it during a period approximately equal to its duration by bone conduction, we must regard this as the normal ratio between hearing by bone conduction and by air conduction. This in otological literature is spoken of as a “positive Rinne.” It may be found, however, that after hearing by b. c. ceases, the patient will no longer be able to hear by a. c. This, of course, points to dis- ease, or at least derangement, of the conducting apparatus. We must now reverse the experiment, holding the vibrating fork first in front of the ear, and transferring it when its sound is no longer heard to contact with the mas- toid. It is possible that its tone will again be heard through the cranial bones during a period about equal to its previous duration by air conduction. This reversed ratio indicates advanced tympanic disease, and is spoken of 90 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS as a “negative Rinne.” This is one of the most reliable and useful tests of chronic middle-ear disease. No other functional test shows so graphically the various stages of functional impairment. Thus, in the earliest stages of tympanic disease the hearing by a. c. will be very slightly diminished while the hearing by b. c. will be very slightly increased. The ratio be- tween b. c. and a. c. will, therefore, not be reversed, the peiiod of hearing by a. c. after hearing by b. c. has ceased being simply shortened. This is spoken of as a “diminished positive Rinne.” The diagnostic significance of the various reactions to this test in uni- lateral aural disease may be stated as follows: A. Hearing noticeably impaired, Rinne negative, the ratio between b. c. and a. c. being reversed; these reactions would point to an advancd lesion of the conducting apparatus. B. Hearing noticeably impaired, Rinne positive, the ratio between b.c. and a. c. being normal, would suggest disease of the labyrinth or auditory nerve. C. Hearing not appreciably impaired, Rinne positive and showing normal ratio, would suggest a normal ear. D. With hearing but slightly impaired, a “diminished positive Rinne” would indicate a comparatively early stage of tympanic disease. In such a case the progress of the lesion is likely to be marked by progressive short- ening of the period during which hearing by a. c. outlasts hearing by b. c. The prognostic value of this test is indicated by the following fact, as to the correctness of which I am sure that all experienced aurists will bear me out,—viz., that when, as a result of chronic or slowly developing tympanic disease, the ratio between b. c. and a. c. is absolutely reversed, the hearing may be improved by treatment, but can never be restored to the normal standard. Weber’s Test.—This consists in holding the handle of a vibrating tuning- fork (128 d. v. or 256 d. v.) in contact with the median anteroposterior line of the vertex of the skull. The sound will be transmitted through the cranial bones, and, since bone conduction is increased in tympanic disease, the sound will be conducted in greater volume to the diseased ear in all uni- lateral lesions of the conducting mechanism. The patient, therefore, has the impression of hearing it altogether with the diseased ear. On the other hand, if hearing by bone conduction is diminished in the diseased ear, as is the case in lesions of the labyrinth or auditory nerve, the sound will be appre- ciated chiefly by the normal ear. In unilateral deafness, therefore, the sound of a tuning-fork held in the mid-line of the skull will be referred by the patient to the diseased ear if the lesion is located in any part of the conduct- ing apparatus, and to the sound ear if the disease is confined to the labyrinth or auditory nerve. It is a recognized fact that in certain individuals with perfectly normal ears the hearing by bone conduction may be referred chiefly to one side or the other, purely as a result of inequalities in the thick- ness, or other anatomical differences, between the opposite sides of the skull. This, however, is exceptional. In the average run of cases Weber’s test is an easily applied and useful corroborative test, confirming what we have TOTAL DEAFNESS 91 already learned as to the relative increase or diminution of bone conduction in one ear as compared with the other. Gelle’s Test.—This test is dependent upon the fact that any force exert- ing sudden inward pressure upon the stapes pushes this ossicle farther into the oval window and, by increasing intralabyrinthine pressure, reduces tone perception, whether the sound wave has reached the tympanum by air conduction or by bone conduction. Gelle’s experiment consists of con- densing the air in the external auditory meatus by means of a Siegel’s speculum and bulb, or similar apparatus, a vibrating tuning-fork being held, meanwhile, in contact with the skull. Normally, as the drum men- brane and ossicles are forced inward, intralabyrinthine pressure is increased and the sound of the tuning-fork is thereby diminished. As the pressure upon the drum membrane is removed, the stapes rr oves outward, intrala- byrinthine pressure regains its equilibrium, and the sound of the vibrating fork increases in volume. In this way the intensity of the sound may be alter- nately increased and diminished. It is held that when tympanic changes causing fixation of tne ossicles have occurred, the labyrinth will not be affected by condensation of air in the external auditory meatus, and hearing by bone conduction will not be diminished. A negative result is, therefore, held to point to ossicular fixation. So far as the writer can see, this test is of theoretic value in only one condition,—viz., when the stapes is firmly fixated or immobilized, within the oval window. It is not of great practical value in diagnosis. Bing’s Test.—This experiment is mentioned in most text-books as a means of differentiating labyrinthine from tympanic lesions. A vibrating tuning-fork is held in contact with the skull,—preferably upon the mastoid process of the ear to be tested. As soon as its tone can no longer be heard, a finger is introduced into the external auditory meatus. It is claimed that the tone will again be distinctly heard if the disease be located within the labyrinth, but will not be heard, or will be heard but faintly and during a diminished period, if the lesion be confined to the tympanum. This test is somewhat unreliable from the fact that in the early stages of either labyrinthine or tympanic disease the sound will recur after closure of the meatus, and in very advanced stages the experiment is likely to give nega- tive results whether the disease be located within the labyrinth or the middle ear. With marked increase in bone conduction, one is not likely to think of labyrinthine disease because the sound of a vibrating fork held against the skull can be prolonged by closing the meatus, nor will one doubt labyrinthine disorder in the presence of marked diminution of bone con- duction because this experiment results negatively. Total Deafness.—In the foregoing pages we have described the various hearing tests which are of use in the analysis of partial deafness,— i.e., the impairment of such patients as are commonly spoken of as “hard of hearing.” Practically all cases of functional impairment due to tym- panic disease, and many cases in which the perceptive mechanism is also involved, come under this classification. There is, however, another class 92 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS of cases in which many of these tests are of little or no value,—I refer to cases of bilateral or unilateral impairment so great as to approach or actu- ally to constitute total deafness. When one ear is very nearly or totally deaf and the other ear retains in large degree its quota of hearing power, the possibilities of error in diagnosis are not inconsiderable. Cases have come under the writer’s observation in which the patient has been sub- jected to much useless treatment simply because a careless or inexperienced practitioner had failed to recognize the fact that one or the other ear was totally or hopelessly deaf. Such profound deafness always means disease of the cochlea or of the auditory nerve. A word must therefore be said as to the determination of profound or total deafness. Total bilateral deafness is not difficult to determine. In the first case, the patient is unable to hear a word that is said, even though it be spoken in a loud voice or shouted close to the ear. With tuning-forks also, unless there be remaining islands of tone perception, he hears no sound. It sometimes occurs with tuning-fork tests that the patient receives the impression that he hears the sound when in reality he only feels the impact of the aerial vibrations against the skull. This is particularly apt to occur when we use a large fork in maximum vibration. We are usually able to detect this error by his inability to describe the sound correctly. With total deafness, bone conduction also is lost. But here again we must guard against apparent contradiction resulting from the patient’s inability to differentiate between his sense of the vibrations against the skull and tone perception. Absolute Deafness in One Ear.—This, when the opposite ear is function- ally normal or nearly so, may be difficult to determine. The tuning-fork tests of tone perception, for example, present the following difficulties. With the normal ear closed by a finger in the meatus, the patient can not hear the lower musical tones,—i.e., tones from 18 to 42 d. v. But when we r6ach 64 d. v., or a little higher, it will be found impossible to exclude its tone from the normal ear, however tightly it be closed. If now he be directed to close both ears, and still can hear the tuning-fork and with equal intensity, we may conclude that it is heard only by the sound ear. Loss of hearing by bone conduction may be even more difficult to deter- mine from the fact that tones of a vibrating tuning-fork held at any point on the skull may be transmitted through the cranial bones to the sound ear. It is best to begin by holding the fork in contact with the mid-line of the skull (Weber). The patient usually states that the sound is heard alto- gether by the normal ear. The experiment is now several times repeated, selecting each time a point nearer the diseased ear. If finally, with the tuning-fork in contact with the mastoid of the diseased ear, the patient still refers its sound to the healthy organ, we may be sure that hearing by bone conduction is completely lost in the ear under examination. Un- fortunately, the value of this test may be negatived by the patient’s inability to interpret correctly his own impressions. With many of these cases the final test of profound or total deafness is MALINGERING; SIMULATED DEAFNESS 93 the patient s inability to hear the conversational voice. V oice sounds may, however, be heard by the sound organ, even though it be closed by a finger tightly pressed into the meatus. To meet this difficulty we have a reliable instrument in Barany’s noise apparatus (Fig. 79). This consists essentially of a small metal box provided with an ear-piece and containing clock-like machinery which when wound up produces a continuous rough metallic sound. It is used as follows: The ear-piece is introduced into the canal of the sound ear and by pressure upon a button the machinery is set in motion. While this sound is being poured into the normal ear, words or numbers are spoken in a loud voice close to the diseased ear. If they are not heard, we may be sure that the ear under examination is totally deaf. If the words are heard, we may be equally confident that they are not heard by the ear into which the noise apparatus is pouring its sound, and that the diseased ear is, therefore, not totally deaf. While the profound type of deafness above described is never met with in lesions confined to the conduct- ing apparatus, it is the rule in certain lesions of the inner ear,— e.g., diffuse suppurative labyrin- thitis. In such cases Barany’s noise apparatus, or some similar instrument, is absolutely essential. Malingering; Simulated Deaf- ness.—Pretended deafness is said to be comparatively common in coun- tries where army service is com- pulsory. In America it is met with chiefly in the caseof impostors seek- ing indemnity on account of pre- tended injuries to one or both ears. Simulated bilateral deafness, if the individual persistently refuses to give evidence of any hearing power, is naturally difficult to detect. To disprove complete bilateral deafness, one must depend on one’s ability to catch the individual off his guard. It has been suggested that by making disparaging remarks about him in the presence of a third party one may be able to determine by changes in his facial expression his ability to hear the conversational voice. Usually, however, the pretense of complete bilateral deafness is too difficult to maintain, and as a rule it is unilateral deafness the genuineness of which the aurist is called upon to determine. There is no absolutely reliable test for feigned deafness, the astuteness of the malingerer and the cleverness and knowledge of the physician being elements at Dlav in everv case. The following are among the tests employed. Fiq. 79.—Barany’s noise apparatus. 1. Assuming in a given case the lesion to be confined to the sound-conducting mechanism, a vibrating tuning-fork is held to the mid-line of the skull (Weber). Its sound should be referred to the side of the lesion; the malingerer naturally states that it is heard by the sound ear. 2. Testing the patient’s hearing for whispered speech through a tube dividing 94 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS terminally into two smaller tubes—one for each ear—he is asked in which ear the words are heard. If the terminal tube communicating with the sound ear be blocked or closed, and he claims that the words are heard only by the presumably sound ear, it is assumed that the deafness in the opposite organ is not real. 3. When only partial deafness is claimed, the various tests—e.g., as to hearing distances, tone limits, etc.—are made. Repeating these tests, the malingerer’s memory usually fails him, and his conflicting statements are likely to show that his answers are not to be relied upon. 4. The individual having been blindfolded, the examiner stands behind him, and alternately tests the two ears rapidly with various forks. This frequently confuses the malingerer and brings answers so conflicting and contradictory as to demonstrate his lack of good faith. 5. A device which the writer recently hit upon wras conclusive so far as the case in question was concerned. The patient had received an injury in the course of his work for a large commercial company, and claimed to have become deaf in his right ear. For this he proposed to sue the company. The drum membrane appeared normal. His answers to the usual tests showed a degree of deafness which could only have re- sulted from a labyrinth injury. Arguing that such a disturbance of the cochlea would be likely to involve also the vestibular mechanism, the writer made a caloric test of the presumably deaf ear. This resulted in a quick and normal reaction, and during the confusion incident to the induced vertigo, it was easy to determine that his apparent unilateral deafness had been assumed. Since the above was written, American aurists have acquired much prac- tical knowledge in the application of these tests in the examination of men striving to evade military service on account of pretended deafness. It may, therefore, be worth while to state briefly the tests which the writer, as a member of an advisory examining board, found most useful, and to describe the routine method of applying them.6 In the first place, let me emphasize the fact that it is important in dealing with a suspected malingerer that he shall receive no slightest hint that he is under suspicion. The more unsuspecting and credulous the examiner may appear, the more readily and conclusively will the suspect respond to the tests. The most glaring evidences of deception should therefore pass without comment or apparent notice until the examination is completed. Most malingerers of deafness who are subject to the military draft know that deafness of a certain grade in either ear will exempt them from service. Complete bilateral deafness is, therefore, for various and obvious reasons rarely, if ever, claimed. Two types of unilateral deafness are assumed, i.e., (1) deafness advanced but not complete; and (2) absolute deafness. My own routine method of examining these cases is about as follows: Only one man at a time is admitted to the examining room. I learn from him which is the deaf or deafer ear, and whether he regards this deafness as partial or complete. If only one ear is complained of, I make a rapid test of the better ear to determine that it is functionally sound or at least only slightly subnormal. This preliminary testing of the sound ear is essential to a proper interpretation of the tests to be applied later. Weber’s Test.—I now apply a vibrating tuning fork of 256 double vi- brations to the vertex of his skull, and if he refers the sound to his supposedly 6 The following pages are taken almost verbatim from a report by the writer made before the American Otological Society in June, 1918. LOMBARD’S TEST 95 deaf ear, I am favorably impressed as to his honesty. If he refers it to his sound ear, I become skeptical, and proceed to the next test. Loud Voice Test.—The suspect’s eyes are now blind-folded. Requesting him to close with a finger his better ear, which has already been determined to be approximately sound functionally, I repeat words and numbers to him at first in a low voice and then in progressively higher and louder tones. If, when I have reached a pitch and intensity at which he should be able to hear and interpret the words with his sound ear even though tightly oc- cluded, he still states that he cannot hear them, I know at least that he is an intentional malingerer. This is a useful test which will expose many impostors. An alert individual, however, may throw this procedure out of court by stating that he hears the sound through his occluded normal ear. Stethoscope Test.—For this the ordinary clinical stethoscope with funnel- shaped chest piece is used. One ear piece is completely occluded with wax. Occlusion with cotton will not exclude the sound. Standing behind the examined, the stethoscope is adjusted with the occluded ear piece in his “deaf” ear. Words in a low voice are spoken into the funnel-shaped chest piece, which naturally he should hear perfectly. The stethoscope is removed for the ostensible purpose of trying some other test, and then re- placed, the occluded ear piece being this time placed in his sound ear. If he is able to hear now approximately as well as before, we have fairly sound evidence that his deafness is either assumed or grossly exaggerated. This is a fairly reliable test. Tests for Eliciting Contradictory Responses.—The eyes are now uncover- ed, the sound or better ear is closed with a finger, and the “deaf” ear is rapidly subjected to the commoner classical tests, e.g., hearing distance for watch, acoumeter, whisper or conversation voice; tuning fork tests to de- termine lower tone limit, etc. His responses, so far as he admits hearing in any of these tests, are carefully noted. Following this, he is again blind- folded and the same tests are repeated many times, fairly rapidly and in varying order. If he is a malingerer and has not in the first instance claimed almost total deafness, his responses will almost surely demonstrate incon- gruous and contradictory variations. Lombard’s Test.—This test, which requires a Baranv noise apparatus, is one of the most dependable means of determining absolute or very ad- vanced deafness confined to one ear. It depends upon the fact that to the normal man the sound of his own voice is necessary to the regulation of its tone and intensity. It is carried out as follows: the noise apparatus is adjusted to his sound ear and its machinery started in order to accustom him to its grating noise. He is given a book and told to read aloud in his nat- ural voice and not to stop reading when the noise instrument is set in action. As soon as the noise begins, a man whose opposite, or open, ear is profoundly deaf will 11 once raise his voice, and if his deafness is absolute he may literally shout. The malingerer, on the other hand, claiming a one- sided deafness which is not real, will continue to read in an even tone or in a tone only slightly elevated. This is a test which a malingerer who has been 96 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS coached may easily turn to his advantage. Otherwise it is one of the mosl useful at our disposal. Cochleo-palpebral Test (Gault).—This test depends on the fact that if a sudden and unexpected noise is produced near either ear, there occurs a slight winking movement, or contraction of the lids, in the corresponding eye. If, therefore, in a case of supposedly unilateral deafness, the sound ear is tightly closed and a slight noise, produced near the ear under suspicion, is followed by a contraction of the lids, however slight, on the same side, this is accepted as evidence of the sound having been heard in the ear in which deafness is claimed. It is clear that this test might be even more valuable in the case of a clever malingerer claiming bilateral deafness, when a notice- able palpebral contraction in response to a slight noise might constitute the only proof of the unreality of the auditory defect. Bilateral Deafness.—Naturally, as there are many cases representing all grades of bilateral deafness, malingering may take the form merely of an exaggeration of an existing defect. If such a person were persistently to assume absolute or very profound bilateral deafness, it is difficult to say what tests would expose the deception. The time-honored tricks of attempt- ing to ensnare him by a sudden and startling question, the use of insulting or disparaging remarks, etc., may be of value in certain cases but are cer- tainly not to be relied upon. The majority of malingerers, however, do not pretend to complete deafness. This is a fortunate fact for the reason that partial though disabling deafness burdens the malingerer with the necessity of maintaining uniformity in his responses to the various tests. The surest means of exposure in such cases is the application of the various classical tests first to one ear and then to the other, and then, after blind-folding him, repeating the same tests and comparing the two sets of responses. In my opinion, the most useful single test is the repeated determination, using a full set of tuning forks, of what he claims to be the lower limit of tone per- ception in each ear. In such repeated tests, a man would have to possess both a phenomenal memory and a wonderfully trained musical ear to avoid conflicting replies. CHAPTER IV. DISEASES OF THE EXTERNAL EAR (AURICLE; EXTERNAL AUDITORY MEATUS). INFLAMMATORY DISEASES OF THE AURICLE. Traumatic Auricular Dermatitis.—This condition is occasionally seen as a result of the slighter injuries to the ear,—i.e., injuries resulting in contusion or abrasion of the cuticle, but not seriously involving the perichondrium. It begins as a simple erythema, is usually accompanied by some degree of pain and sensitiveness to touch or pressure, and soon spreads more or less widely over the auricle. To establish its traumatic origin, it must be traceable to an abrasion or injury of the skin at the ori- fice of the meatus or at some point on the pinna. It may run its course as a simple erythema or, developing localized points of infection, become pustular in character. Such a lesion, unless too long neglected, is usually quite responsive to treatment. The treatment should begin with thorough cleansing of the part. If for this purpose an antiseptic drug is required, a solution of carbolic acid, 1 to 200 parts, is preferable to bichloride of mercury, which in itself is too irritating to the skin. After cleansing, the auricle should be thor- oughly dried, and an antiphlogistic ointment or lotion applied, according to the severity of the inflammation. If of very acute type,—i.e., of suf- ficient severity to cause considerable pain or discomfort,—it is well at the beginning of treatment to protect the ear by means of a large dressing of sterile gauze. The ointment or lotion may be applied upon a thin layer of gauze, and a dry gauze dressing applied over this. It may be said, however, that in many cases dermatitis of this type will make a perfectly satis- factory recovery without other treatment than cleansing of the part and protection from fresh injury. Erysipelas of the Auricle.—This disease may be secondary to the traumatic lesion above described, or it may have its origin in some slight injury or abrasion of the auricle or auditory meatus. Erysipelas of the auricle does not differ materially from the same lesion in other parts of the body. It rarely remains localized in the auricle, usually spreading to some extent to the face and scalp, so that it is apt later to assume the character- istic features of facial erysipelas. The redness, swelling, and tenseness of the skin are much more marked than in the simple traumatic type of erythema, and the line of demarcation between the inflamed and normal areas presents a greater contrast. The pain is usually intense. In addition to the local manifestations, there are usually present fever, accelerated pulse, and other symptoms of systemic derangement. The treatment is that of facial erysipelas: Rest in bed, catharsis, 97 98 DISEASES OF THE EXTERNAL EAR tonics, local cleansing, application of antiseptic or antiphlogistic oint- ments or lotions. Many of the local measures advocated have seemed to the author to exert little or no influence on the course of the lesion, and, though recovery is the rule, one is not always sure to what extent this happy result is due to the remedies applied. The writer is inclined to believe that for severe cases the use of a leucocyte extract (Hiss) will prove to be the treatment insuring the most definitely favorable results. In a later chapter dealing with serum therapy in the treatment of aural disease, the control of erysipelas by the Hiss leucocyte extract will be briefly discussed. Frost=bite.—The auricle from its exposed position is peculiarly vul- nerable to this accident. The symptoms are characteristic, but are often at the time overlooked by the sufferer. The ear, which has been tingling with cold, is suddenly found to be insensitive to touch. On examining the ear, the affected part of the auricle—oftenest the tip of the lobe or margin of the helix, or both—is found to be dead white and absolutely insensitive. The adjoining uninvolved part of the auricle is deep pink or red. Later—unless the circulation is quickly re-established—the frozen part becomes purplish, and still later may become dark brown or black, the part so discolored being afterward separated as a slough. This necro- sis may not involve the cartilage, but simply the superficial tissues. In still milder cases distinct sloughing does not take place, the parts gradually regaining tone and, after desquamation of the skin has taken place, re- turning to an apparently normal condition. That the tissues do not quickly return to an absolutely normal state is shown, however, by the fact that even in very mild cases the parts attacked are usually for a considerable period thereafter particularly vulnerable to the influence of cold, and there- fore to recurrence on comparatively slight exposure. Treatment.—The first indication is to re-establish the local circula- tion in the part frozen. Heat should not be applied, nor should the sufferer be taken into a warm house or room. If snow is on the ground, vigorous rubbing with snow, or better still with the hands after they have been made cold by contact writh the snow, is a time-honored custom, and prob- ably the best method which can be employed. Restoration of the local circulation will be announced by the return of local sensation and pain. Later the ears must be carefully protected from renewed exposure, and, if it becomes evident that sloughing is to some extent inevitable, they should receive antiseptic care and treatment in accordance with the surgical laws governing the management of necrotic or gangrenous wounds. Auricular Eczema.—Clinically, eczema of the external ear is recog- nized in two clearly differentiated forms, the acute and the chronic. Etiology.—The acute form occurs far more frequently in childhood than in adult life, and in the uncared-for and ill-fed children of the tene- ments than among those living under more favorable hygienic conditions. Early childhood and depressed constitutional states must, therefore, be regarded as strongly predisposing factors. Digestive disturbances, and especially intestinal disorders, also seem to influence the development of AURICULAR ECZEMA 99 the disease. The chronic form is seen oftener in adult life and old age, and with particular frequency in those in whom the rheumatic or gouty diathesis is present. Symptoms of Acute Auricular Eczema.—Three stages of the lesion are frequently seen in aural clinics: (1) The erythematous stage, in which the skin is intact, but red, somewhat swollen and angry looking. (2) The vesicular stage, in which the skin is more or less covered with vesicles. From some of these serum exudes which bathes the inflamed surface, finally drying in the form of scales. (3) A stage in which the area involved is completely denuded of its epithelium and presents a raw and bleeding surface. The chief symptom is that of the very distressing local irritation,—i.e. the intolerable itching. This is present in all stages. In the erythematous stage there is sometimes in children very considerable pain, giving rise in some cases to moderate elevation of temperature. The parts most frequently involved are (1) the postauricular sulcus and contiguous parts behind the ear; and (2) the concha and often the outer half of the membrano-cartilaginous meatus. Children find it im- possible to resist the inclination to scratch the intensely itching surfaces, and this often adds a superficial infection to the primary lesion. Treatment.—Fortunately, these cases usually respond readily to proper management. The writer usually begins with internal remedies to cleanse the intestinal tract and regulate the digestion. P'or this pur- pose the following well-knowTn formula for rhubarb and soda gives very satisfactory results: R Extract, rhei fluid., Sodii bicarbonatis, Spirit, menth. piper., aa Aquae dest., q. s. ad 3iv. M. Sig.—One teaspoonful in wineglass of water t.i.d., a.c. The local treatment calls for cleanliness, application of an astringent ointment, and protection from mechanical irritation (scratching, etc.). The parts should be gently bathed with warm water and castile soap, and thoroughly dried. They should then be covered rather thickly with some soothing and astringent ointment. The parents should be instructed to reapply this ointment two or three times daily as may become necessary, and not again to bathe or apply water to the part until so instructed. The ointment which the wrriter is accustomed to prescribe is as follows: R Unguent, zinci oxid., Fetrolati, aa % ss. M. et ft. unguentum. When the skin is very acutely inflamed, much quicker and more satis- factory results are obtained by applying the ointment once daily and protecting the parts in the interim by means of a dressing of sterile gauze. It is surprising how rapidly and completely most cases of acute auricular eczema will clear up under this treatment if faithfully carried out. 100 DISEASES OF TIIE EXTERNAL EAR A condition the treatment of which presents some difficulties is found in cases in which acute eczema of the meatus and auricle coexist with discharge from the middle ear. In such cases the syringing employed to cleanse the canal of pus exerts an unfavorable influence upon the eczema. Under such circumstances the eczematous surfaces should be guarded from the irrigation fluid by thick layers of the protecting ointment. When the aural discharge is not profuse, manual cleansing and drying of the meatus, followed by the introduction of gauze wicks,—the whole ear being covered with a gauze dressing,—may with advantage be substituted for irrigation of the ear. Such a dressing would have to be renewed daily. Chronic eczema of the auricle usually involves also the outer half or third of the external auditory meatus. Two clearly distinguishable types are recognized: (1) The squamous variety, in which the outer part of the meatus and part of the concha are covered with dry, thin scales of exfoliated epithelium. Removal of these scales exposes a sensitive and easily irritated surface. (2) The so-called sclerotic type of eczema, in which the skin lining the outer part of the meatus and covering parts of the auricle is greatly thickened. The calibre of the meatus is in some cases greatly reduced by superposed layers of exfoliated epithelium, removal of which is apt to leave an excoriated and bleeding surface. In both types of chronic eczema, itching is usually a more or less prominent symptom, and the patient’s effort to relieve this by scratching tends to prolong and exaggerate the condition. Treatment.—Tonics and—in cases in which such a diathesis exists— antirheumatic remedies seem to influence some cases favorably. The local treatment calls for the removal of the scales, or exfoliated epithelial layers, lining the canal and concha. Unfortunately, this is often quite difficult or impossible without leaving a raw or abraded surface, which opens the door either to infection or to the formation of scabs or crusts, beneath which epithelial hyperplasia and exfoliation proceed as before. It is well, therefore, in some cases to apply an emollient ointment for several days before attempting to remove the thickened and adherent surface layer. For this purpose the following is quite satisfactory: R Glycerini, gi; Lanolini, 3 iii ; Unguenti petrolati, 3 b M. et ft. unguentum. This should be applied thickly each day until the abnormal surface cov- ering of the canal is softened, and can be easily removed without injury to the underlying skin. The parts should then be thoroughly cleansed with 95 per cent, alcohol, and covered by some protective ointment,— e.g., the zinc oxide ointment, or the following: R Ichthyoli, 31; Acidi salicylici pulv., gr. x; Cj Zinci oxidi, 3ss; Unguent, aquae rosae, o h AURICULAE PERICHONDRITIS 101 Later, occasional swabbing of the ear with alcohol helps to restore to the skin its normal tone. It must, however, be kept soft by frequent applications of some astringent ointment to prevent re-formation of the scales. The condition regularly improves under careful local treatment, but I know of nothing which will absolutely insure against recurrence after treatment has been discontinued. Auricular Perichondritis.—This is an inflammation involving the auric- ular perichondrium, and usually resulting in an effusion of pus or serum between it and the auricular cartilage. It is said in some cases to develop idiopathically, or at least without known cause (Politzer); but in the vast majority of cases it is traceable to a direct infection, spreading either from a neglected furuncle of the cartilaginous meatus, from a lace- rated wound of the auricle, or the infection may be traced to a plastic operation involving the cartilage,—e.g., the plastic work upon the carti- laginous meatus forming part of the “radical operation.” Symptoms.—The onset is announced by gradually increasing auricu- lar pain, which soon becomes exceedingly severe and usually interferes with sleep. Upon examination we find at the beginning a small area of localized swelling. The area involved is dark red or purplish red, is hard, tense, and unyielding to the palpating finger, and is exquisitely sensitive to manipulation or pressure. These changes may at first be confined to a very small area, from which they may spread gradually in all directions over the anterior surface to the extreme limits of the auricular cartilage. With the spread of the lesion, the tumefaction becomes less hard, impart- ing a boggy feeling to the palpating finger,—never that characteristic of fluctuation. Naturally the lobe is never involved, and this supplies a differential point between auricular perichondritis and a severe and exten- sive auricular inflammation of more superficial origin, in which the lobe is apt also to be involved. Fever and accompanying pulse changes are frequently present in some degree at the onset. Terminations.—(A) The lesion may undergo resolution with absorp- tion of pus or serum and a return to the normal. (B) There may be local recovery with considerable permanent thickening and deformity. (C) The presence and pressure of the pus may give rise to necrosis of the cartilage, with very great permanent deformity. Treatment.—The treatment varies with the severity and extent of the lesion, and calls for the surgeon’s best judgment. When the disease is apparently localized in a small area and shows no tendency to spread, the application of a wret dressing,—i.e., of a saturated boric acid solution as hot as the patient can bear, and renewed frequently,—or of a 10 per cent, solution of ichthyol, may help to control the inflammation. When, however, a considerable effusion of fluid has taken place beneath the perichondrium, it is safer to sterilize the part as for a major operation and, with the patient under a general anaesthetic, make a free incision through the perichondrium. After the fluid has been evacuated, a very small gauze drain should be introduced into the wound and for a short distance 102 DISEASES OF THE EXTERNAL EAR between the cartilage and perichondrium, and over this pressure applied by means of a pad of sterile gauze, this being reinforced by a larger gauze dressing. This dressing should be changed daily, and particular care taken to prevent reaccumulation of serum or pus beneath the perichon- drium. If this operation is unduly delayed, more radical measures may become necessary through necrosis of the cartilage. So long as the inflammation is confined to the perichondrium—i.e., so long as the cartilage is not directly involved—through-and-through drainage by an incision passing through the auricular cartilage is not called for. Very great swelling of the auricle is often seen as a result of inflam- matory infiltration of the perichondrium plus an effusion of fluid between it Fig. 80.—Auricular perichondritis. Fig. 81.—Deformity resulting from neglect of lesion shown in Fig. 80. and the cartilaginous plate. In such cases incision of the cartilage does not seem called for. If, however, after incision of the perichondrium, the exposed cartilage is found to have become involved and to have undergone necrosis, there should be no delay in dissecting from it its perichondrial covering and exsecting the necrotic area. Unless this is done promptly, the whole cartilaginous frame may become necrotic, with ultimate very unpleasant permanent deformity. Haematoma Auris (Othaematoma). — This describes a condition in which, as a result of local injury, there has occurred an effusion of blood between the auricular cartilage and its perichondrium. It occurs only on the anterior surface of the cartilage. At first usually localized, it may spread later so as to separate the perichondrium from the entire anterior surface of the auricular cartilage. Etiology.—This is somewhat obscure. Apparently the aged and more especially the insane are particularly prone to certain degenerative changes in the auricular cartilage and perichondrium, in which condition luematoma auris is apparently easily induced by very slight injuries. Its occurrence H2EMATOMA AURIS 103 In this class of individuals has been noted with particular frequency in Germany, and the occurrence there of certain cases in which no history of trauma could be obtained has led to the belief that a certain number of cases occur spontaneously. One wonders, however, whether even in such cases—depending unquestionably in some degree upon degenerative tissue changes—there has not been some slight injury which, though over- looked at the time, has been the directly exciting cause. In this country, so far as the writer knows, the condition is almost always due to direct violence. In twelve ' years of almost daily attendance at aural clinics and hospital wards, no single case has come under his observation which could not be directly traced to local injury. The commonest cause is a fist blow on the ear, but it has occurred also as the re- sult of a hard slap and of violent twisting or pulling of the ear. The accompanying illus- tration is of a prize-fighter in whom the lesion resulted from a blow (Fig. 82). Symptoms.—Following the injury, a tumor upon the anterior surface of the auricle is rapidly formed. At first localized, it may spread rapidly upward and backward to the helix, and downward to the upper boundary of the lobe. The tumor is generally purplish or bluish red, its local temperature is usually elevated, and it presents the peculiar boggy feeling characteristic of fluid confined beneath the perichondrium. If very small and localized, the pain may not be severe. With an effusion of considerable size, the pain is usually intense. Insomnia due to pain, fever, and constitutional depression is apt to be present in severe cases. Terminations.—(1) With a small effusion there may be complete and perfect local recovery. (2) The lesion may undergo resolution, part of the blood being absorbed and the remainder being organized into new connective tissue, which results in permanent thickening and deformity (Fig. 83). (3) Infection may occur, giving rise to destruction of the car- tilage, and ending in final recovery with great permanent deformity. Treatment.—When the collection of blood is small, shows no ten- dency to increase, and is not accompanied by excessive pain, it is well to depend largely upon time to bring about a cure. From the nature of the lesion, it is difficult to see how the application of lotions can be of value, and pressure or manipulation may obviously do harm. In the case of a large effusion of blood, the indications for treatment are well suggested by the statement of Richard Lake, of London, that spon- taneous recovery “is not certain to take place, but if it does, deformity is sure to result.” In such a case a free incision—coextensive with the extent of the effusion—should be made through the perichondrium. A puncture is Fig. 82.—Haematomaauris, result- ing from a blow upon the ear. 104 DISEASES OF THE EXTERNAL EAR worse than useless. The blood or coagulum should then be evacuated, a curette if necessary being used for the removal of firmly organized clot, and the space between perichondrium and cartilage should be lightly packed with sterile gauze. This dressing should be changed daily for several days, after which it may be omitted, and the parts pressed into apposition and held so by a gauze pad and dressing. If, as advised by some surgeons, the cavity is not packed, but is at once subjected to pressure, reaccumulation of blood is more than likely to occur. Differential Points between Auricular Perichondritis and Hcematoma Auris.—While the two lesions present clinically many similar features, they may usually be differentiated by consideration of the following points: (A) History: Auricular perichondritis is usually traceable to a localized point of infection,—e.g., fur- uncle, lacerated wound, plastic surgery involving the perichondrium. Hsema- toma auris is usually traceable to direct violence,—e.g., a blow. (B) Rapidity of development: Following a local infec- tion, the development of auricular peri- chondritis is comparatively gradual and slow. Following an injury, the develop- ment of hsematoma auris is exceedingly rapid. (C) Auricular perichondritis un- der transillumination shows no marked color differences between involved and uninvolved areas. In hsematoma auris transillumination gives a dark purplish color over the area of the blood collection or clot. Lupus. — Tubercular lesions of the skin covering the auricle, while probably fairly common in dermatological practice and clinics, do not come very often before the aurist. Only in cases giving rise to considerable swelling and deformity of the auricle (lupus hypertrophicus, lupus tumidus) is the aurist likely to be called in. The student will, therefore, find more authentic descriptions and directions for treatment of these lesions in works on dermatology. The commonest form (lupus vulgaris), when attacking the auricle is usually seen simultaneously upon other parts of the face. The lesions appear as distinct papules or tubercles, reddish or brownish in color, which may later be covered with dry, brownish scales. A characteristic feature is the tendency to form permanent depressions, the substance of the tubercles apparently in some cases being absorbed or shrinking with- out erosion of the overlying skin. Between these depressions are often formed small cicatrix-like bands. The disease is distinguishable from a syphilitic skin lesion of somewhat similar appearance (a) by absence of Fig. 83.—Final permanent deformity resulting from haematoma auris. Plate V. Fig. 84.—Lupus hypertrophicus auriculae. SYPHILIS OF THE EAR 105 a history or evidence of syphilitic infection, (b) by their slower develop- ment, and (c) by the greater tendency of the syphilitic papules to ulceration. Treatment.—The treatment calls for constitutional building up of the patient by constructive tonics. The local treatment aims at the actual destruction of the diseased tissue forming the basis of each tubercular nodule. For this purpose, the nitrate of silver stick, the sharpened point of which is forced down into the core of each nodule, is said to be effective. Actual surgical removal of the tubercles, the denuded surface being later covered by skin-grafts, is also recommended. The skilful local use of the X-ray is said also to exert a curative action on tubercular skin lesions. Lupus Tumidus (Lupus Hypertrophicus). — According to Politzer, this form of tubercular lesion may result by the following process from the more common variety (lupus vulgaris). The typical superficial tuber- cles, or nodules, becoming confluent, undergo surface necrosis, giving rise to a tubercular ulcer. Within the depths of this ulcerated surface are deposited newly formed tubercular nodules. Following this there is a moderate proliferation of firm granulations which bleed easily. This may result in great thickening or enlargement of the involved portion of the auricle, which usually includes the lobule. The accompanying illustra- tion (Fig. 84) represents a lesion of this nature. Unless brought under fairly prompt control, the cartilage may become involved, and, should it undergo necrosis, great permanent deformity is likely to result. In rare cases a tubercular lesion of the auricle assumes the form of a tumor of considerable size. Tubercular lesions of this form involving the auricle are apparently much commoner in certain parts of Europe than in this country. Treatment.—The treatment recommended for this lesion is prompt and thorough removal of the diseased tissue. The tubercular granulations and nodules are subjected to vigorous curettage with a sharp spoon curette until healthy tissue is reached. This surface should then be painted with a strong solution of silver nitrate, 200 grains to the ounce, in order to destro.y such tubercular tissue as the curette has failed to remove. The parts are then dried and covered with a protective gauze dressing. The above treatment may have to be repeated several times before the disease is eradicated. Finally skin-grafting may be practised in order to hasten the healing process and lessen cicatricial contraction. In severe lesions some deformity is probably inevitable, but is less than if the lesion is allowed to involve the cartilage before treatment is instituted. Syphilis of the Ear.—Primary syphilitic lesions of the auricle, while a few cases have been recorded, are exceedingly rare. The writer in twelve years of attendance in aural clinics and hospitals has not met with a single case. Secondary lesions, however, in the form of papular or pustular eruptions, coincident with similar lesions upon the scalp, fore- head, or other parts of the body, are said to be of fairly common occurrence in dermatological clinics. The severe lesions—i.e., deep ulcerations and condylomata—are more 106 DISEASES OF THE EXTERNAL EAR often seen within the meatus. While the physical appearances may be most suggestive, their specific character can be positively determined only by the association of a reliable history of syphilitic infection, tne presence of other evidences of constitutional syphilis, or possibly by a positive Wassermann reaction. The condylomata are described as “grayish-red, ragged, watery excrescences,” firmer than the ordinary form of inflam- matory granulation tissue, and tending to spread with great rapidity. The formation of gummata upon the auricle or within the meatus is said to be exceedingly rare. A final and confirmatory diagnostic test of these lesions is found in their response to antisyphilitic treatment. The treatment is constitutional rather than local. The local treatment aims chiefly at cleanliness. The chief reliance, however, is to be placed upon the constitutional remedies. Mercurial injections or inunctions with potassium iodide in appropriate doses usually exert a fairly rapid influence upon the local lesion. Salvarsan is even more rapid and positive in its results. Probably the best results will be obtained by fairly large and repeated injections of salvarsan in combination with some form of mer- curial medication. For a general consideration of the value of salvarsan in aural therapy the reader is referred to a later chapter dealing particu- larly with the influence of that drug upon labyrinthine and auditory nerve lesions. Herpes Zoster Auriculae; Herpetic Inflammation of the Geniculate Ganglion (Hunt).—The occasional appearance of herpes upon the auricle, with the coincidence of aural symptoms of varying severity, has long been known to occur, but only since the publication of Dr. J. Ramsay Hunt’s papers on the subject have we possessed any definite con- ception of the nature of the lesion. We now recognize the symptoms as directly due to an inflammation of the geniculate ganglion. According to Hunt, the zoster zone of the geniculate ganglion is sharply confined to the membrana tympani, the walls of the auditory meatus, the concha, tragus, antitragus, antihelix, and helix, rarely extending beyond the boundaries of this area. The herpetic eruption (Fig. 85) may occupy the whole or only a small portion of the geniculate zone. The appearance of the herpes is occasionally preceded by rather severe pain referred to the ear and mastoid region. With the development of the herpes there may be considerable swelling of the canal and pinna. The symptoms may be limited to the aural pain; or the inflammation may spread from the ganglion to auditory and facial nerves, in which case there may be marked disturbance of hearing (cochlear branches of 8th nerve) or symptoms of vestibular irritation,—i.e., nystagmus, vertigo, vomiting, etc. The latter phenomena point of course to involvement of the vestibular branches of the 8th nerve. Since the connection of the geniculate ganglion with the 7th nerve is far more direct and intimate then with the 8th nerve, facial paralysis is far more frequent than are the symp- toms due to disturbances of the 8th nerve, with which the geniculate Plate VI. Jig. 85.—Herpetic eruption due to inflammation of the geniculate ganglion (Hunt). ACUTE CIRCUMSCRIBED EXTERNAL OTITIS 107 ganglion communicates chiefly through the small connecting branch known as the pars intermedia. It is of the greatest practical importance that aurists should be pre- pared to recognize this lesion, for the reason that in a severe case the physical signs may strongly resemble those of a severe tympano-mastoid inflammation, in which rupture of the drum-head has not occurred. The history of aural pain, quickly followed by herpes confined to the geniculate zone and the frequent occurrence of paresis or paralysis of the muscles supplied by the facial nerve, should enable the careful observer to arrive at a correct diagnosis. A careful reading of the papers referred to below is advised.1-2 Malignant Disease of the Auricle: Epithelioma; Cancer of the Auricle.—Epithelioma of the auricle is not very common and, when it does occur, shows no distinctive features directly attributable to its situa- tion. That is to say, it presents the characteristic features common to such growths in whatever region they may appear. Epithelioma origi- nating at some point upon the auricle grows rapidly, and the overlying skin is quickly eroded. The auricular cartilage is soon involved and may be very rapidly destroyed. As to the surgeon’s responsibility in the management of these cases, there is one point which can not be too strongly emphasized,—viz., that an epithelioma originating upon the auricle may in the first stage be re- moved surgically with good chances of a permanent cure. If surgical relief is long withheld, however, the neoplasm may suddenly exhibit very rapid growth, spreading quickly through the auditory canal to the tym- panum, to the parts in front of and behind the ear, and finally may attack and destroy a large portion of the temporal bone. When such extensive involvement has taken place, recurrence is likely to follow any operation which may be employed. INFLAMMATORY DISEASES OF THE EXTERNAL AUDITORY MEATUS. Acute Circumscribed External Otitis; Furunculosis of the Meatus.— A furuncle in the meatus is one of the most painful, as it may be one of the most troublesome, conditions which the aurist is called upon to treat. It in- volves only the outer, or fibrocartilaginous, portion of the canal. It may be single or multiple. It occurs most frequently upon the posterior wall or floor, next upon the roof, and least frequently on the anterior wall. Etiology.—Predisposing Causes.—The number of cases in which the same person in different years has suffered from recurrent furuncles of the meatus, and the still greater tendency of the lesion to immediate recur- rence, impel one to believe that there are certain predisposing factors—■ not always easy to determine—which render certain individuals pecu- 1 Hunt, J. R.: Herpetic Inflammation of the Geniculate Ganglion; Jour, of Nervous and Mental Diseases, February, 1907. 2 Hunt, J. R.: Further Contribution to Inflammations of the Geniculate Ganglion; Amer. Jour, of the Medical Sciences, August, 1908. 108 DISEASES OF THE EXTERNAL EAR liarly susceptible to the disease. People, for example, having the gouty or rheumatic diathesis seem to be particularly frequent sufferers. Depressed constitutional states—e.g., lowered vitality caused by insufficient food or unhealthful surroundings or modes of life—are undoubtedly factors, as is shown by the relative frequency of furuncles of the meatus among the poorer class of dispensary patients as compared with those seen in private practice. It occurs, however, in all classes. Chronic eczematous affections of the concha or meatus also predispose to the development of furuncles, probably by affording denuded points for the entrance of germs. The exciting cause is always a local infection. This may be brought about by a chronic purulent discharge from the middle ear acting upon a denuded area in the meatus. Quite often the lesion may be traced to the habit of scratching the canal wall with a toothpick, hairpin, or even with the finger-nail, this resulting in an abrasion which provides the point of entrance for infective matter. Symptoms.—The symptoms of which the patient complains may be mentioned in the following order: (a) Sensitiveness to slight manipula- tion; (b) pain; (c) tinnitus aurium; (d) impairment of hearing. Discharge, when present, occurs so late in the disease, and is so frequently absent, that it can hardly be regarded as a characteristic symptom. The patient may first be conscious of a sense of occlusion, or “stuffi- ness,” in the affected ear, and with this he may notice that very slight manipulation—e.g., as in drying the ear after the morning bath—gives rise to a sense of soreness or even a sharp pain in the ear. Later this dis- comfort or pain may be induced by extensive movements of the jaw, as in yawning. The next symptom is usually that of constant pain in the ear, at first of moderate grade, but gradually increasing and finally becoming unbearably severe. The pain caused by a furuncle of the meatus is in many cases quite as severe as that accompanying acute otitis media, and is augmented by the intolerable sense of soreness usually present. A charac- teristic feature of this pain is found in the fact that it is usually made worse by movements of the jaw,—e.g., chewing, yawning, etc. This is, of course, explained by the close anatomical relation of the cartilage of the temporomaxillary joint and the cartilaginous framework of the meatus. This phenomenon, when present, is pathognomonic either of acute cir- cumscribed or acute diffuse external otitis, and clearly differentiates these lesions from acute inflammatory conditions confined to the middle ear. Tinnitus aurium is a symptom the prominence of which varies in differ- ent cases from slight head noises, that are overlooked in the severity of other symptoms, to loud ringing noises which add much to the patient’s discomfort. In some degree it is nearly always present. Impairment of hearing is not usually present at the onset, but becomes progressively more noticeable as the calibre of the canal is reduced, and may be very marked if the occlusion of the canal is complete. Physical Examination.—Palpation comes first as a means of deter- mining the presence of a furuncle in the meatus, for the reason that it will ACUTE CIRCUMSCRIBED EXTERNAL OTITIS 109 in many cases elicit tenderness before changes in the contour and color of the canal wall can be detected. The finger should be pressed firmly against the cheek above and in front of the auricle, and brought downward along the line of anterior attachment so as to press the tragus inward. This will surely elicit tenderness if there is a furuncle in the anterior canal wall, and often even though it may be situated elsewhere in the fibrocarti- laginous meatus. If, however,- no pain is caused by pressure on the tragus, the cartilaginous meatus should be moved in different directions,—i.e., forward, upward, and downward. If this procedure causes no pain, we may be quite confident that the disease is not located in the fibrocarti- laginous canal. Inspection by Reflected Light.—In the earliest stage of a furuncle in the canal, inspection may not reveal any localized swelling nor any changes in the color of the overlying skin. In this case the different walls of the canal should be subjected to pressure by means of a cotton applicator wound with cotton. In this way we are usually able to determine the point of local tenderness, which coincides, of course, with the point of infection. Later, inspection will reveal one or more points of localized swelling, according to whether we have to deal with a single furuncle or with a mul- tiple lesion, furunculosis. With the progress of the lesion the canal is always, therefore, narrowed in one or more of its diameters, in accordance with the involvement of the different walls. In severe cases the swelling may be so great as completely to close the canal. Even in such cases, however, it may be possible to introduce a very small speculum beyond the furuncle and thus bring the drum membrane into view. Whenever possible with- out the infliction of too much suffering, this should be done. Careful inspection of the drum membrane is important for the reason that, as soon as we can determine that the membrana tympani is not acutely inflamed, we are in a position to exclude positively the middle ear as the site of intercurrent suppurative inflammation, and this without inspect- ing the drum membrane we are not able to do. Course of the Disease.—In some cases a single furuncle will rupture spontaneously into the canal, and this may, or may not, determine a favorable course toward recovery. Oftener than not, such spontaneous rupture does not provide adequate drainage, and the inflammatory proc- ess continues to spread, foci of infection (i.e., furuncles) developing simultaneously upon other walls of the canal. Quite frequently sponta- neous rupture is so long delayed as to cause the patient excruciating pain, the inflammation finally extending to surrounding structures. Extensions of Inflammation.—The involvement of structures about the ear depends somewhat upon the site of the furuncle. (A) With a furuncle upon the anterior wall, there often occurs very marked swelling of the tissues in front of and below the tragus. In such cases the parotid gland may be distinctly involved. (B) With a furuncle confined to the posterior or posterosuperior canal wall, there is not infrequently very con- siderable oedema over the mastoid region immediately behind the ear. 110 DISEASES OF THE EXTERNAL EAR This commonly results in more or less complete obliteration of the post- auricular sulcus and the production of a very characteristic deformity,— the auricle being displaced forward, or forward and downward, so that it stands out from the head in striking contrast with the opposite sound ear (Fig. 86). Extension of inflammation may also take place through the deeper structures of the auricle itself,—i.e., it may cease to be in any sense a circumscribed inflammation, and spread widely between the perichondrium and cartilage, giving rise to severe and extensive suppurative perichon- dritis (Fig. 87). Fig. 86.—Displacement of left auricle resulting from a furuncle in the posterosuperior canal wall. Fig. 87.—Necrosis of auricular cartilage and deformity resulting from extension of infection from a furuncle in the canal. (Dr. Held’s case.) With a severe infection of the fibrocartilaginous canal, it is not unusual to find the lymphatic glands of the neck, particularly those in front of and behind the sternomastoid muscle of the affected side, enlarged and somewhat sensitive to pressure. Since swelling behind the ear with consequent displacement of the auricle may occur with acute suppurative mastoiditis as well as with furunculosis of the meatus, it may be well to mention here three points which should aid us in differentiating between the two conditions causing this deformity: Postauricular CEdema due to Furuncle of the Meatus. 1. Drum membrane usually intact, and may be normal or only slightly con- gested. 2. Pressure upon tragus and manip- ulation of auricle causing movement of fibrocartilaginous meatus usually cause severe pain. Postauricular Swelling due to Acute Suppurative Mastoiditis. 1. Drum membrane usually perforated, and always shows some of the cardinal signs of suppurative otitis media. 2. Pressure upon tragus and manipu- lation or movement of fibrocartilaginous canal cause absolutely no pain. ACUTE CIRCUMSCRIBED EXTERNAL OTITIS 111 3. Firm pressure over the mastoid process just behind the postauricular sul- cus and opposite the orifice of the meatus will, if so directed as not to disturb the position of the auricle, cause absolutely no pain. The cedematous tissues pit deeply under the compressing finger, after which no bone tenderness can be elicited. Pressure at exactly the same point, but directed slightly forward so as to disturb the auricle, causes severe pain. 3. Firm pressure upon the mastoid process just behind the postauricular sul- cus and opposite the orifice of the meatus usually elicits deep-seated bone tenderness. The practical diagnostic value of the above is well illustrated by the following case. The author was asked by a general surgeon to confirm a diagnosis of mastoiditis in a hospital patient upon whom he was about to operate. The patient, a man of thirty years, presented superficially the following conditions, upon which the diagnosis had been based: (1) he was suffering severe earache; (2) there was very marked oedema behind the left ear and the postauricular sulcus was obliterated; (3) the auricle was displaced forward and stood out from the side of the head in conspicuous contrast with its fellow of the opposite side. The parts about the ear were shaved in preparation for immediate operation. That the mastoid was not involved was clearly shown by the following facts: (a) the drum mem- brane, rather difficult to inspect, was found to be practically normal; (b) the posterior wall of the fibrocartilaginous meatus was intensely in- flamed; (c) any manipulation of the auricle causing movement of the carti- laginous meatus caused intense pain; (d) firm pressure upon the mastoid, so directed as not to disturb the auricle, caused the patient no pain. I learned later that he made a perfect recovery under treatment appropri- ate to furunculosis of the meatus. Prognosis.—The prognosis in this lesion is somewhat clouded by the pronounced tendency to recurrence. A single furuncle may appear to be progressing favorably toward recovery, only to be succeeded by a second furuncle on the opposite wall of the canal. Every aurist can recall cases in which the patient has been afflicted with a series of furuncles,—three, four, five, or more,—each following the other in the same canal and in rather quick succession. It is well, therefore, to acquaint the patient with this danger, and impress upon him the importance of following the pre- scribed treatment to the letter. Treatment.—The marked tendency to recurrence would seem to prove a constitutional basis in many of these cases. Internal, or constitu- tional, remedies should, therefore, play some part in their management. The treatment in every case should begin with thorough cleansing of the alimentary tract. Further than this, it is well to divide these cases into two general classes,—i.e., (1) those presenting evidences of lowered vitality or resistance, for whom simple or constructive tonics should be prescribed; and (2) the overfed, full-blooded, or plethPric class,—the type of individ- ual to whom in the older text-books the term “apoplectic” was applied. Such an individual requires careful regulation of diet, restriction of alco- 112 DISEASES OF THE EXTERNAL EAR holic drinks, and regulation of the bowels. For the latter purpose the administration of small doses of rhubarb and soda three times a day before meals has proved very satisfactory. This rather empirical method of classifying and prescribing for patients suffering from furunculosis of the meatus, has seemed favorably to influence the average results. That the local treatment of this lesion has proved a troublesome prob- lem in otology is shown by the long list of unrelated therapeutic measures which have been proposed for its relief. Many of these remedies have travelled a long journey, passing through one text-book to another, but have found little place in actual practice. Among them we find the fol- lowing: Abstraction of blood by the application of leeches in front of the tragus; abstraction of blood by the so-called artificial leech; application of heat (a) by means of poultices and (b) by fomentations,—i.e., applica- tion of heated lotions; application of cold by means of the Leiter coil; introduction into the meatus of various antiphlogistic agents, among which is mentioned pig’s fat impregnated with opium (Politzer), etc., etc. The writer believes that most of these remedies are worse than useless, and that we but obscure our view of the therapeutic field when we allow our atten- tion to be diverted from the few tried therapeutic measures upon which practical experience has stamped her approval. As the local treatment must necessarily vary with the condition pres- ent, it may be well to re-state briefly the four stages through which a furuncle may pass,—viz.: (1) Initial stage, in which the patient experiences a constant sense of discomfort, but pain only on manipulation of the cartilaginous meatus. Inspection may reveal no noticeable change in the contour or color of the canal, but palpation with a cotton-wound applicator discloses a point of maximum tenderness, representing the focus of infection. (2) Stage of inflammatory infiltration, in which inspection reveals circum- scribed redness and swelling of one or more walls of .the meatus. Palpation shows the tumefaction to be hard, tense, non-fluctuating, and exquisitely sensitive to pressure. This is the most painful stage of the disease. (3) Abscess Stage.—The involved area, representing a circumscribed and encapsulated collection of pus, bulges into the canal, is found by palpation to be distinctly fluctuating, and may point and rupture spon- taneously into the canal. (4) Stage of Surrounding Cellulitis.—Certain cases fail to develop an encapsulated abscess, and extend by invasion of surrounding structures, giving rise to oedema or cellulitis in front of or behind the ear, with con- sequent displacement of the auricle. Local Treatment.—In the initial stage our purpose should be to abort the attack. The entire canal should be thoroughly cleansed of cerumen, exfoliated epithelium, or other impurities. This may be done by first irrigating the canal with warm boric acid solution and then scrubbing it out by means of cotton-wound applicators dipped in 95 per cent, alcohol. After this a pledget of cotton saturated with a solution of carbolic acid, ACUTE CIRCUMSCRIBED EXTERNAL OTITIS 113 1 to 100, should be placed in the meatus and allowed to remain for a min- ute, or until the part begins to tingle. This should leave the canal surgi- cally clean. As a permanent dressing my preference is for a wick of sterile gauze which has been saturated with a carbolic acid solution, 1 in 300, and then wrung out nearly dry. This should be packed rather firmly into the outer (membrano-cartilaginous) part of the canal, the pressure thus maintained seeming to influence these cases favorably. The concha should be filled with a ball of sterile absorbent cotton, which may be held in place by collodion or adhesive plasters. This dressing should be changed daily, the canal each time being thoroughly cleansed and dried. This method of treatment seems in a fair proportion of cases to have the effect of dispersing a beginning infection and bringing about a cure. When, however, this happy result does not follow, the lesion passes into the second stage, and may demand more vigorous measures for its relief. Second Stage.—In this stage the lesion is theoretically a surgical condition for which a free incision would seem the logical procedure, and this indeed may be ultimately necessary in any case reaching the stage of inflammatory infiltration. It is definitely established by experience, however, that a cer- tain considerable proportion of cases are controlled, and re- cover perfectly, under the following simple plan of treatment. The canal is cleansed as described in the last section, or simply by irrigation with a warm boric acid solution. A fold wick of sterile gauze, moistened in some non-irritating solution, is introduced into the canal, not tightly, and cut off so as not to protrude beyond the orifice of the canal into the concha. This wick is to be kept moist (not soaked) by some bland antiseptic solution. For this purpose the proprietary preparation, Cre- satin, gives excellent results. If this cannot be obtained, the following prescription has proved satisfactory in many cases: Acid carbolic gr. i Sodii bicarbonat gr. xx Glycerin 5i Aquae, q. ad 3i Fia. 88.—Furuncle knife. The wick should be kept moist by adding only three or four drops by means of a medicine dropper every two hours or so, a ball or pledget of sterile cotton being placed lightly in the. concha in the intervals. Under this treatment the inflammation and infection is in many cases seen rapidly or at least progressively to subside. If too much of the solu- tion is used, so as to keep the wick soaked, maceration of the cutaneous covering of the canal is likely to occur, causing desquamation of the cuticle, with the added lesion of a diffuse and troublesome dermatitis. As soon as 114 DISEASES OF THE EXTERNAL EAR the localized infection is controlled by the above means, it is better to dis- continue the solution, merely keeping the canal lightly packed with a dry wick of sterile gauze for a few days. If the treatment above outlined fails to control the infection, and particularly if the inflammation is seen to be progressive, a free incision becomes the most rational step toward relief. As this operation, though short, is exceedingly painful, it is always best to have the patient under nitrous oxide anaesthesia. The canal should be previously sterilized by peroxide of hydrogen, followed by irrigation with a warm solution of car- bolic acid, 1 to 200. The point, or focus, of infection having been deter- mined by inspection and palpation, the knife should be introduced into the canal beyond the inflamed area, and the furuncle freely and rather deeply incised as the blade is withdrawn. For this purpose a straight knife (Fig. 88) has always seemed to me more easily controlled, and therefore preferable to the curved bistoury frequently employed. While from the nature of the lesion the depth of the incision cannot be exactly gauged, our purpose should be (1) to have it so placed as to reach the centre of infection, and (2) to carry it through the inflamed cellular tissue and into the perichon- drium without cutting deeply into the cartilage. It is, however, better to cut a little too deeply rather than to err in the other direction with an incision too superficial to reach the source of trouble. An additional and important advantage of having the patient under the influence of an anaesthetic is that it permits one to use pressure for the removal of pus, should it be present, or at least to make sure by the use of a probe that the incision is sufficiently deep. After the patient recovers consciousness, which with nitrous oxide anaesthesia occurs within a few moments, it is well to irrigate the canal again with a carbolic acid solution, 1 in 200, as hot as the patient can bear it without too great discomfort. This second irrigation is distinctly useful, as the heat and the locally anaesthetizing effect of the carbolic acid reduce the sensitiveness of the part and facilitate the subsequent treatment. The canal should now be dried as thoroughly as possible and subjected to rather firm pressure by the introduction of a wick of sterile gauze which has been saturated with cresatin or a weak carbolic acid solution, 1 in 300, and then wrung out nearly dry. If such a patient can be confined to bed for a day or two, the efficacy of this treatment is likely to be enhanced, and in this case it is well to protect the ear with a large dressing of sterile gauze held in place by a bandage. The whole dressing should, of course, be changed daily. With regard to the irrigation fluid to be employed in cases of furuncu- losis, the writer believes that bichloride of mercury, even in weak solutions, should never be used, since it is likely to produce a dermatitis distinctly favorable to the development of secondary furuncles. If for any reason the use of carbolic acid is not advisable, a boric acid solution is non-irritat- ing and usually quite satisfactory. It is hardly necessary to state that carbolic acid in any solution stronger than that indicated in the prescription ACUTE CIRCUMSCRIBED EXTERNAL OTITIS 115 on the foregoing page should never be advocated for home use by the pa- tient or his family. The practice of incising a furuncle, and then directing the patient to syringe the ear at stated intervals, is quite unsurgical, the residual water left in the meatus being apt to macerate the skin covering the healthy portions of the canal, a condition distinctly favorable to the growth of bacteria. Cases so treated will be found to result in a large percentage of recurrences, whereas in my experience immediate recurrence is not frequent when the dry treatment, as above described, is carefully carried out. Routine irrigation of the ears is admissible only in one class of patients suffering from furunculosis of the meatus,—viz., dispensary patients who can be seen only at such long intervals that no other method is available. In such cases the best results will probably be obtained by prolonged irrigation, frequently repeated, with sterile water as hot as the patient can bear it. In advising hot irrigations, the patient should be informed that he will be likely with each repetition to experi- ence distressing vertigo, but that this discomfort will be short-lived and without serious consequences. Third Stage.—When a distinctly fluctuating abscess has formed at the site of the initial infection, the lesion is often no longer excessively painful, and incision usually causes much less pain than in the second stage. Never- theless, it is better, when practicable, to anaesthetize the patient, so that following the incision the pus may be thoroughly expressed and the interior of the cavity scraped out, if need be, by means of a small curette, or swabbed out with a carbolic acid solution, 1 in 20. A small drain may then be intro- duced into the abscess cavity, and pressure applied by means of a wick of sterile gauze. In the fourth stage the treatment does not differ materially from that above described. It is very rarely necessary to incise the oedematous parts behind or in front of the ear, secondary abscesses in these regions being exceedingly rare. Incision at the point of infection in the canal usually relieves tension and provides an adequate pathway for the escape of pus. The application of a wet dressing over the adhacent oedematous areas may, however, prove of value. In the foregoing pages the author has outlined the plan of local treat- ment which in his own experience has seemed to insure the best average results. The best plan of local treatment, however, leaves the patient who has suffered from this painful and depleting lesion particularly prone to recurrences. Against these recurrences I believe that the patient’s most effective defense will be found in the use of an appropriate vaccine. Naturally, whenever pus from the lesion can be obtained, an autoginous vaccine should be prepared. Under present methods, however, the great majority of cases of furunculosis of the canal are controlled without incision. 116 DISEASES OF THE EXTERNAL EAR Stock Vaccines.—Though difficult to explain, it is a fact abundantly established by experience that the vast majority of cases of furuncles of the auditory canal are due to a staphylococcus infection. Utilizing this fact and the large clinical material of her clinics and wards, the Manhattan Eye and Ear Hospital of New York has for several years used for this lesion a stock vaccine made in her own laboratory. ■ This is a composite vaccine, i. e., made from various staphylococcus strains derived from pus taken from various patients suffering from this particular lesion. There is no question that this particular stock vaccine has great value in establishing an im- munity against recurrence of this distressing lesion. For the rationale of this treatment the reader is referred to the short chapter on serum therapy. Note.—-Of recent years the writer has come to regard furunculosis of the meatus as a hospital condition. A few days of absolute rest in bed and the better general and local care which hospital control makes possible undoubtedly help to a quick and per- manent recovery. Acute Diffuse External Otitis.—This, according to my experience, is a comparatively rare condition. It exists whenever, in the absence of determinable foci of infection, the four walls of the canal are in a state of acute inflammation. It differs, therefore, from the occasional diffuse inflammation of furunculosis in the absence of the localized points of infection, single or multiple, which characterize the latter. Another dif- ference between this and the circumscribed form of external otitis (furun- culosis) is the frequency with which the whole canal is involved. That is to say, furunculosis of the meatus is almost invariably confined to the fibrocartilaginous portion, whereas in acute diffuse external otitis the canal in its entire length is usually more or less inflamed. Causes.—Acute diffuse external otitis may occur as an accompani- ment of chronic purulent otitis media, in which the discharge from the middle ear, being allowed to remain in the meatus, gives rise (1) to mac- eration and exfoliation of the cutaneous lining, and (2) acts as a direct irritant of the exposed subcutaneous surfaces. A more characteristic form of acute diffuse external otitis is seen as a result of direct violence, as not infrequently occurs in cases in which a physician with more zeal than skill has attempted with instruments to remove a foreign body from the meatus. Symptoms.—The symptoms are very similar to those observed with furunculosis of the meatus,—i.e., pain, sometimes very severe, increased by extensive movements of the jaw (yawning) and by any manipulations of the auricle which are communicated to the fibrocartilaginous meatus. Pressure upon the tragus always causes severe pain. Inspection by re- flected light shows the calibre of the meatus to be greatly reduced by the diffuse swelling of its walls. Treatment.—'Since the treatment up to a certain point is the same as that outlined for furunculosis of the canal, repetition of details are not called for. Wet dressings by means of gauze and antiseptic solutions as advocated for acute diffuse external otitis, give satisfactory results in a large majority of cases. Fig. 89.—Hyphomycetes, moulds: A, aspergillus nidulans; B, verticillium Graphii. (After Siebenmann.) OTOMYCOSIS 117 In a quite small percentage of cases, the inflammatory process will apparently yield to no treatment short of surgical intervention, which may be summed up in a few words: (1) Thorough cleansing of the canal, after the method described in the treatment of furunculosis. (2) One, sometimes two, longitudinal incisions, by means of the furuncle knife, through what may appear to be the more acutely inflamed wall or walls of the canal. (3) Rather prolonged irrigation with a hot solution of boric acid, or carbolic acid, 1 in 200. The heat thus applied favors free bleeding, thereby relieving tension and tending further to cleanse the parts of bacteria. (4) Careful drying of the canal, followed by the introduction of a wick of sterile gauze, or of gauze which has been impregnated with Dobell’s solution, a solution of boric acid, or a sterile normal salt solution. The dressing should be changed daily, the canal each time being thoroughly cleansed. As soon as the inflammation is apparently controlled, better results are obtained by a dry dressing, the outer cartilaginous canal being firmly packed with a sterile gauze wick. Pressure by this means should be continued two or three days after the symptoms and inflammatory signs have disappeared. Otomycosis.—This term is used to describe the condition in which some form of mould has found lodgement, and conditions favorable for its development, in the external auditory canal. It may be confined to the walls of the bony meatus, or may spread thickly over the drum membrane. The fungus may simply inhabit the meatus without causing any morbid changes in the tissues upon which it grows, in which case it gives rise to no symptoms whatever; and this is the condition found in over one-third of all cases (Bezold). In other cases the hyphomycetes may invade the tissues, the mycelia perforating the lining membrane of the bony canal and the skin covering the drum membrane, and giving rise to an acute inflammatory process. Etiology.—Beyond the fact that the germ requires warmth and moisture for its growth, but little is definitely known as to the cause of its frequent occurrence in the ear. Oils and fatty matter form a suitable nidus for its development, and Bezold obtained in seventy-five per cent, of all cases examined by him a definite history of the patient’s having instilled medicaments containing oil or glycerin into the ear. Many different forms of mould have been demonstrated in specimens taken from the ear. Among them may be mentioned the Aspergillus niger, Aspergillus flavus, Aspergillus nidulans, and the Verticxllium graphii. Symptoms.—As before stated, the fungus may remain long in the meatus and produce absolutely no symptoms. As soon, however, as the mycelia invade the living tissues—i.e., the skin covering the drum mem- brane or walls of the bony meatus—inflammatory changes are induced and the patient experiences more or less discomfort. The symptoms vary from an intense itching and sense of irritation to moderate—sometimes 118 DISEASES OF THE EXTERNAL EAR rather severe—-pain. The hearing may be impaired in cases in which the canal is more or less occluded. Inspection by reflected light reveals a different picture according to the form of hyphomycetes present and the stage of their development. The drum membrane and the walls of the bony meatus may be covered with an adherent growth, the color of which may vary from very dark gray or black (Aspergillus niger) to brownish yellow (A. flavus); or it may be dark green in color (Ferticillium graphii). Should inflammatory changes have taken place, the epithelium covering the drum membrane and canal walls may be thickened or exfoliated, or its removal may leave a red and inflamed surface. Treatment.—Salicylic acid seems to retard or check the growth of the various moulds finding lodgement in the ear. The first step in the treatment is thorough mechanical cleansing of the parts. The mould should first be removed by means of cotton-wound applicators, and the canal walls and surface of the drum membrane then carefully scrubbed with 95 per cent, alcohol. As a further precaution the ear may be irri- gated with a 1 per cent, solution of carbolic acid. Lastly the canal is filled with a 2 per cent, solution of salicylic acid in alcohol, which is allowed to remain in the ear five minutes or more. The patient is given a prescrip- tion for this solution (i.e., 2 per cent, alcoholic solution of salicylic acid) with which he is directed to fill the canal night and morning, allowing it to remain from three to five minutes. This treatment usually controls the affection fairly promptly, but the patient should be seen occasionally during several weeks as a precautionary measure against recurrence. When otomycosis occurs in an ear in which the drum membrane is perforated, the same line of treatment is usually effective. But since the tympanic recesses are not so easily reached, recovery is apt to be less rapid. Croupous External Otitis (Otitis Externa Crouposa).—This is ad- mittedly a rare condition. It may be defined as a diffuse inflammation of the inner, or tympanic, third of the meatus, in which this part of the canal and the surface of the drum membrane are covered by a fibrinous exudate. The membrane is repeatedly thrown off in the form of casts of the canal and drum-head. A new membrane soon forms. This cycle of exfoliation and re-formation may be repeated many times. The condition is some- what anomalous in providing the only instance of a coagulated fibrinous membrane forming upon tissues not covered by mucous membrane. Etiology.—Of this but little is definitely known. There are a few facts, however, which seem to me somewhat suggestive. It is known, for example, that the condition occasionally complicates furunculosis of the canal; that in the past it has occurred with comparative frequency in certain epidemics of influenza (a disease known frequently to cause blebs or bullae of the canal); and that it may be engrafted upon the simple form of acute diffuse external otitis. It is possible that the development of the lesion requires some form of preexisting acute inflammation plus the action FOREIGN BODIES IN THE MEATUS 119 of some germ which has not yet been isolated. This theory may help to explain its gradual disappearance among the affections treated in aural clinics. That is to say, the disease during the past two decades has be- come exceedingly rare, a fact possibly due to the more general and efficient use of antiseptics within that period. In a few instances the staphylococcus pyocyaneus and the streptococ- cus pyogenes have been found in the secretion or casts, but not with suf- ficient frequency to connect them as specific factors in the causation of the disease. The symptoms are those common to acute inflammations of the canal, —viz., pain in the ear, often very severe,—increasing in severity during the formation of new membrane and subsiding as the membrane is dis- lodged. The hearing is naturally interfered with, and varies in accordance with the degree of occlusion of the canal. The course. of the disease, though often protracted, usually ends in recovery. The treatment may be summed up in the word cleanliness. During the acute stage frequent irrigation with boric acid solution will help to hasten the formation and exfoliation of the membrane. During the periods between exfoliation and re-formation of membrane, dry treatment with insufflation of boric acid powder is said to give best results. OBSTRUCTIVE CONDITIONS OF THE EXTERNAL AUDITORY MEATUS. Foreign Bodies in the Meatus.—There is hardly a limit to the vari- ety of foreign substances which may be introduced, either intentionally or by accident, into the external auditory canal. This is the experience of every aurist in hospital practice. Children furnish by far the greater number of patients. The writer personally has removed flies, bugs, glass beads, imitation diamonds, seeds and small fruit kernels, a bullet, a piece of chalk, and a piece of pencil lead. In regard to the influence of a small foreign substance in the auditory canal, and the supposedly urgent need of its prompt removal, two facts should be impressed upon laymen and physicians alike,—viz., (1) that a small foreign body may remain in the canal for a long time, or even indefi- nitely, without injury to the ear and without even causing disturbance of function; and (2) that unskilful attempts at removal have frequently destroyed the usefulness of the organ, and have been the direct cause of not a few deaths. Removal of a Foreign Body by Means of the Syringe.—Fortu- nately, the great majority of foreign bodies finding their way into the auditory canal can be removed without injury to the ear by means of the syringe. This statement applies to practically all smooth substances small enough to enter the bony meatus without having to overcome resist- ance at the isthmus, and to all smooth bodies remaining in the membrano- cartilaginous meatus which are not large enough completely to fill its lumen. The fountain syringe is not suitable for this purpose, a syringe with which the current force can be regulated by hand pressure being 120 DISEASES OF THE EXTERNAL EAR infinitely more effective. Fig. 90 shows a metal syringe which can be sterilized by boiling and which answers this purpose admirably. Before using the syringe the ear should be examined by reflected light to determine as nearly as possible the size, shape, and position of the sub- stance to be removed. If small enough to be freely movable in the canal, a few injections of warm boric acid solution, the stream being directed a little upward and backward along the posterosuperior canal wall, will quickly expel it. When the foreign body has not passed beyond the isth- mus and is so shaped and situated as to leave a demonstrable space be- tween it and one wall only of the canal, the stream of water should be directed against this open space. In such a case, as soon as the water has filled the space between the foreign substance and the drum membrane, the principles of hydraulic pressure are brought into play, and the intruder is thrown out by the force of the increasing volume of water behind it. Were the stream not so directed, it might result in forcing the substance Fiu. 90.—Aural syringe. into the depths of the bony meatus where its expulsion might be less simple. When a foreign body appears completely to fill the lumen of the mem- brano-cartilaginous canal, it is clear that irrigation will not dislodge it and may carry it further into the canal, unless the stream can be made to enter the space between the intruder and the drum membrane. When irrigation is employed in such a case, the auricle should be drawn out- ward and backward, and a rather forcible stream directed inward and a little upward and backward along the posterosuperior canal wall. Fol- lowing this method, the water in most cases reaches the fundus of the canal, and the substance is brought away with the return current. Insects.—'When insects—e.g., bugs—are seen crawling within the canal or upon the drum membrane, it is well before syringing to fill the meatus with olive oil. This dislodges them from their point of attachment and facilitates their expulsion. Seeds, Peas, etc., within the Canal.—Much has been said of the danger in using the syringe of causing such substances to swell and tightly occlude the canal. The question to be considered in such cases is whether the pea or seed has already become swollen, or is so large as to render its. FOREIGN BODIES IN THE MEATUS 121 removal by irrigation doubtful; for in case of failure, the moisture left in the canal will be likely to render subsequent efforts at removal more diffi- cult. When, however, the seed or pea is small and movable in the canal, there can be no possible danger in the use of the syringe. While syringing does not act quite so effectively upon a substance in the depths of the bony meatus, there are in the author’s opinion exceed- ingly few cases in which a foreign body lying free in any portion of the canal cannot by this method be removed without injury to the parts. Cases Requiring the Use of Instruments.—While the syringe is effective in the vast majority of cases, conditions occasionally present themselves in which one may be obliged to resort to the use of instru- ments. In this category may be included the following: 1. Peas, seeds, etc., of such size, or so enlarged by the effect of heat and moisture, as to be no longer freely movable in the canal. Fig. 91. 2. Solid substances which have become so firmly wedged in the canal (e.g., at the isthmus or in the depths of the bony meatus) as to require mechanical dislodgement. 3. Solid bodies of irregular or angular shape, pressure of which is causing inflammatory swelling of the membrano-cartilaginous meatus. A deft use of instruments is often the only means of relieving this condition. 4. Solid substances which have been forced into the bony meatus, and are yet too large to repass the isthmus on the way out except in response to an equal amount of force. Children occasionally furnish such instances. Choice and Use of Instruments.—In the author’s opinion the safest instruments for removing solid substances from the ear are those typified in the accompanying illustrations. The hook (Fig. 91) should present a terminal rectangular bend about 3 mm. in length, the extremity of which is rounded or dull. In using it the hook, or terminal bend, lying flat against the canal wall, is carried past the intruding substance. The handle, or shaft, is then rotated so that the hook squarely engages the foreign body, which can usually be easily withdrawn. This in my experience is a very practical little instrument which can be successfully employed in a majority of cases. Fig. 93. 122 DISEASES OF THE EXTERNAL EAR The dull ring curette (Fig. 92) can be used safely in only one way: it should be introduced either above or behind the body to be removed,—i.e., between it and the roof or the posterior canal wall. The body is then crowded downward or forward against the floo*- or anterior wall, and thus pushed outward toward the orifice of the can i. Pressure with the ring curette from below upward is always dangerous, for the reason that it may force the substance backward upon, and even through, the drum membrane. The author’s adjustable ring curette (Fig. 93) is practically a dull ring curette in which, by sliding forward a movable rod, the ring can be made to assume a position at right angles to the shaft. Its application is obvious. The ring in the straight position is carried beyond the substance to be re- moved, and then changed into the rectangular position, in which it cannot fail to engage the intruder. The writer has purposely not mentioned any form of forceps, because he believes that a forceps should never be used for removing a solid body from the auditory canal. The two main objections to its use may be stated as follows: 1. In removing a foreign body it is particularly important to avoid any injury to the canal. With care it is almost always possible to pass a small instrument between the intruding body and one wall of the meatus without injury to the latter. With the forceps, however, one has in effect simultaneously to pass two instruments—i.e., the two forceps blades —between opposite sides of the foreign body and the corresponding canal walls. Unless the body is so small as to be obviously removable by the syringe, the danger of traumatism is doubled. Bleeding in case of failure renders further effort more difficult. 2. The chief objection to the forceps, however, is the danger of push- ing the offending substance further into the canal. Not infrequently a solid, smooth substance, which seems easily and safely within the grasp of the forceps, slips from its blades and is driven further toward the drum membrane. Successive attempts may result not only in further displace- ment, but often in extensive laceration of the canal. The writer has known more than one case in which the drum membrane has been practi- cally destroyed by this manoeuvre, the foreign body being finally pushed into the tympanic cavity. Every experienced aurist has met with such cases. Surgical Removal of a Foreign Body from the Meatus.—This is advisable whenever it becomes evident that the simpler methods above described cannot be employed successfully or without endangering the integrity of the organ. The conditions calling for operative intervention fall chiefly under two heads,—viz.: (a) Inflammatory swelling of the canal so occluding its lumen that small instruments cannot be manipulated within the meatus without danger of injury to the deeper parts. Under such conditions the attempt to remove a foreign body through the meatus might result in irreparable injury to the ear. REMOVAL OF CERUMEN FROM THE MEATUS 123 (b) The aurist has occasionally to deal with cases in which ill-advised or unskilful attempts at removal have resulted in such traumatism of the canal walls that the exact size and position of the foreign body and the condition of the tympanic structures cannot be determined. Under such conditions further attempts at removal through the canal are apt to result in further injury. It should be accepted as an axiom in practical otology that no instru- ment should be introduced into the meatus except under inspection by reflected light, and under conditions permitting one to know positively its exact position after it has entered the bony canal. Obviously, when the canal is swollen or bleeding, or its walls torn and lacerated, the use of instruments cannot be controlled by the recognition of familiar land- marks. Under such circumstances the attempt to carry an instrument beyond a foreign substance may result in serious injury to important tympanic structures, or even in dislocation of the stapes from the oval window. Bezold is authority for the statement that such accidents have been responsible for many deaths. Students of otology will do well to bear in mind and adhere strictly to the following rule: Whenever the membrano-cartilaginous canal is acutely inflamed, no attempt should be made to remove a foreign body even from the outer, or membranous, portion of the meatus, without having the patient under the influence of a general anaesthetic. With the patient anaesthetized, it is usually possible, even in the presence of moderate inflammation, to remove through the canal a foreign substance which has not passed into the bony meatus. The steps of the operation for removing a foreign body from the depths of the bony meatus are as follows: A curvilinear incision, following the curve of the auricular attachment, is made over the mastoid process. This incision passes through all the soft tissues, including the periosteum, down to the bone. The periosteum is carefully elevated anteriorly, and the lin- ing membrane of the bony canal separated from its walls by means of a small curved elevator. Under traction the membranous canal is usually torn from its attachment to the annulus tympanicus and the drum mem- brane, and the auricle is folded forward upon the face, drawing with it the membranous canal out of the bony meatus. It is now an easy matter to remove the foreign body with forceps or other instrument, unless it has been forced through the drum membrane by previous manipulation, and lies hidden within one of the recesses of the tympanic cavity. After the intruder has been removed, the parts, having been re-sterilized, are re- placed in position, and the posterior wound sutured. The membranous lining of the bony canal is held in place by a light packing of sterile gauze. If asepsis has been carefully observed, the wound resulting from this operation usually heals promptly. In certain cases it will be found that, as a result of previous ill-advised attempts at its removal, the foreign body has been forced through the drum membrane, and therefore lies within the tympanic cavity proper. 124 DISEASES OF THE EXTERNAL EAR Under such conditions it may be necessary to enlarge the opening in the drum membrane or even to remove it in order to locate the object which has been the cause of so much needless injury. In two cases operated upon by the writer, the drum membrane had been torn and lacerated beyond any hope of repair, before the patient came under his care. Removal of Cerumen from the Meatus.—The secretion of cerumen, or “ ear-wax, ” is confined to the area of distribution of the ceruminous glands in the outer part of the membrano-cartilaginous meatus. In amount it varies in different individuals from a very thin layer lining the outer end of the canal to large masses completely occluding its lumen. In a certain proportion of cases there is practical absence of cerumen so far as the eye can detect. These differences may occur in ears which are otherwise perfectly normal. Ordinarily the cerumen is confined to the outer, or membranous, portion of the canal. In some cases, however, in which there is no automatic elimination or extrusion of the cerumen formed, the last to be secreted pushes the previously formed mass further inward toward the drum membrane, and this process, repeating itself, finally completely fills the meatus. When present in the meatus in masses large enough to disturb or endanger the auditory function, cerumen becomes practically a foreign body, which should be removed. The method of removing it calls for but brief notice here, since it is effected by practically the same measures as have been described for removing foreign substances finding their way into the ear. In the vast majority of cases, even large masses of cerumen may be removed easily and without injury to the canal by means of the syringe. As occasional exceptions to this rule may be mentioned the following conditions: (a) The presence of large masses of tightly impacted cerumen com- pletely closing the membrano-cartilaginous canal. In such a case the stream of water from the syringe may play upon the obstructing mass, exerting no influence upon its position. If we can insinuate a dull ring curette or other small instrument between the roof of the canal and the cerumen, we may by crushing the latter downward be able to create a passage by which the irrigation fluid may reach the fundus of the canal. By directing the stream along this pathway, the cerumen will in many cases be quickly expelled. Should this fail, it may be necessary to intro- duce a hook, or the angular ring curette, into the space above described and remove the cerumen by direct traction. (b) A second condition for which the syringe is inadequate is found in cases in which the whole canal from the external orifice to the drum membrane is filled by a solidly packed mass, probably representing the accumulation of years. Such an accumulation is usually composed of cerumen intermixed with layers of exfoliated epithelium, finally becom- ing welded into an exceedingly hard and impervious mass. This condition is made known to us first by the inefficacy of the syringe, and second by the sense of solidity and resistance which it imparts to the probe or curette. EXOSTOSES OF THE OSSEOUS MEATUS 125 In this condition I believe that it is not always best to attempt to remove the entire mass at one sitting. If we can succeed in passing a dull ring curette for a short distance between the canal roof and the obstructing body, we may be able to force the ring down into it, and thus by traction with- draw the entire mass, or a portion of it. If only a part of the mass comes away, we may proceed in like manner to remove piecemeal so much of what remains as can be dislodged without injury to the canal. As soon, however, as we find ourselves in danger of injuring the canal walls, it is better to desist. We now direct the patient to fill the meatus night and morning with a solution of bicarbonate of soda (gr. xx ad gi), and to irri- gate the ear once daily with a warm solution of boric acid (5 j to the pint). If in two days this has not resulted in clearing the canal, we shall in most cases find the mass so much softened that we shall have little difficulty in removing it. In some cases the use of the syringe leaves the drum membrane red and inflamed in appearance, a condition which usually subsides rapidly. Exostoses of the Osseous Meatus; Bony Outgrowths from the Walls of the Bony Canal .—But little is known of the etiology of these growths. According to Bezold, they represent a condition rarely or never developed before puberty. They are multiple oftener than single, appear- ing oftenest on the anterior and posterior walls. When one growth only is present, the anterior wall, near the attachment of the drum membrane, is the most common site. As seen by reflected light, they appear as small, rounded protuberances, covered by normal skin, into the lumen of the canal. Palpation with a silver probe shows them to be hard and rather insensitive to pressure. It is rare for these growths to occlude the canal completely, and the hearing is not usually noticeably impaired. Only in the case of acute middle-ear suppuration do exostoses of the canal cause anxiety, and then only if they are sufficiently large to interfere with drainage or the proper management of the tympanic lesion. Treatment.—Usually none. Unless occluding the canal or unfavor- ably influencing the course of a middle-ear lesion, removal is not indicated. Should conditions arise rendering removal imperative the method of accomplishing this depends upon the character of the growth. If it is attached to the bony canal wall by a slender pedicle, it may be an easy matter to detach it by a single light tap upon a narrow chisel, the edge of which is held in firm contact with the canal wall at the point to which the pedicle is attached. When, however, the growth is attached by a broad base, no attempt should be made to remove it through the membrano- cartilaginous meatus. In such a case it is far safer to make a curvilinear incision behind the ear and carry the auricle forward upon the face, sepa- rating and lifting the membrano-cartilaginous meatus out of the bony canal. The bony growth may then be removed by means of a small chisel or gouge, or it may be practical and safe to introduce a small sharp bone curette and remove it from within outward. CHAPTER V. CAUSES OF ACUTE TYMPANIC DISEASE. The conditions which predispose to, or excite, middle-ear inflammation may give rise to the mildest type of tympanic congestion or to the severest form of suppurative otitis media. That is to say, it is not possible, in the light of our present experience and knowledge, to speak dogmatically of one group of etiological factors as producing the milder ear lesions and of another as responsible for the severer types of tympanic disease. It will, therefore, enable us to avoid much useless repetition, and also conduce to a clearer and more practical view of the subject, to speak first of the causes of acute tympanic inflammation in general. It will then suffice to mention with each recognized of otitis media the causes to which it is most often traceable. Predisposing Causes.—Of predisposing constitutional conditions but little may be said beyond the fact that conditions of lowered vitality render the individual more susceptible to suppurative middle-ear lesions than are the physically and constitutionally robust. Only in this way can be explained the enormous prevalence of suppurative otitis media among the ill-nourished and poorly housed children of the poorer class of tenement- house dwellers in the large cities. The extent of this predisposition is not generally recognized either by the laity or by the medical profession, for the reason that, when drainage from the ear has once been established by a large perforation in the drum-head, the little patients suffer no pain and usually no constitutional symptoms sufficiently pronounced to attract attention. Should any physician in large dispensary practice among chil- dren care to investigate the truth of these statements, he may do so by making systematic aural examinations in any large series of cases. Such a series of examinations, if the results were carefully noted and the number of cases examined were sufficiently large, would not only be in- structive to him, but might form the basis of a record of considerable value alike to otologists and to physicians generally. Age.—Children undoubtedly suffer more frequently from acute middle- ear disease than adults. This is due in part (a) to the influence of pharyn- geal adenoids, which are oftener present during childhood than in adult life; (b) to the greater susceptibility of children to the acute infectious diseases which so often give rise to otitis media; and (c) to certain anatomical dif- ferences in the Eustachian tubes in infancy and young childhood as com- pared with the adult type. These differences are described in the chapter dealing with the anatomy of the conducting apparatus. Nasal Obstruction. — Undoubtedly the most potent predisposing uause of tympanic disease is to be found in conditions interfering with nasal respiration. Here again, with regard to acute otitis media, children 126 ACUTE INFECTIOUS DISEASES 127 are the greater sufferers. The presence in the nasopharynx of large masses of adenoid tissue, with or without great enlargement of the faucial tonsils, constitutes a constant menace to the ears, which can be corrected Only by removal of the growth. The important relation of adenoids to tympanic disease is made clear by the following facts, which may be veri- fied by any physician who will take the time and trouble to do so: (1) A majority of all cases of acute otitis media in children occur in those suffering from adenoids. (2) Conversely, examination of any series of children suffering from adenoids will show in a majority of cases some pathological condition in one or both ears. (3) Children with large adenoid growths rarely pass through a severe exanthematous attack without aural complication,—i.e., without some grade of tympanic inflammation. And, (4) Conversely, children without hypertrophy of the pharyngeal and faucial tonsils, or in whom adenoids have been successfully removed, usually pass through the infectious diseases of childhood without middle- ear inflammation. Among other lesions interfering with nasal respiration are the following, which more commonly give trouble in adult life: Marked deviations to one or the other side of the nasal septum; septal ecchondroses or exostoses (commonly called spurs); hypertrophic rhinitis. These conditions predis- pose primarily to catarrh of the nasopharynx and membrano-cartilaginous portion of the Eustachian tube, and secondarily to middle-ear inflammation. Exciting Causes.—Acute Rhinitis.—Acute middle-ear inflammation occurs very frequently as an accompaniment or immediate sequela of acute coryza, the common “cold in the head.', The author has made a habit of questioning his dispensary patients, as well as those in private practice, as to conditions or causes to which an existing acute otitis might be traced. That it followed “a severe cold” is a very frequent answer, but even more numerous are the cases in which absolutely no data upon which to base a theory as to its causation can be elicited from the patient. These cases can hardly be regarded as idiopathic, and are probably to be explained as having followed a mild coryza, or nasopharyngeal catarrh, which has escaped the patient’s memory. The writer believes that more cases of acute otitis media residt from a simple nasopharyngitis, acting upon an individual in whom strongly predisposing conditions exist, than can he traced to all other exciting causes combined. Acute Infectious Diseases.—Just what percentage of cases of the acute exanthemata give rise to acute aural disease has not been deter- mined. The author, as aural surgeon to the Willard Parker Hospital (New York city hospital for infectious diseases), has had some oppor- tunity of observing the aural complications of certain infections—notably in scarlet fever and diphtheria. Taking these diseases for purposes of comparison, he would say that at least 10 per cent, of all case of scarlatina and 5 per cent, of all cases of diphtheria develop some form of acute 128 CAUSES OF ACUTE TYMPANIC DISEASE tympanic disease. Were the ears of all children suffering from these diseases examined daily, there is little doubt that a larger percentage of cases of acute tympanic disease would be diagnosticated than is repre- sented by those usually attracting the physician’s attention. Measles gives rise to acute suppurative otitis media, often of severe type, and in a percent- age of cases probably falling little short of that associated with scarlet fever. As to the comparative average severity of the aural lesions complicat- ing the various exanthemata, it may be said that the purulent otitis media associated with measles is of severe average type, and that the percentage of cases developing suppurative mastoiditis is particularly large. The tympanic inflammation complicating scarlatina comes next to that associ- ated with measles in the frequency with which the mastoid cells become infected. Another very serious and characteristic feature of scarlatinal otitis media is the astonishing rapidity with which the drum membrane may be actually destroyed. The writer has seen cases in which the pos- terior segment of a perfectly normal drum membrane has undergone almost complete disintegration within a few days of the onset of a scarlatinal otitis media. The destruction of the drum-head is in some cases so rapid and extensive as to render it impossible, after the systemic disease has run its course, for the tympanic defect to be repaired and the middle ear to regain its normal condition. This explains the very large percentage of clinic patients, suffering from chronic suppurative otitis media, wdio trace their aural lesions back to an attack of scarlet fever. As compared with measles and scarlet fever, the aural complications of diphtheria are both infrequent and mild. There is greater danger of extensive destruction of the drum-head than of rapid and serious involve- ment of the mastoid cells. As with other infectious diseases, however, different epidemics vary greatly in the type of aural lesions produced. While in New York during the past three or four years the aural compli- cations of diphtheria have been of comparatively mild type, the author recalls certain seasons in which the disease gave rise to many instances of severe tympanic and mastoid suppuration. Among the further results of such lesions he recalls one fatal case of brain abscess, several cases of purulent leptomeningitis, and a still greater number of cases of infective sigmoid sinus thrombosis. Grippe, or influenza, is a frequent cause of more or less severe purulent otitis media, which in certain epidemics shows a marked tendency to rapid involvement of the mastoid cells. Typhoid fever is a comparatively rare factor in the causation of acute tympanic disease. The aural lesions are in no way distinctive, or different from those occasionally accompanying other wasting diseases. The end of the third week and throughout the fourth week are said to cover the period during which aural lesions are most likely to develop. Parotitis, or mumps, happily seldom causes tympanic suppuration. When the ears do become infected as a result of this disease, the labyrinth as well as the tympanum is not infrequently involved. This form of EXCITING CAUSES OF TYMPANIC DISEASE 129 panotitis may follow the usual course of a suppurative labyrinthitis; or the vestibular symptoms may rapidly subside, leaving in their wake ex- treme or even total deafness. It is one of the unhappy consequences of this lesion that the deafness, if pronounced, is apt to be permanent. Par- tial restoration of the cochlear function is said in certain cases to have been observed. Usually no improvement occurs. External Causes.—Most of these are conditions which give rise to nasal or nasopharyngeal congestion. Thus, sudden or prolonged exposure to cold or getting the feet wet may cause grippe, pharyngitis, or only an acute rhinitis, any of which conditions may lead to acute tympanic disease. Inhalation of irritating vapors may act in much the same way. Thus, the use of fast automobiles by exposing the individual to sudden chilling of the surface or to the inhalation of heavily dust-laden air, has been respon- sible for some cases of acute otitis media. The Nasal Douche.—The nasal douche, so frequently advised by some rhinologists and in some clinics, is doubtless absolutely necessary in certain cases of ozsena or of advanced atrophic rhinitis. It is also, however, a not infrequent cause of acute otitis media. Cases of aural disease originating in this way are known to every aurist. The author knows of at least one case in which the use of the nasal douche was directly followed by acute suppurative inflammation with mastoid involvement of both ears. Opera- tion upon both mastoids revealed pus and extensive caries throughout both processes. In this case the patient said that, on using the douche for the first time, he choked slightly and “felt the fluid go to the ears.” It is certainly safer, so far as the ears are concerned, to prescribe a nasal spray (atomizer) in place of the douche in all cases in which the nasal douche is not absolutely necessary. Swimming or diving in cold water is another prolific cause of acute aural disease, which brings many recruits to the aurist and aural clinic with each return of the swimming season. It is probable that this cause acts in two ways—viz. (1) through water taken into the mouth, some of which is propelled through the Eustachian tubes to the middle ear; and (2) by the impact of the water against the membrana tympani. It is to be guarded against, therefore, (a) by stopping the ears by means of a wad of moistened absorbent cotton, and (b) by care to avoid choking or violent efforts to expel water taken into the mouth or nose while under water. In a general way the above conditions may be said to constitute the chief etiological factors in the various types of acute middle-ear disease. Their importance in otology is obvious. The aurist who relieves the symp- toms of an acute attack, but takes no thought of precautions to prevent recurrences or the development of the insidious chronic processes which may follow, hardly fulfils his whole duty toward the patient. And this obligation can be met only by careful consideration of the underlying causes in each case of tympanic disease. If we consider what might be accomplished in the way of preventing aural disease, the responsibility of the general practitioner is quite as great. In no branch of preventive medi- 130 CAUSES OF ACUTE TYMPANIC DISEASE cine are the possibilities greater. If it were more fully realized that the presence of adenoids, when sufficiently large to interfere in any degree with nasal respiration, almost invariably causes tympanic congestion; that their removal minimizes the danger of tympanic infection; that the infectious diseases of childhood give rise to suppurative otitis media more frequently than acute articular rheumatism gives rise to endocarditis, it is clear that the prevalence of aural disease among people of all ages might be very appreciably reduced. Occupation and Habits as Causes of Aural Disease.—That certain occupations and habits may predispose to, or excite, aural disease, there is no room for doubt. Recognition of this fact and observation of certain forms of aural disorder thus induced have led to their being spoken of as “occupational diseases.” This is an unscientific term which, however, has served a useful purpose in directing attention to certain vicious influences which should as far as possible be guarded against. Certain occupations and certain habits predispose to, or cause, certain forms of aural disease, but there is no evidence that the diseases in question differ in pathology or symptomatology from the corresponding disorders due to other causes. Among the habits or occupations which occasionally cause aural disease or disorder may be mentioned the following: (1) The habitual or frequent use of certain drugs, — e.g., tobacco, alcohol, the coal-tar products (phenacetine, etc.). (2) Occupations in which the individual habitually breathes heavily dust-laden air,—e.g., railroad engineers, firemen, con- ductors, and others employed upon fast-moving trains; chauffeurs; street- sweepers, etc., etc. (3) Occupations subjecting the individual to the constant or frequently recurring influence of loud noises,—e.g., black- smiths, boiler-makers, naval and field officers and men subjected to the reports of heavy ordnance, workers in factories who are subjected to a constant roar of machinery. (4) Occupations requiring sudden or prolonged changes of air pressure, (a) upon the drum membrane, as in the case of caisson workers, or (b) within the tympanum,—e.g., cornet-players and per- formers upon wind-instruments generally. (5) Workers in substances con- taining certain systemic poisons,—e.g., lead, arsenic, phosphorus, aniline, etc. In consideration of the many who, though subjected to one or other of the above influences, escape wholly any untoward result, one is forced to assume that individual idiosyncrasy or especial vulnerability to certain influences, or substantial powers of resistance to the same, must consti- tute in some cases a determining factor. It is also necessary to assume that in many cases the causal factor may act in two ways,—i.e., either upon the sound-conducting mechanism or upon the labyrinth or auditory nerve. As to the varying susceptibility of different individuals to certain influences, tobacco and alcohol furnish notable examples. Thus, one man may be able to smoke habitually large numbers of cigars daily and to drink wine, beer, or whiskey in considerable amount without any determ- inable injurious effect upon his ears, while another suffers regularly from any excessive indulgence in either. 0 C CUP AT 10 X AL CAUSES 131 Tobacco in susceptible subjects may affect the ears injuriously in two ways,—i.e., (a) by inducing venous congestion or catarrh of the tubal mucosa, this giving rise to alterations of intratympanic pressure and ten- sion; or (b) more rarely, may induce a slow and insidious form of auditory- nerve deafness. A colleague of the writer who has been an habitual though moderate smoker of cigars has been obliged to give up smoking on account of the aural symptoms induced. He states that whenever he is tempted to smoke, even in moderation, he regularly experiences tinnitus aurium and a sense of fulness and occlusion of the ears, which as regularly disap- pear after a few days of abstention from tobacco. In such a case the aural symptoms are clearly due to a mechanical interference with the functional activity of the Eustachian tubes. As to the influence of alcohol upon the ears, while it is generally ad- mitted that alcoholic excesses may be injurious to the auditory as to other cranial nerves, a search of the literature yields little that bears directly on the subject. The most authentic and apparently typical cases reported are those of two university students observed by the late Professor Bezold. These patients experienced sudden, very marked loss of hearing. Careful functional tests demonstrated a type of deafness characteristic of labyrin- thine rather than of tympanic disease. Interrogation elicited the fact that both patients had for some months been in the habit of consuming enor- mous quantities of beer. All indulgence in alcoholic drinks was stopped, fol- lowing which there was a gradual but complete restoration of hearing power. Characteristic alcoholic deafness is probably in most cases dependent upon a neuritis of the auditory nerve, which, if the cause is not removed, leads to degenerative changes and permanent deafness. Occupations subjecting their followers to more or less constant breath- ing of dust-laden air—e.g., railway employes, chauffeurs, workers in dust- filled factories, etc.—are naturally productive of nasopharyngeal and tubal catarrh and the type of deafness characteristic of the tympanic changes secondary to such lesions. Occupations in the pursuit of which the individual is subjected to the ear-strain or shock of constant or very loud noises, give rise to two types of deafness, both of which are due to labyrinthine injury or disturbance. Blacksmiths, machine-workers, workers in factories in which a constant whirr of machinery is heard, suffer sooner or later a diminution of hearing which is of the type characteristic of a labyrinthine or nerve lesion. In the case of continuous or frequently recurring noises, it is supposed that the more or less prolonged irritation of the auditory nerve filaments leads in time to degenerative nerve changes of which the loss of auditory acuteness is a logical manifestation. The auditory nerve changes in these cases are probably in some degree analogous to those induced by Siebenmann and Wittmaack in their experiments upon animals. It will be remembered that these investigators, in experiments separately carried out, subjected animals to the continuous sounding of certain musical tones, with the re- sult that pathologic changes were induced in certain definite structures of. 132 CAUSES OF ACUTE TYMPANIC DISEASE the perceptive mechanism, the site of these changes varying with the musical tone employed. Substituting for the prolonged hearing of a single musical tone the constant repetition of loud noises irritating to all parts of Corti’s organ, it is not surprising that morbid changes leading to impaired hearing should result. The cases of sudden, and often very profound, deafness following very loud explosive sounds—e.g., the report of a cannon, the explosion of a mine, etc.—are obviously of quite different origin from those above described, these latter being due most probably to hemorrhage into the labyrinth or to sudden paralysis of the eighth nerve. That the symptoms, in some cases at least, are the result of changes primarily involving the auditory nerve filaments within the labyrinth is evidenced by the fact that the vestibular branch is also frequently disturbed. Occupations requiring sudden or prolonged changes of air pressure upon the drum membrane or within the tympanum, most frequently give rise to morbid changes confined to the tympanum. This is usually the case in occupations calling for frequent increase of intratympanic pressure,—e.g., cornet-players, glass-blowers, etc. The aural lesions to which caisson-workers are subject are also in a majority of cases confined to the tympanum, but occasionally involve the labyrinth. In regard to the aural disorders of caisson workers, a word should be said as to the two very distinct lesions which this occupation may inflict upon its followers. 1. The first, and fortunately the commonest, is due to the great increase of atmospheric pressure to which the tympanic mucosa is subjected. Unless the tubes are absolutely patent the drum membranes are forced inward. In either case the mucous membrane lining the tympanic walls and drum membrane is subjected to enormous uniform increase of pres- sure, which when he leaves the caisson is as suddenly relieved. These sudden changes induce in some cases a most aggravated form of tympanic venous congestion, characterized in some cases by ecchymoses into the drum membrane, or hemorrhage into the tympanum. The symptoms are tympanic in character, alarming to the patient on account of their sudden advent, but usually yielding to time and rational treatment. 2. The second and more serious lesion of the caisson worker is a laby- rinthine disorder the pathology of which is somewhat obscure. According to the theory of those who have made a study of it (Alt, Heller, H. v. Schrotter), the disease is the result of sudden alterations in the composi- tion and density of the blood. As a result of the sudden diminution of atmospheric pressure when the individual leaves the caisson, arterial pressure is increased to the point of causing labyrinthine hemorrhage. Another theory is that the sudden decompression incident to leaving the caisson results in the formation within the blood of gas emboli, lodgement of which within the labyrinth is the direct cause of the lesion. The symp- toms are those characteristic of labyrinthine hemorrhage—vertigo, ataxia, deafness. In severe cases the deafness is profound and may be permanent. CHAPTER VI. THE SUBJECTIVE SYMPTOMS OF AURAL DISEASE. There are just four symptoms referable to the ear of which a patient suffering from any form of aural disease, acute or chronic, may complain,— viz.: (1) aural pain, or earache; (2) impaired hearing, or deafness; (3) aural discharge; and (4) tinnitus aurium, or the subjective sensation of noises in the ear. One or more of these symptoms will be present in any aural disorder. Vertigo and ataxia, which are such important symptoms of certain disorders of the labyrinth, are purposely omitted from this list, which is intended to include only the commoner phenomena which the patient himself would recognize as of aural origin. Before entering upon a discussion of the more important middle-ear lesions, it may be well to consider briefly these subjective phenomena, which convey to the patient the knowledge that his ear is diseased. Aural Pain.—Earache is present at some stage of practically every case of acute middle-ear inflammation. It may also be present (though comparatively rarely) in certain stages of chronic non-suppurative middle- ear disease. It is an invariable accompaniment of acute inflammatory disease of the membrano-cartilaginous meatus, and it may occur in very severe t}rpe as a reflex phenomenon from lesions widely separated from the ear. For purposes of differentiation, all of these types will be briefly discussed. Pain in Acute Otitis Media.—The earache of acute catarrhal or purulent otitis media is described as resembling the pain of a severe tooth- ache,—i.e., throbbing or drawing in character, subject to exacerbations of intensity,—but of greater severity. It is probably one of the most unbearable types of physical pain. Its onset is usually sudden. Follow- ing a few premonitory twinges, the pain quickly attains a degree of inten- sity which makes sleep impossible. It is not influenced by manipulation or movements of the auricle or membrano-cartilaginous meatus. It is due either to increased tension through engorgement of the tympanic vessels, or to pressure and distention by fluid (serum or pus) collecting within the tympanic cavity. It is, therefore, often of short duration, subsiding quickly after spontaneous rupture of the drum membrane. This fact suggests the clearest indication for its relief: Free incision of the drum membrane almost invariably relieves the pain of acute middle-ear inflammation. Pain in Chronic Catarrhal Otitis Media.—Another type of ear pain which may puzzle even the experienced aurist is a form of paroxysmal earache of moderate grade which is far commoner in chronic catarrhal otitis media than is commonly recognized. The patient gives a history of more or less frequently recurring attacks of otalgia, which, however, do not seem ever to be as severe as the pain accompanying acute tympanic 133 134 SUBJECTIVE SYMPTOMS OF AURAL DISEASE disease. The drum membranes may present changes characteristic of chronic catarrhal otitis media, but no sign of acute inflammation. In the mouth and throat are found no lesions of which the ear pain might be a reflex phenomenon. Under such conditions careful testing of the hearing will in many cases show the progress of a chronic middle-ear inflammation, with the periodic extensions of which the pain is probably associated. Pain in Furunculosis of the Meatus.—The earache accompanying this lesion presents certain fairly constant characteristics. It is commonly gradual in its development, beginning as a sense of soreness about the canal, which later changes into a constant, throbbing pain of very severe type. It has frequently this pathognomonic characteristic,—i.e., that it is increased or intensified by wide movements of the jaw,—e.g., in yawning, or even chewing. This practically locates the lesion in the membrano- cartilaginous meatus, though the lesion may be either circumscribed or diffuse. Naturally the pain is intensified by any manipulation of the pinna which moves the cartilaginous meatus. As compared with the earache of acute purulent otitis media, the pain of furunculosis of the meatus is more gradual in its development and often less quickly relieved. While the indication is clearly a free incision through the focus of infection, this does not always furnish immediate relief of the pain. Reflex Aural Pain.—Patients seeking relief from very severe ear- ache, in whom physical examination shows the ears to be practically normal, are by no means uncommon in otological practice. In such cases we must carefully examine the mouth and throat for acute lesions which may be the underlying cause. By far the commonest cause of reflex aural pain is dental caries. Every aurist has seen such cases,—i.e., the patient suffering acutely from aural pain, the drum membranes being practically normal, and one or more teeth of the corresponding side of the jaw being carious. The writer recalls the case of an intelligent, but nervous, woman who rather indignantly combated the suggestion of dental caries as the cause of very severe earache, which, however, was not relieved until a necrotic tooth was removed. The only relief in such cases is obtained through the dentist. Other lesions causing reflex otalgia are severe acute tonsillitis, peri- tonsillar abscess, malignant disease of the base of the tongue. Impairment of Hearing. — Some degree of functional impairment, transient or permanent, is probably present in every case of tympanic disease. Unfortunately, very slight grades of impairment are compionly not recognized by the patient. This is the more unfortunate since the onset of chronic non-suppurative otitis media is the stage in which most could be done to prevent progress of the lesion and the development of disabling deafness later in life. It is important, therefore, that very care- ful hearing tests should be made in all cases of slight aural disorder. In acute middle-ear inflammation the hearing tests are not so important during the attack as after it has run its course, when a careful functional examination may demonstrate a residual disturbance of hearing which AURAL DISCHARGE 135 may be easily corrected by appropriate measures promptly applied. Neglect at this stage may pave the way for chronic changes resulting in marked deafness later in life. Aural Discharge.—Discharge from the ear, resulting from tympanic disease, always signifies partial or complete destruction of the mem- brana tympani,—i.e., a perforation which may vary from a pin-head orifice to practical loss of the membrana tensa. It may be scanty or pro- fuse; serous or purulent, and may be tinged with blood; odorless or ex- ceedingly offensive. Since the character of the discharge necessarily calls for discussion in connection with the various lesions, but little need be said here beyond the mention of certain points in which the discharge in acute otitis media usually differs from that of chronic middle-ear suppuration. Discharge in Acute Otitis Media.—Bacteriologically it varies in accordance with the character of the infection,—i.e., it may contain any of the pus-forming bacteria, or in a purely serous inflammation may be mucoserous and sterile. Usually, however, an aural discharge remains sterile only a short period after incision or perforation of the drum-head, —i.e., it soon becomes infected by germs from without. Except when allowed to remain long in the canal, the discharge in acute otitis media is usually without odor. Following incision of the drum membrane the discharge is often at first very moderate in amount, but rapidly increases during the first twenty-four hours thereafter. Following this initial period, the discharge is usually profuse, and remains so during several days, then showing gradual diminution, and finally, in favorable cases, ceasing altogether at the end of a period varying from one to three or four weeks. The distinguishing features of the discharge in acute otitis media are explained by the fact that they depend upon a lesion characterized by absence of bone necrosis, and which shows a marked tendency to self- limitation. Hence the absence of odor, and the gradual cessation. Discharge in Chronic Suppurative Otitis. — The discharge in chronic middle-ear suppuration may be very profuse or so scanty that the patient may be quite ignorant of its presence. Usually it is subject to variations in this respect, being at times exceedingly profuse and at other times barely noticeable. Rarely does it disappear wholly, however, inspec- tion by reflected light showing more or less destruction of the drum mem- brane and a granulating surface in the depths of the tympanic space, from which foul-smelling pus may be removed by means of a cotton-wound applicator. The odor also varies, being in some cases unbearably offensive and a source of unhappiness to the patient and in others of a sickening but less pronounced character noticeable only when removed from the depths of the canal. These, then, are the characteristic features of the discharge in chronic middle-ear suppuration,—viz. (1) its constant odor and (2) its persistency. As in the case of acute otitis media, the character of the discharge is ex- SUBJECTIVE SYMPTOMS OF AURAL DISEASE 136 plained by the character of the lesion,—i.e., its odor being due to the presence either of carious bone or of necrotic epithelial elements, and its persistency to the progressive character of the disease, which, though quiescent at times, tends rather to further extension and involvement of adjacent structures than to final resolution. In acute otitis media the appearance of an offensive odor in the dis- charge usually means either gross neglect—the pus being allowed to remain for days in the canal—or a change in the character of the lesion—i.e., chronicity due to bone caries. In chronic suppurative otitis media, complete and permanent disap- pearance of odor from the discharge would suggest possible elimination of the necrotic bone, which occasionally is thrown off in the form of minute sequestra in the pus, thus paving the way for final resolution. Such spontaneous cures undoubtedly occur. Tinnitus Aurium. — Of all the symptoms which the aurist is called upon to relieve, tinnitus aurium is the most elusive and difficult to control. It may be caused by any form of tympanic or labyrinthine disease, and may result from other conditions not dependent upon disease of the auditory apparatus. We may cure a tympanic lesion, but fail to relieve the tinnitus. This is a disappointing experience which every aurist has met with. In some cases tinnitus is the only symptom of which the' patient is conscious, and there may be little else that is abnormal either in the physi- cal or the functional condition of the ear. So baffling may such cases prove that it may not be amiss to devote some space to a theoretic discussion of the various conditions which may give rise to this elusive symptom. Obviously the most useful classification of the different forms of tin- nitus aurium would be one based upon the underlying lesions or disorders. I believe that most cases will be found to fall under one or other of the following heads: 1. Obstruction sounds, or noises due to occlusion or impaired mobility of some portion of the sound-conducting apparatus. 2. Blood sounds, or noises produced by the blood current in vessels in or near the ear, and due either to disturbances of the local or general circu- lation, or to abnormalities in the size, shape, or position of the vessels. 3. Labyrinthine sounds, or noises due either to structural changes in the cochlea, or to alterations—either increase or diminution—of intra- labyrinthine pressure. 4. Neurotic sounds, or noises due to abnormal irritability of the audi- tory nerve. 5. Cerebral sounds, or noises due to abnormal conditions acting upon the auditory centres in the cerebral cortex. Obstruction Sounds.—Under this general term we may include the numerous cases in which tinnitus aurium can be traced to its cause in a demonstrable lesion of the sound-conducting apparatus. In acute tubal catarrh, two symptoms chiefly engage the patient’s attention,—viz., TINNITUS AURIUM 137 impaired hearing and tinnitus,—and both disappear as the function of the tube is re-established. Again, in acute purulent otitis media, after the pain has been relieved by incision or rupture of the drum membrane, three symptoms continue to disturb the patient,—viz., impaired hearing, the discharge, and tinnitus aurium,—and all of them may disappear as resolution advances. In such cases the evidence is apparently conclusive that the subjective sounds are the direct result of a disturbed balance of the conducting apparatus. In studying these simpler forms of tinnitus, Panse advanced the theory that the function of the conducting apparatus is not only the transmission of sound waves to the ear, but also the con- duction from the ear of sounds which otherwise would act too strongly upon the perceptive mechanism. As supporting this hypothesis, he quoted the statement of von Troltsch1 that “all noises actually arising in or near the ear must necessarily act more strongly on the auditory nerve if the natural outward sound conduction be in any way diminished.” Another way of explaining this form of tinnitus would be to state that there are always present in the neighborhood of the healthy ear sono- rous vibrations due to certain physiological processes—e.g., the blood cur- rent—which normally do not reach the inner ear; that such vibrations, when they do reach the perceptive mechanism, must do so by bone con- duction; that bone conduction is always increased when the mobility of the ossicular chain is impaired; and, therefore, that sounds accompanying the simpler middle-ear lesions are in many cases the result of normal sonorous vibrations, which by reason of increased bone conduction are permitted to reach and impress the end organs of the auditory nerve. Have a vibrating tuning-fork held in contact with the median line of the skull, until its vibrations cease to be appreciated as sound. It is still vibrating, but now so feebly that the sound is no longer heard. Now close both ears by a finger pressed in each meatus, and the sound of the still vi- brating fork is again distinctly heard, and now also another sound is heard which is produced by the normal blood current in vessels in or near the ear. In other words, we have blocked the natural outward pathway of sound conduction, with the result that vibrations normally imperceptible pass by bone conduction to the perceptive mechanism and are appreciated as sound. It would seem that this theory of the causation of tinnitus might be found to apply to certain sounds for which other causes are sometimes assigned. For instance, it has frequently been noted, that, when the eyes are tightly closed by strongly contracting the orbicularis palpebrarum muscles, a low, buzzing sound is heard. This is supposed to be due to a sympathetic contraction of the stapedius, and is commonly spoken of as a “muscle sound.” But if we will produce this sound by forcibly closing the eyes, and then compare it with the sound produced by placing a finger lightly in each external auditory meatus, we shall find that the two sounds are very similar in quality and pitch, though the latter is of greater inten- 1 Von Troltsch: cited by Panse, Arch, of Otol., vol. xxviii, p. 365. 138 SUBJECTIVE SYMPTOMS OF AURAL DISEASE sity. May not this so-called muscle sound be thought of more correctly as a conduction sound, and as due to a temporary interference with out- ward sound conduction, during the contraction—which lasts but a few moments—of the stapedius muscle? Since tympanic lesions may be accompanied by a high degree of con- gestion and, by pressing the stapes inward, may produce changes of the intra-labyrinthine pressure, it is evident that all cases of tympanic tin- nitus do not necessarily belong to this class. That is, there may be other causative factors at work. The outward conduction of sound may be interfered with by anything which occludes the meatus,—e.g., cerumen, foreign body, furuncle, etc.,— or by anything which interferes with the mobility of the ossicular chain,— e.g., tubal catarrh with retraction of the drum membrane, tubotympanic congestion, fluid effusions within the tympanic cavity, constricting bands binding the ossicles together or to the tympanic walls, etc., etc. Viewed in this way, it is quite logical to treat these conditions locally and expect the tinnitus to subside as the parts regain their normal condition. Blood Sounds.—The so-called blood sounds may be of arterial or venous origin. They may be dependent upon anatomical anomalies and not upon any pathological condition, in which case they are not to be looked upon as a symptom of disease, and are often not amenable to treat- ment. The close relation, for example, of the internal carotid, artery and the internal jugular vein to the tympanum is well known. The anterior wall of the tympanum is separated from the internal carotid by a thin bony plate only, and the tympanic floor is in relation with the jugular fossa, which lodges the bulb of the jugular vein. As an abnormal congenital condition the carotid canal may project into and encroach upon the cavity of the tympanum, and it is not difficult to conceive that any malposition in this direction might give rise to sounds which the patient could not fail to hear. In the tympanic floor, also, dehiscences may exist either as a congenital defect or as a result of an old necrotic process which has under- gone resolution. Many such cases have been observed during surgical operations and in the course of post-mortem examinations. At a meeting of German naturalists many years ago, Professor Korner,2 of Rostock, presented, among other specimens, a temporal bone showing a fissure in the tympanic wall of the carotid canal. Dr. Dench3 has recorded the case of a young woman upon whom he performed the operation of ossiculec- tomy. After removal of the ossicles, “a bluish mass was seen in the floor of the tympanum, which proved to be the bulb of the jugular vein, its exposure being due to a defect in the tympanic floor.” These cases are not unique, and are cited simply to emphasize the fact that tinnitus is not necessarily an evidence of disease. They cor- roborate the statement of Schwartze,4 that “continuous noises may occur 2 Korner: Arch, of Otol., vol. xxxi, p. 119. 3 Dench: Arch, of Otol., vol. xxvii, p. 297. 4 Schwartze: cited by Panse. Arch, of Otol., vol. xxviii, p. 354. TINNITUS AUKIUM 139 during a lifetime in persons of normal hearing, due probably to anomalies in the course of vessels.” A persistent form of tinnitus, which we may also assume to indicate circulatory derangement, is that which may accompany visceral disturb- ances in other parts of the body. It is a well-recognized fact that visceral disorders—notably disorders of the pelvic and abdominal viscera—fre- quently produce aural symptoms. Woakes5 explains this on the hypothesis of a nervous relationship between the viscera in question and the laby- rinth. He points out that the nerves regulating the calibre of the vertebral arteries, and also of the basilar artery and its branches, including the internal auditory which supplies the labyrinth, come from the inferior cervical ganglion of the sympathetic. The stomach and other abdominal viscera are largely supplied by the pneumogastric nerves, and the com- munication between the vagus and the inferior cervical ganglion is estab- lished by means of a fasciculus from the vagus to the ganglion in question. Thus, in certain disorders of the stomach, for instance, impulses may be sent by way of the inferior cervical ganglion to the labyrinth, whereby its arteries are caused to dilate. Woakes claims that under such conditions the blood supply to the area involved “may be ten times as great as” under normal conditions. With this theory in mind it is no tax upon our cre- dulity to accept the statement that “cases of tinnitus from constipation, subacute gastritis, and pathological conditions within the pelvis are of common occurrence.” In such cases it would be logical to expect the tinnitus to yield to treat- ment directed against the existing visceral disorders. Patients with chronic endocarditis form another class who occasionally suffer with tinnitus. When with chronic valvular disease a murmur heard objectively at the base of the heart is transmitted to the vessels of the neck, an accompanying tinnitus may be clearly due to transmission of the cardiac murmur. Strumpel,6 in writing of aortic regurgitation, speaks of cases in which, “ by applying a stethoscope lightly over the femoral, the brachial, and often over the radial and ulnar arteries, a marked valvu- lar sound” is heard. It would be surprising if such a murmur were not transmitted also to the patient’s organ of hearing. A peculiarity of this variety of tinnitus is the fact that in some cases the sound heard by the patient may be heard also by the physician through the otoscope. As illustrating this statement may be mentioned the case of Spirig,7 cited by Panse. His patient, a sufferer from aortic regurgitation, was troubled by subjective noises, at first pulsating, later becoming continuous. Objec- tively it was heard through the otoscope on the right side, a rhythmic, blowing sound; and a similar sound was heard through the stethoscope over the aorta, right carotid, subclavian, and brachial arteries. 6 Woakes: Deafness, Giddiness, and Noises, p. 135. 6Strumpel: System of Medicine, p. 289. 7 Spirig: cited by Panse, Arch, of Otol., vol. xxviii, p. 371. 140 SUBJECTIVE SYMPTOMS OF AURAL DISEASE Another variety of subjective blood sounds which in rare cases may be heard by the physician through the otoscope is that which occurs with intracranial aneurisms. The basilar and internal auditory arteries are the vessels said to be most often affected. Excluding, then, a transmitted cardiac murmur, a pulsating noise synchronous with the pulse, heard sub- jectively and objectively in both ears, would suggest aneurism of the basilar artery; if heard only in one ear, the inference would be of aneurism of the corresponding internal auditory artery. Obviously, in such cases the tinnitus is not amenable to treatment except in so far as cardiac and nerve sedatives may lessen its intensity. Blood sounds are usually of low or medium pitch, and are diagnosti- cated by their character and by the exclusion of other causes. Pulsating noises are of arterial origin, whereas venous sounds are uniform or non- pulsating in character. There should also be mentioned a venous blood sound, which sometimes occurs with chronic or long-continued anaemia. It is a low, continuous hum, supposed to be due to the altered condition of the blood in its pas- sage from the sinus into the bulb of the jugular vein. This sound is prob- ably somewhat analogous etiologically to the haemic bruit which in anaemia is sometimes heard objectively over the large veins of the neck, the so- called bruit du diable. The diagnosis depends upon the character of the sound, the absence of tympanic disease, exclusion by functional tests of labyrinthine disease, and evidences of anaemia as shown by the general symptoms and examination of the blood. Obviously the indications would be for iron, arsenic, tonics, or any treatment looking to the restoration of the blood to its normal condition. Labyrinthine Sounds.—That subjective noises are invariably present at the onset of acute suppurative labyrinthitis is a fact universally recog- nized. This, however, is a class of cases in which by comparison with other more distressing phenomena, the tinnitus becomes a minor symp- tom. The subjective noises accompanying suppurative labyrinthitis will not be considered in this chapter. There are, however, many cases of chronic non-suppurative middle- ear disease in wdiich the accompanying tinnitus seems hardly to be ex- plained as resulting from the tympanic changes alone. There are, for example, cases in which every known local therapeutic measure may be employed without in the slightest degree influencing the subjective noises. In our study of such cases, we must remember that the auditory nerve not only receives and transmits sound impressions in response to sonorous vibrations (its normal function), but may also convey noise impulses to the auditory centres purely as a result of irritation or disturbance of its terminal cochlear fibres (perversion of function). Many investigators (Grant,8 Politzer,9 Gruber10) have placed both 8 Grant, Dundas: The Clinical Journal (London), vol. ix, pp. 241-7. 9 Politzer: Diseases of the Ear, pp. 622-5. 10 Gruber: Diseases of the Ear, p. 514. TINNITUS AURIUM 141 congestion and anaemia of the labyrinth among the causes of tinnitus. George R. Field11 over thirty years ago emphasized his conclusion that “slight variations, either of increase or diminution, in the pressure on the delicate structures (of the labyrinth) may give rise to severe tinnitus.” There is much clinical and some experimental support of this view. Ani- mals killed after frequently repeated doses of quinine, salicylic acid, etc., have shown marked labyrinthine congestion,—congestion sufficiently pronounced to have markedly increased intra-labyrinthine pressure; and these drugs in repeated doses usually cause distressing tinnitus in man. Amyl nitrite is another drug which invariably causes loud tinnitus, and here the effect so rapidly follows the cause that it seems possible to explain it only by reference to the increase in intra-labyrinthine pressure which the drug undoubtedly induces. On the other hand, after severe hemor- rhage, when the patient lies in a condition bordering on collapse from a withdrawal of blood from all the tissues of the body, tinnitus is usually a prominent symptom, and in this case we are obliged to assume a reduction of intra-labyrinthine pressure. Granting, now, that congestive conditions of the middle ear may cause vascular disturbances within the labyrinth, we can easily conceive that the commoner hypertrophic, or hypersemic, form of chronic catarrhal otitis media may, through anastomotic channels, cause and maintain a constant state of moderate labyrinthine congestion. It is a fact long known to pathologists that low grades of hypersemia, long continued, almost invariably give rise to morbid changes in the tis- sues involved. It is probable, therefore, that in cases of obstinate tinnitus apparently dependent upon chronic catarrhal otitis media, we have also to contend with certain structural changes within the labyrinth which, being beyond our reach, account in many cases for our failure to relieve the subjective sounds. I believe that in this form of tinnitus more can be accomplished by regulating the patient’s mode and habits of life, atten- tion to hygiene, and possibly by constitutional remedies, than by local treatment. Neurotic Sounds.—Those subjective noises may be classed as neu- rotic sounds which depend upon a hypersensitive condition of the auditory nerves. The tinnitus in most of these cases is to be regarded as a pure neurosis,—i.e., it is dependent upon a functional disorder of the nervous system in which the auditory nerves share and sympathize. They may present no evidence of organic disease, yet are shown to be in a condition of increased or abnormal irritability. This condition of acoustic hypersesthesia may be produced by toxic matters circulating in the blood, which act as irritants upon the auditory nerves. In this way may be explained the temporary tinnitus occurring in some cases of chronic Bright’s disease, also the tinnitus occurring occasionally without evidence of tympanic disease in the course of acute infectious diseases. “Field: Medical Times and Gazette, June, 1878, p. 616. 142 SUBJECTIVE SYMPTOMS OF AURAL DISEASE The most characteristic cases of neurotic tinnitus, however, are found in patients suffering from neurasthenia or nervous exhaustion. In the diagnosis of these cases the process of exclusion naturally plays an impor- tant part. Thus, on examination of the patient, there may be found no disorder of the general circulation, no evidences of disturbed labyrinthine pressure, no visceral disorders which might affect the ear reflexly. Exam- ination of the ear may reveal nothing abnormal within the meatus or tym- panum, or, as is more common, a tympanic lesion being present, its correc- tion does not result in relief of the tinnitus. Such negative results should suggest, at least, the possibility of a functional nervous disorder. Careful questioning brings out the fact that the noise is made worse by bodily or mental fatigue; thus, it may be absent or hardly noticeable in the morning, after a night’s rest, but reappears or becomes distressing as the day advances. On functional examination, the hearing may at first seem nearly or quite normal. The tone limits are well maintained; lower tone limit nor- mal, upper tone limit unchanged, or may be raised. For certain sounds— usually the higher notes of the musical scale, and such sharp sounds as are produced by the watch and acoumeter—the hearing may be abnor- mally acute,—i.e., those sounds may be perceived further than the normal hearing distance. But while the patient’s hearing power may be normal, or even hyper- acute at certain times, it will usually be found to show great variations, and to suffer rapid diminution as the patient becomes fatigued. Thus, the hearing power may be very much better in the morning than in the late afternoon after the fatigues of the day. It is also characteristic of these cases (Dench12) that the patient may hear very well when conversing with one person, but with great difficulty when engaged in general conversation, the mental effort necessary to this attempt resulting in fatigue, which quickly reacts upon the auditory nerves. Dundas Grant13 has recorded some interesting cases of tinnitus due to nervous exhaustion. Having excluded tympanic lesions and the more usual constitutional causes, he made careful inquiry into the patient’s habits, and in many cases elicited a history of overwork, prolonged anxiety, alcoholism, dissipation, sexual excess, or of some mode of life logically leading to nervous breakdown. Following up this clue, he found on functional examination marked hyperacusis,—a vibrating tuning-fork held opposite the patient’s ear being heard twice the normal period of time, and the watch-tick being heard in some cases “across the room.” In many of these cases the tinnitus was relieved only by regulation of the patient’s life and by treatment appropriate to his nervous disorder. Dana14 places neurasthenia among the chief factors in the causation of 12 Dench: Diseases of the Ear, p. 605. 13 Grant: Loc. cit. 14 Dana: Nervous Diseases, p. 188. TINNITUS AUBIUM 143 tinnitus. He defines neurasthenia as a “ functional nervous disorder, which is characterized by an excessive nervous weakness and nervous irritability, so that the patient is exhausted by slight causes and reacts to slight irritation.” With this definition in mind, it becomes evident that the aural symp- toms are the logical results of the disease; that the tinnitus and hvper- acusis are due to the “nervous irritability,” while the variations of the hearing power under the influence of fatigue are due to the “nervous weakness.” It is probable that there are many cases of tinnitus of mixed origin in which the neurotic element is masked by other causative elements more on the surface; e.g., a tympanic lesion, tubal catarrh, etc. It is the opinion of the writer that cases of tinnitus belonging, at least partially, to this class are far more common, even among the laboring classes, than is usually supposed. For, while neurasthenia is commonly supposed to be a disease to which brain workers and so-called upper classes are particularly prone, we have Dr. Dana’s authority for the statement that sufferers among laborers and artisans are by no means uncommon. Cerebral sounds, or sounds due to irritation of the auditory centres in the cerebral cortex, may be dealt with briefly. This form of tinnitus is not very common in otological practice, and is of interest as much to the neurologist as to the otologist. Most authori- ties agree that complex or elaborated sounds—i.e., sounds taking the form of voices, tunes, distinct words or sentences—are to be regarded as of cerebral origin. The subjective noises which epileptics experience as a warning of impending attacks must also be regarded as due to a central lesion; and it is perhaps important to recognize this premonitory symptom from the fact that its presence is thought to bear somewhat on the prognosis of epilepsy, and to be of ill omen. Gowers15 refers to the fact that “epileptics with such an aura are in greater danger than others of becoming insane.” The hearing of complex or elaborated sounds is also believed by many to carry with it an unfavorable prognosis. While it is generally believed that the hearing of elaborated sounds points to irritation of the cerebral auditory centres, there are others who hold further that this symptom is an evidence of mental instability. Thus, Gruber16 states that “patients who hear human voices, words, conversations, etc., are either mentally diseased or become so later.” It seems hardly justifiable, therefore, to regard such subjective phenomena as aural symptoms, and as otological text-books and literature throw little, if any, light on the proper method of treatment, it would seem to be for the best interests of such patients to refer them to a competent neurologist. In trying to differentiate the various forms of tinnitus in accordance 15 Gowers: British Medical Journal, Nov. 14, 1896. 16 Gruber: Diseases of the Ear, p. 547. 144 SUBJECTIVE SYMPTOMS OF AURAL DISEASE with the underlying causes, we have the following sources of information to draw from: 1. Evidences of disease in any portion of the conducting apparatus as shown by physical examination. 2. History of the case, and character of the sound, as described by the patient. 3. Results elicited by careful functional examination. 4. Evidences of disease in other parts of the body, particularly as to the presence of digestive disorders, circulatory disturbances, blood dys- crasias, or disease of the nervous system. 5. Effect of certain drugs, either in relieving or aggravating the tinnitus. The importance of a careful physical examination of the ear becomes evident from the fact that any appreciable lesion in any portion of the conducting apparatus must act at least as a contributing cause in the production of tinnitus, whatever the character of the sound and whatever the chief factor in its causation may be. CHAPTER VII. ACUTE INFLAMMATORY DISEASES OF THE EUSTACHIAN TUBE, MIDDLE EAR, AND MASTOID PROCESS. Acute Tubal Catarrh; Eustachian Catarrh; Tubotympanic Congestion.—Tubal catarrh is the precursor of almost every form of tympanic disease, and as such deserves a more prominent place than is usually accorded it among diseases of the sound-conducting apparatus. It may be defined as an acute inflammation of the Eustachian mucosa, which may or may not give rise to aural symptoms, according to whether the lumen of the canal is, or is not, occluded thereby. Etiology.—Among predisposing causes must be included all condi- tions interfering with normal nasal respiration. The presence of post- nasal adenoids is, therefore, a particularly potent factor, and children are much more frequently sufferers from tubal congestion and inflammation than is generally recognized. Among adults such obstructive lesions as hypertrophic rhinitis, septal deflections, ecchondroses and exostoses of the septum, etc., are conditions which are apt to induce recurrent attacks of Eustachian catarrh. Of exciting causes by far the most frequent and important is the common “cold in the head,” or acute rhinitis, with which some degree of Eustachian congestion or inflammation is probably always associated. Pathology.1—In a first attack of acute tubal inflammation the lesion is probably in most cases confined to the membrano-cartilaginous, or pharyngeal, portion of the canal. Beginning as a simple venous congestion, the condition is later converted into an acute exudative inflammation. In the great majority of cases it is probable that the lesion never advances to the point of actual tubal obstruction, in which case the tubal functions may not be seriously disturbed, and aural symptoms are slight or absent. The tube may, however, be occluded in one of two ways,—viz. (a) inflam- matory swelling of the parts about the pharyngeal orifice may by pressure close the canal at this point, or (b) the inflammatory changes may extend into the osseous portion of the canal, obliterating its lumen at the isthmus. Tympanic Changes.—So long as the Eustachian canal remains patent, or, rather, so long as it continues to perform its function of supplying air to the tympanic cavity, no changes are observed in the drum membrane. As soon, however, as the tubal function is disturbed,—i.e., when the supply of air to the tympanum is diminished,—the air pressure within the middle- ear cavity becomes negative, and more or less congestion of the tympanic 1 Our knowledge of the morbid changes characterizing this lesion is based largely upon conditions actually demonstrable during the onset and height of the attack, and their analogy with similar processes elsewhere in the body. 145 146 ACUTE DISEASES OF MIDDLE EAK AND MASTOID vessels ensues. This probably explains the prodromal symptom,—the feeling of occlusion or “stuffiness in the ear,” which is sometimes com- plained of. When finally the Eustachian canal is completely occluded, the drum membrane is forced inward toward the inner tympanic wall by the unopposed atmospheric pressure from without. Inspection of the ear may now reveal the picture of a drum membrane showing no color or structural changes, but greatly retracted. It is probably at this point that the onset of aural symptoms is usually experienced. Unless the tubal lesion is promptly controlled, very marked congestion of the tympanic mucous membrane may occur, and the peripheral plexus of veins along the margins of the drum membrane and the attachment of the hammer handle will be greatly engorged. This condition is described in some text-books as a distinct lesion under the name of tubotympanic congestion. It in reality constitutes a later stage of an acute tubal in- flammation, and is a logical result of the lesion when unusually severe and prolonged. Symptoms.—As before stated, complete absence of aural symptoms is by no means inconsistent with moderate grades of tubal catarrh. It is probable, therefore, that most of us are occasional sufferers from this lesion without experiencing symptoms referable to the ear. When occlu- sion of the canal gives rise to tympanic disturbance, the symptoms usually present themselves somewhat in the following order: In a certain proportion of cases the attack is ushered in by a feeling of occlusion of the ear. This rather indefinite symptom is variously described by patients as a sensation of “stuffiness,” or closure of the ear, or of the presence of a foreign body in the canal. This may persist for a few days and then disappear as the canal regains its normal condition; or it may be the forerunner of more definite symptoms of functional disturbance. More commonly, according to the writer’s experience, the first symp- tom complained of is that of marked impairment of hearing. This is often the more noticeable and distressing from its sudden development. The deafness is of the type characteristic of disease in any part of the conduct- ing apparatus. Functional tests show diminished hearing for the watch, acoumeter, and for the conversational voice and whisper. Hearing for the lower musical tones is noticeably lessened, the upper tone limit not being disturbed. Hearing by bone conduction is always increased. With the impairment of hearing the patient usually experiences rather loud subjective sounds, or tinnitus aurium. The noise usually is of high pitch, and is variously compared to the sound of a cricket, the escaping of steam, the noise of a shell against the ear, the sound of the surf, the ring- ing of bells, etc., etc. Quite often there is evident difficulty in recalling any natural sound with which to compare it. In exceptional cases there is slight subjective vertigo, usually lasting but a few seconds, and rarely or never sufficiently pronounced to disturb static equilibrium. This symptom, when present, is presumably due to disturbance of intra-labyrinthine pressure, brought about through retrac- ACUTE TUBAL CATARRH 147 tion of the drum membrane and inward pressure upon the ossicular chain and foot-plate of the stapes. Aural pain is usually absent, practically always so during the first stage of tympanic disturbance from tubal catarrh. There are no consti- tutional symptoms,—e.g., fever, pulse changes, etc.,—unless such are present as a result of intercurrent disorder, or of the disease to which the tubal catarrh is secondary,—e.g., acute rhinopharyngitis, tonsillitis, grippe, etc. Physical Signs.—Following the onset of aural symptoms, inspection by reflected light usually shows a drum membrane which is more or less retracted but otherwise normal. Since one of the most difficult tasks for the beginner is the detection of moderate degrees of retraction, it may be well to speak here of the changes in its physical appearance which usually characterize this condition. Extreme retraction, such as occasionally occurs in the presence of marked atrophy and loss of tension of the mem- bran a tensa, is characterized by such obvious ballooning of the membrane inward and away from its points of attachment as to be easily recognizable even by the beginner. This, however, is an exceptional condition, such extreme displacement of the whole membrane being ordinarily prevented by the resistance which its inherent strength offers to the atmospheric pres- sure from without. It is quite important, therefore, that one should be able to recognize the moderate grades of retraction which are the more usual result of partial occlusion of the tube. Cardinal Signs of Retraction.—Hammer Handle.—It will be remembered that the drum membrane is obliquely placed at the fundus of the bony canal, its outer surface looking outward and also strongly downward and forward. When yielding to pressure from without, it moves inward, backward, and upward, carrying the hammer handle with it. As seen through the canal, the hammer handle appears shorter and having a more decidedly back- ward direction than normally. This foreshortening of the hammer handle is in some cases extremely pronounced, and is one of the characteristic signs of a retracted drum membrane (Fig. 94). There are certain cases, however, in which the distance between the umbo and the promontory is so small that the hammer handle is pre- vented from any extensive inward displacement. Under such conditions, while occupying very nearly its normal position, it is apt to appear ab- normally broad and prominent from the fact that the drum membrane in moving inward is more or less folded about it (Fig. 96). Processus Brevis.—The short process projects from just below the neck of the malleus in a direction both outward and upward. It is held firmly in position by the anterior and posterior ligaments (axis band), which are attached to the malleus a little below the level of the upper surface or point of the short process. In retraction of the drum membrane, the hammer handle moves inward, while the short process rotates outward. The short process appears, therefore, more prominent, as it really is, than when the membrana tensa occupies its normal position. Unusual prom- 148 ACUTE DISEASES OF MIDDLE EAK AND MASTOID inence of the short process constitutes a second sign of retraction (Figs. 94 and 95). Light Reflex.—It will be recalled that this phenomenon of the normal drum membrane is due not to any structural change at this point, but simply to the fact that the drum membrane within this particular space falls into a plane which reflects the light directly upon the eye of the examiner. It is obvious, therefore, that with any change in the position of the lower part of the tense membrane, either the light reflex must be lost or its form changed. It may appear as a single, minute, shining spot immediately in front of the umbo (Fig. 94), or may be divided into two or more points of light. A common type of divided light reflex resulting from Fig. 94. — Retracted drum membrane. Fig. 95. — Retracted drum membrane. Fig. 96. — Retracted drum membrane. retraction occurs as a minute point of light in front of the umbo, and a second crescentic reflex lying near and parallel with the lower anterior arc of the annulus tendinosus (Fig. 95). Another characteristic sign of retraction, which may be difficult to recognize in slight degrees of retraction, but is easily noticeable in cases of marked displacement, is due to the fact that the drum membrane is drawn away from the structures to which it is attached, causing them to appear unusually prominent. Thus, the annulus tympanicus, the anterior and posterior folds and the hammer handle, when this structure is not greatly foreshortened, stand out in exaggerated prominence. This condition is fairly well indicated in Fig. 96. To epitomize: the cardinal signs of a retracted drum membrane are: 1. (a) Foreshortening and rotation backward of the manubrium mallei, or (b) apparent thickening and undue prominence of the same.. 2. Unusual prominence of the short process. 3. Absence, or changes in the form, of the light reflex. 4. The anterior and posterior folds and the annulus tendinosus appear unusually prominent. The Course of the Disease.—According to the development of tympanic changes, the disease may follow one of three roads toward final recovery. 1. In favorable cases the symptoms may last but a few days, disap- TREATMENT OF TUBAL CATARRH 149 pearing completely as the tubal inflammation subsides and the canal regains its normal calibre. 2. In cases of delayed resolution, the negative air pressure within the middle-ear cavity may result in very marked congestion of the mucous membrane lining the tympanum. This condition is usually characterized by engorgement of the venous plexus which is situated along the periphery of the drum membrane and along the margins of the hammer handle. The drum membrane, therefore, exhibits a line of redness in these regions,— i.e., along the edges of the drum membrane and hammer handle. This marginal redness varies in intensity in different cases, but always preserves the characteristic of being differentiated by a distinct line of demarcation from the central area of normal membrane (Fig. 97). The symptoms are those described as belonging to the earlier stage of tubal catarrh, with the difference that aural pain (earache) may be present. It may, however, be absent, and when present is not usually very severe. This condition is spoken of by some authors as “tubotympanic congestion,” a very use- ful and descriptive name, which should not, how- ever, lead us into the error of regarding it as a separate lesion. The tympanic condition and ac- companying symptoms usually subside as the tubal inflammation undergoes resolution. 3. There is still a third possibility in the conversion of the tym- panic congestion into a simple acute inflammation with effusion of serum into the middle-ear cavity. This constitutes the purest form of acute catarrhal otitis media, as distinguished from acute purulent otitis media. Prognosis.—Acute tubal catarrh—i.e., in the first few attacks—tends to spontaneous and complete recovery. Frequent recurrence of tubal inflammation gives rise to chronic catarrhal conditions within the middle- ear cavity, leading to impairment of hearing later in life. Treatment.—The treatment of tubal catarrh may be directed along three lines—viz., (a) internal and local remedies intended to relieve naso- pharyngeal congestion, (b) local treatment of the tube aiming to re-estab- lish its function, and (c) correction of nasal and nasopharyngeal lesions which might act as influences toward recurrence. Treatment of the N asopharynx.—In the first place, if the tubal lesion is very acute and accompanied by pronounced symptoms of nasopharyngeal congestion,—i.e., those of a common “cold,”—the logical treatment is by active measures to combat the latter condition. Therefore, confining the patient to bed, brisk catharsis, and repeated small doses of quinine will do much to shorten the attack. Even when it is not practical to carry out these measures, or when the symptoms do not seem to warrant them, much can be accomplished by the internal administration of appropriate drugs. Thus, quinine in grain Fig. 97. — Tubo - tympanic congestion. 150 ACUTE DISEASES OF MIDDLE EAR AND MASTOID doses repeated every three hours during the day, or three times daily, may aid materially in shortening the attack. Personally the writer believes in the use of atropine or belladonna in acute tubal catarrh, their value being clearly traceable to their blennostatic action upon the nasopharyngeal and tubal mucous membrane. Belladonna may be prescribed with advan- tage in the form of the well-known “rhinitis tablets,” Lincoln’s formula,2 half strength; or the extract of belladonna in gr. % doses may be combined with any of the coal-tar preparations. When the patient, in addition to characteristic tubal symptoms, exhibits the malaise and constitutional depression suggestive of grippe, or marked evidences of acute rhinopharyn- gitis, the following prescription will be found of great value,—particularly if the patient can be confined to bed for a few days. R Capsules or powders, each to contain: Extract, belladonnae, gr. %; Phenacetini, Salol, aa gr. iiss. Sig.—One capsule (or powder) every four hours. As with acute rhinitis, acute tubal catarrh may often at the onset be aborted by the timely use of appropriate drugs. After it has progressed beyond a certain stage, it must run its course, and the best that may be hoped for from internal medication is that the attack may be shortened thereby. Locally, spraying the nose and throat night and morning with a cleans- ing alkaline solution (e.g., Dobell’s solution,3 glycothymolin, etc.) seems in some cases to exert a favorable influence. Alkalol is a proprietary preparation which answers this purpose nicely, and has the considerable advantage of being practically non-irritating. Certain cases of pronounced and intractable nasopharyngeal con- gestion or inflammation will respond favorably to a few repetitions of the following treatment: The nose and nasopharynx are thoroughly sprayed with a 5 per cent, solution of argyrol. This is allowed to remain a few minutes, and then washed out by means of the postnasal syringe with a warm normal saline solution. If the writer has dealt at some length with the treatment of the naso- pharynx, it must be remembered that the tubal inflammation is usually but an extension of a nasopharyngeal catarrh, and that whatever relieves the latter will provide the most logical treatment for the tubal lesion. Inflation.—The first step in the direct treatment of the tube is by some 2 Lincoln’s “ rhinitis tablets,” half strength, contain each: Extract, belladonnae gr. %, camphor, gr. /, and quininae sulphat. gr. )i. 3 Dobell’s solution: R Acid, carbolici, gr. iv; Sodii bicarbonat. Sodii borat., aa gr xl; Glycerini, oz. j; Aquae, q.s. ad oz. iv. TREATMENT OF TUBAL CATARRH 151 form of inflation. While this may be accomplished by the Politzer method, the catheter possesses the following considerable advantages: (1) We are able to inflate each ear singly and to regulate the pressure according to the resistance met with; (2) we obtain much more definite information as to the tubal condition from the clearer ausculatory signs (i.e., through the otoscope); and (3) in our effort to force air through the more occluded tube, we are in no danger of unduly stretching the opposite drum mem- brane, as may easily occur in repeated Politzeration. Local Anaesthesia.—The routine use of cocaine is not either wise or necessary for patients whose treatment requires repeated catheterization. There can be no doubt that repeated use of cocaine for any purpose carries with it some danger of establishing the drug habit. On the other hand, patients are often more or less nervous during a first examination, and it may then be wise to eliminate the discomfort incident to catheterization by applying a weak solution of cocaine. It should not be used in the form of a nasal spray, which anaesthetizes a larger surface than is necessary, and is more apt to cause reactionary engorgement of all the nasal tissues than wrhen the application is limited to the pathway to be traversed by the catheter. This is easily accomplished by passing a cotton-wound applica- tor (Fig. 99) which has been dipped in a 4 per cent, solution of cocaine, through the inferior meatus of the nasal cavity corresponding to the ear to be inflated. The cotton should be passed slowly back and forth three or four times. A minute or two thereafter, it will be found that the catheter can be passed through the nose without causing any discomfort. After this first catheterization, the use of cocaine should be altogether omitted. The technic of catheter inflation has already been described (pages 65 69), and need not be repeated here. It is a procedure which with care and skill can be made practically painless, or in careless or unpractised hands may become a veritable ordeal to the patient. The catheter should find its way easily and without application of force through the inferior meatus, the attempt to force it past any obstacle encountered resulting not only in pain, but in injury to the tissues. When an obstacle is met with in some nasal abnormality,—e.g., a low septal ecchondrosis or exostosis,— it is usually possible, by slowly rotating the catheter, to find a pathway along which the catheter will enter the nasopharynx without force. When this is not possible, catheter inflation will be of no benefit, and we should either resort to the Politzer method or subject the patient to preliminary operative treatment for the correction of the nasal lesion. The latter alternative will generally afford the shortest road to a permanent cure. Auscultatory Signs.—During inflation we may obtain important data as to the exact condition within the tubes from the sounds heard through the otoscope, or diagnostic tube. Thus, there may be (a) complete absence of sound characteristic of air entering the tympanum, this pointing to absolute occlusion of the canal; or (b) the presence of moist rales, changing in character, due to excessive secretion of mucus within the tube; or (c) the sound may be clearly indicative of air entering the tympanum, but 152 ACUTE DISEASES OF MIDDLE EAK AND MASTOID fainter and of higher pitch owing to the reduced calibre of the canal; or, finally, (d) there may be bubbling rales char- acteristic of air passing through fluid, indicating the presence of serum in the lower part of the tympanic cavity. For all the above conditions, which are but stages or phases of the same lesion, the treat- ment is much the same. Inflation per catheter acts beneficially in several ways. Its first result is the re-establishment of the normal air pres- sure within the tympanum and the replacement of the drum membrane in its normal position. This frequently gives immediate relief of the symptoms, and in some cases restores the hearing almost to the normal standard. This improvement, how- ever, is often of very short duration, the discomfort and functional disturbance recurring as the air in the middle-ear cavity is again exhausted. Inflation seems also to act directly upon the tubal mucosa, restoring its tone and aiding in the removal of mucus accumulations which are brought away with the return air current into the nasopharynx. Inflation should at first be practised at short intervals,— i.e., daily or on alternate days,—and later at longer intervals. The improvement under this measure is often very rapid and is clearly indicated by the progressive changes in the character of the sounds heard through the otoscope. Local Application of Drugs.—There can be no doubt of the benefit in acute tubal catarrh from astringent applications to the pharyngeal mouth of the diseased tube. For this purpose the silver preparations give good results,—i.e., nitrate of silver in solution of gr. 10 to 20 to the ounce, or argyrol in 25 per cent, solution. They are best applied by means of a cotton-wound applicator, the end of which is made to describe a curve similar to that of the Eustachian catheter (Fig. 98). This is passed through the inferior mea- tus of the nose and rotated into the pharyngeal mouth of the tube by exactly the same manipulations as are employed in placing the Eustachian catheter. In my experience argy- rol is less irritating, and on the whole more effective, than the nitrate of silver. It can also be used more frequently,—i.e., twice or three times a week, — in appropriate cases, while nitrate of silver, even in weak solutions, should not be applied oftener than once in seven or eight days. Another drug which is efficacious in some cases of Eustachian catarrh is the chloride of zinc in solution of gr. 10 or gr. 20 to the ounce. Fig. 98.—Eustachian cotton applicator. TUBAL CATARRH IN CHILDREN 153 Treatment of Tubotympanic Congestion.—When the lesion has reached the stage described as tubotympanic congestion (Fig. 97), the necessity for prompt therapeutic measures becomes urgent. Usually the treatment already outlined, but pushed rather more actively, will control the con- dition. Catheter inflation of the ear should be performed daily. The application of argyrol, in 25 per cent, solution, should be made to the nasopharynx and mouth of the tube on alternate days. Frequent gar- gling of the throat with alkaline or normal salt solution, as hot as patient can bear it, will in some cases act as a counter-irritant, relieving the tym- panic congestion. Extract of belladonna, gr. %, combined with small doses of quinine, repeated three times a day, or even four times daily, is of undoubted value in acute tubotympanic congestion. Earache, if severe, may be controlled by combining with the above an eighth of a grain of codeine for two or three doses. Finally, should the symptoms be aggravated by an effusion of serum within the tympanum, the best results will usually be obtained by a free incision through the posterior segment of the drum membrane. The incision is exactly the same as that to be described later under the treatment of acute catarrhal otitis media, and the subsequent cleansing of the canal must be carried out in the same way. Correction of Nasopharyngeal Abnormalities. — The acute symp- toms having subsided, it is of prime importance to the patient that the nose and nasopharynx should be carefully examined, and that any condition in this region interfering with nasal respiration or pro- vocative of nasopharyngeal congestion should be corrected. Probably much could be accomplished by the correction of such lesions not only in preventing the recurrence of acute tubal attacks, but also in the larger field of preventing subsequent impairment of hearing,—i.e., deafness in later years. Tubal Catarrh in Children.—Before leaving this subject, the writer wishes to say a word as to the prevalence of tubal disease in young children. Of all the causes of tubal inflammation none is so potent or so wide- spread in the number of its victims as the presence of pharyngeal adenoids. The author has long been convinced that retraction or congestion of the drum membranes constitutes one of the most constant and reliable phys- ical signs of lymphoid hypertrophy in the nasopharynx; or, in other words, that the prevalence of tubotympanic disease in children is almost coequal with the prevalence of adenoids. If this view is correct, it is evident that the subject has not received due attention in otological literature and text-books, and, what is of more serious import, that the condition is more or less ignored or neglected by physicians and otologists alike. There are two predisposing causes which render children particularly prone to tubal congestion,—viz. (1) the greater prevalence of adenoids, and (2) certain anatomical characteristics of the Eustachian canal in infancy and early childhood. 154 ACUTE DISEASES OF MIDDLE EAR AND MASTOID The more important anatomical differences between the infant and adult tubes are clearly indicated in Figs. 99 and 100. The heavy lines representing the Eustachian canals indicate their general direction in Fio. 98.—Skull of infant at term. Line A =level of nasal floor; line B =level of tympanic floor. Fig. 100.—Skull of adult. Line A =level of nasal floor; line B =level of tympanic floor. relation to the horizontal plane,—i.e., they represent merely straight lines passing through the pharyngeal and tympanic orifices of the tube. The line A in each figure represents the level of the nasal floor, and the line B TUBAL CATARRH IX CHILDREN 155 the level of the tympanic floor. It is clear that the canal of the infant at term presents the following differences from the Eustachian tube of the adult: (1) It is shorter (14 mm.) and horizontal in direction, whereas the adult tube is 33 to 38 mm. long, and passes obliquely upward and back- ward to reach the tympanum at a considerably higher level. (2) The tympanic floor in the infant is on a level slightly below that of the nasal floor, while in the adult it is some 20 or 22 mm. above the floor of the nose. (3) The pharyngeal mouth of the infant canal is on about the same level as the hard palate, whereas in the adult it is some 10 mm. above the hard palate. To epitomize: The Eustachian tube of the infant is a short, relatively wide, horizontal canal, the pharyngeal orifice of which lies a little behind the choanae and on a level slightly below that of the hard palate. Its phys- ical characteristics seem, therefore, as compared with the adult tube, partic- ularly favorable to the entrance of germs from the nasal secretion draining posteriorly into the pharynx, and to the development of vascular changes as a result of any pathological condition within the nose or nasopharynx. Absence of Subjective Symptoms.—One reason why tubal catarrh in children is not oftener diagnosticated as such is the absence of such symptoms as a young child would be able to describe, or likely to complain of. Children of a certain age complain promptly of pain, but such indefi- nite symptoms as a sensation of fulness in the ears they probably soon grow tolerant of. We begin life with hearing power so far in excess of our actual need that a child’s ears may be very seriously diseased before his hearing power becomes noticeably impaired. It is clear, therefore, that, if we are to recognize tubal catarrh in children at the stage at which it is most amen- able to treatment, we must make our diagnosis chiefly by the physical signs. Physical Examination.—I have already stated my belief that tubal catarrh is almost invariably present in children suffering from pharyngeal adenoids. Inspection of the ears of children in whom a physical exami- nation has demonstrated the presence of adenoids will, therefore, usually show the drum membranes to be markedly retracted. When the adenoid growth is of such size as to interfere seriously with nasal respiration, the drum membranes are usually retracted to a degree rarely seen in adults. They may also be noticeably congested. Beyond this there may be little to attract attention to the fact that the Eustachian canals are diseased or are not properly performing their function. Treatment.—The treatment is particularly important from the fact that the disease, if unchecked, probably represents the starting-point of morbid processes leading to deafness later in life. The indications are clear,—viz., removal of the pharyngeal growth, especial care being ob- served to avoid injury to the cartilage at the mouth of the tube, and subsequent treatment of the tubal lesion. For inflation of the ears we are usually obliged to resort to the Politzer method, few children being tol- erant of catheter inflation. Aside from the method of inflation, the treat- ment is practically the same as for adult patients. 156 ACUTE DISEASES OF MIDDLE EAR AND MASTOID MYRINGITIS. Acute circumscribed inflammations limited to the drum membrane have been described by Politzer, Schwartze, and other distinguished ob- servers under the name of acute myringitis. Bezold,4 on the other hand, felt so doubtful as to the propriety of separating such a lesion from a possibly coexisting inflammation of the middle ear, that he declined to recognize acute myringitis as a pathological entity. My own observations rather confirm the latter view, or at least convince me that the lesion is one of the rarest of aural diseases. I have seen, of course, innumerable cases in which the physical signs of inflammation were apparently confined to the drum membrane, but exceedingly few in which I was convinced that the middle ear was not also involved. I shall content myself, therefore, with a brief statement of the symptoms as described by others. The condition is said to have been observed with comparative fre- quency in association with influenza. It may be ushered in by a feeling of fulness and discomfort in the ear. This usually gives way to lancinating ear pain of moderate severity. In some cases the earache is of very severe type. With the pain, loud subjective noises often add to the patient’s distress. The hearing is usually only slightly impaired,—so little as often to escape the patient’s attention. In the early stage inspection of the drum- head may show marked injection of the membrana tensa, which is often particularly pronounced in the region of the hammer handle. Later, with exaggeration of the above changes, one or more bullae are seen, usually upon the posterior segment of the membrane. There may be also small ecchymoses, usually located in the posterior segment. The bullae, or blebs, may rupture into the external auditory canal. The course of the affection is usually short, ending in recovery. The disease is differentiated from acute otitis media by (a) the apparent limitation of the inflammatory changes to the external layers of the drum membrane, (b) the absence of bulging of the membrana tensa as a whole, and (c) the very slight impairment of hearing as compared with that usually accompanying acute middle-ear inflammation. The treatment naturally varies with the severity of the attack. The milder cases probably recover with little or no treatment. Moderate pain may be relieved by the application of dry heat,—i.e., lying with the affected ear resting upon a hot-water bag. In cases in which the earache is unbearably severe, the author believes that by far the safest method of obtaining relief is that employed in acute otitis media,—viz., free incision of the drum membrane and subsequent cleansing of the canal by means which will be described in connection with the treatment of acute tympanic disease. This plan of treatment gives prompt relief of pain and at the same time insures against the retention of inflammatory products which may collect within the tympanum. 4 Bezold: Text-book of Otology, p. 123. ACUTE MIDDLE-EAR INFLAMMATION 157 ACUTE MIDDLE-EAR INFLAMMATION. Nomenclature: Significance of Names in Common Use. — Before discussing separately the acute tympanic lesions, we should endeavor to define as clearly as may be just what we intend to convey as to the charac- ter of the lesions by the common terms “acute catarrhal otitis media” and “acute purulent otitis media.” If the question were considered solely from a bacteriological viewpoint, it would be clearly possible to obtain in every case a specimen of the tympanic secretion, and according to the absence or presence of bacteria to say that we have to deal with either a serous or a purulent otitis media. It is neither possible nor desirable, however, in actual practice to base one’s diagnosis wholly upon the bac- teriological findings, and there are obvious advantages in the adoption of a simple classification which may be based upon such data as one may obtain from a careful examination of the patient. According to the investigations of Zaufal and many who have followed his line of work, there are reasonable grounds for questioning whether acute inflammatory processes ever involve the middle-ear cavity in the absence of pathogenic bacteria. He found in a large series of examinations that pus germs were always present in the tympanic secretion taken from acutely inflamed ears; and, per contra, that no cultures could be obtained from secretions taken from apparently normal ears. Accepting this theory as generally correct, we must yet admit that certain congestive conditions —e.g., tubotympanic congestion with effusion of serum—may be accom- panied by distention and vascular engorgement so pronounced as to repro- duce all the clinical and physical phenomena of acute purulent otitis media and to constitute a condition not clinically distinguishable there- from. Bezold, in discussing the nomenclature of tympanic disease, objected to the use of the word “catarrhal” as applied to middle-ear inflammations. He based his objection largely upon certain histological features of the lining membrane of the tympanum which seemed characteristic of a serous, rather than of a mucous, membrane. Thus, while the mucous membrane of the cartilaginous portion of the Eustachian tube is thick, lined by sev- eral layers of ciliated epithelium, and contains many acinous glands, the lining membrane of the tympanum is exceedingly thin, contains no acinous glands, and is devoid of cilia except upon the floor. In the atrium it con- sists for the most part of a single layer of basement cells very closely adherent to the periosteum, and has a decidedly endothelial character. The mucous membrane of the pharyngeal half of the Eustachian canal secretes more or less rather thick mucus, whereas the normal secretion of the tym- panum is very thin and serous in character. Bezold, therefore, proposed to omit the term “catarrhal” from descriptions of tympanic inflammation, and to substitute the word “simplex,”—thus, “otitis media simplex acuta” as differentiated from “otitis media catarrhalis acuta.” The word “sim- plex,” thus used, is in no way descriptive, however, and is open to the 158 ACUTE DISEASES OF MIDDLE EAK AND MASTOID further objection that it would prove in many cases actually incorrect or misleading, since it is often impossible to determine clinically whether an acute tympanic lesion is or is not purulent in character. It would seem better, therefore, not to discard old, time-honored names, which have obtained such widespread adoption, but rather to define clearly the charac- ter of the lesion they are intended to describe. There are three common forms of acute middle-ear inflammation, an appreciation of which helps to a clearer understanding of the varying phases of tympanic disease,—viz. (1) An acute serous otitis media,—i.e. a non-purulent inflammation with effusion of serum into the cavity of the atrium; (2) an acute purulent inflammation confined to the atrium; and (3) an acute purulent inflammation involving both the atrium and the tympanic vault. It may be quite impossible, however, by its clinical manifestations to distinguish an acute serous, or non-purulent, otitis media from an acute purulent otitis media. In either the membrana tensa may be red and bulging, the subjective symptoms are often identical, and the indications for treatment are practically the same. From the standpoint of practical otology, therefore, it seems best to consider acute middle-ear inflammation under two heads,—viz. (1) “Acute catarrhal otitis media,” by which term we shall designate any acute inflammation, purulent or non-purulent, confined to the atrium; and (2) “acute purulent otitis media,” or an acute inflammation involving both the atrium and the tympanic vault. These two conditions undoubtedly represent respectively the simpler and the more serious forms of acute tympanic disease as met with in actual practice. Otitis Media Catarrhalis Acuta; Acute Catarrhal Otitis Media.— These terms we apply to the simpler form of acute middle-ear inflammation, —i.e., an acute inflammatory process confined to the atrium. Etiology.—The causes have already been enumerated in a fore- going chapter. Depressed constitutional states, and therefore exhausting diseases, render the individual more prone to tympanic disease. Obstruc- tive lesions of the nose or nasopharynx—i.e., conditions interfering with nasal respiration—are strongly predisposing factors. Pharyngeal adenoids react injuriously upon the ears, and are responsible in large measure for the prevalence of tympanic disease among children. Exciting Causes.—Gauging their importance as proportional to the number of cases to which they give rise, the exciting causes should be mentioned in the following order: (1) Acute nasopharyngitis,—i.e., the common “cold in the head.” More cases of acute middle-ear inflammation can be accounted for as secondary to this affection than can be traced to any other cause. (2) The acute exanthemata: scarlet fever, diphtheria, and measles cause acute tympanic disease with even greater frequency than is generally recognized by the medical profession. Scarlet fever is accompanied by acute tympanic disease more frequently than is diph- theria, and the proportion of scarlatinal cases which go on to acute sup- purative mastoiditis is considerably larger. Measles is a very frequent cause of acute otitis media of rather severe type in which mastoid suppura- OTITIS MEDIA CATAERHALIS ACUTA 159 tion occurs with marked frequency. Acute epidemic influenza gives rise to acute otitis media, often of very severe type. The proportion of cases in which this complication occurs varies in different epidemics according to variations in the average severity of the disease. (3) The nasal douche: it is a recognized fact that many cases of acute middle-ear inflammation are caused by the careless use of the nasal douche in cases of atrophic rhinitis, ozaena, etc. In the milder cases of nasopharyngeal disease, the nasal spray will be found an efficient, and certainly safer, method of cleansing the nose. (4) Diving or swimming under water: the frequency of tympanic inflammation from this cause is evidenced by the large number of patients presenting themselves each year at the beginning of the swimming season. The injury to the ears may occur in one of two ways,—viz. (a) by expulsion of water taken into the nose or throat through the Eustachian tubes or (b) by impact of the cold water against the drum membrane. The latter danger may be practically eliminated by stopping each auditory canal with a pleget of moistened absorbent cotton. (5) Traumatic injuries of the drum membrane are a comparatively rare cause of acute middle-ear inflammation. Of such injuries the commonest is that caused by a for- cible box or slap upon the ear, the drum membrane being ruptured by the sudden condensation of the air in the external auditory meatus. Micro-organisms found in the Ear during Acute Middle-ear Inflammation. —A very large number of micro-organisms have been found in the secre- tions taken from the ear during acute otitis media. Those most frequently found are the streptococcus, the pneumococcus, and the streptococcus mucosus. Next in frequency are the staphylococcus albus and staphylo- coccus aureus, and after these come the bacillus proteus, the bacillus pyocyaneus, and a long list of organisms which do not call for special mention here. As regards the comparative virulence of these germs in relation to aural disease, there is no longer room for doubt that the streptococcus and pneumococcus give rise to a type of middle-ear suppuration which leads more frequently to intracranial infection than do the tympanic lesions caused by the staphylococci or other germs mentioned. Suepfle, from an analysis of the bacteriological findings in a large series of cases, concluded that cases of acute otitis media due to staphylococcus infection do not give rise to intracranial complications. While this view is extreme, and therefore incorrect, it serves to emphasize the infrequency of intracranial disease secondary to staphylococcus infection. The streptococcus, on the other hand, is unquestionably responsible for a majority of cases of intracranial disease of otitic origin. Accepting the above statements as in the main correct, one must yet acknowledge that one can not prognosticate from the micro-organism found in the tympanic discharge the future course or severity of the aural disease, this being determined quite as much by the patient’s systemic condition,—i.e., the question of normal or lowered resistance. A staphy- lococcus may, therefore, produce clinically an exceedingly severe type of 160 ACUTE DISEASES OF MIDDLE EAR AND MASTOID inflammation; whereas a mild type of acute otitis media may result from a streptococcic invasion of the ear. Anatomical Conditions in Relation to Symptoms.—It may be well, before discussing clinical phenomena, to review briefly certain ana- tomical features of the atrium which bear rather directly upon the symp- toms and course of the simpler form of acute otitis media. It will be recalled that the cavity of the atrium is lined by an exceedingly thin membrane very closely adherent to its walls. Externally the atrium is closed by the tense, inelastic and rather unyielding membrana tensa. Superiorly the atrium is more or less completely separated from the tym- panic vault by the structures massed in this situation,—viz., the neck and short process of the malleus; the lower anterior extension of the body of the incus; the anterior, external, and posterior ligaments of the malleus, and1 the mucous membrane which surrounds them. From the anterior wall of the atrium the Eustachian canal leads forward, inward, and down- ward into the nasopharynx. Germs reaching the tympanum from the nasopharynx by way of the Eustachian tube lodge first, therefore, in the atrium. An inflammatory process originating in and confined to the atrium probably represents changes taking place somewhat in the following order: (1) Marked dilatation and engorgement of the vessels of the lining membrane; (2) transudation of serum and migration of leucocytes from the veins into the tissues of the mucoperiosteal lining. The consequent in- flammatory thickening of the lining membrane has the important mechani- cal effect of rendering the separation of the atrium from the vault more complete. The bony Eustachian tube is also more or less closed by inflam- matory swelling in the region of the tympanic orifice. With the formation of pus or effusion of serum into the atrium, the walls of that cavity are, therefore, soon subjected to pressure, the outer wall, or membrana tensa, being the one which offers least effective resistance. Hence the early spontaneous rupture of the drum membrane—usually in six to twenty- four hours—which commonly occurs in acute catarrhal otitis media. As compared with the vault, the relatively small amount of connective tissue in the atrium (consisting chiefly of its thin and closely adherent lining membrane) constitutes another condition favorably influencing the progress of the disease. That is to say, the fastigium being passed, the tissues more quickly regain an approximately normal condition, the patency of the Eustachian tube being restored, and the mechanical con- ditions favorable to resolution being more quickly established. Symptoms and Signs.—When acute otitis media occurs as a compli- cation of one of the acute infectious diseases, the otitic symptoms may for a time be more or less masked by those of the initial disease. When, on the other hand, the aural disease is not secondary to a systemic infection, the onset is usually sudden and clearly defined. As a prodromal symptom, a sensation of fulness or occlusion of the ear is noted by some authors as of frequent occurrence. This symptom, OTITIS MEDIA CATARRHALIS ACUTA 161 when present, is clearly a result of the tubal catarrh, or congestion, which almost invariably precedes or accompanies acute catarrhal otitis media. According to the writer’s observation, the symptom first experienced, or at least first complained of, by the patient is usually pain. Onset.—The earache is usually sudden in its development. Following a few premonitory twinges, it soon assumes the character of a constant pain, rapidly reaching an unbearable degree of severity. Not infrequently the patient retires at night with no noticeable discomfort, to be awakened during the night or toward morning by the severity of the ear pain. Once established, the pain is usually constant, but is subject to exacerbations of intensity. With the beginning of pus formation, the pain becomes throbbing or “drawing” in character, being sometimes compared by the sufferer to the severe form of toothache usually accompanying an abscess at the root of a carious tooth. Naturally, sleep becomes impossible; and when prompt relief is not forthcoming, the resulting insomnia adds to the nervous strain to which the patient is subjected. The severity of the pain often distracts the patient’s attention from lesser symptoms. If ques- tioned, however, he usually becomes conscious of subjective sounds,— i.e., tinnitus aurium. The hearing is also noticeably impaired, showing certain characteristic changes which will be referred to later. The constitutional symptoms vary widely with the age, and also to some extent with the nervous constitution of the patient. With adults, the temperature may throughout be normal or nearly so, or it may be moderately elevated. With infants and young children, on the other hand, even the mildest type of acute middle-ear inflammation is usually announced by rather high fever,—i.e., temperature ranging from 102° to 105° F. The temperature variations which both adults and children occa- sionally exhibit with mild grades of tympanic inflammation depend probably upon individual differences in the stability of central nervous control. That is to say, it seems necessary in some cases to refer the fever to a reflex disturbance of the cerebral heat centres, rather than to the influence of septic absorption from the ear. Certainly the rapid and considerable elevations of temperature frequently seen in children suffering from the simplest type of acute tympanic inflammation are in many cases most easily explained in accordance with the above hypothesis,—i.e., as a reflex phenomenon. With patients of all ages, adults as well as children, digestive disturb- ances are common during the early stages of an acute catarrhal otitis media. Spontaneous Rupture of the Drum Membrane.—As we have seen, the atrium during acute catarrhal otitis is a small, closed cavity, the outer, membranous wall of which represents the direction of least resistance. Obviously, the membrana tensa must give way before any rapid accumula- tion of pus or serum. Spontaneous rupture of the drum-head usually occurs within six to twenty-four hours after the onset,—or, to be more exact, after the appearance of the initial earache. 162 ACUTE DISEASES OF MIDDLE EAK AND MASTOID With the rupture of the drum membrane and the appearance of aural discharge, there is usually complete cessation of pain. The adult patient usually experiences an immediate sense of relief, and the child, which has been tossing about the bed in distress, now falls into a sleep of exhaustion. The temperature, which in young children is usually elevated, may fall within a few hours to the normal line. With adult patients, two symptoms, probably in some degree present from the onset, are now thrown into bolder relief, and become the patient’s chief cause of concern,—viz., tinnitus aurium and impairment of hearing. Tinnitus Aurium.—The subjective sounds apparently vary greatly in different individuals. On the other hand, it may be that the variations are often more apparent than real, depending upon the natural difficulties in describing a purely subjective sensation. Thus, we are frequently told that the noise is like the “noise of a tea-kettle,” “the escaping of steam,” “whistling of wind in the trees,” “the sound of a cricket,”—all which comparisons may be intended to describe the same character of sound. Again the sound is compared to a ringing of bells or to a shrill whistle,— i.e., sounds of different character. From the average statements of intel- ligent patients, one is led to believe that the sound is usually of rather high pitch. Tinnitus which has made its appearance during, and as a result of, an attack of acute otitis media usually disappears when the last physical evidence of inflammation has gone. It is, however, in my experience often the very last symptom to disappear. Impairment of Hearing.—The hearing is always impaired at the height of an acute catarrhal otitis media. At the onset,—i.e., during the stage preceding the accumulation of fluid in the tympanic cavity—the impair- ment may be slight, or not noticeable. As serum or pus displaces the air in the tympanum, however, the hearing power is usually considerably reduced. The type of impairment assumes to some extent the general character of deafness due to disease in any part of the conducting apparatus,—i.e., hearing by bone conduction is increased, and the ratio between hearing by bone conduction and by air conduction is changed, though not necessa- rily reversed. Bezold called attention to certain features of the disturbance of hearing as characteristic of acute middle-ear inflammation with effusion. In acute otitis media with bulging of the drum membrane, bone conduction is increased, and the tuning-fork held in contact with the mid-line of the skull is referred definitely to the diseased organ. With this increase in bone conduction there is, however, according to Bezold, surprisingly little disturbance of audition for the low musical tones, some of his patients hearing tones as low as 16 d.v. This is the reverse of what one usually finds in chronic lesions of the conducting mechanism, in which the lower tone limit is almost invariably considerably elevated. Bezold explains this difference by reference to differences in the pathology of the two types OTITIS MEDIA CAT A K R H ALIS ACUTA 163 of disease. Thus, in chronic middle-ear disease, either suppurative or non-suppurative, there is usually present either partial destruction of the drum membrane, or fixation of the membrane or ossicles. Either of these conditions would interfere markedly with the slow and extensive movements involved in the production of very low musical tones. In acute catarrhal otitis media, on the other hand, disturbance of function is due largely to the presence within the tympanum of fluid which acts as a weight upon the drum membrane and ossicles, interfering with the acuteness of hearing for all sounds, but not necessarily offering special resistance to the slow and relatively wide vibrations necessary to the transmission of the lower tones of the musical scale. Obviously, the presence of fluid in the tym- panum is not the only factor in the deafness of acute otitis media, the other being the inflam- matory infiltration of the drum membrane and tympanic mucosa. This explains the fact that some degree of deafness often considerably outlasts the cessation of the discharge and final closure of the drum membrane. Physical Changes in the Drum Membrane.—The physical appearance of the drum membrane varies materially with the time which has elapsed since the onset. If seen very shortly after the earache is first experienced, the drum-head will be found deeply injected,—i.e., exceedingly red. When different portions of the tense membrane show variations in this respect, the upper part is usually more deeply injected than the lower portion, which may be nearly or quite normal in color. In other words, the injection is said to appear first above and extend downward; but there is never any line of demarca- tion between the injected and normal portions, the one shading gradually into the other. In a majority of cases, however, the whole membrana tensa when first seen by the physician is uni- formly red (Fig. 101). If the examination be delayed a few hours, inspection of the drum membrane may reveal an entirely different picture,—i.e., the membrana tensa is now not only exceedingly red, but bulges markedly outward into the lumen of the meatus. A slight central depression may be seen in the position of the umbo. Other than this, the normal landmarks, including the short process and handle of the malleus, may be more or less obliterated or hidden from view (Fig. 102). If the examination be still further delayed, we shall be likely to find the Fig. 101. Fig. 102. Fig. 103. Figs. 101, 102, and 103.— Acute catarrhal otitis media. 1st, 2d, and 3d stages. 164 ACUTE DISEASES OF MIDDLE EAR AND MASTOID canal filled with pus, in which case we can, of course, see nothing of the drum membrane until the ear has been irrigated or the meatus otherwise cleansed. It is then possible to locate the perforation, which is situated practically always in the posterior segment of the membrane. Most frequently it is found in the posterosuperior quadrant,—i.e., behind the hammer handle. Occasionally a perforation is so minute that one is not quite sure of its recognition. In such a case, if the patient is required to perform Valsalva inflation while the drum membrane is kept in view, a drop of pus will be seen to exude, thus locating definitely the site of the per- foration (Fig. 103). The Discharge.—Following rupture or incision of the membrane, the discharge may vary considerably, in accordance with certain conditions, —e.g., the constitutional condition of the patient, the character of the in- fection, the time elapsing between the onset of the disease and the rupture of the drum membrane, and, of course, with the efficiency of the treatment. If the inflammation is serous, or non-purulent, and the rupture of the drum- head has occurred early, the discharge may remain serous in character and last but a few days. If, on the other hand, the patient is in a constitu- tionally exhausted condition, or the infection is of virulent type, and par- ticularly if the rupture of the drum membrane has been considerably delayed, the discharge is likely to be more profuse and to persist longer. Taking as an example a case in which an intensely red and bulging drum membrane has been properly incised, the discharge may pursue some- what the following course: Frequently it does not reach its maximum flow during the first twelve or twenty-four hours following the incision. The writer has repeatedly been impressed with the relatively moderate discharge immediately following myringotomy in cases of severe tympanic inflammation. After the first twelve or twenty-four hours it rapidly increases in amount, usually reaching the maximum on the second or third day. From this point it may for a few days be exceedingly profuse, then gradually receding. Its disappearance may be quite rapid, or, for no reason discernible in the physical character of the lesion or the type of infection, be comparatively slow. Finally, after the amount is reduced to an apparent minimum, it may persist obstinately for days, suddenly ceasing with the complete closure of the drum membrane. Following the closure of the incision, the drum membrane may rapidly regain its normal appearance or weeks may elapse before all traces of the recent inflammatory process have disappeared. The above describes somewhat in detail the usual course of an attack of acute catarrhal otitis media. The whole process, from the appearance of the discharge to final closure of the drum membrane, may run its course in a week or less, or may be spread over two or three weeks or more. To understand these otherwise puzzling variations, we must recognize in the patient’s general power of resistance, or departure from the normal therein, a factor quite as potent in deciding the course of the disease as the character of the infection itself. OTITIS MEDIA PURULENTA ACUTA 165 In the writer’s opinion, serious complications of acute catarrhal otitis media rarely occur without previous change in the character of the lesion,— i.e., without extension of the infection to the structures of the vault. The prognosis as to ultimate recovery is good. The drum membrane usually heals without noticeable cicatrices or structural changes. Per- manent impairment of hearing is exceedingly rare. There can be no doubt that a mild attack in which final healing is unduly delayed is more apt to result in some permanent impairment of function than a severe lesion in which prompt local recovery occurs. On the other hand, a very prolonged attack may leave absolutely perfect hearing. Acute Suppurative Otitis Media; Acute Purulent Otitis Media (Otitis Media Purulenta Acuta).—These terms are employed to describe a suppurative inflammation involving both atrium and vault. In many cases the inflammatory process seems to originate in the vault, spreading thence downward to the atrium; in others, an infection of the atrium extends upward to the attic. Etiology.—The causes of acute purulent otitis media are the same as those giving rise to the simpler form of acute tympanic inflammation. They do not, therefore, call for repetition here. So also of the bacteriology, —there is no organism which may cause one grade of acute middle-ear inflammation and not the other. That is to say, the same exciting cause, or the same pathogenic micro-organism, may give rise either to the simpler or the more severe form of otitis media,—this depending perhaps to some extent upon variations in the individual’s vitality or resistance power to disease.5 Anatomical Conditions Influencing the Pathology of the Disease.—The anatomico-surgical features of the vault are perhaps best shown by comparing them with those of the atrium. It will be remem- bered that the atrium contains but little connective tissue other than the thin and closely adherent membrane lining its walls. Inflammation tends, therefore, to be self-limited, by reason of the very limited field involved, and the rather unfavorable nidus provided for the growth of germs. The mechanical separation of the atrium from the vault is rendered more complete by the inflammatory swelling of mucosa, this favoring early rup- ture of the drum-head, with consequent drainage and relief of tension,— i.e., early resolution. As congestion about the Eustachian orifice subsides, the Eustachian canal provides a supplementary drain for the escape of serum or pus. 5 The frequent occurrence of suppurative lesions, apparently originating in the vault, is rather difficult to explain. Why should germs presumably entering by way of the Eustachian canal primarily infect the vault? In trying to account for this phenomenon, the following theory has seemed to the writer the most satisfactory,—viz., that the atrium presents certain conditions unfavorable to the development of purulent inflam- mation which do not exist in the vault; that germs entering by way of the Eustachian canal may pass through the atrium without infecting its mucosa, and, reaching the vault, may find there the conditions favorable for the inception and spread of a suppurative inflammation. 166 ACUTE DISEASES OF MIDDLE EAR AND MASTOID The vault (Fig. 104) presents the following features bearing upon the pathology of suppurative lesions originating therein: (a) It is directly continuous posteriorly with the so-called mastoid antrum. Pus collecting from a primary infection in the vault is not, therefore, quickly subjected to pressure,—flowing rather backward along the pathway of least resist- ance into the antrum. The antrum is early involved in acute purulent otitis media, and from the onset the danger of suppurative mastoiditis is greater. The escape of pus downward into the atrium frequently represents a later stage,—i.e., is subsequent to the accumulating of pus within the antrum. Spontaneous rupture of the drum membrane is often therefore delayed, usually from forty-eight hours to a week, (b) There is no natural path- Horizontal membranous fold, dividing outer chamber of vault into an upper and lower space Artificial opening in malleo-incudal fold, leading into inner chamber of vault Antrum Malleo-incudal fold depending from tym- panic roof and cover- ing upper surfaces of malleus and incus Fig. 104.—Diagrammatic picture of membranous partitions of vault way providing for the free escape of pus from the vault, and even extensive incision of the drum membrane does not provide free and adequate drain- age from the antrum, (c) The lining membrane of the vault is not closely adherent as in the atrium, but hangs in folds from the tympanic roof, covering the head of the malleus and body of the incus, and dividing the attic into an outer and inner compartment. Another fold of mucous membrane is usually present, passing horizontally across the outer cham- ber of the vault, and dividing it further into an upper and lower space. This surplus of vascular connective tissue forms a suitable nidus for the growth of infective germs, and favors the development of suppurative inflammation. The subdivision of the vault cavity into membranous compartments is also distinctly favorable to the retention of pus, and therefore to the spread of infection. Symptoms and Signs.—The subjective symptoms of acute suppurative otitis media do not differ greatly from those of the simpler form. Earache is usually the first purely aural symptom of which the patient complains. OTITIS MEDIA PUKULENTA ACUTA 167 The ear pain resulting from a primary infection of the vault is, perhaps, a little less sudden in its attack, and somewhat slower in reaching its max- imum intensity, than that accompanying a similar lesion confined to the atrium. It is also much less likely to be relieved by early rupture of the drum membrane. It is described as a most unbearable type of pain,— throbbing or boring in character,—and soon reaching a degree of severity rendering sleep impossible. From the onset, the patient usually experiences subjective noises,—this symptom, however, being over-balanced by the severity of the pain, and therefore rarely complained of at this stage of the disease. The hearing may at first be but little disturbed, this depend- ing upon the extension of the inflammation to the membrana tensa and structures about the oval window and incudostapedial joint, and upon the accumulation of pus within the atrium. As the lesion advances, the hearing is always markedly impaired. Some degree of fever is usually present in the acute stage. With adults the temperature may rise to 102° F. or more, or may be but slightly above the normal. With infants and young children, on the other hand, rather high temperature is the rule. Owing partly to the fever, when present, but chiefly to the severity of the pain and the consequent insomnia, there are few circumscribed lesions which will more quickly exhaust the patient than an attack of acute middle-ear inflammation which has not been re- lieved by rupture or incision of the drum membrane. Spontaneous Rupture of the Drum Membrane.—The interval between the initial pain and the rupture of the membrane is usually much longer than in the simpler form of acute otitis media. In my experience, it varies all the way from forty-eight hours to a week. This wide variation is probably explained by differences in the early pathways of extension. If, for example, a suppurative process in the vault extends quickly in the direction of the atrium, or is quickly followed by a secondary infection of the lower tym- panic space, pus collecting there will be likely to cause a comparatively early rupture of the membrane. On the other hand, a primary infection of the vault, spreading chiefly backward in the direction of the antrum, may tor- ture the patient for before pus, accumulating in the atrium, causes rupture of the membrana tensa. Such cases are best studied in dispensary practice, where patients frequently come under observation who have suf- fered three, five, or even six days without rupture of the membrane. It is not difficult to appreciate why final rupture of the membrane in these cases often affords much less relief than that which almost invariably follows the early rupture of the drum-head in acute catarrhal otitis media. Physical Signs.—It is clear that the physical changes in the drum membrane must vary with the progress of the disease. We shall try, therefore, to describe certain conditions, representing progressive stages of the lesion, in the order in which they would be likely to occur. If the patient is seen very shortly after the initial symptom, we may find the following conditions present: 1. The membrana tensa throughout the greater part of its extent may 168 ACUTE DISEASES OF MIDDLE EAR AND MASTOID be quite normal in color and appearance. The upper posterior portion of the tense membrane,—that part immediately contiguous to Shrapnell’s membrane,—and Shrapnell’s membrane itself, are intensely red, and, if not actually bulging, have the appearance of acute inflammatory infiltration (Fig. 105). This condition is very frequently observed in patients who are seen just after the onset, and usually indicates a suppurative process in the vault, which later will extend downward and involve the atrium. 2. A few hours or one or two days later, we may see the following changes: the upper half or whole of the membrana tensa is red, or injected. The injection in the region of Shrapnell’s mem- brane is, however, much more intense, and the inflammatory thickening (infiltration) in this region is so pronounced as to indicate clearly a suppura- tive process behind Shrapnell’s membrane,—i.e., in the vault (Fig. 106). This picture is often seen in acute suppurative inflammation of the attic, and occurs at a period following the onset which in a similar lesion of the atrium would have been marked by noticeable bulging or rupture of the drum membrane (Figs. 102 and 103). 3. The upper posterior part of the membrana tympani—i.e., the part including and immediately adjacent to Shrapnell’s membrane—is markedly bulging, clearly indicating the presence of pus in the tympanic vault (Fig. 107). With this condition, the entire membrana tensa also is invariably inflamed. The bulging, however, is confined to, or most con- spicuous in, the region of Shrapnell’s membrane. 4. The canal contains pus, removal of which reveals the following conditions,—viz., entire drum membrane (membrana tensa and membrana flac- cida) red and bulging. Small perforation in pos- terior segment of membrana tensa. Posterosuperior canal wall—i.e., that part immediately adjoining the drum membrane — is frequently very con- siderably swollen, so that no line of demarcation is here discernible between canal wall and drum membrane (Fig. 108). This condition always indicates a severe suppurative process within the vault, and frequently coexists with inflammation of the mastoid cells. It is commonly spoken of as “sagging of the posterosuperior canal wall.” Fig. 105. Fig. 106. Fig. 107. Fig. 108. Figs. 105,106,107, and 108. —Acute purulent otitis media, 4 successive stages. ACUTE OTITIS MEDIA IK INFANTS 169 Antrum Tenderness.—It must be clear, from a study of tympanic anatomy (Fig. 104), that pus collecting in the tympanic vault must soon find its way into the antrum. The antrum, therefore, is usually to some extent involved in a suppurative inflammation of the vault, and sensitive- ness to pressure over the antrum is rarely altogether absent from the most acute stage of an acute purulent otitis media. Course of the Disease.—The course of an uncomplicated case of acute suppurative otitis media is somewhat similar to that of the acute “catar- rhal” form, but is usually more prolonged. Some very severe cases, how- ever, make surprisingly rapid recoveries. The discharge—increasing dur- ing the first day or two following myringotomy—is usually very profuse at first, its duration depending upon the patient’s constitutional condi- tion, the virulence of the infection, and the extent of the area involved in the vault and antrum. The best possible incision through the drum membrane may not provide perfect drainage of the membranous pockets of the vault, and can not adequately drain the antrum. The process of resolution includes, therefore, the removal of pus in part through an in- cision or perforation of the drum-head, and in part by its elimination through the lymphatic system. In a favorable case, the discharge may cease and the drum membrane close in a period varying from ten days to four weeks. Acute Otitis Media in Infants.—Before leaving the discussion of symp- toms, a word should be said as to the diagnosis of acute middle-ear inflam- mation in infants and young children. It has been frequently stated in otological literature that acute otitis media in young children is invariably announced by a considerable eleva- tion of temperature. This is not strictly true. In the Willard Parker Hospital for Acute Infectious Diseases, the writer has seen a number of cases in which an acutely inflamed ear with bulging of the drum membrane has coexisted with a normal or but slightly elevated temperature. Such cases, however, form so small a percentage of the total number of cases in young children, that they are to be regarded, perhaps, as the exceptions which prove the rule. They are mentioned simply to emphasize the fact that one can not with certainty exclude acute tympanic disease even in young children by the absence of fever. As a general rule, however, it is perfectly correct to say that in the great majority of cases, even the milder grades of acute middle-ear inflammation give rise to a very considerable rise of temperature. In a child of three years or less, the subjective symptoms of acute otitis media are often so indefinite as to be of little or no diagnostic value to the general practitioner. So skilful and experienced an observer as Dr. C. G. Kerley6 has stated his belief that young children do not, as a rule, experience earache with acute middle-ear inflammation. While I have never been able to accept this view as quite justifiable, it is certainly remarkable how 6 Kerley: Symptomatology of Acute Otitis in Children, New York Medical Journal, July 8, 1905. 170 ACUTE DISEASES OF MIDDLE EAR AND MASTOID long a bright little child may suffer from an acute tympanic lesion with- out directing attention to the ear. If earache is not always an avail- able symptom, it is obvious that such subjective phenomena as tinnitus aurium and moderate impairment of hearing are often quite indeter- minable in young children. If I were called upon to enumerate the symptoms of acute tympanic disease in young children, I should give them in somewhat the following order: 1. Fever: high temperature—102° to 105° F.—is present in the great majority of cases. Unexplained temperature should, therefore, call for prompt examination of the ears. 2. Earache, when complained of, is, of course, the most useful sub- jective symptom. 3. Restlessness, shown by irritability of temper, peevishness, loss of interest in play, crying without apparent cause, sleeplessness at night, or restlessness (tossing) during sleep—one or any of these symptoms should, unless otherwise accounted for, be regarded as pointing to possible tym- panic disease. 4. Grabbing at the ears, or rubbing the ears, during sleep or during the waking hours, is regarded as a sign of tympanic pain, and undoubtedly often helps to locate a t3'mpanic lesion. It is often, however, a sign simply of restlessness from other causes, examination showing normal ears. It may, therefore, be a useful sign, but is by no means pathognomonic. Besides those above mentioned, there are of course an army of symp- toms which may be present during acute tympanic disease, but which can not be described as characteristic thereof. I believe very firmly that the routine practice of examining the ears of all sick children would prevent not only much unnecessary suffering, but also some loss of life. Complications of Acute Purulent Otitis Mema.— 1. Acute suppurative mastoiditis: which may give rise to (a) Infective sinus thrombosis. (b) Epidural abscess. (c) Cerebral abscess. (d) Cerebellar abscess. (e) Acute diffuse suppurative labyrinthitis. (f) Acute circumscribed suppurative labyrinthitis. (g) Purulent leptomeningitis. 2. Acute serous labyrinthitis. 3. Acute diffuse suppurative labyrinthitis: which may lead to (a) Epidural abscess. (b) Cerebellar abscess. (c) Purulent leptomeningitis. (d) Infective sinus thrombosis. 4. Direct infection of the jugular bulb (rare). The above are given in what I believe to be the order of their frequency. Some of the lesions included under acute mastoiditis might, theoretically, TREATMENT OF ACUTE OTITIS MEDIA 171 be included among the sequelae of acute purulent otitis media. They occur so rarely, however, without intermediate infection of either the mastoid process or the labyrinth, that the above scheme gives a much more correct view. Acute circumscribed suppurative labyrinthitis is included among the possible sequelae of acute mastoiditis, but not among those of acute puru- lent otitis media, because direct infection of the labyrinth from a tympanic lesion usually proceeds through one of the labyrinthine windows, and is almost invariably diffuse. Acute circumscribed suppurative labyrinthitis results most often from necrosis of one of the semicircular canals, the horizontal canal being the commonest point of attack. This practically never results directly from an acute tympanic lesion. Infection of the jugular bulb as a direct result of purulent otitis media—i.e., without inter- mediate infection of the mastoid cells—is a somewhat rare condition, of which a series of cases have been reported by McKernon.7 Treatment.—Most cases of acute tympanic disease are amenable in some degree both to general and to local treatment. We shall speak first, therefore, of such general measures as are of value in the management of any case of acute otitis media, and then of the local treatment appropriate to each of the two main varieties of the disease. General Treatment.—When the aural lesion occurs as a complication of some systemic disease (e.g., diphtheria, scarlatina, etc.), the general treat- ment must obviously include the treatment of that disease. When not secondary to an infectious disease, the general treatment resolves itself in- to an attempt to place the patient under the most favorable conditions for combating the local infection. In uncomplicated cases, this may be summed up practically in the following indications: (a) rest, (b) catharsis, (c) reg- ulation of the diet, and (d) hygienic arrangement of the sleeping room. Rest.—By this is meant not merely absence from school or business, but absolute rest in bed. This favors recovery in two ways: (1) it secures freedom from the fatigues and excitements of the daily routine, which in the presence of an acute inflammatory lesion entail more than ordinary strain; and (2) it protects the patient from sudden changes in the peripheral body temperature. This is a matter of considerable importance in acute aural disease, where slight accessions of nasopharyngitis may cause rapid extension of the tympanic lesion. With children, it is particularly impor- tant and should be insisted upon. Catharsis.—In hospital practice, the routine treatment begins with the administration of some efficient laxative. Calomel in doses of gr. j to gr. iij according to the patient’s age, and followed in six hours by some drug acting more directly upon the intestines, gives the best results. This routine measure should be prescribed regardless of the presence or absence of constipation or digestive disorder. 7 McKernon: Primary Jugular Bulb Thrombosis in Children as a Complication of Acute Purulent Otitis Media, N, Y. Med. Jour., July 1 and 8, 1905. 172 ACUTE DISEASES OF MIDDLE EAR AND MASTOID Diet.—The digestive function is apt to be easily disturbed during the acute stage of any suppurative lesion. It is a common practice, therefore, to place a patient suffering with acute tympanic disease upon a strictly liquid diet. This, during the first twenty-four hours, is probably, in severe cases, a wise measure. As soon, however, as the patient begins to demand a more generous diet, it should be changed to a light diet of easily digested solid food, from which red meats should, at first, be excluded. Nothing is more senseless or irrational than to deplete the patient’s strength and powers of resistance by a prolonged starvation diet. Arrangement of the Room.—With most cases of acute tympanic disease there is a coexisting tubal catarrh with more or less pronounced naso- pharyngeal congestion. A room overheated tends rather to increase nasal congestion, and is as bad, if not worse, than one in which the temperature is too low. With the patient in bed, the room should be well ventilated, and the temperature in winter kept at about 60° to 65° F.,—the bed, of course, being so placed as to be protected from draughts. Unless these matters are arranged for by explicit directions, it will be no uncommon experience to find at one’s second visit all the windows closed and the temperature of the room at 75° or 80° F.,—a condition in itself capable of inducing pyrexia in one already ill. Non-operative Treatment of Acute Otitis Media.—By this is meant the management of a case of acute middle-ear inflammation without incision of the drum membrane. It is indicated in only a comparatively small per- centage of cases as they are first seen by the otologist. When inspection of the drum-head shows the lesion to be in the incip- ient stage, it may be advisable to try to abort the attack without incising the drum membrane. This is sometimes spoken of as the “abortive treat- ment.” It is admissible only in cases in which there are no evidences of pus accumulation or retention within the tympanum,—i.e.} in which the drum membrane, though red, is not bulging. The abortive plan of treatment is as follows: The patient, whether child or adult, is at once ordered to bed. Calomel in dosage appropriate to the age is administered, and followed in six hours by some drug acting directly upon the bowels. This cleansing of the alimentary tract seems not only to prevent or relieve digestive disturbances, but also in some way to exert a favorable influence upon the tympanic lesion itself. To control pain while the abortive remedies are given time to act, the following prescription is of value, and in itself may influence the lesion favorably: R Codeinae, Extract, belladonna?, aa gr. j; Phenacetini, Salol, aa gr. xx. M.—Divid. in chart. No. viii. Sig.—One powder q. 4. h. During the first twenty-four hours the patient should be placed on a strictly liquid diet, which is then changed to a light diet of easily digestible TREATMENT OF ACUTE OTITIS MEDIA 173 food. Regular diet should be restored as soon as the lesion seems under control. It is certainly irrational to keep a patient suffering from acute middle-ear inflammation upon a continued starvation diet. Relief of Pain.—The meagreness of our resources for the relief of pain constitutes the weak point in this plan of treatment. Opium for the relief of the earache of acute otitis media is to be advised against for the reason that it would mask a very important guide as to the progress of the lesion. Locally our chief reliance is upon the application of dry heat, which, while it may not wholly annul a severe earache, often reduces very materially its intensity. While many appliances have been contrived for applying dry heat to the ear, none is more efficient than the ordinary hot-water bag. It should be only half filled with very hot water, wrapped with one or more layers of flannel, and the patient instructed to lie with the diseased ear in contact with it. With two bags in use, continuous application of heat is easily maintained. Poultices applied to the ear are said sometimes to affect the organ disastrously, and are never used in otological practice. When these measures seem at the end of twelve or twenty-four hours to have controlled the symptoms,—i.e., when the pain is relieved and inspection of the drum membrane reveals no evidences of pus accumula- tion within the tympanum,—the abortive plan of treatment should be continued. In cases responding favorably to this treatment, the pain usually subsides fairly promptly. The subjective noises, on the other hand, may be very persistent, and restoration of the drum membrane to its normal condition and appearance is often very gradual or slow. A possible disadvantage in this plan of treatment is illustrated in certain cases in which recovery, though ultimately complete, has been unduly delayed. There have been cases also in which, after a considerable period during which a favorable result seemed probable, incision of the drum membrane has finally become necessary on account of recurrence or persistence of symptoms. When pain is not relieved within a reasonable period of time, or when the drum membrane, from having been simply injected, is seen to bulge into the canal from the pressure of pus or serum behind it, abortive meas- ures should be abandoned. That this plan of treatment is not more often put into practice by the otologist is due to two facts,—viz. (1) in most cases the patient does not come under his care and observation until after the lesion has passed the stage for which abortive measures are appropriate, and (2) the pain is often so great that the patient demands or requires immediate relief, and this is most promptly and safely secured by incision of the drum membrane. Surgical Treatment of Acute Catarrhal Otitis Media.—When the lesion has advanced to the stage of pus formation and retention, it is clearly a surgical condition. The local treatment in such cases is logically based upon a recognition of two facts: (1) the necessity of providing free drain- age from the tympanum by means of an incision of the drum membrane, and (2) the necessity of keeping the external auditory canal as nearly as 174 ACUTE DISEASES OF MIDDLE EAR AND MASTOID possible free of pus. We endeavor to carry out the second indication by (a) frequent irrigation of the meatus with sterile or antiseptic solutions, or (b) by capillary traction through gauze wicks or some form of sterile gauze dressing introduced into the meatus. Myringotomy. — When inspection of the ear shows the membrana tensa to be bulging (Fig. 102, p. 163), there should be no unnecessary delay in making a free incision through its posterior segment. This opera- tion, though occupying but a few moments, is exceedingly painful. It is much better, therefore, that the patient should be under the influence of a general anaesthetic. For this purpose nitrous oxide is the ideal drug, providing safe anaesthesia easily prolonged to the requirements of an operation on one or both ears, and usually leaving the patient absolutely without discomfort or untoward symptoms. The necessary steps in pre- paring the patient for operation are simple. Having been put to bed, where for the present he is to remain, the auditory canal is filled with peroxide of hydrogen. This is allowed to remain some three or four min- utes, the ear then being irrigated with a warm antiseptic solution,—e.g., bichloride of mercury 1 in 4000, or carbolic acid 1 in 200. A bit of sterile absorbent cotton or sterile gauze is introduced lightly into the outer extremity of the canal, and the patient is ready for the anaesthetic. Since our object is to evacuate pus presumably confined to the atrium, it is not either necessary or desirable that the incision should extend above the posterior fold so as to enter the vault. It is quite important, however, that the cut should be as extensive as possible within the limits of the membrana tensa. The posterior segment of the tense membrane is the broader, and is usually the part most markedly bulging in acute tympanic disease, and it is in the posterior segment that the incision is always made. A mere puncture of the drum membrane or a very short incision may bring temporary cessation of pain through relief of tension, but either closes prematurely or provides such inadequate drainage as not to insure the best resul ts. Another unquestionable disadvantage of a mere puncture of the drum membrane is the fact that, even should it not close prematurely, it is much more apt to result in a permanent perforation than a more extensive incision. The incision should extend from the lower attachment of the posterior segment below to the middle of the posterior fold above (Fig. 109). Removal of Clot following Myringotomy.—Im- mediately following incision of the drum-head, there is always a free escape of blood into the mea- tus, and unless this receives attention, a clot may be left in the depths of the canal, partly or wholly defeating the purposes of the operation. I have known this to occur in cases left to the care of incompetent nurses. It is likely to occur, for example, if the first irrigation is delayed twenty minutes or more after the incision is Fig. 109.—Incision of mem- brana tensa. TREATMENT OF ACUTE OTITIS MEDIA 175 made, and then the fountain bag instead of the hand syringe is used. I personally like to remain five or ten minutes after operating to see this post-operative clot, which is invariably present, dislodged. Once removed, it does not usually re-form. From this stage, the treatment is much the same as that described as the abortive method, plus measures for keeping the canal free of pus. The patient should be kept in bed,8 placed upon liquid or very light diet, and the bowels freely moved. Irrigation. — During the first few days after myringotomy, the ear should be irrigated at rather frequent intervals with some antiseptic solution. Ordinarily, every three hours is often enough, but if the dis- charge becomes unusually profuse, syringing every two hours may give better results. Many bactericidal drugs have been advised by different authors, bichloride of mercury and boric acid being in most common use. Corrosive Sublimate in Aural Therapy.—Admitting that the use of this drug in solutions of proper strength is often followed by satisfactory results, there have in my experience been so many cases which seemed to be un- favorably influenced by it, that I am tempted to record my objections to its routine use. The unfavorable reactions as I have observed them may be mentioned in somewhat the following order: (1) In a certain small per- centage of cases corrosive sublimate even in weak solution has seemed to exert a distinctly destructive action upon the tissues, the incision in the drum membrane showing little tendency to heal, but rather to further enlargement by tissue disintegration. (2) There is a class of cases, par- ticularly numerous among children, in which a bichloride solution of any strength produces a dermatitis of the auditory canal and concha, resulting in an eczematous eruption which will persist so long as bichloride irrigations are continued. (3) Finally there have been cases in which the aural discharge has without other discoverable cause been unduly pro- longed, improvement following quickly upon a change of treatment. The use of this drug and the phenomena above described have seemed to me often to occupy a logical relation of cause and effect. Bichloride of mercury in 1 to 5000 solution, applied frequently to the hands, will produce a dermatitis. Taken into the stomach, it would not only prove toxic by absorption, but would quickly produce severe gastro-enteritis by its local action upon the mucosa. Entering the tympanum through the incision in the drum membrane, it is probable that the advantage derived from its bactericidal action is more than offset by its corrosive action upon the tympanic mucosa. Certainly many cases of acute otitis media— particularly in children—do better as soon as bichloride of mercury is discontinued. Personally, the writer believes that in the cases in which routine irri- gation is successfully employed, its happy effects are due very largely to 8 While it is not always possible to insist upon confinement to bed in the case of a busy man or woman, there can be no doubt that it may play an important part in hastening recovery, and that its neglect is not without risks to the patient. 176 ACUTE DISEASES OF MIDDLE EAR AND MASTOID its mechanical results in cleansing the meatus of pus, and only in minor degree to the germicidal action of the drug used in solution. He therefore prefers boric acid as less irritating than bichloride of mercury, and is inclined to believe that water absolutely sterilized by boiling might prove as effective as either. As soon as there is a noticeable diminution in the discharge, the fre- quency of the irrigations should be reduced,—e.g., three times daily, twice daily, once daily, etc. Practical Suggestions.—I believe that every practical aurist will agree with me that the value of routine irrigation in acute middle-ear disease depends much less upon the frequency than upon the thoroughness of the irrigation. The object in view is simply the complete removal of pus from the meatus. If this can be accomplished by a single forcible compression of a small rubber syringe, we gain nothing by repetition of this procedure. If the contents of a vessel containing two quarts—e.g., the rubber bag of the ordinary fountain syringe—have been allowed to flow in and out of the ear, leaving a residue of thickened pus at the fundus of the canal, nothing of value to the patient has been accomplished. With an adult, some form of hand syringe by which current force can be controlled gives satisfactory results. The auricle should be drawn somewhat upward and backward, and a stream of some force directed along the posterosuperior canal wall toward the drum membrane. Properly used, the contents of an ordinary coffee-cup usually suffice thoroughly to cleanse the canal of pus. After the irrigation, a ball of sterile absorbent cotton should be placed in the concha (not introduced into the meatus), and the head turned side- ways so that the irrigated ear is directed downward. The cotton is removed as soon as the surplus moisture from the irrigation has been absorbed. With nervous or very young children, the hand syringe is often diffi- cult for the nurse to manage effectively, and then the fountain syringe may be used instead. When the fountain syringe is employed, it is better to use a larger quantity of water,—i.e., one or two quarts,—and the bag should be held or secured on an elevation at least three feet above the patient’s head. I have known a vigorous infant to resist even the fountain syringe so effectively as to make irrigation very difficult even by this method. In such a case the child should be tightly wrapped in a sheet, the hands and arms being pinioned to the side of the body, and the sheet held by safety- pins. By this procedure resistance is rendered impossible, and it is sur- prising how soon the most unmanageable child realizes the painlessness of the measure and ceases to object to it. No matter how carefully the nurse may perform her duties, it will be found that the fountain syringe will in certain cases leave a residue of thickened pus at the bottom of the canal. This is a common cause of failure in children. It is due often to the thick, adhesive character of the pus rather than to a faulty method of syringing the ear. This difficulty may be eliminated by preliminary use of a few drops of hydrogen peroxide TREATMENT: CAUSES OF FAILURE 177 poured into the meatus and allowed to remain four or five minutes pre- vious to the irrigation. The value of the peroxide is not so much from its bactericidal action as from its power of dissolving thickened secretions at the fundus of the canal, thus facilitating their expulsion. The theory that this use of peroxide of hydrogen may cause a spread of the infection by the evolution of gas within the tympanum is not supported by any observed facts in actual practice. When satisfactory results do not follow the irrigation method of cleans- ing a discharging ear in acute tympanic disease, we should look for a pos- sible cause of failure in one or other of the following conditions, viz.: 1. Faulty Technic. — Direct the nurse to irrigate the ears as usual, and immediately thereafter examine the ears by speculum and reflected light. If a residue of pus remains in the depths of the canal, the procedure is worse than useless. This is undoubtedly a common cause of failure. 2. The discharge may be so profuse as to require more frequent irri- gations than are being employed. In this case, increasing their frequency to the point necessary to keep the meatus free of pus may give better results. 3. The incision in the drum membrane may have prematurely closed to a point no longer adequately draining the tympanum. While gradual closure of the perforation belongs to the normal process of repair, yet, if it occurs without proportionate diminution in the amount of pus secreted, a second incision of the drum membrane may be necessary. 4. Finally, there are certain cases in which one is forced to conclude that frequent irrigations tend to retard tympanic resolution. Such a conclusion being reached, the irrigations should be discontinued or modi- fied by combination with other measures. Wick Treatment in Acute Otitis Media. — Personally I believe that there are few cases of acute middle-ear inflammation which do not sooner or later reach a stage in which the wick treatment may with advantage be substituted for irrigation, or combined with it. By this method we depend partially upon capillary traction by means of sterile gauze to take up the pus draining into the meatus. Technic. — Free drainage from the tympanum being assured, the meatus is cleansed by means of pledgets of sterile absorbent cotton wound about applicators,—first dry and then dipped in alcohol. A prepared wick or strip of absolutely sterile gauze is then carefully introduced into the meatus so that its end is in contact with the perforation in the drum- head. The whole canal is thus filled with gauze, lightly packed. The outer end of the wick or gauze strip should not protrude from the meatus. The concha should now be filled with a small pad of sterile absorbent cotton. In the case of a restless child or nervous adult, who would be likely to disturb this dressing, the wick may be allowed to protrude from the meatus, and this and the whole ear may be covered with handkerchiefs of sterile gauze such as are used in covering a mastoid wound, the whole being held in place by a narrow gauze bandage. With the average intel- 178 ACUTE DISEASES OF MIDDLE EAR AND MASTOID ligent adult, however, the simpler dressing answers every purpose and possesses some advantages. Within twelve to twenty-four hours, this dressing should be removed and the wick carefully examined for the amount of pus that has come away with it. Frequently the wick and cotton in the concha are found completely saturated with pus at the first change of dressings. This, of course, is what one would expect. The meatus is now cleansed as before with alcohol and sterile absorbent cotton, and the drum membrane inspected to make sure that the incision is not prematurely closing. Drainage being adequate and the patient’s general condition being satisfactory, a sterile wick exactly similar to the first should be applied. These dressings should be changed at regular intervals of twelve to twenty-four hours, according to the copiousness of the discharge. Each dressing removed should be carefully scrutinized for changes in the amount of pus. In a favorable case, a distinct diminution will soon be noticeable. The use of wicks may be combined with irrigation by syringing the ear at each change of dressing, a plan wThich often gives exceedingly satisfactory results. In some cases it will be found necessary to abandon the use of wicks altogether. In the writer’s hands, however, it has been of undoubted value in shortening many attacks, and he is convinced that it has turned the scale in some cases which were not progressing favorably. The chief disadvantages in the wick treatment are the difficulties in correctly carrying out its provisions. It can be employed safely only in such cases as can be kept under the physician’s close personal care and supervision. The writer regards it as contra-indicated in (a) acute infec- tious diseases complicated by acute middle-ear inflammation, and (b) in cases of acute tympanic disease accompanied by high fever or other signs of septic absorption. Catheter Inflation in Acute Tympanic Disease.—The Eustachian cathe- ter has a distinct field of usefulness in the treatment of acute middle-ear inflammation. That it is so seldom used is due probably to the fear that the current of air may carry pus from the tympanum into the mastoid cells. This, in the writer’s opinion, is a remote possibility. In the normal ear the atrium is more or less separated from the vault by the structures massed at the boundary line between the two (see Fig. 27). During an acute middle-ear inflammation the swelling of the tympanic mucosa must tend to render this separation more complete. If inflation were performed in a case in which no adequate opening in the drum membrane had been provided, it is possible that harm might result from the displacement of pus. After free incision of the drum-head, however, it seems clear that air entering the tympanum from the Eustachian catheter must find its path of least resistance through the incision in the drum-head, carrying with it some of the pus or fluid in the tympanum. Upon physical grounds, there- fore, it would seem that catheter inflation may be used to advantage in certain stages of acute tympanic inflammation. For example, when diminution in the amount of discharge has warranted us in reducing the number of irrigations to twice or three times daily, we have reached a TREATMENT OF ACUTE PURULENT OTITIS MEDIA 179 point from which further progress is in some cases rather slow. Suppose, in such a case, that after irrigation we inspect the drum membrane and, by wiping out residual moisture, satisfy ourselves that the canal is free of pus. We may now cleanse the nose and nasopharynx by alkaline sprays and carefully inflate the ear by catheter, using not too much force. If subsequent inspection shows a residue of pus thrown out into the meatus, we may easily wipe this out with sterilized cotton. If now we introduce a sterile gauze wick into the canal and leave this in contact with the drum-head to take up pus as it escapes through the perforation, it is clear that we have left both canal and tympanum in a con- dition more favorable for prompt resolution than if irrigation alone were depended upon. I am con- vinced that the course of the disease may in many cases be materially shortened by these measures. Treatment of Acute Purulent Otitis Media.—The treatment of acute suppurative otitis media may be dealt with briefly, since it is necessary only to point out wherein it differs from that of the milder form. In the first place, there is no stage of the disease for which palliative, or abortive, measures are either adequate or safe. Infection of the vault is in itself an indication for incising the drum membrane. In practically all cases, therefore, the treatment begins with a myrin- gotomy. The incision should begin near the lower marginal attach- ment of the posterior segment below, and extend upward to and through the posterior fold so that the knife may enter and provide drainage from the vault (Fig. 110). When, in addition to the inflammatory changes in the drum membrane, the postero- superior canal wall is noticeably inflamed or swollen, this also should be incised. This is accom- plished by rotating the knife so that its cutting edge is directed backward, and dividing the adjacent inflamed portion of the canal wall as the blade is withdrawn (Fig. 111). This inflammatory condition of the meatus resulting from acute suppurative otitis media is prac- tically always confined to the soft parts covering the posterosuperior Fig. 110. — Incision indi- cated in acute purulent otitis media. Fig. 111.—Incision through drum-head and posterosuperior canal wall. 180 ACUTE DISEASES OF MIDDLE EAR AND MASTOID wall of the bony meatus. The incision, to give maximum relief, should divide all tissue down to the bone. Following myringotomy, the measures advocated for the milder form of the disease are of equal or even greater importance here. Absolute rest in bed, catharsis, and careful regulation of the diet may exert a decided influence upon the course of the disease, or at least upon the duration of the attack. The ear should be irrigated every three hours with a sterile or antiseptic solution,—a boric acid solution (dr. ss ad oz. viij) being the writer’s preference. Later, when the amount of the discharge has become noticeably diminished, the frequency of the irrigation should be reduced,—e.g., to one, two, or three times a day. I believe that the ear should not be syringed oftener than is necessary to keep the canal fairly free of fluid pus. With diminution in the amount of the discharge, the use of gauze wicks may be combined with periodic irrigation. By this plan the ear is irrigated once or twice daily,—once being usually sufficient,— the canal in the interim being filled with a strip of sterile gauze. In addition to the above measures, occasional catheter inflation to clear the atrium and hypotympanic space will influence some cases favorably. It must be employed with care,—i.e., with only moderate force,—and only after the acute stage is well passed, the physician having assured himself that an adequate opening in the drum membrane remains. The objection that inflation, even though practised with gentleness, may in these cases carry pus from the antrum to the mastoid cells is, I believe, founded on theory rather than fact. Antrum Tenderness.—At the height of an acute suppurative otitis media of average severity, some degree of tenderness over the antrum is usually present. This physical sign undoubtedly denotes an extension of the inflammatory process from the tympanic vault backward to the ant- rum, but does not necessarily mean suppurative involvement of the mastoid cells proper. I believe that this condition—i.e., tenderness localized over the antrum and occurring early in a suppurative middle-ear lesion—is one for which the application to the mastoid of the ice-bag or Leiter’s coil may be of positive value in limiting the process and preventing spread of infection throughout the mastoid cells. All, however, that can be accomplished by its use is obtained by twenty-four hours of continuous application, after which it may be distinctly harmful in lowering the vitality of the part. Occasional Necessity for Re-incising the Drum Membrane.—The normal drum membrane exhibits a remarkable tendency to rapid healing after puncture or incision, provided infection has not occurred. I have seen a drum membrane, after free incision for the relief of severe earache in the initial stage of acute catarrhal otitis media, practically healed at the end of forty-eight hours. This tendency to quick healing occasionally works to our disadvantage in the treatment of acute purulent otitis media, in which closure of the incision advances more rapidly than repair of the sup- purative process within the tympanum. I wish to emphasize the fact that ACUTE MASTOIDITIS 181 in cases of retarded resolution following myringotomy, if inspection shows that the opening in the drum-head is no longer affording adequate drain- age, there should be neither hesitation nor delay in re-incising the mem- brane. Nor can we formulate any rule as to the number of times it may be necessary or wise to repeat this operation. Even in cases in which my- ringotomy has been repeated one or more times, should evidences of pus retention within the tympanum recur, reopening of the drum membrane will often lead to recovery. There can be no doubt that delayed resolution is due in a certain proportion of cases to the fact that the individual’s vitality or power of resistance is below par, and it is a reasonable hypoth- esis that the same causes might unfavorably influence the process of repair following operation upon the mastoid. The measures outlined above, if thoroughly and conscientiously carried out, will bring about recovery in all cases of acute middle-ear inflammation except in those in wdiich the process of repair is interrupted by one or other of the following conditions: (a) Acute suppurative mastoiditis. (b) Caries of tympanic structures leading to the condition known as chronic suppurative otitis media. (c) Spread of the infection to the labyrinth or to one or other of the intracranial structures. The symptoms by wrhich such extension of the disease is announced will be discussed in connection with the lesions mentioned. After Treatment.—After the discharge has ceased and the drum mem- brane is completely healed, the after treatment, if any be required, is the same whether the lesion has been of the catarrhal or purulent type. If the hearing is perfect and no subjective symptoms persist, no treatment is called for. On the other hand, if tinnitus or other- subjective symptoms persist, or if the hearing remains below par, it may be necessary to practise occasional inflation by catheter to break up newly formed adhesions and correct any remaining congestion within the tympanum and Eustachian tubes. Quite often, however, these conditions correct themselves without treatment. ACUTE MASTOIDITIS. Etiology.—Acute suppurative mastoiditis is practically always sec- ondary to a suppurative lesion of the middle ear. While cases have been reported in which the drum membrane has presented no signs of inflam- mation, past or present, there is no evidence in such cases that a tympanic lesion has not preceded, and given rise to, the mastoid disease. Primary mastoiditis due to syphilitic or tubercular infection, while theoretically conceivable, is so rare as to be practically negligible. It is not seen in actual practice. Traumatic mastoiditis is among the rarest lesions. In short, the mastoid process seems to enjoy immunity from acute disease except as a result of infection from a diseased tympanum. Pathology.—We shall obtain a much clearer conception of the pa- 182 ACUTE DISEASES OF MIDDLE EAR AND MASTOID thology of this rather grave lesion if we bear in mind two facts, namely: (1) The so-called mastoid antrum should not be regarded as one of the mastoid cells, but simply as the posterior end of the tympanic vault. In the foetus at term, the mastoid process as such does not exist, yet the antrum is already a large and easily demonstrable cavity. (2) In acute purulent otitis media, the inflammatory process and the flow of pus must quickly invade the antrum. This, however, does not of itself constitute a true suppurative mastoiditis. Acute mastoiditis may be defined as an acute inflammatory process originating in the antrotympanic cavity and spreading thence to the mastoid cells proper. It is probable that the in- flammatory process passes in most cases through certain fairly well defined stages,—viz. (1) stage of vascular engorgement and cell infiltration; (2) suppurative stage, characterized by the presence of fluid pus; and (3) the stage of osseous necrosis or softening. These three stages are clearly and easily recognized macroscopically during operations upon patients in dif- ferent stages of the disease. Probably there is no well recognized lesion which presents such wide variations in the rapidity or slowness with which the disease advances. Thus, in one case weeks may elapse without the development of symptoms justifying a decision to operate, while in another case, operated upon but a few days after the onset of the tympanic disease, the cells throughout the mastoid may be bathed in pus. If one will refer to Plate III, page 33, showing recognized structural variations, or types, of the normal mastoid,— or, better still, if one will examine any fairly large series of bone sections,— these variations in the pathology of the disease will be more easily under- stood. Thus, it is clear that in a temporal bone characterized by a large antrum in close relation to large pneumatic spaces separated only by thin lamellae of bone, a suppurative process would logically advance with far greater rapidity than in a bone presenting a very small antrum and a sclerotic mastoid. On exposing the mastoid cortex, we find in a majority of cases no changes indicative of the pathologic changes within the bone. In adults, only if the lesion is of comparatively long duration, are cortical per- forations likely to be present. The most common site of such cortical defects is the space slightly above and behind the spine of Henle; but they may occur at any point upon the outer cortex from the temporal ridge above to the tip below. Perforation may also occur through the thin bony plate forming the inner covering of the mastoid tip (Bezold’s perforation or abscess). In young children, owing to the comparative thinness and softness of the outer covering, cortical perforations are by no means uncommon. On removing the cortex, we may find any of the following conditions, which, in the order named, represent roughly the successive stages of the lesion: (a) Antrum more or less filled with fluid pus draining back- ward from the tympanic vault. The mastoid cells contain no pus, but their mucous lining is red, swollen, and bleeds easily and pro- ACUTE MASTOIDITIS: SYMPTOMS 183 fusely, showing great vascular engorgement. (b) Cells adjacent to the antrum, and also the large cell at the tip, contain a variable amount of fluid pus. (c) Mastoid cells throughout contain pus and exuberant granulations, (d) Intercellular bone substance is softened or completely disintegrated, (e) In the later stages necrosis of the intercellular bone substance may co-exist with intact inner plates, or the latter may exhibit areas of necrosis. Pus, being present within the mastoid, may be removed wholly or in part by absorption through the lymphatics, or may find a pathway of escape through perforation of the bone brought about through osseous necrosis. The various pathways of escape, and the lesions to which they give rise, will be spoken of in a later chapter. Symptoms.—The symptoms of acute mastoiditis are usually engrafted upon those characteristic of acute purulent otitis media. We have, there- fore, to ask ourselves what symptoms, or modifications of symptoms, occurring during an attack of acute middle-ear suppuration, or during convalescence therefrom, should lead us to suspect suppurative involve- ment of the mastoid cells. Pain and Insomnia.—The patient, who has been comparatively com- fortable, may suddenly experience deep-seated pain in the region of the mastoid process. Or, in the absence of actual pain, there may be a dis- tressing sense of fulness, soreness, or discomfort referred to the mastoid. On the other hand, there are many cases in which the patient complains little either of mastoid pain or discomfort. In the presence of mastoid pain or discomfort, and in proportion to its severity, insomnia is usually present, and sudden inability to sleep at night is in some cases a useful guide to arrested resolution. Fever.—Elevation of temperature, usually of moderate degree, may be more or less continuously present during suppurative disease of the mastoid. When present it is a most important symptom, and one which, unless yielding fairly rapidly to rational non-operative measures, calls more or less imperatively for surgical intervention. Fever, however, is in one sense a most unreliable symptom, in that many cases of severe mastoiditis exhibit throughout no noticeable elevation of temperature. That extensive necrosis of the mastoid cells may coexist with a practically normal temperature curve is a fact now fortunately recognized. In the author’s experience fever is absent, or so slight as to be of no special diagnostic value, in a majority of cases. Absence of fever is, therefore, no evidence that the mastoid cells are not extensively diseased. Aural Discharge.—The aural discharge may undergo certain quantita- tive changes which wrould lead an experienced aurist to suspect mastoid involvement. For example, a rather copious discharge may suddenly cease, this abrupt cessation being accompanied by no amelioration of the patient’s condition and being followed within a few days or hours by a renewed flow of pus. Or, again, a moderate discharge may suddenly or 184 ACUTE DISEASES OF MIDDLE EAR AND MASTOID gradually increase in volume until it becomes necessary upon purely physical grounds to assume involvement of the mastoid cells in order to explain the amount excreted in the twenty-four hours. In still another group of cases, the long persistence of the discharge may of itself force the inference of a focus of disease beyond the limits of the small tympanic cavity. Changes in the Drum Membrane and Sagging of the Posterosuperior Canal Wall.—While cases have been observed in which the tympanic condition has improved simultaneously with the advance of a suppura- tive process within the mastoid, such cases are exceedingly rare. As a rule, the drum membrane presents the picture of severe suppurative otitis media. It is usually perforated, red, and markedly bulging in the upper posterior quadrant. That these tympanic changes are often a result of the disease within the mastoid is frequently demon- strated by the rapidity with which the diseased drum membrane regains its normal condition and appearance after operation upon the mastoid. A very common feature of these cases is a noticeable inflam- matory thickening of that portion of the posfcerosuperior canal wall which immediately adjoins the drum membrane, so that the one gradually merges into the other, there being no distinguishable line of demarcation between the two. This is undoubtedly due to a periostitis in this situation, and is so frequently seen in cases of acute purulent otitis media complicated by mastoid suppuration that it is by some authors regarded as pathognomonic of the latter condition. Taken in connection with other symptoms, it is of considerable diagnostic value; alone, it is not a reliable sign of mastoid disease. Mastoid Tenderness.—Undoubtedly the most reliable sign of acute mastoid disease is sensitiveness to pressure over the mastoid cortex. This varies in different cases from moderate tenderness elicited only by firm pressure to extreme sensitiveness even to very light pressure. In some degree it is usually present in every case of suppurative mastoiditis. In many cases it seems to reach its height during the early (vascular) stage, becoming less marked as these initial inflammatory changes are past. Most aural surgeons have been occasionally surprised in operating upon cases in which intense mastoid tenderness has been present to find an absence of pus, the most conspicuous macroscopic change being extreme vascular engorgement. During the later progress of the lesion, exacer- bations of mastoid tenderness may occur, being due probably to an occasional extension of the inflammatory process to cells not hitherto involved, or to the influence of pus temporarily retained under pres- sure in certain cells. Undoubtedly, the degree of mastoid tenderness is in some degree related to the type of bone involved. For example, it seems a logical deduction that a suppurative inflammation involving a mastoid process of thin cortex and pneumatic structure (see Plate III, page 33) would give rise to greater sensitiveness to pressure than would a similar process ACUTE MASTOIDITIS: SYMPTOMS 185 within a sclerotic mastoid, or one having a very thick cortex. From this relation, one may in some cases reach a practical inference from one’s clinical data as to the type of the diseased mastoid, and therefore as to the character of the lesion. Thus, in a case in which symptoms of mastoi- ditis with very marked mastoid tenderness follow rapidly upon the onset of the tympanic lesion, one may infer with considerable confidence that one has to deal with a pneumatic mastoid having a comparatively thin cortex. On the other hand, with symptoms of more gradual development and with well-marked mastoid pain or discomfort coexisting with very slight sensitiveness to pressure, one would expect to find a mastoid of sclerotic type, or one having a thick cortex. Clearly the latter may be the more serious condition. It will be seen from what has been written that the clinical picture includes only a limited number of symptoms which can be said strictly to characterize the disease. To epitomize: The symptoms to be looked for are mastoid pain, with consequent insomnia; elevation of temperature; certain quantitative changes in the character of the discharge; mastoid tenderness, and bulging of the pos- terosuperior canal wall. The above rather meagre clinical picture may be said to comprise practically all the symptoms which are characteristic of an uncomplicated case of acute mastoiditis. Unfortunately, many cases of acute mastoiditis run their course with complete absence of one or more of the above symptoms. For example, neither elevation of temperature nor mastoid pain may be present. When fever is absent and pain inconsiderable, the subjective and constitutional phenomena are naturally not very characteristic. Even in such cases, however, there is usually some feature in the clinical picture which will cause the experienced observer to suspect that recovery is being inter- rupted by the advance of a suppurative process within the mastoid. For- tunately, there is one physical sign which is seldom or never wholly absent. Some difference in the sensitiveness of the two mastoids to pressure can usually be demonstrated by careful palpation. There remain to be described certain changes in the position of the auricle and in the contour of the soft parts about the ear, which are among the more unusual accompaniments of mastoid inflammation. Auricular displacement is a comparatively rare result of mastoid inflammation in adults. When present it constitutes a very characteristic deformity. It may be produced in one of two ways,—viz.: (1) Subperiosteal Abscess.—The suppurative process within the mas- toid gives rise to a perforation in the mastoid cortex. Pus escaping through this perforation elevates the periosteum from the surrounding bone, and, being confined beneath the periosteum, constitutes what is known as a subperiosteal abscess. As this abscess is usually in close proximity to the posterior attachment of the pinna, the postauricular sulcus is often obliterated and the auricle markedly displaced. If the perforation is behind the centre of the postauricular attachment, the auricle is pushed 186 ACUTE DISEASES OF MIDDLE EAR AND MASTOID directly forward, standing prominently outward from the side of the head. When the perforation is at a higher level, the auricle is displaced both forward and downward (Fig. 112). (2) Postauricular OEdema.—In another class of cases the acute inflam- matory process extends through the mastoid cortex without causing a perforation. This extension of inflammation involves the periosteum and overlying soft tissues, which become markedly swollen or cedematous. This condition gives rise to a deformity similar to that above described, though usually less pronounced. While auricular displacement is in adults comparatively rare as a result of mastoiditis, it occurs very frequently in the mastoiditis of infants and young children. It will also be recalled that a similar deformity is a very common feature of furunculosis of the meatus in adults. The two lesions are very different, however, in their surgical significance, for whereas the postauricular oedema and consequent displacement resulting from furun- culosis of the canal are usually relieved by incision of the focus or foci of infection within the meatus, the subperiosteal abscess or oedema result- ing from mastoid suppuration is a positive indication for opening the mas- toid. Hence the importance of being able to make a correct diagnosis. It may be well therefore to repeat briefly the chief differential points be- tween the two conditions. Auricular Displacement in Furunculosis. 1. Common in adults; rare in children. 2. Pain always severe; increased by movements of the jaw. 3. Any manipulation of the auricle causes excruciating pain. 4. Speculum examination shows fu- runcular swelling situated always in fibro- cartilaginous portion of canal. 5. Drum membrane may be, and usu- ally is, intact. 6. Discharge, if present, comes from furuncular perforation in membrano-car- tilaginous canal. 7. Pressure upon the mastoid, so di- rected as not to move or disturb the auri- cle, causes no pain. Pressure at same point, but directed slightly forward so as to disturb the auricle, causes great pain. Auricular Displacement in Suppurative Mastoiditis. 1. Very common in children; com- paratively rare in adults. 2. Pain not usually severe, and may be absent; not influenced by movements of the jaw. 3. Manipulation of the auricle causes absolutely no pain. 4. Inspection of meatus shows absence of inflammation in fibrocartilaginous part of canal. Inflammation, if present, con- fined to lining membrane of posterosupe- rior wall of bony canal. 5. Drum membrane almost invariably perforated. 6. Discharge from the tympanum through perforation in drum membrane. 7. Pressure upon the mastoid elicits deep bone tenderness. Bezold’s Abscess.—A more unusual complication of suppurative mastoiditis was first described by the late Professor Bezold, and is known as a Bezold abscess. This condition is caused by a perforation in the bony plate forming the inner surface of the tip of the mastoid. It occurs pre- sumably in cases in which the tip cells are especially large and in which Fig. 112.—Auricular displacement resulting from postauricular subperiosteal abscess. Fig. 113.—Aural ice-bag. Fig. 114.—Lei ter’a coil. MASTOIDITIS IN INFANTS AND YOUNG CHILDREN 187 the bony plate forming the inner or medial wall of the tip is very thin, and the outer cortex thick. Pus escaping through such a perforation burrows downward in the neck beneath the sternomastoid, or may be con- fined between layers of the deep cervical fascia. It presents a prom- inent, elongated swelling below the mastoid in the neck, which, if other symptoms of mastoid disease were not clear, might present difficulties of diagnosis. It renders the surgical treatment of the disease rather more troublesome by the occasional necessity of extensive incisions in order to provide adequate drainage from the cervical spaces involved. Paralysis of the Ahducens (6th) Nerve.—A somewhat puzzling compli- cation, which the aurist has sometimes to deal with, is the development dur- ing the course of a suppurative mastoiditis of paralysis of the 6th cranial nerve. It will be recalled that this is purely a motor nerve and that it supplies only one muscle, the external rectus muscle (occuli). Origin and Position.—According to Gray, the deep origin of the 6th nerve is from the gray substance of the fasciculus teres by a nucleus com- mon to it and to a part of the 7th (facial) nerve. It is said also to be con- nected with the nuclei of the 3rd and 4th nerves. Its superficial, or appar- ent, origin is from the upper constricted portion of the medulla just behind the pons. The trunk, as it passes forward along the inner wall of the cav- ernous sinus to enter the orbit through the foramen lacerum anterius is in more or less close relation with the molar occuli (3rd), the pathetic (4th) and the ophthalmic branch of the trifacial (5th). It is also in relation with the cavernous portion of the internal carotid artery. Within the orbit it is distributed solely to the inner surface of the external rectus muscle, con- traction of which rotates the eye outward. Pressure by tumors, the exudates of a basilar meningitis or of cerebro- spinal syphilis may disturb its function. The diagnosis of 6th paralysis is simple. The patient usually com- plains of the discomforts incident to double vision. When any small object, e.g., a pencil, is held directly in front of him,—i.e., in the median plane of vision,—it is seen as a single object. So also when it is moved laterally in the direction corresponding to the sound nerve. When, however, it is moved in the opposite direction, diplopia is complained of as soon as the median plane of vision is passed, when it will be seen that the eye corre- sponding to the paralyzed nerve remains stationary in the median position, while the sound eye follows the moving pencil as normally. The path of infection from mastoid to 6th nerve is usually obscure. Theoretically, one may say (1) that the nerve may be compressed by disease (thrombosis) of the cavernous sinus; (2) that it may be subjected to pressure by a thrombus in the anterior end of the inferior petrosal sinus (Page’s case9); (3) that the nerve sheath may be involved in a meningitis spreading inward from a necrotic tagmen antri; (4) that a suppurative labyrinthitis may give rise to a subtentorial leptomeningitis which, extend- ing forward, may involve the nerve sheath; (5) that the nerve lesion may be 9 Page: Thrombosis of Jugular Bulb; Paralysis of External Rectus Occuli; Annals of Otol. Rhinol. and Laryng., June, 1910. 188 ACUTE DISEASES OF MIDDLE EAR AND MASTOID an extention by continuity from disease involving the apex of the petrous bone (Gradenigo). While some of these roadways of infection seem to have been definitely established in recorded cases, they are usually in actual practice merely hypotheses, which do not throw much light upon the path- ologic aspect of the case in hand. In 1918 the author10 published the history of a case in which a paralysis of the 6th nerve which had existed at least two weeks, disappeared completely on the third day after a mastoid oper- ation; but the pathway of infection could not be determined. The number of such cases which have been recorded is quite large. In 1910 Dr. C. E. Perkins 11 of New York published a very interesting review of the literature of this subject up to that time. His report embraced sixty cases, in twenty-nine of which, the mastoid was operated upon, no operation having been performed in the remaining thirty-one cases. Of the cases operated upon, there were one death, one failure (i.e., of restoration of nerve function) and twenty-seven complete recoveries. Of the thirty-one cases treated non-surgically there were four deaths, three failures and twenty-five (sic) recoveries. So far as any deductions are permissible from these figures, they would seem to be; that in suppurative mastoiditis associated with 6th nerve paralysis, the mortality is far greater and the percentage of 6th nerve recoveries far less in cases not operated upon than in those in which a mastoid operation has been performed. The author believes, therefore, that even in cases in which the symptoms referable to the mastoid are not very marked, the association of a homolateral para- lysis of the external rectus muscle should be regarded as a positive indica- tion for the mastoid operation. Gradenigo’s Symptom-Complex. —Before leaving the subject of abducens paralysis a word should be said as to the surgical import of what is known as Gradenigo’s symptom complex. Gradenigo attributed to it a surgical significance only in the presence of a suppurative lesion of the mastoid. This complex is present when with evidences of middle ear or mastoid infection, there is associated a homolateral paralysis of the 6th nerve, eye pain or facial neuralgia and also severe frontal headache. This is thought to point strongly to necrosis or at least to a suppurative lesion of the apex of the petrous bone. It is clear that such a diagnosis would place upon the surgeon a very grave responsibility. It is important to bear in mind, therefore, that this syndrome might easily represent the combined results, or symptoms, of separate and distinct lesions. For example, should mastoiditis co-exist, as is not very uncommon, with suppurative disease of the ethmoid cells or sphenoid sinus, it is quite conceivable that the abducens paralysis might be a product of the mastoid lesion, while the sensory components (eye pain, facial neuralgia, frontal headache) might have their origin solely in the diseased ethmoid or sphenoid. Mastoiditis in Infants and Young Children.—Before leaving the sub- 10Kerrison: A case of abducens paralysis complicating mastoiditis: brief discussion of this complication as a surgical indication; Medical Record, November 30, 1918. 11 Perkins: Abducens Paralysis and Otitis Media Purulenta; Annals of Otology, September 1910 MASTOIDITIS IN INFANTS AND YOUNG CHILDREN 189 ject a word should be said as to the symptoms as observed in young children. Since the mastoid process as such does not exist during the first months of infantile life, it seems paradoxical to speak of mastoidectomy as occa- sionally called for at this period of development. It is an established clinical fact, however, that even in the first months of life, acute middle- ear inflammation may give rise to necrosis of the outer wall of the antrum and consequent subperiosteal abscess, and this condition for convenience of description is spoken of as mastoiditis. Antritis would be a scientifically more correct term. The symptoms of mastoiditis in infancy and early childhood resemble those of adult life, with the following differences: 1. The child suffering from acute aural disease is usually unable to differentiate between pain referred to the antrum and pain localized in the tympanum. Antrum pain is therefore of little diagnostic value in determining mastoid inflammation. 2. Fever is usually present rather persistently duving the acute stage of an acute purulent otitis media. After its recession a subsequent rise of temperature may easily be due to a slight exacerbation of the tympanic lesion. Fever, therefore, is hardly a reliable sign of mastoiditis in children. 3. Occasional symptoms suggesting cerebral irritation,—e.g., convul- sions, sudden vomiting, chills, hyperpyrexia, etc.,—while naturally causing anxiety, are of less serious import than if occurring in an adult patient suffering from mastoid inflammation, for the reason that the cerebral centres presiding over these disturbances of function are more subject to reflex irritation from slight peripheral causes than in the adult. Such symptoms are not, however, even in very young children, to be consid- ered lightly, and the child exhibiting them should be very carefully watched. A conspicuous difference in the Physical signs of mastoiditis in early life depends upon the fact that the outer wall of the antrum in infants, and the outer mastoid cortex in children of two or three years, are softer, more vascular and spongy, and infinitely thinner than in later life. As a result of these structural peculiarities, perforation of the cortex with consequent subperiosteal abscess is a comparatively frequent and early manifestation of mastoid disease in early life. As a matter of fact, the diagnosis of mastoiditis in young children is frequently not made until after the appearance of postauricular oedema or subperiosteal abscess. Prognosis.—Most cases of acute mastoiditis which are brought under the care of a competent aurist recover without operation upon the mastoid. Of the minority which do not respond to non-operative measures, but which present no evidences of intracranial complications, the prognosis as to recovery after operation is very favorable. Taking any large series of such cases operated upon by competent aural surgeons, the percentage of mortality probably does not exceed 1 or 2 per cent. In those cases in which, either before or after operation, the intracranial structures become involved (brain abscess, meningitis, sinus thrombosis), the mortality is exceedingly large,—depending in part upon the character of the lesion, and in part upon the amount of surgical skill and judgment which are brought to their care. 190 ACUTE DISEASES OF MIDDLE EAR AND MASTOID Treatment.—The patient should be ordered to bed, and kept there until all physical signs of mastoid inflammation have subsided. An active cathartic should be administered. During the first day or two, he should be given a liquid or very light diet. Early Myringotomy.—Irrespective of a previous incision of the drum membrane, it should again be incised under nitrous oxide anaesthesia, unless tympanic drainage is obviously adequate. The ear should be irrigated with boric acid solution at regular intervals, the frequency of the irrigations being regulated in accordance with the amount of the discharge. A ball of sterile absorbent cotton may, however, be placed lightly in the concha to protect the ear from fresh infection from without, this being changed as often as it becomes saturated with pus. Application of Cold to the Mastoid.—If the surgeon believes the inflam- matory process to be in the incipient stage, the application of an ice-bag or of Leiter’s coil may be of positive value in retarding, and perhaps abort- ing, the attack. It should be used not longer than twenty-four hours and once removed should not be reapplied. After the stage of fluid pus formation is reached, it may reduce the vitality of the part of the degree actually favoring bone necrosis. The application of leeches to the mastoid, scarification, and blood- letting by means of the so-called “artificial leech,” and the old practice of blistering the mastoid, while mentioned in some text-books, are practically without value, and are to be condemned as likely to produce a local sen- sitiveness to pressure which might obscure an important physical sign,— i.e., either increase or diminution of true bone tenderness. The administration of opium in acute mastoiditis is particularly inad- visable, for it may not only mask important symptoms, but, if repeated, soon reduces the patient to a condition of nervous irritability unfitting him for anaesthesia and surgical intervention, should these later become necessary. The successful non-operative treatment of acute mastoiditis depends largely upon the maintenance of free drainage from the vault until the processes of repair within the mastoid are established. If, therefore, during this critical period evidences of premature closure of the postero- superior quandrant of the drum membrane arise, there should be no hesi- tation or loss of time in re-incising it. The writer has seen many cases in which this simpler surgical measure has saved the patient from the major operation upon the mastoid. As to the criteria by which the results of non-operative treatment are to be judged, it is best to avoid dogmatism. The patient should, of course, be seen and examined carefully each day. If at the end of three or four days the discharge is less profuse and mastoid tenderness less marked, I should regard these conditions—fever, of course, being absent—as dis- tinctly favorable, and should these conditions show further improvement at the end of a week, I should look upon recovery without operation as probable. On the other hand, if a week passed without improvement in the patient’s condition, and particularly if mastoid tenderness remained INDICATIONS FOR MASTOIDECTOMY 191 unchanged or had become more pronounced, I should feel that the patient’s safety called for operative intervention. The indications for operating in acute mastoiditis may be summed up somewhat as follows: 1. The development during acute mastoid disease of auricular dis- placement as a result either of postauricular oedema or subperiosteal abscess,—furunculosis of the canal being eliminated as a possible cause. 2. The development during acute purulent otitis media of symptoms of vestibular irritation—e.g., vestibular nystagmus, vertigo, etc.—'Calls for prompt opening of the mastoid in order to relieve the vestibular walls of the pressure or presence of confined pus. 3. Marked tenderness on pressure, extending well beyond the limits of the antrum, and showing no tendency to diminution within five or six days following the incision of the drum membrane, would point to an active inflammatory process within the mastoid cells, calling for surgical intervention. 4. Marked variation in the quantity of pus discharged, its maximum flow being apparently too great to be explained by the tympanic lesion, its periods of diminution being coincident with the development of mastoid pain or tenderness (or both). Such a combination of symptoms consti- tutes one of the most positive indications for opening the mastoid. 5. Mastoid symptoms having been present and having disappeared, a discharge from the tympanic vault which resists all rational non-opera- tive measures may, by reason of its persistence, justify the hypothesis of a necrotic area beyond the limits of the antrotympanic cavity. In such cases an operation is often the only means of saving the integrity of the organ and preventing serious impairment of function. 6. Finally, evidences of mastoid disease having been present, the development at any time during convalescence of symptoms of septic absorption—e.g., chills, sweats, septic temperature, etc.—would, in the absence of other concurrent disease, constitute a positive indication for immediate operation. In speaking of the above as positive indications for opening the mastoid, it must be understood that we are speaking from the view-point of the patient’s safety,—i.e., with the view of correcting a lesion which has be- come dangerous before danger signals proclaim that his life is already in jeopardy. Every aurist has seen cases of mastoid suppuration of the severest type, in which operation seemed clearly indicated, recover without operation. He has also, however, seen patients by whom operation was delayed or rejected, return later with symptoms of intracranial infection. The aural surgeon is, therefore, frequently confronted with a grave respon- sibility. If he waits in all cases until symptoms are present rendering surgical intervention absolutely obligatory, he will frequently find, when these symptoms appear, that the question is shifted from the advisability of opening the mastoid to a far more serious one,—i.e., the possibility of saving the patient’s life by any means at his command. CHAPTER VIII. CHRONIC MIDDLE-EAR SUPPURATION. Otitis Media Purulenta Chronica.—This term is applied to any tym- panic inflammation giving rise to a perforation of the drum-head which shows no tendency to heal and through which there is a more or less constant flow of pus. Etiology.—Probably every case of chronic purulent otitis media has its origin in one or more attacks of acute tympanic disease. As a rule, however, these patients apply for relief only after months or years of constant or intermittent otorrhoea, so that the early changes marking the conversion of the acute into the chronic form of the disease rarely come under actual observation. All observers who have had an opportunity of watching the ear changes in any large series of cases of the acute exanthemata must have been impressed with the remarkable rapidity with which the drum membrane is frequently destroyed in acute tympanic lesions complicating scarlet fever and diphtheria. In some cases this tendency is so pronounced that nothing the physician may do seems to exert the slightest influence upon the rapid and permanent destruction of tissue. Measles and influenza also contribute their quota to the number of cases of acute tympanic disease which ultimately become chronic. Probably from 18 to 20 per cent, of all cases of chronic middle-ear suppuration are traceable to the infectious diseases of childhood. Adenoids predispose the child so markedly to acute middle-ear disease and interfere so effectively with spontaneous recovery that they must be included among the active causes of chronic purulent otitis media. This explains in some degree the greater frequency with which the disease develops in childhood as compared with adult life. An occasional cause of the disease in adult life is found in the atrophic changes in the drum membrane occurring in some cases of non-suppurative middle-ear catarrh. The drum membrane in such cases may be exceed- ingly thin, transparent, and retracted, or may be apparently thickened and relaxed. Probably most aurists have seen cases in which, during an attack of acute purulent otitis media of apparently moderate severity, the mem- brana tensa has undergone rapid disintegration about the site of the perfor- ation, which has subsequently shown little tendency to regeneration. The rapid loss of tissue in these cases is probably due to atrophy of the normal fibrous layers of the membrana tensa, which are ordinarily so strongly resist- ant to the influence of an acute suppurative process within the tympanum. Giving due weight and consideration to other causes, there can be little doubt that the great majority of cases are directly traceable to neglect or un- skilful management of an antecedent attack of acute purulent otitis media. Pathology.—The drum membrane is necessarily perforated in every 192 MARGINAL PERFORATION OF DRUM-HEAD 193 case of chronic purulent otitis media. In the great majority of cases the perforation is central,—i.e., does not at any point ipvolve the marginal attachment to the annulus tympanicus. In size it may vary from a minute pin-point orifice to practical destruction of the greater portion of the mem- brana tensa. It may also vary in shape from a small circular or oval opening to the larger crescentic or horseshoe-shaped defects involving both anterior and posterior segments. When the membrane bordering the perforation is relaxed and indrawn, and the tympanic mucosa is swol- len and denuded of its surface layer of epithelium, adhesions may form between the margins of the perforation and the inner tympanic wall. Perforation of Shrapnell’s membrane seldom or never occurs during acute purulent otitis media, but is found in about 3 per cent, of cases of chronic middle-ear suppuration (Bezold). While an artificial opening in Shrapnell’s membrane would lead into Prussak’s space, that occurring in chronic purulent otitis media invariably forms a direct communication with the vault, and therefore with the aditus and antrum. Marginal perforations—meaning thereby perforations in which there is at some point absolute destruction of the peripheral edge—are found in a cer- tain proportion of cases of long-standing middle-ear suppuration. They also occur primarily in certain cases of very rapid destruction complicating pro- found systemic infection, notably in cases of scarlet fever or diphtheria of unusual severity. Generally speaking, a marginal perforation of the drum membrane must be regarded as pointing to a more serious lesion of the tym- panum than a central perforation, for the following reasons: (1) in a large percentage of cases, a marginal perforation indicates necrotic changes in the bone adjacent to the perforation: (2) the great majority of marginal perfora- tions involve either Shrapnell’s membrane or the upper posterior margin of the membrana tensa, in either case leading directly into the vault, aditus,and antrum; and (3) a marginal perforation involving Shrapnell’s membrane or the posterosuperior segment of the membrana tensa, or both, constitutes the ideal condition for extension of the epidermis of the meatus into the antro- tympanic cavity. This leads in some cases to a proliferation of epithelial ele- ments within the antrum, and provides the most favorable nucleus for the sub- sequent formation of cholesteatomatous masses within that cavity. Accord- ing to the author’s experience, marginal perforations always mean osseous necrosis, the structures most commonly involved being the malleus and incus and the contiguous portions of the tympanic ring and Rivinian segment. The Mucosa.—The changes in the mucous membrane may vary in different cases from simple hypersemia with infiltration of leucocytes to practical destruction. In the simplest form of the disease, the mucosa may be greatly swollen so as to encroach considerably upon the cavity of the atrium, yet may preserve intact its surface layer of ciliated epithelium. This condition may persist for long periods without actual destruction of tissue. In the severer forms the epithelial covering is lost over consider- able areas, in which situations granulations form and there is a marked tendency to adhesions with adjacent structures. 194 CHRONIC MIDDLE-EAR SUPPURATION Bone Changes.—It is quite possible for a chronic purulent otitis media to exist for a considerable period without producing caries of the bony structures of the tympanum. For example, erosion of the superficial epithelial layer of the mucosa may be followed by the formation of firm granulations which protect the periosteum and underlying bone. When, however, the entire thickness of the tympanic lining membrane is at any point destroyed, the exposed bone, being deprived of its periosteal support, must depend chiefly upon its own arterial supply. Whether in such a case the denuded bone has been able to maintain its own nutrition, is usually indicated by the character of the granulations: e.g., fairly rapid formation of a covering of firm, apparently healthy granulations usually indicates normal repair, whereas the slow formation of loose, friable granulations, through which a probe passes without appreciable resistance to bare bone, commonly indicates bone caries. This process involving the bony capsule of the laby- rinth—e.g., the promontory or the outer wall of the horizontal semicircular canal—may be self-limited, the diseased layer of surface bone being thrown off in the pus in the form of minute sequestra, and the bone being grad- ually covered by healthy granulations; or the necrotic process may involve the entire thickness of the labyrinthine wall, giving rise to a suppurative labyrinthitis. The latter result occurs in 1 per cent, of all cases of suppura- tive otitis media (Hinsberg). Destruction of the mucous membrane lining the vault, aditus, or antrum leads usually to a more destructive form of os- seous disease, from which spontaneous local recovery is comparatively rare. In the cellular bone surrounding the bony capsule of the labyrinth, and in that bounding the aditus and antrum, the disease in many cases involves a dual process, osseous necrosis or softening being apparently accompanied, or closely followed, by a proliferative osteitis, in consequence of which the diploic or pneumatic bone substance is ultimately replaced by very hard, compact bone. As a result of an extension of this process, the mastoid cortex is often greatly thickened, and the cellular character of the bone to a very considerable extent lost. Much has been said as to the influence of this pathological osteosclero- sis upon the gravity of the disease. Undoubtedly the marked increase in the thickness and density of the outer cortex renders an escape of pus thropgh a perforation in this direction less likely to occur. On the other hand, it must be remembered that the process is not confined to the outer cortex, but occurs with equal regularity and frequency in the cellular bone surrounding the labyrinthine capsule, which it probably serves to protect. Bezold regarded it as a conservative process tending to limit the advance of a suppurative lesion in all directions. Granulations; Polypi.—Whenever in the tympanum there is actual ero- sion or destruction of tissue, however superficial, the process of repair is in- augurated by the formation of new granulations, which may later become organized into firm fibrous tissue. The presence of a certain amount of firm granulation tissue points, therefore, not so much to the disease itself, as to the effort on the part of the organism to repair or replace that which has been EPIDERMIZATION AND CHOLESTEATOMA 195 destroyed. On the other hand, the proliferation at certain points of loose, exuberant granulations, through which a probe at once passes to contact with rough denuded bone, is distinctly characteristic of osseous necrosis. Aural polypi may assume almost any shape within the limits of the tympanum and auditory meatus. They may be single or multiple; may consist simply of masses of granulation tissue, or may become partially organized, covered by squamous or ciliated epithelium, and assume some- what the character of fibromata. They may be attached by a compara- tively broad base or by a very small pedicle. They may spring from any denuded surface,—e.g., from the margins of a small perforation, from necrotic ossicles, from the promontory, or from the diseased tympanic margin, or tympanic ring. They are not infrequently attached to a denuded wall of the bony meatus near its tympanic margin. Very frequently they originate in the tympanic vault or the aditus. In the author’s experience, aural polypi point almost invariably to bone necrosis. While occasionally springing from the promontory, this site is exceedingly rare as compared with the outer wall of the vault or the diseased inner margin of the bony meatus. Aside from actual observa- tion and experience, the comparative rarity of polypi springing from the promontory may be inferred from the rarity of suppurative involvement of the labyrinth as compared with the frequency of polypi as a manifestation of chronic middle-ear suppuration. That is to say, if any considerable proportion of the polypi observed in chronic purulent otitis media had their origin from a diseased promontory, one would expect more frequent suppurative invasions of the labyrinth than are known to occur. Epidermization and Cholesteatoma.—A noticeable change in certain cases of chronic purulent otitis media is the conversion of the tympanic mucosa into a grayish-white, non-secreting membrane bearing some resemblance to the skin of the meatus. It is seen oftenest in association with marginal perforations involving Shrapnell’s membrane and the upper posterior periphery of the membrana tensa. It may, however, occur with large central perforations. This so-called epidermization of the middle- ear cavity is inaugurated by extension of the epidermis of the meatus and drum membrane over the edges of the perforation and into the tym- panic cavity. This process, by converting the recesses of the tympanum into dry cavities lined with a protective, non-secreting membrane, may be nature’s method of limiting the spread of the disease. There can be no doubt that in many cases spontaneous recovery has resulted from this process (Schwartze). Unfortunately, this happy sequence of events is not always realized. Let us imagine a case in which the epidermis of the canal, having entered the tympanum through a marginal perforation, extends by way of the aditus to the walls of the antrum. The new lining membrane, perhaps becoming macerated by pus from a deep-seated focus of suppuration, is ultimately exfoliated, leaving, however, a similar epithelial layer beneath. Successive layers, being similarly thrown off, finally become welded into a 196 CHRONIC MIDDLE-EAR SUPPURATION rather compact mass which can not be expelled through the aditus, and must inevitably increase in size. Such a mass has received the name of cholesteatoma. Examined under the microscope, it usually contains numerous pus germs, some cholesterin crystals, and quantities of epi- thelial cells. The outer surface usually preserves the arrangement of concentric epithelial layers, which are easily separable one from the other. The influence which cholesteatoma exerts upon the surrounding bone is one of gradual disintegration or absorption. The term absorption is in many cases more descriptive of the actual process than necrosis, since the latter destroys first the membranous lining or covering of the bone attacked. Cholesteatoma, on the other hand, may eat its way into contiguous bone, without the usual signs of suppuration, the enlarged and enlarging bone cavity retaining everywhere a well-defined epidermal covering. In such cases there may be little or no demonstrable discharge through the meatus, or there may be occasional very slight discharge consisting chiefly of the secretion from the newly-formed membrane mixed with decomposing epithe- lial cells. Such a discharge, when removed by means of a cotton-wound applicator, is usually unbearably offensive. In other cases the cholesteato- matous absorption of bone coexists, or rather alternates in different parts of the bone cavity, with the usual form of suppurative necrosis. The pus from such a lesion is often so indescribably offensive as to constitute in some degree a social barrier between the patient and his fellows. Illustrations of these two types of the disease are found in two cases operated upon by the writer. In one, a man over fifty years of age, the radical operation was performed on account of some of the more common- place symptoms of chronic middle-ear suppuration. On removing the cortex, the antrum, greatly enlarged, was found to contain a large choles- teatomatous mass, around which was a limited amount of secretion the stench of which was almost overpowering. In this case the operation was completed by the formation of a large meatal opening, and the patient made a perfect recovery. The second case was that of a strong Irish woman, a domestic, who suffered from a more or less constant discharge of so offensive a character that she found it difficult to retain any position longer than a few weeks. In this case cholesteatoma was found side by side with the usual signs of suppuration,—i.e., pus, granulation tissue, and necrotic bone in adjacent spaces. Removal of these products of dis- ease by the radical operation resulted in permanent cessation of the dis- charge. In both these cases, the evidence of progressive disintegration or absorption of bone rendered the danger of serious intracranial involve- ment, had surgical relief been withheld, very great. The serious nature of these cases depends upon a fact now fortunately recognized by all experienced otologists,—viz., that cholesteatoma con- fined in parts of the ear not accessible through the external auditory meatus, may lead to dangerous spread of the infection,—e.g., through the labyrinthine capsule, causing suppurative labyrinthitis; to the middle fossa of the skull, causing epidural or temporosphenoidal abscess; to the CHOLESTEATOMATOUS DESTRUCTION OF BONE 197 posterior fossa, giving rise to infective sinus thrombosis or more rarely to cerebellar abscess. Before leaving this phase of the pathology, it may be admissible to mention certain very exceptional cases in which the cholesteatomatous mass has caused such extensive destruction of the posterosuperior wall of the bony canal as to accomplish practically the mechanical results of a radical operation. Probably most aurists have seen one or more such cases. The writer some years ago had referred to him a patient whose aural lesion presented the following interesting features: The patient, a man of fifty years, had suffered since boyhood from occasional discharge from his right ear. Inspection revealed such extensive destruction of the posterior wall of the bony meatus that it was not difficult to remove from the antrum through the canal an epithelial mass the combined bulk of which equalled that of a chestnut. The cavity from which this mass was removed was apparently lined throughout with an epidermal covering which could easily be reached through the meatus. After removal of the growth, this patient was practically without aural symptoms up to the Fig. 115.—Bone absorption resulting from cholesteatoma: a, cholesteatomatous mass; b, remains of canal roof; c spine of Henle; d, posterior canal wall. time of his death from pneumonia some years later. Bezold was among those who recognized this condition as one reasonably insuring the patient’s safety. The accompanying picture, drawn from a specimen in the writer’s collection, illustrates very nicely a stage of the process by which this mechanical result is reached (Fig. 115). 198 CHRONIC MIDDLE-EAR SUPPURATION Symptoms and Signs.—A suppurative process which by extension may reach the labyrinth, the brain cavity, or may infect the large venous channels of the brain, may obviously be the primary cause of many varied and complex phenomena. We shall limit our remarks, however, to a brief statement of the symptoms characterizing a suppurative lesion absolutely confined to the tympanum and adjoining mastoid cells. For the sake of brevity, it may be well to state in advance, that, aside from the discharge and the physical changes observed through the aural speculum, many patients endure this lesion for years without pronounced symptoms, either systemic or subjective. While it would seem reasonable to assume that a lesion capable of maintaining a more or less constant purulent discharge might also cause considerable systemic disturbance, it is a clinical fact that constitutional symptoms are in most cases absent. This fact is so universally recognized among aurists, that the development of constitutional symptoms—e.g., fever, pulse changes, etc.—would suggest to an experienced observer either an intracranial complication or some unrelated intercurrent disease. This does not necessarily imply that a chronic suppurative otitis media may not in some cases react unfavorably upon the patient’s vitality, but simply that it rarely or never gives rise to characteristic symptoms of sepsis or of systemic disorder. The two symptoms of which these patients usually complain are the discharge and the impairment of hearing. The Discharge.—The aural discharge varies greatly in different cases of chronic middle-ear suppuration, and is of some diagnostic significance. In the first place, the discharge has in the great majority of cases a dis- tinctly offensive odor, whereas the discharge in acute purulent otitis media is usually odorless. It has been proved, however, that a mucopurulent secretion, unmixed with detritus resulting from necrotic bone or discarded epithelial elements, may be quite without odor. In certain neglected cases of chronic purulent otitis media, the exceedingly foul odor is due not so much to the tympanic changes as to the admixture with the tympanic secretion of decomposing epithelial cells from the diseased lining membrane of the bony canal. In such cases, measures applied to keeping the canal free of pus greatly modify the offensive character of the discharge. Chronic suppurative lesions characterized by deep-seated areas of bare and necrotic bone may give rise to moderate discharge of very offensive odor. In such cases, the secretion may be so limited in quantity that its odor becomes noticeable only when the aurist attempts to wipe out the tympanic cavity for purposes of examination. Finally there is a class of cases in which the foul character of the discharge may be a constant cause of discomfort and chagrin to the patient,—i.e., cases in which the aditus and antrum are filled with cholesteatomatous masses, decomposing particles of which are constantly being washed out in the aural discharge. In these cases the peculiarly offensive nature of the discharge, and the presence in it of choles- terin crystals and quantities of broken-down epithelial cells, are of con- siderable diagnostic importance in determining the character of the lesion. SYMPTOMS A YD PHYSICAL SIGNS 199 Physically the discharge may be thick or exceedingly thin; profuse or may consist merely of a few drops of viscid secretion confined to the recesses of the tympanic cavity, the presence of which may be unknown to the patient. The frequent or occasional presence of blood in the discharge points, as a rule, to the presence of polypi or exuberant, vascular granulations. Micro- scopic examination of the discharge in cases of chronic purulent otitis media practically always shows a mixed infection. Deafness.—To some extent the hearing is impaired in almost every case of chronic suppurative otitis media. The functional loss depends on two conditions,—viz. (a) the partial or complete destruction of the mem- brana tensa and elimination of the malleus and incus from the function ol sound transmission; and (b) hyperplastic changes in the region of the oval window interfering with the mobility of the stapes. Fortunately, complete loss of the drum membrane and also of the malleus and incus is by no means inconsistent with very good hearing,—i.e., impairment so slight as to interfere but little or not at all with the patient’s enjoyment of life. On the other hand, the formation of organized fibrous bands binding the crura of the stapes to the niche of the oval window may cause very dis- abling deafness. It is not always possible to determine the presence or extent of these hyperplastic changes by inspection alone. Thus, in two cases with extensive destruction of the membrana tensa and practical disarticulation of the ossicular chain by necrosis of the long arm of the incus, one patient may exhibit remarkable acuteness of hearing while the other may be exceedingly deaf. In each case the niche of the oval window may be filled with granulation tissue almost or quite hiding the stapes. In such contrasting cases, labyrinthine disease being excluded, we can explain the deafness of one patient as compared with the auditory acuteness of the other only by assuming that with the former fibrous adhesions between the stapes and the oval niche or window have taken place, while in the case of the latter the stapes is surrounded and covered by a mass of unorganized granulation tissue which acts vicariously with the stapes in the collection and transmission of sound waves from without. This hypothesis receives support from the numerous cases of chronic suppurative otitis media with retention of good hearing in which the hearing power has failed after spon- taneous recovery and epidermization of the inner wall of the tympanum. It is worthy of note that the deafness due to fibrous ankylosis of the stapes resulting from chronic middle-ear suppuration is regarded by Polit- zer as the type of deafness most amenable to treatment by surgical means, —i.e., by division of adhesive bands passing between the head and crura of the stapes and the walls of the oval niche. The impairment of hearing in these cases is of the type generally characterizing lesions of the sound-conducting mechanism. In those cases showing large perforations or practical destruction of the membrana tensa, the perception of the lower musical tones is always very considerably reduced. This is in accordance with the investigations of Helmholtz, cor- roborated by Bezold and others, which showed that the drum membrane is 200 CHRONIC MIDDLE-EAR SUPPURATION particularly essential to the transmission of low musical tones. The middle and upper register may on the other hand be heard with apparently normal acuteness. In testing cases in which the sound waves were transmitted wholly by the stapes acting alone, the writer has met with a few instances in which there seemed to be some hyperacusis for the very high tones of the scale,—e.g., the whistle. Hearing by bone conduction is regularly increased. Physical Signs.—On attempting to inspect the ear by reflected light, the depths of the canal—i.e., drum membrane or exposed inner wall of the tympanum—may be hidden from view by inflammatory products filling the auditory meatus. The canal may contain pus, detritus formed of pus mixed with exfoliated and decomposing epithelium, or may be occupied by a polyp partially or completely obstructing its lumen. The pus and epi- thelial debris are, of course, easily removed by the syringe or may be wiped out by means of a cotton-wound applicator. The removal of an aural polyp is not so simple a matter. Large aural polypi—i.e., polypi which nearly or completely fill the canal—are usually easily recognized at a glance. On the other hand, a small polyp, occupying the tympanic space or confined to the inner ex- tremity of the bony meatus, may be somewhat puzzling to the student or beginner: he may find some difficulty in determining whether such a growth is a polyp, a swollen inner tympanic wall, or a bulging and raw, or denuded, drum membrane. Diagnosis.—An aural polyp, large or small, presents the following physical characteristics: (1) It usually appears, as in most cases it is, nearer the orifice of the meatus, and therefore nearer the eye of the exam- iner, than either the bulging drum or the swollen tympanic mucosa. (2) It presents a raw and granular surface, usually easily distinguishable from the denuded drum membrane on the one hand and the swollen but intact tympanic mucosa on the other. (3) It is comparatively insensitive to palpation by the tympanic probe, provided the probe does not touch the canal wall, whereas the drum membrane and tympanic mucosa are ex- tremely sensitive to pressure. (4) It is usually freely movable in the canal. (5) The probe, carried beyond the polyp, may be passed in all directions around it, except where it is attached to the wall of the bony meatus or to the tympanic ring, at which point the probe will be arrested. If the polyp is attached to some point on the inner wall of the atrium,the prom- ontory (rare),—the probe will pass completely around it in either direc- tion. In these manipulations great care must be observed to avoid bruising the polyp, or free hemorrhage is likely to occur, making further examina- tion for the time being difficult or impossible. The question of removing the polypi through the canal, either for therapeutic purposes or to facilitate further examination, will be spoken of in connection with the treatment of chronic middle-ear suppuration. The auditory canal being free of pus or other foreign matter, one is able to determine the position and size of the perforation. Only rarely is the drum membrane completely destroyed, the tough peripheral edge CENTRAL PERFORATIONS OF DRUM MEMBRANE 201 (annulus tendinosus) being very resistant to suppurative disintegration. The majority of perforations are central apertures confined to the mem- brana tensa. They occur most frequently in the posterior segment (Figs. 116 and 117), but are also found in the anterior segment (Fig. 118). With large perforations of the anterior segment, the posterior margin, drawn inward by the hammer handle, is often adherent at the level of the umbo to the promontory (Fig. 119). Perforations involving both anterior and Fig. 116. Fig. 117. Fig. 118. Fig. 119. Fig. 120. Fig. 121. Fig. 122. Central perforations. Fig. 123. Fig. 124. posterior segments are not uncommon, and are seen chiefly in three forms, apparently representing different stages of the destructive process: viz., (a) the kidney-shaped perforation confined to the lower part of the mem- brana tensa (Fig. 120); (b) the horseshoe-shaped perforation involving large central portions of both anterior and posterior segments, the manu- brium mallei remaining approximately intact (Fig. 121); and (c) the large irregularly heart-shaped perforation which is so often seen in cases of long- standing suppuration in which the hammer handle has been to a great 202 CHRONIC MIDDLE-EAR SUPPURATION extent destroyed by the necrotic process (Fig. 122). All of the above examples fall under the head of central perforation when the peripheral edge is not at any point destroyed. There is usually no great difficulty in mapping out the boundaries or limits of a central perforation so long as the surrounding surface of drum membrane is covered by normal or at least recognizable epidermis. The margins of a perforation of long standing are commonly thickened and easily distinguishable from the tympanic surface beyond. A condition which is sometimes difficult to interpret correctly is found in cases in which the membrana tensa is not only perforated but also denuded of its epidermal covering, its outer surface being everywhere covered with fine granulations. When with this condition the mucosa covering the inner tympanic wall is swollen, granular, and crowded against the margins of the perforation, even the most experienced aurist may be unable to gauge correctly the extent of the injury until the remaining portion of the drum membrane has been restored by treatment to an approximately normal condition (Fig. 123). The inner tympanic wall seen beyond the margins of a large central perforation may have the appearance of fairly normal mucous membrane, or may be so swollen that the normal elevations and depressions are to a great extent obliterated. Or, again, the mucosa may for the most part be replaced by granulation tissue (Fig. 124). In some cases the lining membrane appears as a grayish-white, com- paratively dry membrane having some resemblance to the skin of the canal. This change in the tympanic lining is brought about in part bjr the in- growth through the perforation of the epidermal covering of the drum- head, and in part also by the action of the air upon the tympanic mucosa after the suppurative process as such has run its course. By this process, which is usually spoken of as epidermization, spontaneous recovery is brought about in certain cases. Marginal Perforations.—It is clear that any central perforation, by extension of the destructive process, may be converted into a marginal perforation. The commonest and most characteristic marginal perfora- tions are those in which the peripheral edge of the upper posterior segment of the membrana tensa and the adjacent part of Shrapnell’s membrane are destroyed, leaving bare the bony ring to which they were attached (Fig. 125). In the majority of such cases, according to my experience, the adjacent portion of the bony frame is also diseased and very fre- quently to some extent destroyed. Thus, through a marginal perforation including and extending somewhat behind Shrapnell’s membrane, one is occasionally able to see a considerable portion of the head of the malleus and body of the incus. This invariably indicates destruction of the inner, or tympanic, margin of the roof of the bony meatus (Fig. 126). With marginal, as with central, perforations, the landmarks of the tympanum may be completely hidden by granulation tissue or polypi (Fig. 127). In marginal perforations exposing the normal structures of the vault,— PEBFORATIONS OF SHRAPNELL’S MEMBRANE 203 e.g., head of malleus or body of incus, or both,—these bones and the ex- posed tympanic cavity are seen in some cases to be covered by a white and apparently dry skin-like membrane. This condition has a different surgical significance according to the presence or absence of discharge. If there is, and for a considerable period has been, complete absence of discharge, it may represent the final stage of local resolution by the conversion of the vault recesses into dry skin-covered cavities (Fig. 128). On the other hand, a constant or even occa- sional flow of offensive pus from the aditus may be due to a cholesteatomatous collection within the antrum constituting a constant menace to life through .its possible invasion of the labyrinth or intracranial cavity. Perforations of Shrap7ielVs Membrane.—These little perforations seem pathologically and clini- cally to constitute a class by themselves. They Fig. 129. Fig. 130. Fig. 125. Fig. 126. Fig. 127. Fio. 128. Fig. 131. Marginal perforations. Perforations of Shrapnell’s membrane. are seen chiefly in three situations,—viz., immediately above the short process of the malleus (Fig. 129), above and a little in front of the short process (Fig. 130), and perforations extending backward through the posterior stria of Prussak (Fig. 131). While comparatively uncommon, a considerable number of these minute perforations can be seen during the year in any large aural clinic. The membrana tensa may be intact and apparently normal. Discharge from the vault may be fairly abundant, exceedingly slight, or wholly absent. Discharge being absent, there may 204 CHRONIC MIDDLE-EAR SUPPURATION be a history of past tympanic suppuration. Quite frequently no such history is obtainable. The exact pathogenesis of this condition has been, and still is, a sub- ject of controversy. The statement of Dench1 that “a perforation above the short process always means intratympanic caries, and usually indicates that the malleus is affected,” is incorrect and might lead to surgical error. The ossicles may be, and in some cases certainly are, necrotic, but in many cases observed by the writer they were not. Two facts must be taken into account in any attempt to determine the origin of these perforations, viz., (1) that they rarely occur during an acute middle-ear suppuration, and (2) their frequent presence in individuals whose ears present no evidences of tympanic suppuration either past or present. Bezold stated that he had looked diligently for years for such a per- foration occurring during acute suppurative otitis media, but had never seen one. He connected their origin etiologically with chronic obstruc- tive lesions of the Eustachian tube, as a result of which Shrapnell’s mem- brane is first retracted, then becomes markedly atrophic, and finally breaks down. This theory seems in part to have been held by Hartmann (quoted by Politzer), who stated that he had repeatedly observed the coincidence of a perforation of Shrapnell’s membrane and a membrana tensa intact but retracted and adherent to the inner tympanic wall. Politzer states that he has more than once seen the development of a perforation in Shrapnell’s membrane during chronic middle-ear catarrh. His theory is that the membrana flaccida is first drawn into the depres- sion above the processus brevis, where it subsequently breaks down under the influence of compression by epithelial masses, there accumulating from the skin of the auditory canal. One of the most interesting contributions to the study of these minute perforations is found in a paper by Professor Schmiegelow,2 published as far back as 1891. In it he described the physical changes in certain cases of acute suppurative otitis media in which a perforation of Shrapnell’s membrane provided the only pathway for the escape of pus. Two of these cases recovered promptly under rational treatment, leaving, however, the perforation of Shrapnell’s membrane as a permanent result. There is obviously no reason why such a perforation should be regarded as pointing to ossicular necrosis. There are of course cases in which perforations of the membrana flaccida are clearly associated with ossicular necrosis. Returning to the symptoms of chronic middle-ear suppuration, we must repeat the statement that, aside from the discharge, the impair- ment of hearing, and the physical changes in the ear itself, these patients are often practically without symptoms. Pain is not usually present in chronic suppurative otitis media, except as betokening one or other of the following conditions,—viz., (a) retention 1 Dench: Diseases of the Ear, p. 399. 2 Schmiegelow: Perforations of the Membrana Flaccida Shrapnelli, Arch, of Otology, vol. xx, No. 3, pp. 228-256. INTRACRANIAL COMPLICATIONS 205 of pus somewhere within the tympanic vault, aditus, or antrum; or (b) acute exacerbations of inflammation, usually involving the mastoid cells. As a rule, pus under pressure quickly finds a pathway of escape, with prompt relief of pain. Many cases exhibit periodic variations in the amount of discharge, these changes being influenced by changes in the weather and other con- ditions causing nasopharyngeal congestion or inflammation. Acute exacerbations, accompanied by mastoid tenderness, are always to be regarded seriously in cases of long-standing middle-ear suppuration, for the reason that an acute inflammatory process confined within bone spaces, which may have been the seat of extensive previous disease, may naturally be separated only by thin barriers from vitally important intra- cranial structures. The course of the disease is very slowly progressive, and seems in many cases to be in some degree self-limited. That is to say, either by the pro- cess of osteosclerosis (eburnation) or by the formation of resisting walls of granulation tissue, the disease is in many cases confined during the major part of the patient’s life to the antrotympanic cavity. This fact should be considered in its relation to the necessity for operative intervention. It does not, however, relieve the patient of the possibility of intracranial complication, which may ultimately occur in any case of chronic purulent otitis media. Complications.—The complications of chronic purulent otitis media may be mentioned in the following order: (a) Suppurative labyrinthitis, usually diffuse, rarely remaining cir- cumscribed. (b) Cerebellar abscess, infection very frequently by way of the labyrinth. (c) Cerebral abscess. (d) Meningitis, most often accompanying some suppurative lesion of the brain. (e) Infection of the sigmoid (lateral) sinus. There is no longer any doubt, that, in a very large percentage of cases of intracranial disease of otitic origin, the infection of the brain or men- inges is secondary to suppurative labyrinthitis. That this relation has not been more commonly recognized is due to the fact that the phenomena of labyrinthine disease have only recently received adequate recognition. Undoubtedly many cases of intracranial suppuration have been operated upon, and ended fatally, without any suspicion on the part of the medical attendants of a pre-existing suppurative labyrinthitis. Treatment.—The treatment of chronic purulent otitis media con- sists essentially of local treatment of the various morbid changes present, and in no disease do the physical changes vary so widely. Polypi, if present, must be removed, either through the canal or by radical opera- tion; ossicles, if to a certain extent diseased, must be removed; cholestea- toma must be dealt with radically. The ear should be irrigated in some cases, whereas in others irrigation is contra-indicated. Finally, there are certain cases which, in the author’s opinion, call for little treatment other 206 CHRONIC MIDDLE-EAR SUPPURATION than certain simple measures for cleansing the ear, in which the patient should be instructed. Obviously no routine method of treatment can properly be described for this disease. For example, routine irrigation of the ears with antiseptic solutions does not assure surgical cleanliness and rarely results in recovery. Clearly we must classify our cases before we can suggest rational lines of treatment. I. Let us consider first, the simplest form of the disease,—viz., a case of comparatively short duration,—i.e., not over one or two years,—and presenting the following conditions: central perforation of small or medium size which refuses to heal; discharge persistent but moderate in amount and free from the offensive odor characteristic of bone necrosis. Such a lesion falls under the head of chronic purulent otitis media when it has passed the stage in which spontaneous recovery may be hoped for. In searching for the chief obstacle to local recovery in a case of this character, we may find it in one or other of the following conditions: (a) In the first place, the mere presence of a small perforation subjects the middle ear to constant reinfection from the nasopharynx. With an intact drum membrane, occasional condensation of the air in the nasopharynx does not affect the tympanum further than to produce temporary increase of intratympanic pressure. With a perforation, on the other hand, every such condensation, as when the patient sneezes or blows his nose, carries a stream of air, impregnated with the impurities of the nasopharynx, through the tympanum, (b) The epidermal covering of the drum mem- brane may have extended over the edges of the perforation, rendering its closure by cicatricial tissue no longer possible; and (c) the lower part of the tympanic cavity may contain residual pus which the perforation by reason of its position can not drain. Routine irrigation with any solution is without value in such cases, and not infrequently is distinctly injurious. Bone disease being excluded by the character of the discharge, the treatment should aim at protection of the tympanum by closure of the perforation. As an initial measure, the canal should be wiped free of pus and dried. The nose and nasopharynx should be sprayed with some mild cleansing solution, the ear carefully inflated per catheter, and the drum membrane reinspected. Ordinarily a certain amount of pus or mucus will have been blown out into the canal, giving some idea of the condition of the lower (hypotympanic) space. The canal and drum membrane are again wiped out, swabbed with alcohol, and the canal lightly packed with a wick of sterile gauze. This is to remain in the canal until the patient is seen by the aurist on the following day. This treatment should be repeated for several consecutive days, when we shall have gained fairly accurate knowledge of the tympanic condition. If the discharge is veiy slight, so that the canal and wick are found practically clean at the daily dressing, we may proceed at once in our efforts to close the perforation. If, on the other hand, a considerable amount of secretion is discharged daily, it may be necessary to obtain better drainage by a free incision through the membrana tensa, after which the wick treatment is continued as before. TREATMENT 207 When the discharge is reduced to a minimum, it may be found that the perforation is gradually closing under the stimulation of the daily cleansing and inflation. If no tendency to closure is observed, it may be that this is prevented by epidermization of the edges of the perforation. To correct this the edge of the perforation should be very lightly cauter- ized. For this purpose trichloracetic acid is the best agent. It is applied in the following way: The drum membrane is cleansed and thoroughly dried. A fine-pointed cotton applicator is tightly wound with a minute amount of absorbent cotton, which is dipped in sterile water, the excess of which is removed by sterile gauze. The cotton-wound end of the applicator is then plunged into a bottle containing crystals of trichloracetic acid, and rotated several times. Any adherent crystals are removed. Under inspec- tion by reflected light, the edges of the perforation are very lightly touched with the applicator. The influence of the acid is seen at once in slight whitening of the edges. The perforation may then be closed by a disk of paper prepared as follows: A disk of thin paper is cut of a size to extend slightly beyond the edges of the perforation; this is soaked in 95 per cent, alcohol, and then carried to its position covering the perforation by means of tympanic forceps or on the point of a cotton-wound applicator. Such a disk, if properly applied, adheres closely to the drum membrane. If no inflammatory reaction results, it should be allowed to remain in position until carried outward to the canal wall by the outward growth of epidermis covering the membrana tensa. Quite frequently the perforation will be found greatly reduced in size or may be closed. This, by protecting the tympanic mucosa, may end the lesion as a suppurative process. In some cases this treatment may have to be repeated several times before the perforation is closed. In still other cases it may be impossible to obtain complete closure of the perforation, the dry, cleansing treatment resulting, however, in cessation of discharge. While a perforation per- sists, however, the patient remains subject to recurrences through infec- tion from without, or from the air current from the nasopharynx. II. Large Central Perforations without Polypi or Excessive Production of Granulation Tissue.—It will be remembered that a central perforation may mean destruction of the entire membrana tensa with the exception of the marginal or peripheral edge (annulus tendinosus). In this condition restoration of the drum membrane is no longer possible. Under this head I wish to refer briefly to a class of cases with which all aurists are probably familiar, but which have, as a rule, received scant attention in otological literature. The physical picture is somewhat as follows: There is extensive destruction of the membrana tensa and fre- quently also of the hammer handle, the remnant of which may be adherent to the promontory. The tympanic walls are covered with mucous mem- brane or a layer of firm granulation tissue which does not disguise the landmarks of the inner tympanic wall,—e.g., promontory, niche of round window, etc. (Figs. 117 and 122). Rough, denuded bone is nowhere demonstrable either by inspection or by the tympanic probe. The dis- 208 CHRONIC MIDDLE-EAR SUPPURATION charge or tympanic secretion may be slight, or may appear abundant simply as a result of neglect. In the latter case rational cleansing treat- ment soon reduces its amount. There are no evidences of labyrinthine involvement. Hearing tests may demonstrate a very fair degree of hear- ing power, the patient being at no disadvantage in communicating with his fellows; or the hearing may of course show considerable impairment. How shall we interpret this condition for ourselves and to our patients? Personally I believe that it in many cases represents a suppurative process which has run its course, or at least has become stationary, having erected its own barriers, either in the condensation of the bone itself, or in the production of firm granulation tissue between the focus of disease and surrounding structures. So long as the tympanum is lined by mucous membrane or granula- tion tissue, there must of necessity be some secretion or discharge, though this may be very limited in amount. This discharge can be absolutely terminated only by converting the tympanic spaces into skin-lined cavi- ties. But we can not be sure that such epidermization may not result in very considerable reduction of the patient’s hearing power. Every aurist knows of cases in which this has occurred. The point I wish to make is this: We should not be slaves to the dogma, too often repeated in otological literature, that aural discharge is neces- sarily of itself a danger signal, or one which when persistent calls for operative intervention. If we can satisfy ourselves that the discharge is simply the logical product of exposed mucous membrane or healthy granulation tissue, and that there is no evidence of an active suppurative process involving the bone itself, we should not be too ready to interfere with nature’s method of conservation. Treatment.—In my experience, the condition just described is not, as a rule, improved by routine, frequent irrigations. If when first seen the canal and tympanum show the result of neglect in residual pus,—usually very offensive in odor,—this should be removed by means of sterile cotton on applicators. The canal should next be filled with hydrogen peroxide, which should be allowed to remain at least five minutes. The ear is then syringed with a warm solution of boric acid, after which the canal is filled with 95 per cent, alcohol, which in turn is allowed to remain a few minutes. The alcohol, itself an efficient cleansing agent, by its quick evaporation leaves the canal comparatively dry. Finally the canal and tympanum are “dusted” with boric-acid powder, introduced by a powder-blower. The canal is lightly filled with sterile gauze or the concha filled with sterile cotton. The patient is instructed to return at regular stated intervals for observation, at first on consecutive days. This treatment has the un- doubted advantage of reducing the amount of the discharge. When, finally, the physician has through careful treatment reduced the amount of discharge to a minimum, the patient should be instructed in keeping the ear clean. Many cases do well on the following routine treatment: Regularly once a week, the patient is to cleanse the ear by the TREATMENT 209 method first described,—using first hydrogen peroxide, then thorough boric-acid irrigation, and lastly alcohol. Following this the ear is to be dried with sterile absorbent cotton. While out of doors, the ear should be protected by a bit of sterile cotton in the concha, but not introduced into the meatus. Once daily, preferably at night, the meatus should be filled with an alcoholic solution of boric acid (gr. xx ad Sj), which is retained in the ear a few moments only. If the alcohol causes severe “burning,” it may be diluted with sterile water, half and half. Under this treatment many patients suffer little or no discomfort, and the lesion remains qui- escent or its character may finally be changed by epidermization of the tympanic cavity. In some cases the frequency of the irrigations may be reduced to once in ten days; in others its repetition every three or four days may be required. It should, however, be repeated no oftener than is necessary to free the canal and hypotympanic space of residual pus. It is, of course, not claimed that the treatment above outlined 'will prove successful in every case presenting the physical characteristics described. There are some cases, for example, in which the discharge, whether it be scant or profuse, is perpetuated by a diseased condition at the tympanic mouth of the Eustachian tube. The tubal lesion may con- sist of an area of superficial osseous necrosis easily within the reach of a Fig. 132.—Yankauer’s Eustachian curette. curette through the meatus; or, again, one aspect of the tube may be denuded of its mucous lining while a persistent mucosa of the opposite wall prevents the fibrous closure of the tube which is the first step toward permanent cessation of the discharge. When it can be determined that the principal seat of disease is located here, thorough curettage of the tubal region may bring about a cure. The purpose should be not only to remove any small focus of necrotic bone, but absolutely to remove the mucosa from that portion of the canal curetted. Possibly the best method of accomplishing this end may be that proposed by Yankauer. This proced- ure is carried out by means of a specially devised curette in the following way: The tympanic cavity, including both atrium and vault, is very care- fully cleansed. The Eustachian canal is cocainized by means of a 10 per cent, solution of cocaine, carried through the tube first by a cotton-wound applicator and then introduced through the Eustachian catheter. The tympanum and pharyngeal end of the tube are also cocainized. The Eustachian curette (Fig. 132) presents a shaft so curved that it may be introduced through the meatus and tympanum into the tube as far as the isthmus or slightly beyond. The cutting part consists of a terminal disk attached centrally to the end of the shaft. When carried to its position in the tube at or just beyond the isthmus, the shaft is rotated slightly back and forth so that a circular cut through the mucous membrane, is 210 CHRONIC MIDDLE-EAR SUPPURATION made. When the surgeon is satisfied that the mucosa is completely di- vided throughout the entire circumference of the canal, the instrument is sharply withdrawn, separating the mucosa from the bony canal, and in some cases bringing it out inverted into the tympanum. This in favorable cases induces the formation of healthy granulations and subsequent per- manent closure of the tube. When this result is obtained, discharge from the tube naturally ceases, and the tym- panum is no longer subjected to this source of reinfection. III. Aural Polypi and Granulations (Fig. 133).—Polypi occluding the audi- tory canal interfere not only with drain- age but also with any plan of treatment. Polypi must therefore be removed either through the canal or by more radical operation. The first step is the deter- mination of the point of attachment by means of the probe. Most polypi are attached to the tym- panic ring, the posterior wall of the bony meatus, or spring from some point in the aditus. In these situations, they can usually be removed either in part or whole by means of the snare or a sharp ring curette, the latter instrument be- ing carried beyond the polyp and pressed against the bone surface to which the pedicle is attached. Unfortunately, such removal is very often followed by rapid re-formation of the growth. As a comparatively rare condition, polypi of considerable size have been found depending from the edges of a small perforation in the drum membrane. In such a case, the careful use of the probe detects the sur- rounding membrana tensa. Removal of the polyp in such a case has re- sulted in a cure (Bezold). Polypi springing from the promontory or other part of the inner tym- panic wall are rare as compared with the marginal attachments above referred to, and also represent a more serious condition. It must be remembered that the appearance of a polyp springing from any bone surface invariably represents nature’s effort to limit a necrotic process at that point. The attempt to remove a polyp springing from the promon- tory or the region of the oval window through the external auditory canal may be mechanically successful, but may too easily give rise to a laby- rinthine fistula, and consequent suppurative labyrinthitis, to appeal to me as good surgery. I am inclined, therefore, to regard polypi attached to the inner tympanic wall—the labyrinth itself having escaped invasion— as valid and sufficient grounds for performing a radical operation. Fig. 133.—Aural polyp. TREATMENT 211 Polypi not being present, or having been removed, the landmarks of the tympanum may be obscured or hidden by exuberant granulations (Fig. 124). This condition may be largely the result of neglect, the probe finding everywhere beneath the granulations a firm bed of healthy tissue, or, in other words, an absence of bare, necrotic bone. In this case, careful cleansing treatment, with occasional judicious use of astringents,—e.g., nitrate of silver, preferably in the form of a bead fused upon the end of an applicator,—may soon bring about a healthier condition. I have seen cases, in which the granulations were apparently exuberant and the dis- charge exceedingly offensive, show marked and quick improvement as a result of the following plan of treatment: The ear having been cleansed by the usual method and dried, boric-acid powder in considerable quantity is introduced into the tympanum, not by a powder-blower, but by means of a spatula. With a probe or other blunt instrument, the powder is well distributed over the tympanic surface, a central space being made for a sterile gauze wick. The wick is packed rather firmly in the tympanic cavity and loosely in the meatus. It is a mistake to believe that boric acid thus used may act as a dangerous obstruction to the flow of pus. Some of the powder is apparently always absorbed, and pus escapes through or around the remainder and is taken up by the gauze wick. The action of boric-acid powder thus directly applied is usually to cleanse and deodorize the cavity of the tympanum, and also in many cases to cause noticeable shrinkage of the granulations. In other words, it is both dis- infectant and astringent. In other cases the probe quickly reveals a lesion of different character, —passing without sense of resistance through the granulations to bare, necrotic bone. In this condition I can see no safe method of treatment short of a radical operation. IV. Marginal Perforations.—In the great majority of cases marginal perforations are accompanied by evidences of bone necrosis. Nearly always the contiguous portion of the tympanic ring is diseased, and the tympanic end of the roof of the bony meatus is occasionally eroded to a very considerable extent. In the latter instance the tympanic vault may be open to inspection, and the head of the malleus or body of the incus brought into plain view (Fig. 126). When the posterosuperior canal wall is to a considerable degree destroyed, we are frequently able to introduce a bent tympanic probe backward and slightly upward into the aditus and antrum. This condition, while giving evidence of the destructive power of the lesion, frequently adds to the patient’s safety by providing free drainage from the antrum and upper mastoid cells. Another frequent site of osseous necrosis is found in the ossicular chain. Almost invariably with large marginal perforations involving both membrana tensa and mem- brana flaccida, the malleus and incus will be found diseased. They may be completely destroyed. The incus, from its position in relation to the aditus and antrum and from its poorer blood supply, is the most frequent victim of the necrotic process, the malleus coming next. The stapes, by 212 CHRONIC MIDDLE-EAR SUPPURATION some fortunate provision of nature,—probably its abundant blood supply through the annular ligament,—is only rarely involved. The writer recalls at least three cases, however, upon which he performed a radical operation, in which no vestige of any ossicle, malleus, incus, or stapes, was present. In two of the three cases the labyrinth was involved in the suppurative process; in one the labyrinth was not involved. The treatment indicated varies somewhat in accordance with the fol- lowing conditions,—viz., (A) The presence of bare necrotic bone, (B) evidence of pus retention in the vault, (C) necrosis of the head of the malleus and body of the incus, and (D) recurring polypi or exuberant granulations in the aditus and vault. A. Osseous necrosis is evidenced in some cases by the constant recur- rence of exuberant granulations at some point, in others merely by the presence of bare rough bone. The significance of an area of necrotic bone as a surgical indication varies with the region involved. Thus, in surface necrosis of the promontory or region of the oval window, the danger of labyrinthine fistula and suppurative labyrinthitis calls for surgical intervention. On the other hand, a large marginal perforation involving both membrana tensa and Shrapnell’s membrane, and causing destruc- tion of the upper posterior segment of the bony ring, may, by providing free drainage from the vault, aditus, and antrum, render the condition much less dangerous (Fig. 134). When with this condition the promontory is not diseased, and the antro attic cavity is not occluded by polypi, a bent probe passing without resistance backward and upward into the aditus and antrum, it is usually possible to cleanse the whole antrotym- panic cavity by the measures already advocated in the treatment of large central perforations. Such a case—particularly if functional tests dem- onstrate fairly good hearing power—should, in my opinion, be subjected to careful and rather prolonged cleansing treatment before a radical- opera- tion is decided upon. B. Another variety of the lesion, by no means uncommon, is one in which, with extensive destruction of the membrana tensa below the pos- terior fold, that portion above the posterior fold and also Shrapnell’s membrane remain intact. The lower margin of this remnant of membrane, being more or less indrawn and adherent to contiguous structures, gives rise to occasional pus retention within the vault (Fig. 135). These patients suffer from periodic attacks of earache,—during which antrum tenderness is usually demonstrable,—these acute symptoms being usually relieved only after a free flow of pus from the vault is re-established. I believe that this'is one of the most dangerous forms of the disease. An incision through the bulging remnant of membrane, the knife being carried upward into the vault, relieves the pain of the acute attack, but does not provide against recurrences. When operated upon radically, the aditus and antrum, and frequently the mastoid cells, are found to be extensively diseased. In the writer’s opinion, these cases represent the type of lesion in which extension of the suppurative process to intracranial TREATMENT 213 structures is most likely ultimately to occur. The safest treatment lies, therefore, in surgical intervention,—i.e., the radical operation. C. Necrosis of the Malleus and Incus.—Necrosis of the bodies of the malleus and incus is usually accompanied by the presence of surrounding polypi or exuberant granulations. The ossicles themselves may, there- fore, be hidden from view, even when the attic is exposed by erosion of the tympanic end of the roof of the bony meatus. The ossicles may be only slightly eroded or may be to a very great extent destroyed. In this con- dition granulations springing from the diseased ossicles, and also from the adjacent walls of the attic and aditus, may interfere very seriously with drainage of pus from the antrum (Fig. 136). Fia. 134. Fia. 135. Fig. 136. Perforations of long standing Fig. 137. D. A somewhat kindred condition is that in which, evidences of ossic- ular necrosis being absent, the vault is filled with unhealthy granulations, apparently springing from the walls of the aditus (Fig. 137). The treatment of these conditions by any means short of surgical intervention requires patience and carries with it prolonged uncertainty as to whether an operation will not in the end become necessary. When the disease is perpetuated chiefly by ossicular necrosis, the logical means of relief would seem to be surgical,—i.e., either the removal of the ossicles through the auditory canal, or the more complete removal of all diseased structures by the radical operation. The relative value of these opera- tions will be referred to later. When the chief obstacle to drainage is found in polypi or exuberant granulations springing from the walls of the aditus, and a large marginal 214 CHRONIC MIDDLE-EAR SUPPURATION perforation brings this region into the practical reach of instruments, an attempt may be made to remove them through the canal, though I believe it is better surgery, and will prove in the majority of cases to the advantage of the patient, to proceed at once to the radical operation. Technic.—To begin with, the ear should be irrigated with bichloride of mercury solution (1 in 4000) , and dried. A gauze wick, saturated with 10 per cent, solution of cocaine, should be packed rather tightly against, and if practicable behind, the granulations and allowed to remain some ten minutes. We may then try to remove the granulations with a sharp curette. The ring of the curette should be carried in front of and beyond the granulations, and an effort made to remove them with one stroke of the instrument. With the cutting edge directed backward and outward against the inner surface of the tympanic ring, no damage can be done, whereas pressure of instruments inward against the inner tympanic wall is fraught with dangers outweighing in importance the advantages to be gained. Even after the use of cocaine, the first stroke of the curette is usually followed by free hemorrhage, interfering with the further exact use of instruments,—unless much time be allowed for repeated application of adrenalin, cocaine, etc. Enough may be removed, however, to provide drainage of the attic and spaces behind. Following this curettage, the wound is again irrigated, dried, and lightly packed with sterile gauze. For some days thereafter the patient should be seen daily. One of the best dressings in these cases is by a fairly thick covering of boric-acid powder, against which a wick of sterile gauze is lightly packed. This dressing should at first be changed daily, the ear being cleansed and dried each day before the wick is replaced. Under this treatment the tympanic condi- tion may change markedly and fairly rapidly for the better. When finally the use of wicks is discontinued, we should adopt as nearly as possible a dry method of treatment, frequent irrigation with warm solutions unques- tionably favoring the re-formation of redundant granulations. Should the granulations re-form within the aditus, it will usually be better to resort to the radical operation. V. Perforations of Shrapnell’s Membrane.—Perforations confined to Shrapnell’s membrane may for practical purposes be divided into two classes, viz., (1) those associated with a suppurative process within Prus- sak’s space, the tympanic vault, or even in the aditus or antrum beyond; and (2) those in which all signs of tympanic suppuration are absent. The writer personally believes that these small perforations without any evi- dences of present suppuration represent in many cases the result of a past infection of one of the membranous spaces of the vault; and further that such lesions, if circumscribed, may be credited with a certain tendency toward spontaneous resolution. This hypothesis seems justified by the number of such cases (Figs. 129, 130 and 131) in which, with a history of acute tympanic disease long since ended, discharge is absent or negligible, and the hearing but little or not at all impaired. These little perforations are in many cases so inconspicuous as to be easily overlooked unless systematic search is made for them. TREATMENT OF ATTIC SUPPURATION 215 When the discharge is continuous and profuse, one may be obliged to infer that the attic, and probably also the aditus and antrum beyond, are involved in the suppurative process. Treatment.—When the hearing is good and the discharge very slight, I am inclined to let these ears very much alone. Occasional irrigation by the physician himself by means of the attic syringe or cannula may be of value. I believe that this should be repeated only when there is evidence of pus collection behind the perforation. The use of alcohol, or alcoholic solution of boric acid, the canal being partly filled therewith once or twice daily, is of distinct value in some cases. When the discharge is so profuse as to constitute a proof of extensive suppurative involvement of the vault, surgical intervention may be called for. In this condition, I am inclined to believe that a radical operation is in many cases not indicated, and that a rational procedure, and one which does not endanger the hearing power, is by a simple mastoidectomy, the aditus being very carefully and thoroughly cleared of granulations and diseased bone. The aditus should be kept open until all evidences of attic suppuration have disappeared. I have used this method in a few cases of long-standing attic suppuration with very good results. Obviously there will be cases in which this operation will fail on account of necrotic changes requiring more radical treatment than a simple mas- toidectomy makes possible. When the simpler operation proves success- ful, the gain to the patient in the saving of drum membrane and ossicles and the preservation of function is very great. For this reason, the simpler operation is not only justified, but, in my opinion, indicated in cases in which it offers fair promise of success. The patient, however, should be fore- warned as to the possible necessity of later recourse to the radical operation. Cholesteatoma.—The presence of cholesteatoma within the antrum can not always be determined. In some cases, howrever, characteristic masses may be seen projecting into the vault from the aditus, and in others their presence may be inferred from the persistently offensive character of the discharge or the occasional presence therein of characteristic epithelial elements. Systematic examination of the discharge under the microscope for cholesterin crystals and broken-down epithelial cells would probably indicate its presence in many unsuspected cases. The treatment of cases in which the presence of cholesteatoma can be determined may be summed up in three words,—the radical operation. Such a growth, from its power of causing osseous disintegration or absorp- tion in any or all directions, constitutes a condition in which the patient is constantly exposed to the danger of intracranial infection. The operation in these cases should provide for an enlarged meatal opening through which all parts of the tympanomastoid cavity can be reached, and subse- quent cholesteatomatous collections prevented. Operative Indications.—From a descriptive view-point it is clear that “chronic purulent otitis media” is an elastic term covering a variety of conditions. While some of these constitute a positive menace to the life 216 CHRONIC MIDDLE-EAR SUPPURATION of the patient, in others the danger of intracranial invasion is exceedingly remote. The responsibility of the surgeon in the matter of his advice to the patient is, therefore, not small. If his duty in some cases is to state posi- tively his belief that the patient/s safety demands surgical intervention, there are others in which it is no less his duty to state with equal frank- ness his belief that operation is not required, and this without emphasis upon remote eventualities which the patient is not likely to experience. In this connection I am reminded of a remark of Professor Korner of Rostock, in watching whose work I had the privilege of spending a very instructive week some years ago. Upon my expressing the hope that I might see him perform a radical operation, he said: “Well, wre may have to wait for the proper case. There are so many cases of chronic purulent otitis media, but so few in which the radical operation is really indicated.” The radical operation is an attempt at once to remove all diseased bone and to provide absolutely free drainage of all infected recesses of the antro- tympanic cavity by way of the external auditory meatus.3 Many attempts have been made to formulate the indications for this procedure, resulting in some cases in lists of considerable length. In the writer’s opinion there are comparatively few conditions which can safely be given as positive indications for this operation. These may be mentioned somewhat in the following order: 1. The persistent recurrence of exacerbations of acute inflammation accompanied by mastoid tenderness or pain and physical evidences of pus retention in the vault. In these cases we may assume that the antrum and mastoid cells are the seat of a subacute suppurative process, an advance of which may be recorded with each succeeding attack. I believe that these recurrent attacks indicate one of the most dangerous forms of the disease, and that they should be regarded as a positive indication for the radical operation. 2. Evidences of fistula leading from the mastoid cells either through the posterior wall of the bony meatus or through the outer cortex. The latter condition gives rise either to marked postauricular oedema or to subperiosteal abscess. Mygind,4 analyzing 100 cases of subperiosteal abscess treated in the Copenhagen Commune Hospital, observed 22 cases in which the cortical perforation resulted from an acute mastoid inflam- mation complicating chronic suppurative otitis media. In 16 of these cases (75 per cent.) the vault and mastoid cells were filled with choles- teatoma. This would apparently indicate that postauricular swelling points usually to a more serious condition in chronic middle-ear suppura- tion than in primary acute disease of the tympanum and mastoid. It is a positive indication for immediate surgical intervention. 3. The dangers of cholesteatoma within the antrum or mastoid cells have already been explained. Hinsberg, Neumann, and others who have 3 The radical operation is described in detail in the section devoted to Aural Surgery. 4 Mygind: Subperiosteal Abscess of the Mastoid Region, Annals of Otology, 1910, pp.529-540. INDICATIONS FOR THE RADICAL OPERATION 217 studied the etiology of suppurative labyrinthitis, have found that a large percentage of cases are traceable to the action of cholesteatoma upon the bony capsule of the labyrinth. The determination of cholesteatoma is, therefore, a positive indication for the radical operation. 4. Polypi springing from the promontory or region of the oval window can not be removed through the auditory meatus without great danger of producing a labyrinthine fistula. They are, therefore, an indication for a very careful radical operation. 5. Persistently recurring polypi from any part of the tympanum— showing bone necrosis which non-operative treatment fails to eradicate— constitutes a logical reason for performing the radical operation. 6. Very profuse and persistent discharge,—either by reason of the patient’s discomfort or the evidences it may afford of deep-seated bone disease, may constitute a valid reason for surgical intervention. 7. Facial paresis or paralysis, occurring during the course of chronic middle-ear suppuration, evidences of suppurative labyrinthitis being absent, is a positive indication for very careful performance of the radical operation. If in the above list the author has omitted certain conditions usually included among the indications, he has done so with intention. For example, one writer, for whom the author entertains the greatest respect, includes “recurrent attacks of dizziness, nausea or headaches” occurring in chronic purulent otitis media as the operative indications. These symp- toms may or may not call for the radical operation. If due, for example, to suppurative labyrinthitis, the radical operation alone would be most positively contraindicated. This brings us to the consideration of a rule which all aural surgeons will do well to respect,—viz.: No patient should be subjected to the radical operation until his labyrinth has been carefully tested for evidences of suppurative labyrinthitis.5 Ossiculectomy.—Before leaving the subject of treatment, a word should be said of the operation of ossiculectomy. This operation proposes to provide freer drainage from the vault, aditus, and antrum by the removal of the diseased malleus and incus and incidentally of diseased remnants of the drum membrane which might interfere with the escape of pus from the vault. It is, therefore, in a way a substitute for the radical operation. If it were possible to determine that the diseased ossicles were the sole obstacles to resolution, or that their removal would insure resolutions in spite of infection within the mastoid cells, the arguments in favor of this procedure would have a more logical basis. I know, how- ever, of no positive indication for the selection of this operation, for the reason that there is no way of positively excluding deep-seated foci of bone disease which also might require surgical eradication. For this reason I have personally preferred the radical operation in all cases of 8 The various tests for suppurative disease of the labyrinth are given in the chapter dealing with Suppurative Labyrinthitis. 218 CHRONIC MIDDLE-EAR SUPPURATION chronic purulent otitis media in which surgical intervention was deemed necessary. I can, however, conceive of many cases in which the slighter operation might prove successful, and in this event the advantages to the patient might be very considerable. The most favorable cases for the operation are those in which, with evidences of ossicular necrosis, there is no demonstrable exposure of bare bone in other directions, and in which the patient has retained good hear- ing power. In such a case I see no objection to this operation, the patient being made to understand that the results are somewhat uncertain and that in case of failure a radical operation may later become necessary. CHAPTER IX CHRONIC NON-SUPPURATIVE DISEASES OF THE MIDDLE EAR; OTOSCLEROSIS. Chronic catarrhal otitis media is an elastic term rather indefinitely applied to a variety of tympanic conditions not easily classified. There can be little doubt that many of the conditions resulting in impaired hear- ing, and described in text-books under different names as pathological entities, are in reality but different stages of a slowly progressive lesion. Our knowledge of these conditions is based very largely upon clinical study of cases, and observation of such morbid changes as can be seen in the living patient, and only to a limited extent upon actual study under the microscope of the tissue changes involved. It is clear, therefore, that, whatever classification may be adopted, the different groups will be found more or less to merge one into the other, and it is by no means im- possible that future investigation may show more definitely either their pathological relationship or independence. The chronic non-suppurative lesions of the ear may be considered under the following heads: 1. Chronic tubal catarrh without marked tympanic changes other than those due to retraction of the drum membrane. 2. Chronic catarrhal otitis media. 3. Chronic hyperplastic otitis media; dry catarrh of the middle ear. 4. Otosclerosis. CHRONIC TUBAL CATARRH. Obviously a catarrhal condition of the Eustachian tube may exist for a considerable period without producing ear symptoms. Only those cases, therefore, are likely to come under the otologist’s care in which the calibre of the tube is so reduced as to interfere with the passage of air to the tympanum. The causes of chronic tubal catarrh are exactly the same as those mentioned as predisposing factors to the acute type, and need not be re- peated here. In nearly every case will be found some condition either in the nose or nasopharynx interfering with nasal respiration. The history in characteristic cases is that of very moderate impair- ment of hearing characterized by periods of amelioration. The patient may tell you that there are considerable periods during which he is not conscious of any loss of auditory acuteness; or he may associate his periods of improvement with periodic changes of residence,—e.g., as related to vacation periods in the mountains or at the sea-shore. Usually the hear- ing is very considerably influenced by weather conditions, improving in dry clear weather and relapsing with the reverse conditions. With the 219 220 NON-SUPPURATIVE DISEASES OF MIDDLE EAR impairment of hearing, and often changing with its variations, tinnitus aurium is almost invariably present. Interrogation usually elicits the fact that the patient suffers at times from difficulty in nasal respira- tion, and physical evidences of some degree of nasal obstruction are usually present. Functional examination shows very moderate impairment of hearing of the general type characteristic of disease confined to the conducting apparatus,—e.g., slight loss of hearing for the lower musical tones and some increase in hearing by bone conduction. The ratio between hearing by air conduction and bone conduction is never reversed in a chronic lesion confined to the Eustachian canal. On physical examination the drum membrane is found to be retracted. In adults suffering from chronic tubal catarrh of not very long standing, the retraction may be of moderate grade, more pronounced displacement being at first opposed by the natural strength and resistance of the mem- brana tensa. Children, on the other hand, not infrequently exhibit with chronic tubal disease very extreme grades of retraction. A very characteristic feature of chronic tubal catarrh is found in the fact that the patient’s sense of functional loss or disturbance is frequently out of all proportion to any functional changes which may be demonstrated by the usual hearing tests. Conversational and whispered speech and the acoumeter may be heard at distances only moderately under the normal, and the change in the lower tone limit may be so slight as to leave one in doubt as to its significance. If the lesion be unilateral, however, there is a demonstrable difference—i.e., increase—in bone conduction in the in- volved ear. As compared with these rather negative findings, the patient himself is in no doubt as to his sense of diminished hearing power. I believe that a recognition of this seeming paradox or contradiction is extremely important, for otherwise we may believe, and assure the patient, that his auditory disturbance is transitory and of little importance, whereas his aural disorder is in reality at just that stage requiring most careful study and attention in order to avert changes leading to later serious functional loss. Another characteristic feature of this lesion is the very marked sub- jective sense of functional improvement resulting from inflation. The impairment, it must be remembered, is a mechanical one, due, in the early stages of the disease, not to pathologic changes within the middle ear. but to partial fixation of the membrane and ossicles by unopposed atmos- pheric pressure from without. If the impairment is slight, the hearing may be practically restored to the normal, and if of more advanced grade, the improvement resulting from a first inflation is very much more pro- nounced than that which occurs in chronic lesions of the tympanum. This point is, therefore, an important one both in the diagnosis and prognosis of these cases. Under chronic tubal catarrh, it may be admissible to recognize three conditions causing retraction of the drum membrane,—viz. (a) nasal CHRONIC TUBAL CATARRH 221 obstruction, the tube remaining patent; (b) tubal congestion; and (c) constriction due to actual hypertrophy of the tubal mucosa. Nasal Obstruction.—There are certain cases in which, as a result of an obstructive nasal lesion, the tubes remaining open, the air in the naso- pharynx is more or less rarefied with each inspiration. In consequence of this, the air-pressure within the tympanum becomes constantly negative, and retraction of the drum membranes and some impairment of hearing result. In such a case, inflation per catheter results in a fairly good current of air to the tympanum, replacement of the drum membrane, and prompt relief of the subjective symptoms. The relief thus afforded is, however, exceedingly short lived, the patency of the tubes conducing to the quick reduction of the tympanic air-pressure under the influence of the naso- pharyngeal lesion. Obviously, in such a case, no amount of local treat- ment of the ears by inflations, pneumatic massage, etc., will be of any permanent value until the nasal lesion, whatever its nature, has received attention. Chronic Tubal Congestion.—Belonging more properly to this group are those cases in which the tubal mucous membrane is the seat of chronic venous congestion. These patients present symptoms and physical signs almost identical with those just described. Inflation, however, gives unmistakable signs of obstruction due to congestion, the sounds through the diagnostic tube being at first muffled, rasping, or accompanied by moist rales, then becoming clearer as air enters the tympanum in greater volume. Inflation results in marked temporary relief of symptoms, and the gradual improvement in the auscultatory signs resulting from repeated inflations shows more or less clearly that the lesion is chiefly one of chronic venous congestion. Another method of determining the character of the occlusion is by applying a 4 per cent, solution of cocaine by means of a bent cotton- wound applicator to the mouth and walls of the pharyngeal end of the tube.1 Instead of cocaine, a 1 in 1000 solution of adrenalin may be used, but cocaine is preferable. If the action of the cocaine or adrenalin, thus applied, is exerted rapidly—i.e., in one or two minutes—throughout the canal so as to restore its lumen to a practically normal calibre, we may assume that the obstruction is due chiefly to venous congestion. On the other hand, if inflation, following this application, does not demonstrate a notable effect upon the calibre of the canal, we may assume that the lesion is one of structural thickening, inflammatory infiltration, or at least of tissue changes more complex or advanced than simple venous engorge- ment. If, finally, the application of cocaine or adrenalin exerts no appre- ciable influence upon the calibre of a constricted tube, we must infer ten- tatively that the lesion is one of cicatricial or hyperplastic narrowing or stenosis. This deduction must not, however, be accepted as conclusive until we have further investigated the tubal condition by means of a 1 The cotton applicator for the local application of drugs to the pharyngeal end of the tube is described on page 152. 222 NCN-SUPPURATIVE DISEASES OF MIDDLE EAR Eustachian bougie. It may be that the congestion or inflammation in the pharyngeal end of the tube or in the neighborhood of the isthmus is so great as to have limited the action of the cocaine strictly to the pharyngeal end of the tube, yet this localized obstruction may yield readily to the gentle passage of the bougie. Combining these methods it is usually possible to interpret correctly the nature of the tubal lesion. The importance of this careful preliminary investigation of the character of the tubal disease must be obvious to the reader, since it is clear that we can not determine upon a rational method of treatment until we knowr the character of the lesion which is to be the object of our attack. Treatment. — Cases of tubal venous congestion usually respond readily to rational treatment. This should include correction of any con- dition within the nose or nasopharynx which might act as an excitant of tubal congestion; application of astringents to the inflamed pharyngeal end of the tube; occasional catheter inflation for the purpose of restoring the membrana tensa to its normal position. For adult patients, inflation by catheter possesses among others the following advantages over the Politzer method: It enables one, by means of clearer otoscopic sounds obtained, to determine with greater accuracy the condition of the tube, and to measure the progressive improvement resulting from successive treatments. It eliminates the danger—where one ear only is diseased—of producing undue relaxation of the opposite drum membrane. With children, on the other hand, it is nearly always necessary to depend upon Politzerization. Many of these cases require no other treatment than the use of anti- septic sprays and the local application of astringent drugs, e.g., silver nitrate, argyrol, etc., to the naso-pharynx and pharyngeal ends of the Eustachian tubes. Structural Narrowing of the Tube.—There is still another class of cases coming under the general head of tubal catarrh,—viz., cases in which the obstruction depends not merely upon venous congestion, but also to some extent upon actual increase in the normal tissue elements (hyper- trophy). In more advanced cases the process may have given rise to a proliferation of new connective tissue (hyperplasia). The disease may occur as a uniform thickening of the tubal mucosa, or as localized deposits hav- ing a tendency to contract. During inflation the sounds through the oto- scope are insufficient, high-pitched or may be almost whistling in character, clearly indicating the reduced calibre of the tube. With such a lesion, we are justified in grouping under the general heading of chronic tubal catarrh only those cases of very moderate impairment of hearing which show sufficient improvement after inflation to exclude serious involvement of the tympanic structures. In the great majority of cases, however, these pa- tients do not come under the observation of the otologist until evidences of organic disease within the tympanum are also well marked. These advanced lesions of the tube will be considered in connection with the tympanic lesions to which they give rise. CHRONIC HYPERTROPHIC OTITIS MEDIA 223 CHRONIC NON-SUPPURATIVE TYMPANIC DISEASE. In attempting to describe the two main types of chronic middle-ear catarrh,—viz., chronic hypertrophic otitis media and chronic hyperplastic otitis media, or dry catarrh,—it must be understood that they probably in most cases represent different stages of the same disease; or, in other words, that one is sequel to the other. However this may be,—i.e., whether they in some cases represent the gradual conversion of a simple exudative inflammation into a hyperplastic condition in which the normal tissue elements are to a considerable extent replaced by new connective tissue, and in others originate independently as separate lesions from their incip- iency,—there can be no doubt that as seen by the aurist they occur as conditions having a different pathologic basis, and also differing substan- tially in their response to treatment. Chronic hypertrophic otitis media may be defined as a chronic exudative inflammation of the Eustachian tube and tympanum, whereby the lining membrane of both is greatly thickened and the calibre of the tube re- duced, with resulting impairment of hearing. Etiology.—Unfortunately, the lesion is frequently so advanced when first seen by the aurist that it is difficult or impossible to determine the original cause. Undoubtedly many cases are traceable to the presence of adenoids in early life. Among adults probably many cases originate in one or other of the following conditions, — viz., (1) recurrent attacks of subacute catarrhal otitis media, in which resolution is never quite complete; (2) frequent attacks of acute rhinitis, each attack giving rise to more or less tubotympanic congestion; and (3) obstructive naso- pharyngeal lesions resulting in chronic tubal catarrh which later involves the tympanum. The influence of gout and rheumatism is clearly a factor in some cases of chronic middle-ear catarrh, and such a diathesis should be taken into account as suggesting certain lines of treatment which may be indicated. Pathology. — Pathologically this lesion is characterized by morbid changes within the Eustachian tube and also within the tympanum. The middle ear, as well as the Eustachian canal, is the seat of a subacute in- flammation involving primarily the mucous membrane. The character- istic changes are congestion and round-cell infiltration, leading later to the formation of a variable amount of new connective tissue. As a result of these changes, the mucous membrane everywhere throughout the tubo- tympanic space is greatly thickened. The calibre of the tube is there- fore considerably reduced, and may be practically closed to the auto- matic passage of air to the tympanum. Within the tympanic cavity the most pronounced changes, according to Politzer, occur in the neighborhood of the labyrinthine windows and in those situations where the ossicles are in contact with the tympanic walls. Diffuse inflam- matory thickening, then, is the earliest characteristic feature of this 224 NON-SUPPUEATIVE DISEASES OF MIDDLE EAR lesion. Naturally such changes can not fail to interfere with the mobility of the ossicles. In addition to the diffuse changes above described, there are occasion- ally developed certain secondary products of inflammation, instances of which have been seen and recorded by Toynbee, von Troltsch, Politzer, Moos, Bezold, Gradenigo, and others. These secondary changes usually take the form of adhesive bands between adjacent structures,—e.g., be- tween the crura of the stapes and the walls of the oval niche, between one or both arms of the stapes and the long arm of the incus, between the hammer handle and the promontory, or between adjacent surfaces of the ossicular joints. Contraction of these bands tends to limit still further the mobility of the ossicles. When adhesions occur between the hammer handle and promontory, the inward curvature of the mem- brana tensa is increased and the tensor tympani may be permanently shortened. Symptoms. — A consideration of the varied morbid changes which may occur in the course of this lesion makes clear to us the wide varia- tions in symptoms which different cases present. Usually the symptoms are very gradual in their development, so that the lesion may be well advanced before the patient applies for treatment. The first subjective symptom to attract his attention may be either impaired hearing or tinnitus aurium. Impairment of Hearing.—Deafness in chronic catarrhal otitis media is usually of very gradual development and never becomes complete,—i.e., unless disease of the auditory nerve or labyrinth is superadded to the tym- panic lesion. If the patient comes under the aurist’s care during the incip- iency of the disease, the loss of hearing will be found very slight. For example, there may be no appreciable reduction of hearing power for the conversational voice, the initial loss being shown only by a very slight reduction of the hearing distance for such sounds as the watch or acoumeter. At this stage loss of acuteness for the lower musical tones and increase in bone conduction are too slight to be demonstrable. The writer has, however, frequently examined patients who could hear tones as low as 18 d. v. or 20 d. v., yet showed a beginning depreciation of one ear as com- pared with the other by stating that the sound was distinctly fainter in the ear involved. This of course represents the stage of the disease most favorable for a practical and permanent cure. As the lesion advances, the deafness becomes more noticeable, and the functional reactions assume a more characteristic type,—e.g., the lowest musical tones are no longer heard and hearing by bone conduction is increased. The high musical tones, on the other hand, are heard with undiminished acuteness. In- crease in bone conduction usually advances with the progress of the lesion. I believe, however, that Bezold was justified in his conclusion that the ratio between air conduction and bone conduction is never absolutely reversed until some structural change—e.g., inflammatory adhesions, fibrous hyper- plasia, or the formation of new bone (otosclerosis)—has occurred within TINNITUS AURIUM 225 the oval window or niche, very markedly interfering with the mobility of the stapes. If we accept this view,—i.e., that a negative Rinne means stapedial ankylosis, partial or complete,—it is clear that this test acquires added importance as throwing some light upon the character of the lesion, and therefore upon the prognosis. If the disease is unilateral or decidedly more advanced in one ear than the other, a vibrating tuning-fork held in contact with the mid-line of the skull is usually referred by the patient to the more diseased ear (Weber’s test). Occasionally, however, it gives anomalous or contradictory results, presumably as a result of differences in the thickness, solidity, and conductility of the two sides of the skull. It is, therefore, of value chiefly when considered in connection with results of other tests. What is of greater concern to the patient is the progressive loss of auditory acuteness for all sounds by air conduction. Usually his first intimation of impaired hearing for the conversational voice comes when he first experiences auditory strain at the theatre or in church, or at about this time he may notice that he occasionally loses the drift of a general conversation,—e.g., at a dinner party. Yet in talking with one or two persons he experiences absolutely no difficulty. From this stage, years may elapse before the deafness reaches the point where even with one or two persons conversation becomes difficult. It is, unfor- tunately, at this advanced stage that many patients first apply to the aurist for help. As in tubal catarrh, but to a smaller degree, the deafness in these cases varies from time to time,—e.g., with the season of the year, with weather changes, and to some extent with changes of climate. As the lesion ad- vances and the deafness becomes more pronounced, these periods of tem- porary improvement become less frequent and noticeable. Tinnitus Aurium.—Patients suffering from chronic catarrhal otitis media differ very greatly in their subjection to this troublesome symptom. To some extent it is present in nearly every case. In some cases, however, the subjective noises are so slight as not seriously to disturb the patient, and sometimes he is obliged to concentrate his mind upon them before he can affirm that they are present. In other cases the loud head noises are the patient’s chief concern, and, if he be a nervous individual, they may become a veritable scourge. In nearly all cases the subjective noises vary greatly at different times, or at least the patient is more troubled by them at certain times than at others. The character of the sounds varies greatly, as described by different individuals. Usually they are high-pitched. Sometimes the patient describes two distinct sounds which are heard synchronously in the same ear. While treatment which is successful in improving the hearing frequently relieves also the subjective noises, this is not by any means invariable. It is best, therefore, to discourage the patient from concentrating his attention too closely on this illusive symp- tom, which may be among the last to be relieved. Pain.—While it is true that earache is not a characteristic symptom of chronic middle-ear catarrh, I do not believe that ear pain should be 226 NON-SUPPURATIVE DISEASES OF MIDDLE EAR entirely omitted from the symptomatology of the disease. The writer, who has himself suffered from chronic catarrhal otitis media, has occasion- ally experienced pain in the ear,—sometimes starting quite sharply, but usually soon assuming the character of a dull, trying, but not unbearable earache, lasting a few hours or sometimes a day or two. I know that many sufferers have these periodic ear pains in chronic catarrhal otitis media. Many do not. In those cases in which they occur, I believe that they are in some way related to periods of active progress or exacerbation of the lesion. Vertigo. — A comparatively rare phenomenon in chronic catarrhal otitis media is subjective vertigo. Usually it amounts to little more than slight dizziness lasting but a few moments. Apparently it is not rotary in character,—i.e., it is not attended by the impression of the rotation of surrounding objects,—but is rather a momentary “light-headedness,” induced by suddenly rising from a stooping or the recumbent position,— e.g., after stooping to tie the shoes, on getting out of bed in the morning, etc. The exact causation is not known, the theory usually advanced, that it is caused by disturbance of intra-labyrinthine pressure brought about by inward displacement of the ossicles, being merely a hypothesis, and far from convincing. Physical Signs.—Inspection by reflected light reveals almost invari- ably a retracted drum membrane, the short process appearing more than usually prominent, and the hammer handle being displaced inward and backward. In some cases the hammer handle is so far rotated inward as to appear much foreshortened, or to occupy nearly a horizontal position. In others, in which inward rotation is less marked, the hammer handle appears much broader than in the normal ear, this being due possibly to slight rotation upon the long axis, or to the folding about it of a thickened and relaxed membrana tensa. The light reflex is almost invariably changed, —being either absent, or reduced to a mere line or point, or broken up into two or more points of light. The commonest type of divided reflex is seen at a point of light in front of and below the umbo, and a second crescentic or curvilinear reflex lying parallel with the peripheral edge of the membrana tensa in the antero-inferior quadrant. When retraction is marked, the posterior fold and the annulus tendinosus appear unusually prominent. The physical signs of retraction are practically the same as are seen in acute tubal catarrh (Figs. 94, 95, and 96). In some cases the earliest stages of the disease are attended by an effusion of serum into the tympanic cavity. This fluid rarely or never fills the cavity, but may rise well above the level of the floor of the bony canal. A condition described in many text-books, but rarely seen, is that of a hair-like line running more or less horizontally across the membrana tensa, representing the upper surface level of this fluid. Naturally such a line would change its direction with changes in the position of the head. Other than the physical signs of retraction, the drum membrane may PHYSICAL SIGNS 227 )resent no visible evidences of disease. On the other hand, there may be :ertain abnormalities due to structural changes. Calcareous Thickening.—The drum membrane may present the ap- pearance of being thickened within certain well-defined areas as if bv a chalky deposit upon its inner surface or within ts structure. These localized deposits are often prescentic in shape and confined to the posterior segment (Fig. 138), but may take any form and occupy any part of the membrana tensa. They are commonly regarded as calcareous deposits resulting from a rheumatic diathesis. Appar- ently they do not per se cause much disturbance of function, since they are frequently seen in persons of normal hearing. Tubal Conditions.—During catheter inflation the sounds through the diagnostic tube may be faint, indistinct, and distant,—indicating an obstructed tube through which little or no air enters the tympanic cavity. This, after several compres- sions of the bulb, may be succeeded by a blowing sound, giving the impression of sound originating in or near our own ear, indicating that the tube has suddenly opened under the pressure of air from the inflating apparatus. This sudden and very marked improvement in the character of the sound while inflation is in progress usually means that congestion plays a prominent part in the tubal lesion. In other cases air may be heard entering the tympanum from the start, the sounds being unmistakably tympanic in character, but accom- panied by moist rales. Such sounds usually indicate an exudative inflam- mation of the tube, accompanied by an increased secretion of mucus, which partly occludes its lumen. Not infrequently such rales disappear or become fainter and less frequent during inflation, as a result of displacement of the tubal secretion which is expelled into the pharynx by the return air current. Structural narrowing of the tube is characterized by a sound of tym- panic quality, but fainter and of higher pitch than is normally heard,— fainter by reason of the small volume of air entering the tympanum, the higher pitch being explained by the reduced calibre of the tube. Absolute closure of the tube, which is exceedingly rare, would be indicated by complete absence of sound characteristic of air entering the tympanum. Obviously no trustworthy deductions can be drawn from catheter inflation until the student has acquired sufficient technical skill to feel confident of his ability to place the tip of the catheter in its correct posi- tion in the pharyngeal end of the tube. Besides determining the tubal condition, the otoscope also throws some light upon the tympanic lesion, particularly as to the presence of two conditions occasionally resulting from this lesion,—viz., the pres- ence of fluid and relaxation of the drum membrane. Fig. 138.—Thickening due to calcareous deposits. 228 NON-SUPPURATIVE DISEASES OF MIDDLE EAR In some cases of chronic hypertrophic otitis media, a limited amount of mucoserous fluid collects in the lower part of the tympanic cavity. Usually it is not sufficient in amount to influence the position of the drum mem- brane, and may be quite indeterminable by inspection. In such a case the inflation sound is modified by a series of bubbling rales. The sound is so distinctly characteristic of the passage of air through fluid as to be quite unmistakable. As a comparatively rare result of inflation in these cases, a number of bubbles may be blown up upon the inner surface of the mem- brana tensa, which then become visible through the membrane by reflected light. Relaxation of the drum membrane is demonstrated during inflation when each otoscopic sound begins with a distinct snap. Inflation of the normal ear does not give rise to a percussion sound due to the impact of air upon the drum membrane; it begins and ends as a moderately low blowing sound. With moderate relaxation of the drum-head, there is heard with each inflation a short snap, immediately followed by the characteristic “blow.” With extreme relaxation, there are two distinct and characteristic flapping sounds,—one at the beginning of inflation as the relaxed membrane is blown outward, and a second at the end, due to its recoil. In this way we frequently become aware of marked changes in tension which may be absolutely indeterminable by inspec- tion alone. This loss of normal tension, or relaxation, may be further corroborated by means of Siegel’s otoscope.2 Through the speculum of this instru- ment the relaxed membrane is seen to execute exaggerated movements,— inward against the inner tympanic wall and outward into the auditory canal,—as the air in the meatus is alternately compressed and rarefied. At the same time we may note a characteristic of the relaxed drum membrane which accounts in large part for the resulting deafness,— viz., the relatively small influence which wide movements of the relaxed membrane exert upon the hammer handle, and therefore upon the ossic- ular chain. The hearing in chronic hypertrophic otitis media is in nearly all cases improved as an immediate result of a first inflation. In the early stages this improvement is especially marked. As the disease advances and the pathologic changes within the tympanum involve more seriously the ossicular joints, the functional gain following inflation is naturally less pronounced. Chronic hypertrophic otitis media tends to gradual but progressive impairment of hearing. Whether the functional loss finally disables the patient for enjoying the society of his fellows depends to some extent upon W'hether he is fortunate enough to come early under proper care, and also upon the character of the lesion. It is conceivable that two cases developing with the same initial severity may within the same period of * See Fig. 59, page 59. TREATMENT 229 years reach very different grades of deafness, from the fact that the hyper- trophic process may in one case involve chiefly the regions of the ossicular joints, and in the other may be spread over regions of less functional im- portance. Fortunately, the disease may enjoy periods of apparent qui- escence, and, even when this can not be affirmed, the patient may be well past middle age before his deafness becomes a serious handicap in life. There is, however, a numerous class of patients with whom impairment of hearing begins very early in life and progresses rapidly, so that the indi- vidual is seriously hampered at a time when his career is still in the forma- tive stage and his best energies still called for. Prognosis.—In the very early stages the disease is probably a curable one. In its later stages, when the pathologic basis of the symptoms is found in gross morbid changes which can no longer be corrected, the patient’s symptoms may be relieved and his hearing for a time improved, but the lesion is no longer curable. Treatment.—It is clear that this lesion may give rise to conditions differing widely in their mechanical influence upon sound-conduction. Thus, in one case deafness may be due very largely to tubal obstruction causing retraction of a relatively normal drum membrane, while in another the tube may be patent and the deafness due chiefly to abnormal relaxa- tion of the drum-head. In still a third variety neither tubal obstruction nor relaxation of the drum-head may be marked, the deafness depending chiefly upon adhesive processes involving the oval window and stapes. Obviously successful treatment demands recognition of the mechanical cause of deafness. Care of the Nose and Nasopharynx.—As a preliminary measure, the nose and nasopharynx should be carefully examined and any lesion or condition interfering with nasal respiration, or acting as a predisposing cause of tubal congestion, should be corrected. Preliminary to the use of the catheter, the nose and nasopharynx should be sprayed with some alkaline cleansing solution (Dobell’s, alkalol, normal salt solution). This periodic flushing of the nasal spaces is in itself distinctly beneficial in some cases. When the turbinates and the nasal mucosa are in a state of chronic con- gestion or turgescence, the occasional application of argyrol is often of value. Under its influence, the congestion usually subsides and the mucous membrane regains a more normal tone and appearance. Argyrol may be applied twice or three times a week,—either locally in 25 per cent, solution by means of a cotton applicator, or in 5 per cent, solution in the form of a spray. The home use by the patient of cleansing sprays followed by oil sprays leads to improvement in some cases, in others seeming rather to excite or perpetuate a subacute form of nasal congestion or irritation. Their results should, therefore, be carefully watched. Local Treatment.—The Eustachian tube is probably in most cases the starting-point of this lesion and is our logical point of attack. If the condition here is chiefly one of venous congestion, it will in most cases 230 NON-SUPPURATIVE DISEASES OF MIDDLE EAR respond to the measures outlined under chronic tubal congestion, which need not be repeated in detail here. In all cases in which the tubes are partially occluded, the local treat merit should begin with inflation, preferably by catheter. Inflation should be repeated at regular intervals, at first on alternate days, this being con - tinued as long as progressive improvement in hearing can be demonstrated. By occasional retesting, the results being compared with those of the ori- ginal functional examination, it will be easy to gauge the results of treat- ment. When the functional gain reaches a point beyond which no improve- ment can be demonstrated, the inflations should be stopped, or practised only at considerably longer intervals. In many cases the disturbance of the tubal function is due largely to per- sistent inflammatory changes in the pharyngeal end of the tube, in which case the local use of astringent drugs forms an essential part of the treat- ment. They are applied by means of a cotton applicator bent to a curve similar to that of the Eustachian catheter, and introduced catheter-fashion into the mouth of the tube. In my experience, nitrate of silver in solution of gr. x-xxx ad 5j, and argyrol in 25 per cent, solution, are the drugs which give the best average results. While nitrate of silver is usually well tolerated by the tubal mucosa, it is best to begin with a weak solution,—e.g., gr. x ad 3 j, —and later increase the strength to gr. xxx to the ounce, which accomplishes all that would result from a stronger solution and is less irritating. This drug should not, as a rule, be applied to the tube oftener than once in seven days. It causes considerable burning discomfort at the time, which, however, usu- ally subsides within from thirty minutes to an hour, leaving the tubes clearer. Its value may be considered proved in those cases in which the beneficial results of inflation are thereby prolonged or rendered more stable. There are cases, however, in which nitrate of silver increases tubal conges- tion and is distinctly harmful. I have personally found argyrol of more uni- versal value than nitrate of silver. It is quite as astringent as the latter, has very decided antiseptic value, and, so far as I have been able to observe, is practically non-irritating. It may be used in solutions from 25 to 50 per cent., and as often as twice or three times a week. Next to nitrate of silver and argyrol, I have found chloride of zinc in 2 to 4 per cent, solutions of most value in these cases. Should inflation and the local use of astringents fail to restore the func- tional activity of the canal, the Eustachian bougie must be employed. In the author’s opinion, there are but three clearly defined indications for the use of the Eustachian bougies: (1) to determine and locate a point of local narrowing, or constriction; (2) to overcome a constriction due to inflamma- tory adhesions within the membrano-cartilaginous portion of the tube; and (3) in certain cases of obstinate tubal congestion, in which the passage with- out force of a small bougie helps to re-establish the tubal function and opens the way for the local or direct application of astringent drugs. Other than the above definite and distinct indications, I believe that the frequent use of bougies is likely to do more harm than good. Eustachian bougies are made of whalebone, celluloid, or certain com- USE OF EUSTACHIAN BOUGIE: TECHNIC 231 positions in which gum elastic is a prominent constituent. They all terminate in an olive-shaped enlargement or bulb. This terminal enlarge- ment is of diagnostic value in determining the exact position of any local- ized constriction, in that the stricture offers resistance to its passage inward, and again to its withdrawal. Thus, a bougie may pass easily through the tube until it meets resistance from a localized constriction. Passing this, it may enter the tympanum without further opposition or it may encounter and pass a second stricture. Owing to its terminal bulb, its withdrawal is again opposed at the points of resistance previously noted. In this way one or more strictures may be determined. The size is measured by the diameter of the terminal bulb, and varies from a half millimetre or less to one and a half millimetres, the latter measurement being the largest that should be used. Of the different kinds of bougies, the celluloid are much more pliable than the whalebone, following the curve of the tube better, and being therefore less likely to create a false passage. Most of the composition bougies are open to the objection that they soon become rough, increasing the danger of injury to the tubal mucosa. As to the size of bougie to be used, whoever attempts this rather deli- cate procedure should remember that the average normal tube at the Fig. 139.—Celluloid bougies (calibre and length reduced). isthmus is one and a half millimetres in diameter; some are smaller. If we employ a bougie which is too large for the tube, we may by the applica- tion of force carry it beyond the isthmus, but in doing so may crush or cut the mucous lining against the beginning of the bony tube, giving rise to an annular cicatrix whose subsequent contraction may cause the most in- tractable kind of stricture. Ordinarily a bougie with a bulb one millimetre in diameter should first be tried. If it meets too much resistance at the isthmus, it is better that it be withdrawn and a smaller one substituted. Technic.—As a preparatory step, we will assume that the nose and nasopharynx have been thoroughly sprayed with Dobell’s or other cleans- ing solution; that the catheter of malleable silver has been sterilized by boiling; that the celluloid bougie, which cannot be boiled, has been cleansed in alcohol and dried with sterile gauze. We must also assume that the physician has clearly in mind the fol- lowing facts, without which he cannot work intelligently: 1, that the Eus- tachian tube in adults varies from 31 millimetres to 38 millimetres in length; 2, that its narrowest part, the isthmus, is at the junction of the bony with the membrano-cartilaginous portion of the tube; and 3, that the end bulb of the bougie will reach the isthmus when it has passed beyond the terminal opening of the catheter to a distance varying between 20 and 25 millimetres. Obviously we must adopt some method by which the physician may know at any time just how far the bougie has passed out of the catheter and into the Eustachian canal. In practice I meet this necessity in the NOY-SUPPUKATIVE DISEASES OF MIDDLE EAE 232 following way. Taking, for example, a celluloid bougie, I pass it through the catheter end to a length of about 38 millimetres, or about one and a half inches (Fig. 140). Practice soon enables one to gauge this measure- ment quite accurately by eye. I now bend the opposite, or proximal, end quite sharply downward over the edge of the large end of the catheter. The bougie retains this bend or angle (6). Now, when the catheter is Fig. 140.—Eustachian catheter and bougie. in proper position in the patient’s nose and pharynx and I have intro- duced the bougie, I know, when my guide-bend is 38 millimetres from the outer extremity of the catheter, that the tip of the bougie is just enter- ing the canal. As the bougie is advanced into the canal, I am able at any time to compute the distance it has traversed by mentally deducting from 38 millimetres the distance remaining between the expanded extremity of the catheter and the bend in the bougie. The bougie should be passed very slowly and with little application of force. If one uses a very small bougie, it may traverse the whole length of the canal with no appreciable resistance. With a terminal bulb one milli- metre in diameter, one will almost invariably meet with a sufficient in- crease in resistance at the isthmus to inform one that the bougie has reached this narrowest point of the canal. If the isthmus can not be passed without the use of considerable force, it is better to withdraw the bougie and either employ a smaller one, or try the same bougie at a later sitting after very thoroughly shrinking the canal with cocaine or adrenalin. In many cases the passage of a bougie of proper size is followed within a few days by a very noticeable improvement in the patency of the tube. Yankauer3 has devised a set of Eustachian applicators, bougies, and sounds, and described in detail a systematic method of dilating a constricted tube, which, while founded upon methods long in use, represents a useful technical advance. By this method it is possible not only to locate, but also to determine the extent, measured in millimetres, of the constricted portion of the tube. This constricted portion is then anesthetized and exsanguinated by a 5 per cent, solution of cocaine in adrenalin, 1 to 2000, carried into the tube by a specially devised cotton applicator. Following this, inflation demonstrates whether the constriction is due to congestion or to inflammatory infiltration of the tubal mucosa. If due to the former, 3 Yankauer: The Isthmus of the Eustachian Tube, A Contribution to the Pathology and Treatment of Middle-ear Disease, Laryngoscope, July, 1910. TREATMENT OF EUSTACHIAN STENOSIS 233 application of 25 per cent, or 50 per cent, argyrol solution is made to the diseased portion. If dependent upon inflammatory infiltration, the appli- cation of argyrol is preceded by the passage of the Eustachian sound, which is allowed to remain in place five or ten minutes. While this method represents a useful initial measure in certain cases, its frequent repetition as advised by Yankauer, does not impress the writer as advisable, or as altogether without risks. The handles of Yankauer’s instruments are provided with a graduated scale, enabling the physician to tell at any moment the exact distance to which the bougie or sound has entered the canal. The Electric Bougie (Duel).—Still another method of dilating an obsti- nate stricture of the tube is by the so-called “electrolytic method” devised by Dr. A. B. Duel, of New York. Basing his experiments upon the hypoth- esis,—which is an accepted fact in electrotherapeutics,—that contact of the negative pole of a galvanic current favors absorption of inflammatory products, he subjected a number of patients, with tubal strictures which had resisted other methods, to the following treatment: Using a galvanic battery provided with a reliable rheostat and milliamperemeter, a bougie constructed of gold wire was connected with the negative pole, the positive electrode being held in the patient’s hand. This bougie was passed through a silver catheter, insulated by a covering of rubber tissue, and slowly advanced until its progress was blocked by the stricture. The current was then gradually turned on to a strength varying between two and five milliamperes. In many cases it was found that at the end of from two to five minutes the bougie could be advanced without force. A somewhat alarming accident, which has been recorded by several aurists, is the breaking or separation of the distal end of the bougie within the Eustachian tube. This has never occurred in the writer’s experience, and he has found this treatment of decided value in certain cases in which all other methods of dilatation had failed. It is an agent which should not be used carelessly, and whoever wishes to employ it should follow carefully the technic as described by its sponsor.4 The patency of the tube having been restored so far as catheter inflation may indicate, the patient should for a time be carefully observed for the purpose of determining whether the tubal function has also been re-estab- lished. Every aurist has had experience with cases in which inflation results in an apparently normal air current to the tympanum, yet with each return of the patient the drum membrane is found retracted. Func- tional improvement following inflation is, therefore, only temporary. This condition would seem fairly positive proof that, while the tube itself is patent, its function has not been resumed. Upon such a case a com- parison of the results of inflation by catheter and by the Politzer method may throw considerable light. Supposing, for example, in a case of uni- lateral disease that catheter inflation reveals a normally patent tube and 4 Duel: The Technic of Eustachian Electrolysis, Trans. Am. Lar., RhinoL, and Otol. Society, 1909. 234 NON-SUPPURATIVE DISEASES OF MIDDLE EAR yet by the Politzer method little or no air reaches the tympanum, the evidence of obstruction at the pharyngeal mouth of the tube would seem to be clear. The mechanical cause of this obstruction may or may not be visible by means of the postnasal mirror, being due possibly to one or other of the following causes,—viz.: (a) remnants of adenoid tissue remaining in the fossa of Rosenmuller, occasional congestion of which closes the tube by pressure; (b) chronic oedema or swelling of the lips of the pharyngeal mouth of the tube, giving them a valvular action under pressure; (c) un- relieved oedema within the mouth of the tube, beyond which the catheter passes; and, lastly, (d) there may possibly be cases in which, as a result of hyperplastic thickening or induration of the nasopharyngeal and tubal tissues, the pharyngeal muscles no longer act effectively upon the pharyn- geal end of the tube. These conditions suggest their appropriate treatment. When finally the function of the Eustachian canal has been re-estab- lished, the further treatment will naturally depend upon the interpretation of the tympanic condition. If the subjective symptoms have been relieved and a reasonable improvement of hearing obtained, it may be better to suspend all treatment, instructing the patient to return within three to six months in order that the permanency of the results may be tested. On the other hand, if symptoms are present depending apparently upon tympanic hypertrophy or congestion, a persistent effort should be made to correct these conditions. Since any further treatment which may be required in these cases conforms in a general way to that indicated in the hyperplastic form of chronic otitis media, the subject may with advantage be deferred to be considered jointly with the treatment of that disease. Chronic hyperplastic otitis media (sometimes called dry catarrh of the middle ear) is characterized by an excessive production of new connective tissue within the tympanic mucosa. In the drum membrane this hyperplasia may involve not only the mucous membrane, but also the fibrous layers of the membrana tensa, which may to a greater or less degree be replaced by new connective tissue. The mechanical results of tnese changes vary logically with the regions and tympanic structures in- volved. Wherever the joint structures of the ossicular chain are involved, the contraction of new connective tissue may react unfavorably upon ossi- cular mobility. With the membrana tensa, on the other hand,while con- nective tissue hyperplasia may lead to apparent thickening, the loss or atrophy of the normal fibrous layers may, and usually does, result in a loss of normal tonicity, or relaxation, which constitutes one of the chief factors in the mechanics of obstructive deafness. All authors agree that the condition above described is often a late stage of the hypertrophic form of chronic middle-ear catarrh, beginning with well-marked round-celled infiltration, and ending in the conversion of the newly formed round cells into fibrous connective tissue. The same process, taking place within the Eustachian tube, may give rise to widely different end-results,—e.g., (a) the deposition of new tissue may be so extensive as CHRONIC HYPERPLASTIC OTITIS MEDIA 235 nearly to occlude the isthmus of the tube, resulting in an organized obstruc- tion or stenosis very difficult to correct; or (b) the hyperplastic process being less marked, contraction of a moderate amount of new connective tissue gives rise to an abnormally wide and open tube. The lesion may be further complicated by the presence of fibrous bands passing between the ossicles and adjacent tympanic surfaces. They may, for example, bind the head or crura of the stapes to the walls of the oval niche, adding greatly to the impairment of hearing. Such adhesive structures probably always represent an earlier hypertrophic or exudative stage in which swelling or oedema was a more or less prominent feature. Symptoms. — Since they in many respects resemble those already described under chronic hypertrophic otitis media, the symptoms may be dealt with briefly. Usually when the diagnosis is made the hearing is already considerably impaired, there being noticeable loss of hearing for the lowest musical tones, and hearing by bone conduction being appreciably prolonged. The ratio between hearing by air conduction and bone conduction may or may not be reversed, actual reversal not taking place until the deafness is very pronounced. As compared with chronic hypertrophic otitis media, it has seemed to me that sufferers from this lesion show often a loss of hearing for the conversational voice and whisper out of proportion to the demonstrable changes in tone limits and bone conduction. For example, the patient may have difficulty in hearing a moderately loud whisper at 5 or 6 feet, and yet may hear forks as low as 36 or 40 double vibrations per second, and bone conduction may be only moderately increased. The degree of deafness is also less variable, neither weather conditions nor changes of season or climate influencing it so markedly as in the hypertrophic form of middle-ear catarrh. Paracusis (Willis).—A condition which sometimes accompanies the deafness of this lesion is known as paracusis Willisii. It is present when an individual with advanced deafness can understand conversational speech better in the presence of loud surrounding noises than in a quiet room. Thus, some patients, who are ordinarily extremely deaf, hear with com- parative ease while traveling in a railway-car or when walking in a noisy street. There are two theories in accordance with which this phenomenon is explained,—viz.: (1) The tympanic theory,—i.e., that, with pronounced tympanic changes, the ossicular chain loses the power of responding ade- quately to the conversational voice; but that, when set in motion by such gross sounds as the noises of the street or of a railway-car in motion, they regain for the time their responsiveness to the more delicate sound waves involved in conversational speech. (2) The labyrinthine theory is that in cases of very advanced deafness, even though the lesion may be of tympanic origin, the auditory nerve becomes more or less torpid and irre- sponsive to the voice sounds, but that when stimulated by loud noises it becomes simultaneously more responsive to the more delicate and complex sound waves of the conversational voice. NON-SUPPURATIVE DISEASES OF MIDDLE EAR 236 Paracusis is seldom present in chronic hyperplastic otitis media except in the advanced stages in which the ratio between air con- duction and bone conduction is reversed (negative Rinne). It is also very commonly present in advanced stages of otosclerosis. It is probably, therefore, in some way related to conditions bringing about fixation of the stapes, and to this extent is of some importance as bearing upon the prognosis. Tinnitus aurium, though usually present, varies greatly in different cases, either in its intensity or in its impression upon the patient. Some patients, while stating that the subjective noises are continually present, do not seem to be greatly disturbed thereby. Others, either by reason of their loud character or through anxiety as to their significance, are made exceedingly nervous or unhappy by them. A not uncommon impression among those who suffer from tinnitus is that their difficulty in hearing is due chiefly to the confusion incident to the subjective noises, rather than to actual impairment. “I could hear perfectly if it were not for these head noises,” is a statement with which every aurist is familiar. Fortu- nately, many people with incurable ear lesions become so accustomed to continual head noises as actually to be unconscious of them during the day, when the noises of the street and the interests of the hour serve to distract their attention. Undoubtedly individuals of trained will power are less disturbed than the weak, nervous, or neurasthenic. As with chronic hypertrophic otitis media, vertigo is a comparatively rare phenomenon, and when it does occur is usually little more than a momentary dizziness, sometimes, however, recurring with annoying per- sistence. When severe attacks of vertigo, accompanied by disturbance of static equilibrium, occur in this lesion, careful functional examination will usually establish other clearly defined evidences of labyrinthine involvement. Physical Appearances of the Drum Membrane.—While the Eus- tachian canal may be not only patent but abnormally wide, it is a curious fact that the drum membrane is in most cases distinctly retracted. The frequent coincidence of a widely open tube and a retracted membrane may in some cases be accounted for as being the result of adhesions between the hammer handle and promontory, shortening of the tensor tympani, etc. Probably much oftener it is the result of an earlier hypertrophic stage, during which tubal obstruction led to prolonged retraction of the mem- brane, the resulting loss of resiliency preventing its subsequent return to the normal position. The most characteristic appearance, however, is that of moderate thickening,—the membrana tensa appearing to be not only thicker but to have lost in some degree its characteristic sheen or lustre. This con- dition is usually the result of an increase of connective tissue at the ex- pense of the normal fibrous layers of the membrana tensa. The apparent thickening is often most marked at the periphery and in the central area immediately surrounding the umbo. In some cases the deposition of new connective tissue may be plainly seen in the form of opaque lines running PHYSICAL SIGNS 237 in various directions through the tense membrane, most often radiating from the umbo or hammer handle to the periphery. Such a drum mem- brane, if examined with Siegel’s otoscope, will not infrequently be found to be abnormally relaxed, both anterior and posterior segments making exaggerated movements as the air in the auditory canal is alternately compressed and rarefied. Atrophy of the Drum Membrane.—The drum membrane may present exactly the opposite appearance to that just described, the whole mem- brana tensa being abnormally thin and transparent. This change is probably the result of atrophy and partial disappearance of its fibrous layers under the pressure of a moderate deposition of new connective tissue. The membrane in consequence is exceedingly thin, transparent, and so relaxed as to exhibit in some cases exaggerated degrees of retraction. Tympanic structures not clearly visible through the normal membrane come therefore plainly into view through the depressed and attenuated membrane. Thus, the incudostapedial joint and niche of the round win- dow may be quite prominent, the membrane being applied so closely to the inner tympanic wall as almost to give the impression that one is look- ing directly at the tympanic structures. This is the type of membrane which may be easily ruptured by catheter inflation even with moderate pressure. Naturally the physical picture is greatly altered by inflation, but the lack of normal tension favors quick return to the condition of exaggerated retraction. There are also cases in which the membrana tensa undergoes atrophy only in certain regions, the rest of the membrane being apparently normal. This condition is in some cases easily recognized by the greater trans- parency of the area involved; in others, there may be no structural change which the eye can appreciate, the condition being detected only while examining the drum membrane with a Siegel otoscope, when the atrophied part is seen to balloon out into the meatus independently of the surround- ing normal membrane. The immediate effect of inflation upon the hearing depends upon a variety of conditions,—e.g., patency or structural narrowing of the tube; the degree of relaxation of the membrana tensa; and, more than any other condition, upon the presence of adhesive processes involving the stapes and margins of the oval niche. Whatever the condition may be, the immedi- ate effect of a first inflation is usually in the direction of an improvement in hearing. As a rule, however, the functional gain is not so pronounced as that which is obtained in chronic hypertrophic otitis media. This is to some extent a differential point between the two conditions. When the tube is greatly narrowed at the isthmus, the otoscopic sound during infla- tion is of reduced volume and higher pitch than is normally heard. On the other hand, with an abnormally wide tube, one hears a very low, full, and often rough, blowing sound. A very common accompaniment of the pathologically wide tube is marked relaxation of the drum membrane. During inflation one may hear, therefore, not only the low, rough, blowing 238 N0N-SUPPURAT1VE DISEASES OF MIDDLE EAR sound of the wide and probably dry canal, but in addition the character- istic flapping sound of the relaxed membrane. In such a case the increased calibre of the tube and loss of tension in the membrana tensa are each in their way expressions of the same morbid process,—viz., atrophy and partial disappearance of normal tissue elements. The use of Siegel’s otoscope is an important part of the examination of these cases, enabling the physician to detect adhesions between the hammer handle and promontory, or between the drum membrane and intratympanic structures. During rarefaction of air in the meatus, the free portions of the drum membrane are sucked outward into the canal, leaving the points of adhesion depressed and in conspicuous view. The Siegel otoscope also enables one to determine loss of tension—i.e., relaxation—of the membrane, either localized or involving the whole membrana tensa. Course of the Disease; Prognosis.—The tendency of the disease is toward slowly increasing deafness. The possibilities of treatment depend in each case upon the stage of the disease, the degree of deafness, and the physician’s ability to interpret correctly the mechanical cause of the deafness. In some cases local treatment fails utterly to influence the symptoms. In most cases, however, something may be accomplished either in the way of improving the patient’s hearing or conserving that which remains to him. Treatment.—Since the treatment of chronic hypertrophic otitis media has been described somewhat in detail, it will suffice here to speak briefly of the chief indications in this form of chronic middle-ear disease. As with all forms of tympanic disease, the Eustachian canal should receive first attention. If the tube is found to be structurally narrowed, an effort should be made to re-establish its normal patency. For this purpose some form of mechanical dilatation is essential. Preparatory to the introduction of a bougie, the nose should be thoroughly sprayed with some cleansing solution (Dobell’s, Seiler’s, alkalol), and a 4 per cent, solution of cocaine should be applied to the pharyngeal end of the tube. Using the ordinary celluloid or whalebone bougie, it is best to employ first one of the smaller sizes, gradually advancing to the largest size which will pass the isthmus without much force. A weak point in this type of dilator is in the form of the bougie,—i.e., a terminal enlargement or bulb attached to a narrow shaft,—limiting the dilation to the passage back and forth of the bulb. To meet this difficulty Yankauer has devised a Eustachian sound, the tubal part of which is of uniform calibre, enabling one to maintain uniform dilatation throughout the constricted portion of the tube. This in some cases gives better re- sults than the ordinary bougie. Whatever instrument is used, its calibre should not be larger than can be made to pass the isthmus with comparative ease,—i.e., without risk of injury to the tympanic mucosa. The effort by suddenly applied force to pass a large bougie beyond the isthmus may give rise to traumatism TREATMENT 239 and subsequent cicatrization, leading ultimately to an annular constric- tion, or stricture, far more difficult of correction than that which we set out to relieve. Following the sound or bougie, the application of a 25 per cent, solu- tion of argyrol throughout the entire length of the canal by means of a Eustachian applicator may add to the efficiency of this treatment. The use of bougies has been advocated by various authorities and for various purposes. It has been used, for example, as a means of massaging the tubal mucosa, for which purpose a bougie as large as will pass the isthmus without force is introduced, and allowed to remain in the tube five minutes or more. Professor Urbantschitsch advised that its stimulating action be increased by friction, the bougie being moved rapidly back and forth in the dilated tube, a measure which would seem to the author to be Fig. 141.—Eustachian applicator made of No. 5 piano wire contraindicated by the inherent risks. With the same end in view, the tubal end of the bougie may be dipped into a solution of arygrol or ichthyol or into a weak solution of nitrate of silver, and passed thus into the canal. Albert A. Gray, of Glasgow, advises that the end of the bougie be smeared with an ointment having a one-half per cent, nitrate of silver content, the vehicle being lanolin. The bougie thus medicated he allows to remain in the tube twenty minutes or longer. All of these measures have in view the purpose of increasing the local blood supply of a wide-open and sclerotic canal. Probably the most effective mode of stimulating the tubal membrane, and certainly the best way of applying drugs locally to the canal, is by means of a suitable Eustachian applicator. A perfectly practical applicator and one which can be easily prepared by the physician, is that long since de- scribed by Dr. Dench. It consists simply of a piece of No. 5 piano wire cut to the proper length, the end of which to a length of about one millimetre is sharply bent backward so as to lie in contact with the main wire (Fig. 141). 240 NON-SUPPURATIVE DISEASES OF MIDDLE EAR A very small pledget of sterile cotton wound about this is firmly engaged by the terminal hook, and cannot be dislodged in the tube. Yankauer’s appli- cator has the advantage of a convenient handle and greater flexibility (Fig. 142). With either of these instruments drugs may be applied throughout the entire length of a patent tube. In the author’s experience, argyrol in 25 to 50 per cent, solution is the drug giving best results in these cases; it is both astringent and stimulating, possesses considerable antiseptic value, and is practically non-irritating. It may be applied as often as twice or three times a week. After all that seems possible in re-establishing normal conditions within the Eustachian canal has been accomplished, there is still the question of the tympanic cavity proper, and what may be done to restore its lining membrane to a condition more nearly approaching the normal standard. Upon purely theoretic grounds it would seem that drugs which have proved their value as applied to the tube should have a similar field of usefulness as applied to the tympanic cavity. That they are not equally available is due not to any difference in their local action in the two situa- tions, but to the comparative difficulty in applying them to the tympanic walls. While the introduction into the tympanum of various drugs in solution has been mentioned by many distinguished aurists, I have always felt that this might be attended with certain risks. My own experience has, therefore, been confined largely to the use of one drug, argyrol, ap- plying it in the following way,—viz., the Eustachian canal having been cocainized, a few drops of a 25 per cent, solution of argyrol are taken up in the end of a catheter, which is then introduced and inflation performed in the usual way. In this way a drop or two of the solution reaches the tympanum, probably in the form of a spray. If the drum membrane is inspected a minute or two thereafter, it will be found to be markedly congested. The patient usually experiences a burning sensation, but rarely pain. Both the sensation of heat and the redness are temporary, and the congestion will usually have disappeared when the patient is again seen by the physician. Certain cases have been benefited by argyrol used in this way. Catheter Inflation.—According to my experience the value of catheter inflation in the treatment of deafness is distinctly limited. The prolonged routine use of catheter, repeated at short intervals, has practically no value in correcting ossicular rigidity, and is likely to produce structural changes in drum membrane leading ultimately to definite diminution of hearing. Fig. 142.—Yankauer’s Eustachian applicator. AUDITOBY MASSAGE 241 While in a general way it may be stated that most cases of chronic hyperplastic otitis media are benefited by occasional catheter inflation, this statement calls for an accompanying word of caution. Inflation, like every other therapeutic measure, has its indications and its contra- indications, and there can be no doubt that many cases of “chronic deaf- ness” have been made permanently worse by irrational, routine use of the catheter. For example, let us consider a case of extreme atrophy of the drum membrane in which the membrana tensa is attenuated, trans- parent, and appears as if plastered against the promontory. Such a drum membrane may be easily ruptured by catheter inflation, and, if this acci- dent does not occur, the already pathologically relaxed membrane may be still further stretched. I have seen cases presenting this extreme degree of attenuation and retraction in which a very fair amount of hearing power was retained, the drum membrane of course having ceased to fulfil any, other purpose than that of a protective covering, and the sound waves being taken up directly by the ossicles beneath,—possibly being trans- mitted directly to the incudostapedial articulation. Under these condi- tions, it may be well at very considerable intervals—certainly not oftener than once or twice a month—to practise very gentle inflation simply to lift the membrane away from its contact with tympanic structures and thus prevent adhesions which, becoming organized, might add seriously and permanently to the impairment of hearing. Another condition more easily overlooked is that in which the drum membrane, though thickened by connective-tissue hyperplasia, has suf- fered a coincident loss of tension,—i.e., is relaxed. In this condition it is clear that catheter inflation is an exceedingly dangerous procedure, since its mechanical results are more in the direction of a further reduction of tension than of effectively exercising the ossicular chain. If, as sometimes occurs, some degree of relaxation of the drum-head coexists with tubal or other conditions calling for catheter inflation, it may be well to apply a coating of collodion to the membrana tensa. This in contracting tends to draw the drum membrane outward into its normal position, and to protect it from further stretching under gentle inflation. Auditory Massage.—A somewhat perplexing problem in the treatment of these cases is the necessity of combating tympanic and ossicular rigidity by some form of passive exercise. The method which has been most extensively employed for this purpose is what is known as pneumatic massage. Pneumatic massage is a term applied to passive movements of the drum membrane by means of any instrument producing alternate conden- sation and rarefaction of the air in the external auditory meatus. A very large number of such instruments have at various times been placed on the market. They are all somewhat similar in design, in that they combine the principle of a Siegel otoscope with that of an electric or other motor by which the piston is moved rapidly back and forth. Such instruments seem to be based upon the theory that whatever 242 NON-SUPPURATIVE DISEASES OF MIDDLE EAR will move the drum membrane and ossicles will improve the hearing. They quite ignore the ease with which the adjustment of so finely balanced a mechanism may be disturbed. Let us recall for a moment the character of this mechanism,—i.e., a system of delicate and sensitively mobile levers capable of responding to the slightest movements of the drum membrane, and designed to respond to such movements, and to no others, through life. Obviously the perfect execution of this function must call for a defi- nite and proportionate degree of tension in both drum membrane and ossicular chain, that of the latter being maintained by the tympanic muscles. Clearly the movements of a relaxed membrane can be but im- perfectly transmitted to a system of heavier bone levers. If, therefore, we close the meatus and subject the drum-head to a series of crude exer- cises in which the ossicles can not possibly take part, it is obvious that the net result will be undue relaxation of the membrana tensa and further impairment of hearing. In any system of tympanic massage we should bear in mind the very limited maximum excursions which, according to the investigations of Helmholtz, Politzer, and others, the individual ossicles can make in re- sponse even to experimental movements of the drum-head,—i.e., hammer handle, three-fourths of a millimetre, stapes one-fourteenth of a millimetre. In some cases a very noticeable gain in hearing has resulted from a first treatment by this method. This initial gain has rarely proved perma- nent, and progressive improvement has never to my knowledge resulted from repeated use of this measure. The unsatisfactory results of this form of massage are probably ex- plained by two facts: (1) The movements of the membrana tympani are not those which nature requires of it or which are necessary to the trans- mission of sound waves, and do not therefore exercise the drum membrane and ossicles in their normal function. (2) The undue strain to which the drum membrane is subjected tends to produce alterations in tension, reducing still further the patient’s hearing power. It may seem from the above that my purpose is to discourage all efforts to exercise the drum membrane and ossicles through the external auditory meatus. This, however, is not my intention, since I believe this to be one of the most important problems before otologists to-day. Preobraschensky, of Moscow, who has made systematic investigations of the various methods in use, records his belief that vibratory massage with any instrument which fits into and tightly closes the meatus, produces such rough and exaggerated movements as to constitute an insult to the delicate mechanism involved. With this view I have long been in accord.5 Undoubtedly there are many cases which call for some form of ossicular massage beyond that which catheter inflation affords. In trying to meet this indication, we should bear in mind the following points: The ear- 6 Kerrison: Notes on Some Very Simple Experiments as to the Influence of Sound Waves on Ossicular Rigidity, Jour. Amer. Med. Assoc., December 1, 1906. RATIONAL USE OF TRIED REMEDIES 243 piece of the instrument should not be introduced into the meatus so as to close the canal. Either it should be held slightly separated from the ear, or the ear-piece should be perforated. Tight closure of the canal produces exaggerated movements of the drum-head which are distinctly injurious. Since the loss of mobility is usually greatest in response to the relatively slow vibrations concerned in the production of low musical tones, it would seem more rational to employ a rather low vibration rate, using vibrations of considerable force or amplitude, rather than very rapid vibrations to which the ear still responds with apparently normal ease. For the same reason, low musical tones may of themselves be of value in exercising the ossicles in cases of beginning tympanic deafness. From the foregoing pages it will be seen that the writer has made no attempt to describe an inelastic course of treatment which would fit all, or even a majority, of these cases. He has tried rather to describe certain morbid conditions which may be met with in either the hypertrophic or hyperplastic form of chronic otitis media, and to suggest the more rational means for correcting the same. I believe that we should not make use of too many therapeutic agents simultaneously, since by so doing we shall inevitably mask the results of the different agents employed. For example, in a foreign clinic the writer once saw a considerable number of patients under treatment by a galvanic current of moderate strength applied alternately in front of and behind the ear for a period of five or ten minutes. To determine the value of such treatment, other measures should for the time being be excluded. If at one sitting we inflate the tympanum, pass a bougie for purposes of tubal dilatation or massage, and supplement these measures by some form of external vibratory massage, we shall certainly be at a loss in analyzing our results,—whether of functional gain or loss. I believe, therefore, that if we are endeavoring to restore the normal calibre of a restricted tube, it is best to postpone other local treatment until we are satisfied with the mechanical widening of the tube, and are able to determine what functional gain, if any, has resulted from this change. Following this plan, and weigh- ing results by frequent hearing tests, we shall soon know definitely (1) whether the patient is being benefited, and (2) to what particular agent a demonstrable improvement is due. Before leaving this subject, a word must be said as to the constitutional or general management of these cases. Undoubtedly some cases of chronic middle-ear catarrh have a constitutional basis in subacute or chronic gout or rheumatism. When such a diathesis can be determined, the care- ful physician will recognize its possible bearing upon the tympanic lesion and the importance of constitutional remedies. In a majority of cases it is difficult or impossible to trace any relation between the aural disease and any constitutional disorder. The general treatment often narrows itself, therefore, to a regulation of the patient’s mode of life,—this including such minutiae as clothing, diet, use of tobacco or alcholic drinks, habits of open-air exercise on the one hand or of over- OTOSCLEROSIS 244 work and excessive confinement to office or business on the other. These influences vary so greatly in different cases that they can not be disposed of dogmatically. In the case of tobacco, for example, we know that many excessive smokers go through life without discoverable ear lesion or dis- order. When, therefore, a patient with chronic aural disease acknowledges to a moderate use of tobacco, I believe that we should investigate rather carefully its possible influences before depriving him of a comfort for which a more harmful substitute may be found. If we believe that even moderate smoking is in a given case harmful to the individual, it should undoubtedly be advised against. Excessive smoking is always harmful to these patients, either in its effect upon the tubal mucosa or in the influence of the tobacco upon the auditory nerve. Since all these matters must be discussed more at length in connection with otosclerosis, the student is urged to a careful consideration of the treatment of that disease. OTOSCLEROSIS. While no pathological relationship between otosclerosis and disease of the middle ear has been demonstrated, the clinical resemblance is in many cases so great as to render a differential diagnosis no easy matter. It seems best, therefore, that it be considered side by side with the other lesions commonly leading to impaired hearing or deafness. Definition.—The term otosclerosis is employed to describe the con- dition in which, independently of the health or intercurrent disease of the tympanum, the bony capsule surrounding the labyrinth is the seat of chronic non-suppurative disease interfering with the function of hearing. Etiology.—With reference to the etiology, it is well to acknowledge at once that we have as yet no definite knowledge as to the exciting causes of this disease. It has occurred with sufficient frequency in syphilitic subjects to lend some weight to the conjecture that syphilis in some way influences its inception. Habermann0 is among those who have held that syphilis is a direct cause of the disease. Korner,7 on the other hand, in analyzing the grounds for this belief, could find therein no proof that otosclerosis is ever of syphilitic origin. Professor Denker,8 of Halle, made a thorough and careful investigation of 27 cases in which the clinical histories were recorded during life and in which the tissues were examined post mortem under the microscope. As a result of these studies and a review of the literature, Denker concludes that there is no proof that syphilis is ever a direct cause of otosclerosis. It now seems probable that syphilis is a factor in the progress of the lesion rather than in its causation. Thus, otosclerosis in an individual suffering from constitutional syphilis is said frequently to run a rapid course leading early to marked deafness. Naturally gout and rheumatism are present in a certain proportion of 6 Habermann: Arch. f. Ohrenh., Bd. lx. 7 Korner: The Heredity of Otosclerosis, Arch, of Otol., Amer. Edition. 8 Denker: Die Otosklerose, p. 81-84. ETIOLOGY; PATHOLOGY 245 cases, but if they have any causal relation to the disease, it is probably an indirect one exerted through the anaemia and lowered physical state to which they give rise. While the disease is sometimes seen in patients who also present evi- dences of tympanic disease, it seems probable that the two lesions are in most cases quite unrelated. Certainly many cases of otosclerosis have been observed in which there was complete absence of all signs of tympanic disease, past or present. As to whether tympanic disease is ever the direct cause of the lesion under discussion, there is still some difference of opinion, with the consensus of opinion steadily turning to the belief that otosclerosis is a pathological entity never secondary to a tympanic lesion. This question will be referred to later. An etiological factor which heretofore has received scant attention, but which is destined to have greater consideration in future, is the influence of poisons conveyed through the blood stream from extraneous foci of infec- tion. If infected tonsils, carious teeth, or pus foci in any part of the body may cause inflammatory changes in the articular structures of the larger joints, why not also in the joint structures of the ossicular chain? And why may not the same metastatic poisons influence—at least in some cases—the initial changes in the bony labyrinthine capsule leading eventually to the characteristic features of otosclerosis? I believe that the tonsils are des- tined in future to come more frequently, and 1 hope earlier, under suspicion in their possible relation to otosclerosis. While it is conceded to be a disease of middle life, usually commencing after the twentieth year, Korner has shown that it may occur much earlier, recording two cases from his own practice in which the disease was present at ten years and fifteen years respectively. Sex seems to influence predis- position to the extent that women are more frequently sufferers than men,) e.g., 58.2 per cent, in women, 41.8 per cent, in men (Denker). Her- edity undoubtedly plays an important part in the spread of the disease, as has been proved by Hammerschlag, Korner, Gray, and others, who have published family trees showing remarkable reproduction of the disease. Morbid Changes Affecting the Mobility of the Stapes.—In the minds of many, the association of otosclerosis with bony fixation of the stapes is a fixed idea; hence the determination in any case of stapedial ankylosis is apt to suggest the presence of otosclerosis. It is obvious that such de- ductions may lead to faulty diagnosis. Firm fixation of the stapes in the oval window or niche may be caused by many conditions,—as, for example, the fibrous bands sometimes re- sulting from chronic hypertrophic otitis media, which may give rise to a very high degree of stapedio-vestibular ankylosis. Such processes have been very clearly demonstrated by Politzer 9 and others. Another form of stapedial fixation occasionally results from middle-ear suppuration, in which masses of granulation tissue occupying the oval window recess may be transformed first into fibrous tissue, and later as a result of inflammatory 9 Politzer: Diseases of the Ear, p. 278. 246 OTOSCLEROSIS changes in the surrounding bone may even be converted into bone (Pritchard).10 It is needless to say that such conditions have no relation to true otosclerosis. Pathology.—Otosclerosis is a lesion originating, so far as we know, in the bony capsule surrounding the labyrinth, and varying in its mechani- cal results according to the region chiefly involved. Occurring in the region about the oval window, it may give rise to ossification of the annular liga- ment, or rather to its absorption and replacement by bone, with resulting osseous fixation of the stapes. In other recorded cases, the morbid pro- cess has involved intra-labyrinthine structures,—-e.g., the spiral membrane, —and thus caused deafness without producing stapedial fixation. Fur- thermore, since foci of the disease have been observed in widely separated portions of the petrous bone, there can be no doubt that characteristic changes may occur in parts of the labyrinthine capsule not closely related to structures essential to the cochlear function, in which case the patient would still have otosclerosis, though a diagnosis would not be made on account of the fortunate absence of symptoms. The morbid process seems to lack any of the characteristic features of an inflammatory process. It consists essentially of the absorption of the old bone in the region involved and its replacement by new spongy bone. The new spongy bone is characterized by Havarsian canals of abnormal width, and by large medullary spaces containing numerous multinuclear cells and large thin-walled blood-vessels. The new bone is also characterized by its strong affinity for haematoxylin and carmine dyes. It is differentiated by a distinct line of demarcation from the surrounding healthy bone. It may retain its spongy character, or may in time be con- verted into dense bone. These changes may occur in any part of the bony capsule of the labyrinth. The commonest point of attack is that portion of the labyrinthine capsule just above and in front of the oval window. Occurring in this region, the upper and anterior margins of the window undergo the characteristic changes. Absorption of any portion of the margin of the oval window cuts off the nutrient supply of the contiguous portion of the annular ligament of the stapes (Gray). The ligament, therefore, is also absorbed, its place being occupied by new spongy bone, which later may be converted into compact bone. The foregoing paragraph appeared in the first edition of this book and is as pertinent today as when it was written. In his more recent work on otosclerosis, Gray discusses the origin and pathology of the disease more from the biologic viewpoint. Drawing upon the storehouse of his exten- sive knowledge of comparative anatomy, he pictures for us the gradual evolutionary development of the labyrinth. From its most elementary type in certain primative fish forms, the labyrinth, then embracing only a rudementary vestibular apparatus, is gradually evolved, finally reaching in the more highly organized fishes the most highly developed and complex form of vestibular mechanism. Only with the appearance of the amphibia 10 Pritchard: Fixation of Stapes, Trans. Otol. Society United Kingdom, Vol. vii, p. 60. Fig. 143.—Horizontal section through oval window (right), dividing stapedial foot-plate, vestibule, and basal turn of cochlea. (After Paul Manasse.) A, newly formed bone in region of anterior margin of oval window; B, foot-plate of stapes. Stapes itself is not involved, nor is the annular ligament destroyed. Stapes is therefore not anky- losed. Coincidently there is complete atrophy of Corti’s organ. Fig. 144.—Horizontal section through stapes and basal turn of cochlea. (After Paul Manasse.) The characteristic bone changes are seen in the foot-plate of the stapes, extending thence in front of anterior border of oval window through the entire thickness of the cochlear capsule to its inner per- iosteal lining. The posterior end of the stapedial foot-plate is enormously thickened by the outgrowth of the new bone and the annular ligament is destroyed, giving rise at this point to complete osseous ankylosis. At the anterior margin of the oval window, the annular ligament, though bounded on either side bv newly formed bone, still persists. The auditory nerve and spiral ganglion are atrophied. GRAY’S THEORY 247 does the adjunct mechanism of hearing, the cochlea, begin to appear. From this we see that the vestibular and semicircular canal system is older by untold ages than the cochlear mechanism. This fact, as will be shown later, may be not without bearing upon the pathogenesis of otosclerosis. Gray 11 regards otosclerosis as a degenerative process, in which evi- dences of inflammatory changes, past or present, are completely absent. It is, moreover, according to Gray’s view, a degenerative process dependent upon certain inherent defects in the bone cells or bone structure of the organ of hearing. Regarding such structural defects or errors as develop- mental variations, and recalling that such variations are particularly prone to involve structures of comparatively recent biological descent, we are provided with a hypothesis by which to explain the frequency of sclerotic changes in the cochlea, and their comparative rarity in the structures of the vestibular mechanism. Gray apparently believes that these biologic or developmental defects in the labyrinthine capsule play a major part in the prevalence of the disease. If the developmental defects are sufficiently pronounced, the individual is not likely to escape otosclerosis; if they are completely absent, no exciting cause will induce the disease; between these two extremes are individuals who may or may not escape the disease, and in whom inter- current conditions—e.g., acute otitis media, toxic agents in the blood, syphylis, etc.—may be the deciding factor. With Dr. Gray’s view as to the incidence of the disease, Dr. J. S. Fraser seems not to be in complete accord in that he apparently believes that an exciting cause of extra-labyrinthine origin is necessary to its incep- tion; and among such causes he gives acute inflammatory lesions of the middle ear a very important place. This view, whether accepted in whole or part, calls for serious consideration, on account of its important bearing upon the question of prevention or prophylaxis. That the process is one of absorption of the normal bone and its replace- ment by new spongy bone, rather than rarefaction or spongification of the old bone, is clearly shown by the accompanying illustrations (Figs. 143, 144, 145). Two of them represent cases of otosclerotic stapedial ankylosis. In each it is seen that the new spongy bone occupies not only the position of a previously existing normal structure, but extends far beyond its normal limits. It is clear, therefore, that the lesion may give rise to exos- toses from different parts of the bony capsule. These growths may pro- trude externally from some aspect of the promontory encroaching upon the tympanic space, or internally into the vestibulum. Extending from one or both walls of the oval niche, this recess may be so narrowed as to lock the stapes in an immovable grip. Or the cartilage covering the foot-plate of the stapes may be absorbed, and its place occupied by a bony growth extending into the vestibular cavity (Fig. 144). Obviously stapedial fixa- tion may be produced in two ways,—i.e., (1) by osseous union to the 11 Gray: Otosclerosis; H. K. Lewis & Co., London, 1917. Gray: Otosclerosis; Review of J. S. Fraser: Journal of Laryng. and Otol., Vol. XXXIII, p. 16. 248 OTOSCLEROSIS margins of the oval window, and (2) by pressure of bony growths from other parts of the labyrinthine capsule (Fig. 143). Politzer has recorded a case in which, in addition to characteristic changes involving the stapes and oval window, the scala vestibuli was completely filled by compact bone. Contemplation of the character of the lesion is enough to convince one of the'futility of local treatment. The causes and conditions which inaugurate these changes are still a fruitful subject of investigation. Siebenmann’s investigations led him to believe, as Gray now holds, that otosclerosis is a developmental abnor- mality rather than a disease in the ordinary sense. He regards it as a last stage in the process of the development of the labyrinthine capsule,—a stage which ordinarily does not take place. He believes that the process ori- ginates not in the bony capsule, but in the layer of cartilage-cells lying be- tween the original membranous capsule of fetal life and the surrounding bony capsule later developed from the connective tissue of the skull. Ac- cording to this view, otosclerosis is in reality a process which, while abnor- mal in the labyrinthine capsule, is the rule in the other bones. To under- stand this theory we must remember that the bony labyrinth attains approximately its maximum size at birth. This, of course, is the reverse con- dition to that governing the other bones of the skeleton, which from birth to maturity must constantly increase in size while maintaining their presribed form.This process of growth is accompanied by a continual loss and regen- eration of tissue. Similar changes occurring in the fixed and closely confined bony labyrinth cannot fail to result in distortion or obliteration of normal structures. Siebenmann’s theory, while never generally accepted, seems to have commanded the respect of Korner and many other distinguished students of otology. Apparently we are on the threshold of a period of renewed interest and activity—at least throughout the Anglo-Saxon world of otologists— in the study of the causes and pathogenesis of this at present rather hope- less disease. Unfortunately the enormous amount of work which in the past has been focused upon the pathology of otosclerosis, has yielded results of academic interest, rather than of practical value to suffering humanity. We know (something of) the histologic character of the lesion, and we are provided with fairly convincing theories as to the pathogenesis; but as to treatment or prevention we have only hypothesis based for the most part on pure conjecture. There is nothing in the way of evidence that any causal relation exists between tympanic lesions, inflammatory or suppurative, and the characteristic bone changes of otosclerosis. While such hypothesis may furnish useful bases for a perfectly justifiable empir- icism, they may never-the-less be misleading and may involve the dis- advantage of retarding work in a direction of effort to establish a more solid basis for treatment, preventive or corrective. In the solid work of Gray, Siebenmann, Manasse, Korner and others we have the ground work for the next advance. GRAY’S THEORY AS TO PATHOGENESIS 249 A more recent hypothesis is that advanced by Gray, of Glasgow,11 who connects the lesion with failure of the local blood supply, and in this way brings it into some etiological relation with depressed systemic con- ditions, and particularly with those in which amemia is a prominent feature. Fig. 145.—Horizontal section through right oval window. (After Paul Manasse.) Widespread and characteristic bone changes are seen involving the foot-plate of the stapes, the entire thickness of the cochlear capsule, and the outer wall of the vestibule. The more lightly stained areas represent the changes of long standing, the dark areas the more recent proliferation of new bone. Total destruction of annular ligament and complete osseous ankylosis of stapedial foot-plate are seen at posterior margin of oval window; the same process, though in a less advanced stage, being in evidence at the anterior margin of the oval window. The membranous labyrinth and both branches of the auditory nerve are atrophied. In support of this view, Gray marshals the following facts: (1) the well recognized absence of any evidences of inflammatory action; (2) the char- acter of the initial change,—i.e., absorption of bone and cartilage through- out small circumscribed areas of bone, which are differentiated by 11 Gray: Transact. Otol. Soc. United Kingdom, vol. vii, pp. 76-79 250 OTOSCLEROSIS well-marked lines of demarcation from surrounding healthy hone; (3) the deposition of new spongy bone to replace the structures which have been absorbed; (4) the fact that this absorption without inflammatory reaction and the subsequent replacement by spongy bone are what might be ex- pected in a tissue in which the local blood supply had failed; (5) the charac- ter of arteries supplying bone,—i.e., that of vessels incapable of changes in calibre in response to variation in arterial force; and, finally, (6) the anatomical peculiarities of the bony capsule,—i.e., very dense bone in which the calibre of the Haversian canals is much smaller than in any of the other bones of the body. This reduced calibre of the Haversian canals increases the friction which the heart action has to overcome. Gray, therefore, believes that, when for any reason the arterial force is markedly reduced, and particularly if the quality of the blood is pathologically changed, the conditions become ripe for stagnation of the blood in the vessels traversing the bony capsule, with possibly resulting thrombosis. Thrombosis in these minute vessels effectually cuts off the blood supply from certain circumscribed areas of bone, in which consequently are inaugurated the characteristic changes of the disease. Gray holds that this theory explains in part the greater predisposition of women to the disease, women being more subject than men to various forms of anaemia. It does not, on the other hand, coincide with the strong influence which heredity is known to exert upon the incidence of the disease. Symptoms and Diagnosis.—All observers agree that a perfectly uncomplicated case of otoslcerosis, with bone changes confined to the stapedio-vestibular region, is easily diagnosticated. There are in the main but two varieties of the disease which present special difficulties of diag- nosis,—namely: (1) otosclerosis with foci of disease so distributed as to involve directly the cochlear structures, and (2) otosclerosis complicated by chronic catarrhal otitis media. We shall begin, therefore, with the symptoms which characterize the lesion in the most uncomplicated form, —viz., otosclerosis with deafness dependent upon fixation of the stapes. History.—In characteristic cases there is usually a history of very gradual development of symptoms. Frequently there are no intercur- rent diseases or disorders with which the patient associates his aural complaint. If the lesion is advanced, both ears are almost invariably involved. According to Bezold, the lesion is bilateral in 88 per cent, of cases. In the early stages, however, evidences of the disease may be con- fined to one ear. Frequently the ear in which symptoms appear last is the one in which the progress of the lesion is subsequently most rapid and the deafness or impairment most pronounced. The history may be abso- lutely negative as to catarrhal or suppurative conditions having involved the tympanic cavities. In a word, there may be no account of any con- ditions within the nose or nasopharynx, or in the Eustachian tubes, with which the aural lesion can be in any way associated. Symptoms.—The patient usually complains of two symptoms,—namely, impaired hearing and tinnitus aurium, Either one may be the first to SYMPTOMS: BEZOLD'S SYMPTOM COMPLEX 251 attract his attention, though impairment of hearing is probably always the first symptom. It is conceivable that an adventitious subjective sound might disturb the patient while moderate recession of the normal hearing power might escape his notice. This probably explains the occasional statement that tinnitus was present long before the hearing became impaired. Deafness.—The impairment of hearing is frequently so gradual in its advance as to be fairly pronounced before the patient is fully aware of his functional loss. In the early stages the impairment of hearing may be manifested by slight loss of auditory acuteness for the watch, acoumeter, and the conversational voice, and by very slight increase in hearing by bone conduction. Thus, the sound of a vibrating tuning-fork in contact with the mid-line of the skull may seem louder in the ear first affected, or in the one in which the lesion is more firmly implanted. In advanced stages of the disease, the hearing tests give the following fairly definite reaction: The hearing distances for the watch, the acou- meter, and for the whisper and conversational voice are very considerably reduced. The lower tone limit is always elevated, and loss of hearing for progressively higher tones in the musical scale usually advances with the progress of the lesion. The perception of the higher musical tones is, on the other hand, well maintained, and the upper tone limit may be abso- lutely normal. The period of hearing by bone conduction is always defi- nitely, and usually very considerably, prolonged. This brings us to Bezold’s triad symptom complex,—viz., (a) loss of hearing for the lower musical tones, (b) prolonged period of hearing by bone conduction, and (c) negative Rinne. Bezold claimed that the pres- ence of this syndrome, in cases presenting no evidences either of tympanic disease or of disease of the auditory nerve, could be positively relied upon as pointing to otosclerosis with stapedial fixation. As a corroborative measure, Gelle’s test should be applied. If conden- sation of the air in the auditory meatus exerts no influence upon the intensity wdth which sound is heard through the cranial bones, the diag- nosis of stapedial fixation is strongly confirmed. Tinnitus Aurium.—There is no aural disease in which the subjective sounds are more constant or persistent. Fortunately, there are many cases in which the patient is apparently not greatly disturbed by them,— either by reason of their moderate intensity or from the fact that custom and possibly a strong will enable him to ignore them. In other cases the head noises are the most distressing feature of the disease, sometimes rendering life a burden. Unlike the impairment of hearing, the head noises are, fortunately, subject to periods of comparative amelioration, or at least to periods during which the patient is less disturbed by them. There is, however, no promise that they will disappear as the disease advances; and if the lesion is confined to the region of the oval window, they are not unlikely to increase as the hearing power recedes. This, in the writer’s opinion, constitutes one of the most alarming possibilities of 252 OTOSCLEROSIS this dreadful disease,—a possibility which with nervous or mentally unstable individuals may far outweigh the serious one of prospective loss of hearing. Vertigo.—While vertigo is not a particularly prominent feature of the disease, moderate dizziness is complained of in a certain proportion of cases (22 per cent., Bezold). It usually does not amount to more than slight subjective vertigo, lasting but a few moments. In others, it assumes so severe a character as to overbalance all other symptoms, and to justify even the most drastic surgical measures for its relief (Lake). Paracusis Willisii.—This condition has already been described as an occasional symptom of hyperplastic otitis media with fibrous fixation of the stapes. It is a much more frequent phenomenon of otosclerosis unac- companied by disease of the auditory nerve. The next step is the examination of the ears both by inspection and by catheter inflation. Inflation usually reveals a tube of normal calibre, and is practically without influence upon the deafness,—i.e., no note- worthy improvement results as in the case of chronic catarrhal otitis media. This is an important diagnostic point. If, in addition to this, the drum membranes are seen to occupy approximately their normal position and to present no changes characteristic of chronic middle-ear disease, the diagnosis of otosclerosis may be regarded as proved. There is one physical sign which is regarded as more or less strongly indicative of otosclerosis,—viz., the presence of a reddish or pink blush, seen upon, or rather through, the membrana tensa, usually behind the umbo (Schwartze). It is in many cases absent. When present it is sup- posed to be due to congestion of the mucous membrane covering the promontory, secondary to pathological changes in the bone beneath. Before leaving this subject the writer wishes to revert for a moment to a consideration of Bezold’s syndrome,—viz., prolonged hearing by bone conduction, elevation of the lower tone limit, and reversed ratio between hearing by air conduction and bone conduction. This combination is present also in any tympanic lesion giving rise to stapedial ankylosis. It is, therefore, of special value as pointing to otosclerosis only in cases in which tympanic disease can be definitely excluded. Since disease of the auditory nerve regularly results in reduction of hearing by bone conduction, Bezold’s syndrome must be lost or changed whenever the lesion involves the cochlear filaments of the nerve. It is, therefore, of considerable value in determin- ing whether the lesion is confined to the stapedio-vestibular region or is so distributed as to involve also the cochlea. To epitomize: The characteristic features of the disease may be summed up as follows: History of hereditary predisposition (frequently obtain- able); history of very gradual, but progressive, bilateral impairment of hearing, not subject to marked variations in response to external condi- tions; tinnitus present and usually persistent; paracusis present; absence of physical signs of chronic tympanic disease; patent Eustachian tubes; catheter inflation followed by little or no real functional gain. Deafness SYMPTOMS: HARTMANN’S DIFFERENTIAL TEST 253 characterized by auditory failure for low musical tones, upper tone limit remaining normal or nearly so; bone conduction increased; Rinne negative. Intensity of sound as conveyed through the cranial bones uninfluenced by compression of air in auditory meatus (Gelle). With such a picture the physician who fails to recognize otosclerosis with stapedial fixation is certainly not a practical otologist. Otosclerosis with Involvement of the Cochlea.—In describing the pathology of otosclerosis, it was pointed out that the disease may attack any portion of the labyrinthine capsule; and that while the region of predilection is found in the immediate neighborhood of the stapedio- vestibular articulation, the lesion may be so distributed as also to involve the intracochlear structures. In this way may be inaugurated changes affecting the cochlear nerve filaments, leading to many of the symptoms characteristic of a primary nerve lesion. Obviously such extension of the disease must produce some modification of the clinical picture. Symptoms.—For emphasis and comparison, let us consider first a case of otosclerosis with extensive involvement of the cochlea and in which fixation of the stapes has not taken place. As in the type first described, the patient usually complains of impaired hearing in both ears, and sub- jective noises. The deafness is at first very gradual in its advance, but later may be subject to very marked periodical changes for the worse,— i.e., loss of hearing which is never thereafter regained. The tinnitus is usually a distressing symptom. It may be very persistent, or may become less severe with the progress of the disease, finally subsiding as the patient approaches absolute deafness. This, however, is not invariable, cases having been recorded in which patients have become absolutely deaf yet continued to suffer from the most distressing head noises. Paracusis Willisii is not present. There may be no history of past or present tym- panic lesions having any etiological relation to the disease. Examination of the ears reveals comparatively normal drum mem- branes,—i.e., drum membranes fairly normal in position and showing no marked structural changes. The characteristic red “blush'’ behind the umbo may or may not be present. The Eustachian tubes are patent, and catheter inflation exerts no influence on the hearing. Deafness.—In advanced stages the hearing tests show the following characteristic changes: The lower musical tones may be well perceived and the lower tone limit but little changed or practically normal. The upper tone limit is lowered, and all the higher tones are heard with re- duced intensity. The period of hearing by bone conduction is reduced, and Rinne remains positive or normal. Bezold’s triad syndrome is there- fore absent. Hartmann's Differential Point.—A rather striking differential test, based upon the normal hearing periods for the different tuning-forks by aerial conduction, was first announced by Ed. Hartmann. He found in lesions involving the cochlear nerve not only that the higher tuning-forks were heard during a much shortened period, but also that the relative 254 OTOSCLEROSIS curtailment as compared with the normal hearing periods become progres- sively more marked as we ascend in the musical scale. Exactly the reverse is the case with otosclerosis confined to the stapedio-vestibular region. The experiment may be stated briefly as follows: In otosclerosis confined to the stapedio-vestibular structures, the hearing periods are greatly reduced for the low musical tones, but gradually approach the normal as we ascend in the musical scale. In otosclerosis with involvement of the cochlear nerve (the stapes remaining mobile), the hearing periods are progressively reduced as we ascend from the lower to the upper end of the musical scale. In the above we have taken two extreme types of the disease in order to bring out more clearly and graphically the clinical features character- istic of stapedial ankylosis on the one hand, and disturbance of the coch- lear nerve on the other. In a majority of cases, however, in which post- mortem findings have demonstrated the presence of intracochlear disease, there have been coincident changes in the region of the oval window result- ing in fixation of the stapes. It is clear, therefore, that we shall find in many cases functional reactions characteristic both of stapes ankylosis and of disease of the cochlear nerve. Thus, both upper and lower tone limits may be curtailed, and the tendency to increase in bone conduction commonly resulting from stapedial fixation may be counteracted by the cochlear lesion. With such contradictory reactions, it may be difficult to differentiate between otosclerosis and a lesion primarily involving the cochlear branch of the auditory nerve. As bearing upon such a problem, a possible history of heredity, a history of gradual bilateral onset, and the determination by functional tests of greater disturbance of hearing for the lower musical tones than would ordinarily result from a primary nerve lesion, may aid us in reaching a correct diagnosis. The course of the disease varies greatly in different cases. In some cases the disease progresses rapidly from the start, leading within a com- paratively short period to very marked—sometimes to profound—deafness. Such rapid advance in the lesion and its resulting deafness has been ob- served to occur with greater frequency in patients suffering also from constitutional syphilis. Politzer states that women suffering from oto- sclerosis often show a considerable permanent increase in the deafness with each childbirth. When, without intercurrent constitutional disease, the aural disease runs a particularly rapid course, the inference seems admissible that the lesion is so distributed as to involve early the perceptive mecha- nism proper. Fortunately, there is a large class of cases in which the disease is very gradual in its advance. In some cases years may elapse without apparent progress in the lesion. To this extent, however, the prognosis is always bad,—namely, that individuals in whom the lesion has produced marked impairment by middle life will probably in old age reach a very distressing grade of deafness. The most hopeful prognosis belongs to those cases in which the disease develops late in life, or rather in which the func- tional disturbance then demonstrable is of moderate grade. Such a case TREATMENT 255 may be so gradual in its advance as to bring the patient to old age without disabling deafness. Otosclerosis Complicated by Chronic Catarrhal Otitis Media.— When chronic catarrhal otitis media coexists with otosclerosis, the one lesion may so obscure the other that a positive diagnosis of the two condi- tions can not be made. Certainly such a diagnosis is quite impossible as a result of a single examination, no matter how careful this examination may be. As pointing to otosclerosis we may in some cases have the fol- lowing somewhat indefinite facts,—viz., (1) the deafness may be more pronounced than would be expected from the tympanic lesion alone, and (2) local treatment may exert less influence upon the symptoms than would be expected in uncomplicated tympanic disease. With well-marked evidences of tympanic disease the early stages of otosclerosis can not be diagnosticated. The opinion expressed by Whiting, that profound deafness is always due to labyrinthine or nerve disease, is a belief probably subconsciously held by most otologists. With respect to tympanic disease, there is a degree of deafness which probably is never reached unless the movements of the stapes within the oval niche or window are mechanically restrained. Personally, I believe that a reversed Rinne always means stapes fixation. But with the physical evidences of chronic non-suppurative tympanic disease, whether a negative Rinne points to fibrous immobilization or to osseous union resulting from otosclerosis, is a question which is not always soluble. Treatment.—If we accept Siebenmann’s theory that the disease is simply an abnormal stage of development, all treatment seems useless. If we agree with Gray that the disease may be in some degree dependent upon depressed systemic conditions giving rise to anaemia, the prospect seems more favorable. In its most typical form,—i.e., otosclerosis without evidences of tympanic disease,—I can see no possible influence which local therapeutic measures can exert upon the progress of the lesion. The occasional statements of well-known otologists as to cases of otosclerosis which have responded favorably to local treatment are probably to be regarded as cases of mistaken diagnosis. Such experiences are not, how- ever, to be altogether ignored, since they serve to emphasize two facts,— viz., (1) that cases of deafness apparently traceable to otosclerosis are sometimes on further investigation found to be cases of temporary deafness dependent upon transient causes, which yield readily to local treatment; and (2) that the deafness of otosclerosis is sometimes markedly increased by certain obscure but transient conditions within the tympanum, such cases showing rapid improvement as a result of local treatment. As illustrating the class just referred to may be mentioned the following ex- perience of the writer: A patient referred to him by another physician gave a history of slight impairment of hearing of two or three years’ stand- ing which had recently become very marked in the left ear. Both drum membranes were practically normal in appearance. Functional tests showed 256 OTOSCLEROSIS in the left ear a type of partial deafness characteristic of disturbed sound conduction. Little or no improvement resulted from the first inflation. As a result of these findings a tentative diagnosis of otosclerosis was made, the patient being advised to submit to a short course of treatment in order to prove definitely the character of the disease. To the writer’s surprise, the hearing very rapidly improved under the plan of treatment usually employed in chronic catarrhal otitis media, soon reaching a degree of acute- ness which, though slightly below the normal standard, might be regarded as little more than the physiological impairment due to his fifty-five years. In this case the writer did not flatter himself that he had relieved a case of otosclerosis, but rather that he had relieved some transient condi- tion within the tympanum, the nature of which he had not been able to determine. Leaving such exceptional cases out of our consideration, we must come back to the regrettable fact that otosclerosis is a lesion which ordinarily is not helped by local treatment of any kind. Catheter inflation usually reveals open tubes and to some extent exercises the drum membranes, but can have no influence upon the progress of the disease. Politzer states that vibratory massage through the external auditory meatus is of value in the early stages of the disease,—i.e., before osseous union between the foot-plate of the stapes and margin of the oval window has taken place. He also recommends the administration of iodide of potassium in 5-grain doses three times a day, this to be continued through 25 or 30 days, and to be repeated two or three times during the year. Politzer believes that this periodic use of the iodides helps in beginning otosclerosis to stay the progress of the disease. Siebenmann advocated small doses of phosphorus, to be given more or less continuously over a period of years. It is worthy of note that neither the iodide of potassium nor the phosphorus was expected to result in improvement of hearing, but simply to retard the progress of the disease. Couple this fact with the statement of Bezold that a large number of cases become stationary with only moderate impairment of hearing, and we have a commentary on the difficulty of determining the real value of these or other drugs in this disease. While otosclerosis is a disease for which local treatment promises little, there is much that can be done for such a patient. In the first place, we are able in many cases to assure him that his deafness will in all probability be very gradually progressive, and that it may never reach a degree inter- fering seriously with his usefulness. There is no question that much need- less suffering has been caused in certain cases by a frankly unfavorable prognosis, the correctness of which has been disproved by subsequent events. The writer has under his care a patient for whom another aurist eight years ago predicted rapidly progressive loss of hearing. And yet during the past eight years this man’s hearing has not changed demon- strably for the worse, and during this period he has been able to accomplish a very considerable amount of useful work. I believe, therefore, that when TREATMENT 257 the hearing is only moderately impaired, we should acquaint the patient with the nature of the lesion only to the extent of making him appreciate the importance of carrying out such general provisions as may seem best for him, and that their neglect carries distinct danger of serious deafness. There is probably no disease in which hygienic measures and a wise regulation of the patient’s mode of life are of more importance than in otosclerosis. This view seems admissible when we consider the following facts: It is known that constitutional syphilis, if not a cause of the disease, is at least a factor influencing its rapid advance; that anaemia influences its progress; that with women the onset of the disease seems frequently to be associated with the age at which they are most subject to chlorosis; that women suffering from otosclerosis commonly show a definite advance of the lesion, as evidenced by permanent increase in deafness, after each childbirth. Presumably these conditions influence the disease either through lowered vitality or through the anaemia which is their common characteristic. If these depressed constitutional conditions hasten its advance, it seems a logical deduction that by the reverse process, of build- ing the patient up to his maximum of physical health, we may to some extent hold the disease in abeyance. In the section dealing with the etiology, reference is made to tonsillar infection as a possible and probable factor in the incidence of certain cases of the disease. Naturally if such a causal relationship could be established in any large series of cases, the importance of tonsillectomy in the control of the disease would be evident. There is at hand no data justifying any statement more definite than that the tonsils should be carefully studied in the early stages of all cases of otosclerosis. Three cases reported by Mr. Richard Lake of London are of sufficient interest to justify their inclusion in brief outline here.12 Case I. Was that of a young woman, oet. 24, who presented characteristic symptoms of otosclerosis. Removal of the tonsils brought marked im- provement, both in the hearing and as to the physical appearance of the drum-membranes. A relapse was traced to an infected maxillary sinus, disinfection and treatment of which resulted once more in marked auditory gain. Case II. “Women, aged about 25, with recent history of rapidly in- creasing deafness; both ears showed red reflex. Tonsils removed without delay. Two weeks later, redness of fundi gone and hearing as good as ever.” Case III. Woman of thirty years, suffered from deafness diagnosti- cated as due to otosclerosis. Treatment by various methods resulted only in moderate and temporary improvement in hearing. Finally the tonsils were removed, with a gain in hearing which up to the time of the report had been maintained. There is no doubt that overwork, mental or physical, the strain of busi- ness anxieties, excessive confinement to business, unrelieved by regular hours of exercise in the open air, may unfavorably influence the disease. As 12 Richard Lake: Journal of Otology and Laryngology, vol. XXXVII, 1922, p. 361. 258 OTOSCLEROSIS nearly as the individual’s circumstances admit, it should be insisted upon, therefore, that his business activities be brought within reasonable limits, and he should be made to understand that any indulgence in such business excesses may in the end be paid for dearly by serious loss of hearing. Tobacco and alcohol, when they influence the hearing injuriously, do so chiefly through their action upon the auditory nerve. It is clear, therefore, that excessive smoking or drinking may have disastrous results in a lesion in which the end organs of the nerve may be maintining their function under conditions which have already become abnormal. Tobacco and alcohol should, therefore, be indulged in only with the greatest moderation. Drugs, other than such tonics as may be occasionally indicated, have little or no specific value in otosclerosis. The patient should be instructed that quinine, the salicylates, and most of the coal-tar derivatives induce intra-labyrinthine congestion, and are under ordinary conditions distinctly contra-indicated. Gray places great emphasis upon the importance of combating anaemia in any form; and it may be that periodic blood examinations—particularly young women suffering from otosclerosis—might suggest measures which would prove of value in maintaining these patients in the best condition or combating the advance of the aural lesion. Dr. J. A. Stucky of Lexington, Kentucky, believes an important factor in the progress, if not in the causation, of otosclerosis to be the circulation in the blood of toxins resulting from errors of diet. He has recorded his experience with a series of cases which he has had under observation during many years, and in which he is convinced that systemic care in preventing this form of auto-intoxication has played an important role in staying the progress of the disease. The patient should be seen from time to time, and the hearing retested in order to determine the progress or the comparative quiescence of the lesion. It is of course particularly important that any catarrhal condition within the tubes or tympanic cavities should have prompt and efficient treatment. The plan above outlined suggests in a general way what seems to the writer the best way of caring for these patients. While active local treat- ment is, as a rule, not indicated, it is important that the patient should consider himself constantly under the care of a competent aurist. By this is meant that he should return at stated intervals for examination and advice. This shifts the responsibility of his condition from his own shoulders, and, what is of considerable importance in these cases, elimi- nates the risk of much useless and possibly harmful treatment by ignorant or unscrupulous practitioners. In what has been said above, the writer has had in mind the rather large class of cases in which the hearing is only moderately impaired, the lesion being apparently quiescent or very slowly progressive. There is, unfortunately, another class of patients,—i.e., those whose deafness is either progressing rapidly from bad to worse, or whose hear- ing is already so far lost as to render conversation exceedingly difficult or impossible. Such patients should be told frankly of the incurable nature >f their disease, and encouraged to make use of artificial aids to hearing, rhe very best advice that can be given to such a patient is that he apply limself diligently under the advice of a competent teacher to the task of inquiring the art of lip-reading. Only in this way can he rob his infirmity )f its most unbearable hardship,—that of practical isolation among lis fellows. Surgical Measures for the Relief of Deafness.—Before leaving this sub- ject, a word must be said as to the various surgical measures which have been proposed from time to time with the purpose of relieving ossicular ankylosis and thereby improving the hearing. They may be mentioned in the following order: 1. Mobilization of the stapes by passive movements by means of instruments introduced through a window in the drum membrane. The best opening is secured by a horseshoe-shaped incision in the postero- superior quandrant (Fig. 146). The flap of drum membrane thus formed is then folded downward, leaving the incudo- stapedial articulation in view and accessible to instruments. The head of the stapes is then gently moved in different direc- tions as far as its attachment to the lenticular process of the incus will allow without danger of injury to the annulai ligament or of disarticulatior from the incus. The results of this procedure have not given it a per- manent place in aural therapy. 2. Reduction of abnormal ossicular tension by division of the tendons of the tensor tympani and stapedius muscles. The fact that this operation has no champion among recognized authorities points to the disappoint- ing results obtained. 3. Division of fibrous bands binding the crura of the stapes to the walls of the oval niche. Politzer makes the point that this operation, while without proved value in the fibrous fixation of chronic catarrhal otitis media, is in certain cases quite successful in the fibrous ankylosis follow- ing suppurative otitis media. . 4. Removal of membrana tensa, malleus, and incus,—the stapes being left in situ. This procedure was based upon the hypothesis that the drum membrane, malleus, and incus, when incapacitated by disease for the function of sound conduction, should be removed in order that the stapes, acting alone, may be permitted to receive directly the sound waves from without and transmit them to the inner ear. The ultimate results of this operation proved so disastrous to the auditory function, that it has no advocates among the otologists of to-day. These operations, mentione for their place in otological history, are quite obsolete today. SURGICAL TREATMENT OF DEAFNESS 259 Fia. 146.—Diagrams showing line of incision, and the resulting flap, deflected. CHAPTER X. THE ANATOMY AND PHYSIOLOGY OF THE LABYRINTH. The inner ear, or labyrinth, embraces two distinct mechanisms,—viz., the cochlea, or essential organ of hearing, and the vestibular apparatus (saccule, utricle, and three semicircular canals), a contributory organ of equilibrium or orientation. These structures are contained within a series of little communicating cavities in the petrous portion of the temporal bone, known as the osseous labyrinth. Within the cavities of the bony labyrinth and surrounded by a supporting fluid, the perilymph, are the essential structures known as the membranous labyrinth. The inner cavities of the membranous labyrinth also contain a fluid which, to distinguish it from the surrounding perilymph, is called the endolymph. In form the membranous labyrinth follows rather closely the contour of the bony spaces in which it is contained. Anatomically the labyrinth is separable into three main portions,— viz., a central cavity, the vestibule; an anterior portion, the cochlea; and a posterior superior portion, the semicircular canals. The vestibule lies just internal to the tympanum, with which, but for the foot-plate of the stapes, it would communicate by means of the oval window. Anteriorly it communicates with the cochlea, and posteriorly with the semicircular canals (Figs. 147 and 148). Fig. 147. Fig. 148. Fia. 147.—Bony capsule of labyrinth. Fio. 148.—Drawn from metal cast of labyrinthine cavity, a, three semicircular canals; b, vestibule; c, cochlea. The Osseous Labyrinth.—The cochlea consists of a bony tube measuring about llA inches in length, and coiled two and a half times about a central rod or cone into a form somewhat resembling a snail-shell. The diameter of the tube near its opening into the vestibule is about 2 mm., but from this point its calibre rapidly diminishes, so that after the first turn the average diameter is not more than 1 mm. The central axis of the cochlea—i.e., from the centre of the base to the apex—lies in the hori- zontal plane and is directed forward and outward. Passing horizontally through the cochlea from base to apex is a central cone-shaped body known 260 THE OSSEOUS LABYRINTH 261 as the modiolus. The modiolus is really a hollow central cone around which the spiral tube of the cochlea is coiled. Passing outward from the modiolus into the spiral canal of the cochlea is a lamina of bone called the spiral lamina (Fig. 149). The spiral lamina projects only half-way across the lumen of the cochlear canal. From its outer edge a delicate and important membranous structure, the basilar membrane, passes in the recent state to the outer wall of the cochlear canal, completing its division into two Internal auditory meatus * Lamina spiralis - Scala vestibuli ‘ (in second whorl) Tympanic vault Mastoid antrum Vestibule (roof, removed) Fig. 149.—Horizontal section through internal auditory meatus, cochlea, and vestibule. channels,—an inner, communicating with the tympanum through the round window, and known as the scala tympani; and an outer, opening into the vestibule, the scala vestibuli. Note.—In most text-books the scala tympani is spoken of as the lower cochlear channel, and the scala vestibuli as the upper space. This method of description prob- ably arose from the habit of illustrating the subject by diagrams of the cochlea with the apex uppermost. This, however, is not only incorrect but confusing to the student, whose effort is, and should be, to learn not only the relation of the various labyrinthine structures to each other, but also their relation to the various planes of the skull. With the head erect, the modiolus, representing the central axis of the cochlea, is not vertical but horizontal, and its direction from the vertical anteroposterior plane of the skull is horizontally forward and outward. The spiral cochlear tube winds around this hori- zontal body, and the spiral lamina, projecting vertically into its lumen, must neces* sarily divide it not into an upper and lower, but rather into an inner (basal) and outer (apical) space. This point is made clear by Fig. 150. 262 ANATOMY AND PHYSIOLOGY OF LABYRINTH The scala tympani and scala vestibuli communicate with each other at the apex of the cochlear pyramid through a small opening known as the helicotrema. On the floor of the scala tympani, not far from its beginning at the round window, is a small opening leading into a short canal, the aquceductus cochleae. This minute channel provides under certain condi- tions so dangerous a pathway of infection that the student should have a clear appreciation of its possible significance in disease. Beginning in the floor of the scala tympani near the round window, the osseous canal leads inward and slightly downward through the petrous bone to emerge by a Scala vestibuli Spiral lamina Inner surface of squama Scala tympani- Head of malleus (in vault) Internal auditory meatus Space surrounded by three semicircular canals Fig. 150.—Horizontal sections through modiolus from base to apex (all structures enlarged), x—y, line giving direction of anteroposterior axis of skull. triangular opening at the outer edge of the jugular foramen. The termination of the bony aqueduct is seen, therefore, on the basal surface rather than the interior of the skull. But while the bony aqueduct terminates at this point, the membranous canal is continued inward through the jugular foramen into the cranial cavity and perforates the dura to communicate directly with the subarachnoid space (Politzer. Schwalbe, A. A. Gray). According to Politzer, colored fluid introduced into the subarachnoid space quickly enters the cochlea and vestibule. The cochlear aqueduct is sometimes called aqueduct of the 'perilymph, because through it the cochlear perilymph may pass into the sub- arachnoid space. The important influence of this communication upon the possible consequences of a suppurative invasion of the labyrinth is obvious. The central canal of the modiolus begins in a depression in the anterior wall of the internal auditory meatus near its fundus, called the fossa coch- THE VESTIBULE 263 learis (Fig. 151), and gives passage to the cochlear branches of the audi- tory nerve. Surrounding the orifice of the central canal, the base of the modiolus (i.e., fossa cochlearis) is perforated by numerous very minute foramina, leading into little canals which radiate outward between the bony layers, or plates, of the spiral lamina. These little canals receive the branches of the cochlear nerve, which in turn perforate the outer (apical) plate, or surface, of the osseous spiral lamina, to pass to their distribution in the basilar membrane and organ of Corti. Wire passed through ampullar end of anterior vertical semicircular canal Orifice of entrance of facial nerve ' Tympanic vault Fossa cochlearis- Ampulla of horizontal semicircular canal Internal auditory., meatus 'Section of facial canal Orifice of Eustachian tube Fig. 151.—Vertical section through tympanum, vestibule, and internal auditory meatus. The Vestibule.—The position of the vestibule in relation to the middle- ear cavity is indicated by the fact that the oval window opens into it and marks the centre of its outer wall. It measures 5 to 6 mm. in length (f.e., from before backward), and approximately 4 mm. each in width and height. On the inner vestibular wall, and nearer the anterior than the posterior wall, is a slight ridge, approximately vertical in direction, known as the crista vestibuli. In front of this ridge is a small circular depression, the recessus sphericus, which in the living subject lodges the saccule. Behind the crista vestibuli is an elliptical depression, which lodges the upper part of the utricle, and is called the recessus ellipticus. Openings into the Vestibule (Figs. 151 and 152).—The vestibule presents the five openings of the three semicircular canals. Each canal expands at one end into a bulbous enlargement known as the ampulla. The am- pullae of the horizontal and of the anterior vertical canals are situated near each other, these canals entering the vestibule through its superior wall, or roof, above the oval window (Fig. 151). The ampulla of the pos- 264 ANATOMY AND PHYSIOLOGY OF LABYRINTH terior vertical canal is found in the floor (F'g. 152, a). Behind this—i.e., on the posterior wall near the roof—is the opening of the small end of the horizontal semicircular canal (c). Further inward—i.e., near the angle formed by the junction of the inner and posterior walls with the roof—is the common opening of the anterior and posterior vertical canals (6). In the anterior and outer corner of the vestibule,—i.e., where the anterior Wire passed through small opening (x) of horizontal canal (c) Wire passed through common opening ■Or) of the anterior and posterior vertical canals (6) Ampulla of posterior vertical canal, opening in floor (a) Fig. 152.—Labyrinthine vestibule (d) with roof removed. and outer walls join the floor,—is the opening into the scala vestibuli. Still another minute opening is found on the inner wall of the vestibule leading into the aquseductus vestibuli. The crista vestibuli, recessus sphericus, and recessus ellipticus are perforated by numerous very minute foramina, constituting the so-called maculae cribrosce. They give passage to the saccular and utricular branches of the vestibular nerve. The semicircular canals are about 1 mm. in diameter, except at their ampullae where their calibre is about doubled. With the head erect and with chin indrawn, the horizontal, or external, semicircular canal lies very nearly in the horizontal plane. The two other canals are both vertical, the anterior vertical canal lying in a vertical plane directed from within outward and forward, and the posterior vertical occupying a vertical plane at right angles with that of the anterior vertical,—i.e., directed outward and backward. It is obvious, therefore, that each canal lies in a plane at right angles to the other two (Fig. 153). In every case the ampullar end is situated further forward than the small end of the canal. In the case of the horizontal and anterior vertical canals this is made evident by a glance at any model or prepared specimen. With the posterior vertical, on the other hand, this fact is demonstrated only by tracing its lower, or ampullar, end to its opening in the floor of the vestibule, and there com- paring its position with the common opening of the two vertical canals (Fig. 152). The posterior vertical canal is on a much lower plane than THE MEMBRANOUS LABYRINTH 265 the anterior vertical (Fig. 153). The anterior vertical canal is, therefore, by many authors called the superior vertical canal, the posterior vertical being called the inferior vertical canal. Anterior vertical and posterior vertical are, however, much more descriptive, and therefore more useful Juncture of the two vertical canals to form their common small opening into the vesti- bule Bony covering of sig- moid sinus Ampullar end of an- terior vertical canal ■ Horizontal semicircu- lar canal Posterior vertical canal The Membranous Labyrinth.—The membranous labyrinth is every- where partly surrounded by a supporting fluid, the perilymph. I say “partly” for the reason that it is in most regions connected at some point with the endosteum lining the walls of the osseous labyrinth. Owing to this intervening layer of perilymph, the various portions of the membranous labyrinth are necessarily much smaller than the bony spaces in which they are contained. The membranous semicircular canals, for example, are attached to the endosteum along the outer convex wall of the bony canals, being separated elsewhere by a considerable amount of perilymph. The membranous canals are, therefore, for the most part very much smaller than the osseous tubes in which they lie. Only at*their ampullae do they enlarge sufficiently to fill approximately their expanded bony compart- ments. Wherever in the labyrinth filaments of the auditory nerve per- forate the bony capsule to reach the membranous labyrinth, the mem- branous parts so supplied are attached to the bone surface thus perforated, —e.g., the cristae acusticae of the ampullae and maculae acusticae of the utricle and saccule. The membranous vestibule is found within the central cavity (vestibule) of the osseous labyrinth, and is partly surrounded by perilymph. It con- sists of the saccule and utricle and the vestibular structures by which they communicate with other parts of the membranous labyrinth. The saccule communicates directly with the scala media of the cochlea (ductus coch- learis) and only indirectly with the utricle. The utricle communicates by five openings with the three semicircular canals. Fig. 153.—Relative positions of three semicircular canals. 266 ANATOMY AND PHYSIOLOGY OF LABYIHNTH The utricle, about 5 mm. in length, is attached to the posterior part of the inner wall of the bony vestibule. Its upper half is lodged in the reces- sus ellipticus, behind the crista vestibuli. The portion of the utricle which rests against the recessus ellipticus is called the recessus utriculi. The recessus ellipticus is perforated by numerous small foramina for the passage of the utricular branches of the vestibular nerve; and where these nerve filaments enter the utricle, its inner wall is greatly thickened so as to project somewhat into the cavity of the utricular sac. This thickened area is covered by a highly specialized form of neuro-epithelium, and is known as the macula acustica of the utricle. The cavity of the utricle communicates by five openings with the three semicircular canals (Fig. 154). The ampullar ends of the horizontal and Saccule Anterior vertica semicircular canal Crista acustica of the anterior vertical canal Crista acustica of the horizontal canal External (horizontal) semicircular canal Posterior vertical canal Utricle Crista acustica of the posterior vertical canal Aquaeductus vestibuli Saccus endolymphaticus Cochlear canal Canalis reuniens Fig. 154.—Membranous labyrinth (after Schafer). anterior vertical canals open into its roof; the ampullar end of the posterior vertical perforates the utricular floor, and the small opening of the hori- zontal canal and common opening of the two vertical canals enter the posterior wall. From the lower anterior end of the utricle is given off a small membranous tube which passes forward, inward, and downward and unites with a similar tube from the saccule to form the aqucedudus vestibuli. The aqueduct of the vestibule enters a very small opening on the inner wall of the bony vestibule, and traverses the bone in a curved direction inward and somewhat backward to emerge by a slit-like opening upon the posterior surface of the petrous bone, some 7 or 8 mm. behind the internal auditory meatus. It here expands into a closed sac, the saccus endolymphaticus. The endolymph spaces of the labyrinth do not, there- fore, communicate directly with the cerebrospinal channels or subarach- noid space. The perilymph of the labyrinth may, on the other hand, escape through the aquseductus cochlese to mingle directly writh the cerebro- spinal fluid. The Saccule.—The other membranous compartment of the vestibule is lodged in the recessus sphericus, a somewhat circular depression on the inner wall of the osseous labyrinth, in front of the crista vestibuli. The saccule is only partly separated by the crista vestibuli from the utricle, THE CKIST.E ACUSTICAE AND MACULAE ACUSTICA 267 these bodies being in contact above (Schafer), but having no direci communication. The recessus sphericus, sometimes called the fovec hemispherica, and the anterior surface of the crista vestibuli preseni numerous small perforations through which the saccular branches o: the vestibular nerve pass. These nerves penetrate the contiguous surfac( of the saccule, and there give rise to pronounced structural changes which will be described later. As a result of these localized changes the cavity of the saccule presents a circumscribed bulging of th( inner wall, known as its macula acustica. Very similar changes art found in the ampullae of the three semicircular canals, being there spoken of as the cristce acusticce. From the lower part of the saccule a minute membranous canal, the canalis reunions, passes downwarc to enter the scala media of the cochlea just above its closed vestibulai extremity. Another small membranous tube leaves the lower posterior aspect of the saccule and passes downward and backward to unite with a similar canal from the utricle. The union of these little canals forms the aqueedudus vestibuli, already described. The aquaeductus vestibuli is also spoken of as the aqueduct of the endolymph. The junction ol the two canals by which it is formed provides the only communication between the utricle and saccule. The Cristce Acusticce and Maculce Acusticce.—The cristae acusticae oi the canals and maculae acusticae of the utricle and saccule are structu- rally very similar. The crista acustica of each semicircular canal is situated in that part of the membranous ampulla which is attached to the outer wall of the osseous ampulla,—i.e. that aspect of the bony ampull; which is continuous with the oute convex wall of the bony canal Each crista acustica occurs as ; transverse elevation or ridge acros; its ampulla (Fig. 155). The macuh acustica of the utricle is attacher to the posterior surface of the crisfo vestibuli and the recessus ellipticus behind it; that of the saccule is attached to the anterior surface of the crista vestibuli, and in front ol this to the recessus sphericus. Both maculae occur as irregularly rounc or oval elevations which project from the inner walls into the cavities of the saccule and utricle respectively. In the cristae acusticae and maculae acusticae alike, the following layers may be recognized: 1st, an outer layer of loose fibrous tissue which receives the blood-vessels and branches of the vestibular nerve; this layei is directly connected with the endosteum covering the contiguous bone surface; 2d, a clear or nearly transparent structure known as the tunica propria; and, 3d, the inner layer, consisting of so-called neuro-epithelium, which is made up of the following structures: superficially, a surface layer of elongated pear-shaped, or “flask-shaped,” cells, known as the hair-celk Fig. 155. — Diagrammatic section of ampullar end of horizontal semicircular canal showing posi- tion (a) of crista acustica. 268 ANATOMY AND PHYSIOLOGY OF LABYRINTH (Fig. 156, a). They are arranged parallel to each other, their long axes being at right angles to the free epithelial surface. Their lower rounded extremities do not extend downward as far as to the tunica propria. From the upper extremities of these cells, hair-like processes project into the Fig. 156.—Structures common to the cristse acusticse and maculse acusticse (after Retzius). a. Hair-cells; b, supporting cells of Retzius; c, outer fibrous layer; e, nerve-fibres which, before leav- ing the fibrous layer, lose their medullary sheaths; /, otoliths. cavity of the organ of which they form a part,—i.e., ampulla, utricle, or saccule. In the crista} acusticse of the ampulla}, the processes are covered by a gelatinous substance which is spoken of as the cupola. In the maculae acusticse of the utricle and saccule, they project into the gelatinous cov- ering in which are contained the small bodies known as otoliths. Between the hair-cells and the tunica propria, and in contact with the latter, are elongated nucleated cells known as the fibre-cells of Retzius (Fig. 156, b). They are regarded as supporting structures, analogous in this respect to Deiters’s cells in the organ of Corti, the sensory function being credited solely to the hair-cells. The outer fibrous layer is rich in blood-vessels and receives the branches of the vestibular nerve. In it the arteries break up into a network of fine branches. The nerve-fibres, as they leave the fibrous layer, lose their medullary sheaths, the axis-cylinders being continued upward into the epithelial layer, where their branches pass between and in contact with THE MEMBEANOUS COCHLEA 269 the cells. They have not, however, been traced into the hair-cells, and the exact distribution of their terminal filaments has not yet been determined. The structural arrangement above described characterizes both the cristse acusticae of the ampullae and the maculae acusticae of the saccule and utricle. In the gelatinous substance covering the latter, and in con- tact with the hair-cells, clusters of minute bodies, known as otoliths, are always present. They consist of crystals of carbonate of calcium. Otoliths are not regularly found in the cristae acusticae of the ampullae, though their occasional presence in small numbers has been observed (Schafer). The Membranous Cochlea.—It will be remembered that the spiral tube of the cochlea is divided by the spiral lamina and basilar membrane into two channels,—viz., an inner tube, the scala tympani; and an outer, known as the scala vestibuli. There remains to be described a third channel, the scala media, which contains the organ of Corti, the essential structure in the organ of hearing. The spiral lamina (Fig. 157, j) is composed of two bony plates between which are channels transmitting the branches of the cochlear nerve. In /Labium vestibulare (c) /-Membrana tectoria (d) Scala media, ductus -'cochlearis (e) Membrane of Reissner (b)' of Corti (/) Scala vestibuli (a) -Spiral ligament (9) -Spiral groove (m) ■Labium tympanicum (h) Scala tympani (») Cochlear nerve (1) '•Lamina spiralis (J) ''Spiral ganglion (A) the dry or macerated bone, the outer edge of the lamina spiralis presents simply a rather sharp edge. In the recent state, however, the outer part is covered with a rather thick layer of connective tissue, and presents on section a grooved formation, described as suggesting the letter C. The lower margin of this groove, which extends further outward toward the outer wall of the spiral tube than the upper, gives attachment to the basilar Fig. 157.—Diagrammatic cross-section of cochlear canal 270 ANATOMY AND PHYSIOLOGY OF LABYPINTH membrane. It is called the labium tympanicum (h). The upper margin is called the labium vestibulare (c), and the groove between the two, the spiral groove (m). The labium vestibulare, with the thickened surface immediately behind it, is called the limbus. The limbus is formed of firm connective tissue, which, however, disappears after maceration. The limbus gives attachment to the membrana tectoria (d). From the upper surface of the lamina spiralis, a little behind the attachment of the mem- brane tectoria, a delicate connective-tissue membrane passes obliquely outward to the outer wall of the spiral tube. This is known as Reissner’s membrane (6). It encloses a third channel, triangular in form, and situ- ated in the outer part of the cochlear tube between the scala vestibuli and the scala tympani. This is called the scala media, canal of the cochlea, or ductus cochlearis (e). The ductus cochlearis runs through the spiral tube from the cochlear base to its apex, and encloses the organ of Corti (/), to be described later. Its apical extremity ends in a blind sac which is attached to the cupola. The basal or vestibular end also presents a closed extremity, though it receives a little above this a small membranous canal from the saccule, the canalis reuniens. The ductus cochlearis con- tains the endolymph of the cochlea, as distinguished from the scala vesti- buli and scala tympani which contain perilymph. The spiral membrane separates the cochlear duct, or canal, from the scala tympani. Along the line of its attachment to the outer wall of the spiral tube of the cochlea, the lining membrane of the latter is greatly thickened so as to present on section a triangular surface. This spiral projection or ridge is known as the spiral ligament (g). Structurally the spiral membrane consists of a homogeneous substance in which innumerable radiating fibres (about 24,000 in all, Retzius) are stretched from the free edge of the spiral lamina to the spiral ligament. It is narrowest at the basal or vestibular end, from which point it becomes gradually wider, reaching its greatest width near the helicotrema. Within the cochlear duct (scala media) and resting upon the basilar membrane is the organ of Corti (/). The Organ of Corti (Fig. 158) occurs as a rather broad elevation or ridge resting upon the basilar membrane throughout the entire length of the cochlear duct. On cross-section, and under high magnifying power, the following structures are observed: Resting directly upon the spiral membrane and near its attachment to the lamina spiralis are two striated rod-shaped structures, known as the rods of Corti (I.R.C., O.R.C). That nearest the limbus is called the inner rod of Corti, and the one external to this, the outer rod. Below, as they rest upon the spiral membrane, there is a distinct space between them, but above they incline toward each other so as to meet at their upper extremities. The inner rod is described as resembling the human ulna in form, presenting an upper extremity somewhat similar to the head of that bone. The upper end of the outer rod is compared to the head of a swan,—the back of the head representing the part which fits into the concavity on the upper end of the inner rod, THE ORGAN OF CORTI 271 and the projecting part, resembling the swan’s bill, being directed back- ward (Fig. 159). The rods, both inner and outer, are arranged in single parallel rows extending throughout the entire length of the organ of Corti, and the inner and outer rows enclose between them a triangular space, known as Corti’s tunnel (Fig. 158, T. C.). Covering the organ of Corti on both sides of the rods of Corti are the characteristic cell-bodies known as the hair- cells (I. H. C.. O. H. C.). These are somewhat columnar-shaped cells, narrow above, expanded and rounded below. From their upper extremities tufts of hair- processes project. There is a single row of hair-cells internal to the inner rod of Corti and four rows external to the outer rod. These are known as the inner hair-cells and outer hair- cells respectively. Beneath the hair-cells, and between them and the basilar membrane, are a number of supporting cells of very different type, known as Deiters’s cells. These cells are cylindrical below and rest directly on the basilar membrane. Above they become narrowed, each into a slender process which extends upward between the hair-cells, there expanding into a thickened extremity, known as the pharyn- geal process. These processes of Deiters’s cells with their terminal enlargements, or phalanges, enter into the formation of a reticulum surrounding the hair-cells and presenting spaces above through which the hair-processes project. External to the hair-cells and supporting cells of Deiters are several rows of elongated cells which form the outer edge of Corti’s organ. They are known as Hensen’s cells (H. C.). External to this, the basilar membrane is covered by a single row of cubical cells, called the cells of Claudius (Cl. C.). The membrana tectoria (Fig. 158, M.T.) is a peculiar structure described by Schafer as being composed of “fine fibrils embedded in a gelatinous matrix.” It is attached by a thin edge to the limbus external to the orison Fig. 158.—Organ of Corti (after Schafer). R, Membrane of Reissner; L, limbus; N, cochlear nerve; Lam.sp., lamina spiralis; I.H.C., inner hair- cells; 0. H. C., outer hair-cells; I. R. C., inner rod of Corti; O.R.C., outer rod of Corti; T.C., tunnel of Corti; M.sp., membrana spiralis; D.C., cells of Deiters; H. C., Hensen’s cells; Cl. c., cells of Claudius; Lig. sp., ligamentum spirale. Fio. 159.—Inner (a) and outer (6) rods of Corti (after Retzius). 272 . ANATOMY AND PHYSIOLOGY OF LABYRINTH of Reissner’s membrane. From this point it extends outward over the organ of Corti. From its attachment to the limbus to its outer ex- tremity, it increases greatly in thickness. Its upper surface is somewhat convex; its under surface—i.e., that apposed to, or covering, Corti’s organ —is irregularly concave. Owing to its varying appearances in different preparations, its dimensions are variously described by different authors. Thus Schafer states that it extends externally only over the region of the outer hair-cells, while A. A. Gray states that it extends outward as far as the extreme outer limit of the organ of Corti. As seen in microscopic sec- tions a very considerable space usually intervenes between the free surface of Corti’s organ and the superimposed tectorial membrane. Apparently most observers believe, however, that the normal relation of the two structures during life is one of actual contact (Schafer, A. A. Gray, Shambaugh). The Cochlear Nerve.—The cochlear branches of the auditory nerve enter the cochlea by numerous minute perforations in the circular depres- sion at the base of the modiolus (fossa cochlearis, Fig. 145, a). This depres- sion is situated in the anterior wall of the internal auditory meatus, near its fundus, and below the opening of the facial canal from which it is sep- arated by a prominent ridge. It presents a central orifice leading into the central canal of the modiolus, around which are ranged the minute per- forations, or foramina (tractus spiralis foraminosus), through which pass the branches supplying the first two turns of the cochlea. The nerve- fibres entering this tract pass directly to the base of the spiral lamina. At the base of the spiral lamina as it winds around the modiolus is a spiral space in which are collected ganglion-cells, forming the spiral ganglion of the cochlea (Fig. 157, k). From the cells of this ganglion nerve-fibres radiate outward in the channels between the plates of the spiral lamina, perforating its outer plate to reach the basilar membrane and organ of Corti. On entering the neuro-epithelium of Corti’s organ, the nerve- filaments lose their medullary sheaths, their axis-cylinders then passing between, and in contact with, the supporting cells of Deiters,. the rods of Corti, and the hair-cells. They have not, however, been traced directly into the hair-cells, and their exact terminal distribution is not yet known. The nerve-fibres passing through the central canal of the modiolus are distributed to the last half-turn of the cochlea. Vestibular Nerve.—The distribution of the peripheral branches of the vestibular nerve has already been described in connection with the cristse acusticse and macuke acusticse of the vestibular apparatus. In the in- ternal auditory meatus the vestibular portion of the auditory nerve is divided into two branches,—i.e., an upper branch which supplies the utricle and ampulla? of the horizontal and anterior vertical canals, and a lower branch which supplies the saccule and ampulla of the posterior vertical canal. Central Fibres.—Within the internal auditory meatus the cochlear and vestibular branches are traced to their common trunk, which passes in- THE BLOOD-VESSELS OF THE LABYRINTH 273 ward across the subarachnoid space toward the restiform body. Accord- ing to Dana, the nerve enters the medulla by two roots,—viz., a lateral or posterior root, composed chiefly of auditory, or acoustic, fibres, and a median or anterior root, made up chiefly of vestibular fibres. These roots communicate with three nuclei,—(1) the central nucleus (acoustic tubercle), situated on the floor of the fourth ventricle; (2) the ventral or accessory nucleus, which springs from the lateral root and lies between it and the median root; and (3) the large-celled nucleus (Deiters’s nucleus), which lies external to and below the central nucleus. The lateral root (auditory) communicates chiefly with the accessory nucleus, but is connected also with tfye other nuclei. From the central and accessory nuclei auditory fibres are sent to the temporal lobes of both hemispheres, but more fibres go to the opposite than to the corresponding side of the brain. The cor- tical centre for hearing is located in the first and second convolutions of the temporal lobe; and, since the basal nuclei of either ear send more auditory fibres to the opposite side of the brain than its own, it is clear that destruction of the cortical centre on one side will result in impairment of function which will be more pronounced in the ear opposite to the cortical lesion. The median root of the auditory nerve, composed chiefly of vestibular fibres, is principally connected with Deiters’s nucleus and, through fibres leading from Deiters’s nucleus, with the cerebellum. The Blood-vessels.—The arteries supplying the labyrinth are derived from one vessel,—the internal auditory artery, a branch of the basilar artery. This vessel breaks up within the internal auditory meatus into branches which in a general way follow the course of the branches of the auditory nerve. To the vestibule it supplies three branches,—one to the utricle and the horizontal and anterior vertical canals, another to the posterior vertical canal, and a third to the saccule. The cochlear division, before entering the spaces in the spiral lamina, breaks up into a network of anastomotic loops, from which small terminal vessels are sent to supply small circumscribed areas of the basilar membrane, organ of Corti, and outer wall of the cochlear duct (Shambaugh). According to Siebenmann, the venous blood is returned mainly along three channels,—viz., veins leading from the cochlea into the internal auditory meatus, and veins leaving the labyrinth by the aquaeductus vestibuli and aquaeductus cochleae respectively. Shambaugh,1 who made careful studies of the blood-vessels of the labyrinth in the pig, sheep, and calf, found in these animals but one venous channel, which left the "labyrinth along the aquaeductus cochleae and apparently drained the entire labyrinth. He refers to the work of Eichler upon the blood-vessels of the human ear, who “found but two routes by which the venous blood left the labyrinth, the vein of the aquae- ductus cochleae and the vein of the aquaeductus vestibuli.” Eichler’s conclusions have received the support of Politzer. 1Shambaugh: Some Relations of the Blood Supply of the Inner Ear, Arch, of Otol., vol. xxxv, No. 1, 1906. 274 ANATOMY ANI) PHYSIOLOGY OF LABYKINTH Physiology of Sound Perception (Cochlear Function).—In attempting to place before the reader a brief synopsis of this rather difficult subject, it may be well to acknowledge that the modern conception of the physiology of sound perception is based largely upon hypothesis and only to a limited extent upon demonstrable facts. There are, however, a few basic facts relating to the cochlear function, acceptance of which may now be assumed. We know, for example, that the cochlea is supplied by the cochlear branch of the auditory nerve, and that, when this cochlear nerve is completely destroyed or divided, total deafness of the correspond- ing ear results. We know also that destruction of the cochlea, either by disease or by surgical removal, invariably gives rise to total deafness. Of this there can be no shadow of doubt. The occasional leports of cases in which there has been apparent retention of hearing after surgical removal of the cochlea are unquestionably to be explained by the failure of the observer to exclude the compensatory function of the sound ear. Since, therefore, we may produce deafness by destroying either the cochlea itself or the cochlear nerve before it enters the cochlear fossa at the base of the modiolus, and since the branches of the cochlear nerve have been traced to the basilar membrane and organ of Corti, we may confidently assume that the basilar membrane and organ of Corti are structures which are essential to the function of tone perception. So far we are dealing with indisputable fact. Attempting to go beyond this, we come quickly upon Helmholtz’s theory of tone analysis, a hypothesis which has formed the basis of most subsequent investigations which have yielded practical results. Up to the time of Helmholtz’s investigations, the study of the physi- ology of the cochlea had been obscured by certain mistaken views as to the anatomy of the labyrinth. In the seventeenth and eighteenth cen- turies it was generally believed that the labyrinth spaces contained air instead of fluid; and later the conception of the cochlear function was distorted by the belief that the fibres of the basilar membrane were longest at the cochlear base and diminished gradually as the apex was approached. We now know that exactly the reverse is true. Helmholtz's theory is to the effect that the perception of musical tones is brought about by vibration of the basilar membrane in response to sound waves from without, and that the analysis of musical sound into tones of different pitch is explained by the hypothesis that different parts of the basilar membrane vibrate in response to sound waves of different pitch. In other words, thata soundwave consisting of a certain number of rhythmic double vibrations per second can induce movements only in certain fibres of the basilar membrane, other fibres being stimulated only when the number of rhythmic vibrations is either increased or diminished. And since the radiating fibres of the basilar membrane—i.e., stretching from the outer edge of the spiral lamina to the spiral ligament—are longest at the apex of the cochlear pyramid and shortest at the tympanic-vestibular end, it is assumed that the highest tones of the musical scale are produced WITTMAACK’S EXPERIMENTS 275 by movements of that portion of the basilar membrane nearest the vestibu- lar and round windows, and that the lowest tones correspond to vibrations of portions of the membrane nearest the apex or helicotrema. The Helmoltz theory is the theory of sympathetic vibration; i.e., it proclaims that only certain parts, or certain fibres of the basilar membrane can respond to, or vibrate in response to, an serial stimulus, or vibration, of given pitch, or vibration rate. At best it is a hypothesis, but a hypothesis which threw enormous light upon the significance of the structurally com- plex mechanism of the organ of Corti. The objections to it have been chiefly upon physical grounds; e.g., the unsuitable conditions for vibration, as we understand it, inherent in, and surrounding, the radiating fibres of the basilar membrane. This, it seems to the writer, is in accordance with a naive and common human propensity, which insists upon literal translation of terms, and accepts with difficulty any thesis which cannot be explained by analogy with commonly known facts and phenomena. Admittedly the radiating fibres of the basilar membrane are not analogous to the strings of a piano in their mode of sympathetic response to sonorous stimuli from without. That certain definite areas of the basilar membrane and organ of Corti have to do with the perception of certain tones has been supported by the studies of Wittmaack.2 Wittmaack’s experiments consisted in subjecting animals during prolonged periods to hearing constantly a certain note,—• e.g., 256 d.v., 1024 d.v., etc.,—the animals later being killed and the coch- lear structures examined under the microscope. It was found that certain definite areas of Corti’s organ, corresponding constantly to certain tones, gave evidence of pathologic change as a result of the prolonged stimulation or strain; and, further, that high tones produced morbid changes near the vestibular end of the scala media, and that low tones gave rise to changes nearer the helicotrema. These results have been confirmed by the investi- gations of Siebenmann. A belief which has become part of the accepted hypothesis is to the effect that some interaction between the organ of Corti and the membrana tectoria is essential to the proper transmission of auditory impressions to the brain,—or, to be more explicit, that friction or impact of the project- ing hair-processes of the hair-cells covering the organ of Corti against fhe under surface of the tectorial membrane is in some way essential to the function of tone perception. As to the method, or process, by which this contact or friction is brought about, the consensus of opinion among physiologists has strongly supported the view that sound waves, propagated through the perilymph and reaching the under surface of the basilar mem- brane, have there caused vibration or displacement of certain of its fibres thus carrying the corresponding hair-processes of Corti’s organ against the tectorial membrane. Naturally many theories and modifications of theories of sound per- 2Wittmaack: Ueber Schaedigung des Gehor durch Schalleinwirtung, Zeitsch. f. Ohrenheil., Bd. 50, 1908. 276 ANATOMY AND PHYSIOLOGY OF LABYRINTH ception have from time to time been advanced which, though exceedingly- interesting, cannot be brought within the limited space of this handbook. The theory of Sir Thomas Wrightson and Sir Arthur Keith is based upon an intensive study of wave forms and elaborate experiments to deter- mine the direction of fluid sound waves within the cochlea and to explain mechanically the influence thereby exerted upon the essential structures of the organ of Corti. It is assumed that each inward movement of the stapedial foot plate imparts to the cochlear fluids an impulse which is immediately transmitted throughout their entire mass. According to this theory, the fluid sound wave travels, not by way of the scala vestubuli and through the helicotrema to the scala tympani, but passes directly through Reissner’s membrana and the scala media to the scala tympani, this mass movement being, of course, compensated for by an outward movement of the membrane of the round window. With these mass movements of the cochlear fluids the basilar membrane and the organ of Corti are depressed inward toward the scala tympani. The interaction of the hair-cells of Corti’s organ and the membrana tectoria are brought about by the to and fro movements of the basilar membrane. An effort is made to bring the movements of the hairs of the hair-cells into relation with what Wrightson calls the four phases of a simple sound wave, or rather the four phases of a single double vibration. Wrightson’s theory apparently relegates Reissner’s membrane and in fact the scala media to a status of complete functional insignificance. Though ingenious and interesting, it is, in the author’s opinion, unconvincing. The theories of Siebenmann and Shambaugh, giving a major function in vibration to the membrana tectoria, have found comparatively few followers, one obstacle to their acceptance being the apparently inherent unfitness of this structure to assume this role. Of modifications of the Helmholtz theory, the most satisfying, in the author’s opinion, is that of Dr. Albert A. Gray of Glasgow. According to this theory, the basilar membrane may vibrate in response to a sound wave over a considerable area; but there is a point of maximum amplitude of vibration, varying with the pitch or vibration rate. In other words, while the vibration may involve considerable portions of the basilar membrane, the point of maximum amplitude varies with each change of pitch, or vibra- tion rate; and it is the note corresponding to this point of maximum vibra- tion which is recorded in the cerebral hearing centre, and therefore appre- ciated as a musical tone. This theory is the more satisfying for the reason that, while robbing the Helmholtz theory of none of its essential features, it removes one of the chief obstacles to its acceptance, i.e., the conception of vibrations propagated through the cochlear perilymph which would not 3 Siebenmann: Bardelben’s Handb. d. Anat. d. Menschen. 1897. 4 Shambaugh: Physiology of the Cochlea, Annals of Otol., Sept., 1910; Physiology of Tone Perception, Dec., 1910. 6 Gray: Various Theories of Hearing; Journal of Laryngol. and Otol., p. 391. PHYSIOLOGY OF THE VESTIBULAR APPARATUS 277 induce movements in the basilar membrane more extensive than are allowed for in the Helmholtz hypothesis. The Vestibular Apparatus.—'The membranous vestibular apparatus consists of the utricle, saccule, and three semicircular canals. Whatever may be their exact function in health, it is probable that these structures act in concert. Injury to any one canal causes subjective and objective phenomena very similar to those following injury of the other two, or to the parts resting within the bony vestibule. The phenomena of vestibular irritation have been carefully studied both experimentally and clinically by Flourens, Goltz, Breuer, Crum-Brown, Ewald, Barany, Neumann, Ruttin, Hinsberg, Jansen, and a host of observers in different parts of the world. These observations, while of immense value in their bearing upon the symptoms of acute tympanic disease, have thrown but little direct light upon the vestibular function in health. They will not, therefore, be considered in the present chapter. We know that the vestibular mechanism is not an organ essential to man’s power of equilibration, for after its complete removal the individual’s equilibrium is soon re-established. By a somewhat similar course of logic the theory of Ewald—i.e., that the vestibular apparatus is in some degree responsible for the tone of the skeletal muscles—must be discarded, for destruction of the canals does not seem to influence muscular tone inju- riously. The author has had the opportunity of examining two individuals, a man and a woman, in whom the function of both labyrinths was absolutely and apparently permanently ablated, and these patients seemed to be rather above the average in muscular strength and potential efficiency. It is probable that the vestibular mechanisms are in one sense organs of orientation, in that they enable man under all conditions,—i.e., in light or darkness, and in whatever position his body may be placed,—subcon- sciously and without effort to determine the position of the different parts of his body. It is the sudden withdrawal of this power which places the individual after removal of one or both labyrinths, and even after he has recovered from the first vestibular disturbances incident to the operation, in some danger of serious accident. That he soon learns to guard against such mishaps under all or any conditions does not disprove the value of these organs in health. It proves simply that certain other faculties—• e.g., the so-called muscle, arthrodial, and tactile senses and the sense of sight—’have so enlarged their scope as to compensate for that which he has lost. Viewed in this way, it would seem that, if we permitted outselves to speak of the cochlear branch of the auditory nerve as the auditory branch, we might with equal propriety regard the vestibular branch as the nerve of orientation. The Otolith Apparatus.—In recent years there have been recorded several observations of a peculiar form of nystagmus, somewhat resembling, yet clearly distinguishable from, that induced by rotation. Barany 6 6Barany: Disease of the Otolith Apparatus; Journal of Laryng. and Otol., vol. XXXVI, p. 229. 278 ANATOMY AND PHYSIOLOGY OF LABYRINTH recorded the case of a man suffering from multiple sclerosis who, if the head was inclined toward the right shoulder, no matter how slowly, regularly exhibited a marked horizontal nystagmus to the left. That it was not due to displacement of endolymph in the semi-circular canals, but rather to the effect of position, was proved by the very gradual changes of position which caused it and also by its long persistence, i.e., provided that the inclined position of the head was maintained. This phenomenon is believed to be brought about through a disturbance of the so-called otolith apparatus or, to be more exact, of the saccule and utricle, though the exact nature of the imbalance by which it is produced has not been determined. During the past few years, much experimental work has been done chiefly in the University of Utrecht and under the direction of Professor Magnus and Dr. deKleijn, to determine more definitely the exact function of the Saccule and Utricle. While these experiments are interesting, their practical bearing upon health and disease has not yet been sufficiently established to call for their inclusion in a handbook on otology. Students who wish to follow these investigations in detail will find in the short and interesting monograph of Dr. Alex. H. Tweedie 7 of Nottingham, England, a brief outline of this work, to which has been appended a rather compre- hensive bibliography. Whatever the exact function of the vestibular mechanism may be, it is fairly certain that the essential structures are the cristae acusticae of the semicircular canals and maculae acusticae of the saccule and utricle. Both histologically and physiologically there appears to be a certain analogy between these structures and Corti’s organ. Thus, both the organ of Corti and the cristae and maculae acusticae are covered by a highly-organ- ized neuro-epithelium, of which the surface strata are composed of hair- cells from which hair-processes project. In each of these organs the hair- processes project into, or toward, an important superimposed structure, friction or impact against which is essential to its proper performance of function. Thus the hair-cells of the cristae acusticae do not project directly into the endolymph of the ampullae, but into the soft cupola terminalis covering them. The hair-cells of the maculae acusticae are in contact with the otolith-holding membrane, while the hair-cells of Corti’s organ project toward the under surface of the membrana tectoria. According to Sham- baugh, the relation of the free surface of the organ of Corti and the tectorial membrane is one of actual contact. In the organ of Corti, impact of the hair-processes against the membrana tectoria is brought about through the agency of sound waves propagated through the labyrinthine fluids. In the case of the cristae acousticae and maculae acusticae, interaction is brought about between their hair-processes and the cupola terminalis and the otolith membrane by sudden changes in the position of the head. The importance of this structural and physiological analogy between the different parts of the membranous labyrinth has been emphasized by Shambaugh. 7Tweedie: Saccular, Utricular and Allied Reflexes; Journal of Laryn. and Otol., 1922, p. 213 CHAPTER XI. INFLAMMATORY AND SUPPURATIVE LESIONS OF THE LABYRINTH. Suppurative labyrinthitis is unquestionably one of the most dan- gerous lesions with which the physician has to contend. The disease is practically always secondary to purulent disease of the middle ear or mastoid. The initial symptoms—i.e., those which announce the actual invasion of the membranous labyrinth—are invariably such as may be attributed to vestibular irritation. Unfortunately, universal familiarity with the phenomena of vestibular irritation can not as yet be assumed. It may be well, therefore, before discussing the clinical aspects of the disease, to review briefly certain experiments, facts, and accepted theories upon which our present knowledge of suppurative labyrinthitis depends. The experiments of Flourens1 upon pigeons and rabbits, published in 1824, established the fact that section of any one of the semicircular canals gives rise to uncontrollable movements of the head and eyes in the plane of the canal experimented upon. Breuer in 1888 demonstrated that similar phenomena could be induced by simple irritation of a canal without caus- ing its actual destruction,—e.g., by electrical, thermal, or chemical irritants. In 1892, Professor Ewald, of Strasburg, carried these experiments further, corroborating the results of Flourens, Breuer, and others, and establishing further the relation between endolymph movements in the different canals and the character and direction of the resulting nystagmus. These latter experiments are so clearly the basis of our present knowledge of the phenomena of vestibular irritation that we shall take time to describe them briefly. Ewald’s Experiments (Fig. 160).—Ewald2 experimented upon pigeons in the following way: Having exposed the canal selected for investigation, a small hole was drilled into it near its small end, and the lumen of the canal was obliterated at this point by the introduction of a lead mass. A second opening was next made between the small occluded end and Fig. 160.—Semicircular canals of pigeon (after Ewald). 1 Flourens: Les propri£tes et les fonctions du systeme nerveux, pp. 454-482. 2 Ewald: Physiologische Untersuchengen liber das Endorgon des Nervus Octavus, pp. 255-266. 279 280 LESIONS OF THE LABYRINTH the large, or ampullar, end of the canal. Into this second opening was introduced and fixed one end of a small hollow cylinder, open at both ends, the outer end of which communicated by means of a piece of narrow rubber tubing with a compressible rubber ball or bulb. The interior of bulb, tubing, and cylinder being now directly continuous with the lumen of the canal, it is clear that compression of the bulb must necessarily cause displacement of the endolymph in the membranous canal involved; and, since the small end of the canal has been obliterated, it is obvious that during compression, the endolymph movement must be toward and through the ampulla and into the cavity of the utricle. Beginning with a partially compressed bulb, it is equally clear that release of pressure will cause a movement of endolymph from the utricle toward and through the ampulla and in the direction of the small end of the canal. Ewald by this method experimented separately on the three semi- circular canals, and obtained the following results: Right Horizontal Canal.—Compression of the bulb (causing endolymph displacement toward the ampulla) was invariably followed by a slow strong movement of the head, exactly in the plane of the canal, toward the left. Coincidently with this head movement, the eyes were moved, also in tho plane of the canal, to the left. On release of pressure the head and eyes quickly returned to their normal position. Suction (causing endolymph movement from the utricle through the ampulla and toward the small end of the canal) was followed by slow turning of the head and eyes, always in the plane of the canal, to the right. This experiment upon the left horizontal canal gives rise to similar movements of the head and eyes, but in reversed directions. Right Posterior Vertical Canal.—Compression (i.e., endolymph displace- ment toward and through ampulla) is followed by gradual movement of the head and eyes exactly in the plane of this canal and in the direction of its ampulla,—i.e., to the right. Suction gave rise to movements in the same plane, but in the opposite direction,—i.e., to the left. The reactions of the anterior vertical canal are similar to those of the posterior vertical, varying only in accordance with its different plane. Ewald’s experiments established definitely the following important facts: (1) Excitation of any single canal can produce nystagmus only in a plane parallel with the plane of that canal; (2) the relation between the direction of the endolymph movement in any canal and the direction of the resulting nystagmus is definite and constant; and, consequently, (3) by reversal of the endolymph movement in any canal we can reverse the direction of the induced nystagmus. The analogy between these experimental phenomena in the lower animals and vestibular nystagmus in man is now clearly established. As we shall see later, vestibular nystagmus in man is characterized by a quick movement in one direction and a slow movement in the opposite direction. With pigeons both head and eyes move in response to vestibular irritation, whereas in man the nystagmic movements are confined to the eyes. With CALORIC REACTIONS 281 regard to Ewald’s experiments, it is important that we bear in mind the fact that the slow movements of head and eyes caused by either compression or suction correspond to the slow component of a vestibular nystagmus. We are accustomed to name the direction of a vestibular nystagmus in accordance with the direction of the quick eye movement,—e.g., nystag- mus to the right, or nystagmus to the left. The quick eye movement does not, however, represent the vestibular impulse, which is responsible only for the slow eye movement in the opposite direction, the quick recoil movement being under the control of the central nervous system. Note.—The differentiation of the vestibular from the cerebral component of a vestibular nystagmus has been beautifully demonstrated in certain cases in which the caloric experiment—next to be described—has been employed upon a patient under deep anaesthesia. Narcosis having been pushed to the point where the peripheral reflexes are abolished, the caloric test has been applied in the manner usually giving rise to a ves- tibular nystagmus toward the opposite ear,—let us say to the left. Under these condi- tions, the vestibular activity being retained and the central nervous control having been suspended, the eyes, instead of executing successive quick movements to the left, are slowly rotated to the right and remain in that position. As the influence of the anaes- thetic wears off and the central reflexes are restored, the eyes are suddenly jerked from their position of deviation to the right, and execute the characteristic quick movements to the left. Or, if the narcosis is prolonged, the influence of the vestibular impulse may wear itself out, and the eyes return to their normal position. Barany’s Experiments; the Caloric Reactions.—It has long been known to otologists that irrigation of the ears for the removal of pus or cerumen will in some cases give rise to nystagmus, vertigo, and disturbance of equilibrium. This remained an unsystematized fact of no practical value in otology until the discovery by Barany, of Upsala, that these phenomena were not haphazard occurrences, depending upon individual idiosyncrasy, but were constant reactions having a definite relation to the temperature of the water used. The caloric reaction may be briefly stated as follows: If we irrigate either ear of a person with normal labyrinths with water of body tempera- ture, no subjective or objective symptoms are experienced. If we use water considerably below blood heat,—i.e., 86° F., or lower,—we invariably obtain the following reactions,—viz.: (a) rotary nystagmus of which the quick movement is in the direction away from the ear irrigated; (b) the patient experiences subjective vertigo, and (c) exhibits marked disturb- ances of equilibrium. Substituting hot water,—i.e., at 110° F.,—we obtain exactly the same phenomena with the exception that the direction of the nystagmus is now toward the ear irrigated, and the ataxia shows certain changes in accordance with laws governing its relation to the nystagmus present. These reactions are very nearly invariable with normal persons. Their diagnostic value depends upon the fact that when the static labyrinth (vestibular apparatus) has been destroyed, either surgically or by disease, the vestibular nerve can no longer respond to stimulation by heat cr cold,, and the caloric reactions are absent. 282 LESIONS OF THE LABYRINTH Note.—Barany’s explanation of these phenomena in accordance with Ewald’s experiments is interesting and on the whole convincing. We must regard the whole labyrinthine cavity as an irregularly shaped vessel containing fluid (perilymph, endolymph), the temperature of which is presumably that of the blood. If, now, we bring hot or cold water in contact with one wall of this vessel, the temperature of that part of the contained fluid nearest this wall will be raised or lowered. In other words, its specific gravity here will be increased or diminished, and it will sink or rise according to the physical laws governing fluids of different specific weight. Now, the parts of the semicircular canal system nearest the surface of the inner tympanic wall are the anterior half of the horizontal canal and the anterior or outer third and ampulla of the anterior vertical canal (Fig. 161). These parts are, there- fore, first influenced by the hot or cold water used in irrigating the ear. With the head erect, sudden cooling of the endolymph in the external (horizontal) semicircular canal does not give rise to an endolymph movement, this being pre- vented by its horizontal position. In the case of the anterior vertical canal, on the other hand, the part nearest the tympanum—viz., the outer or ampullar end—points directly downward. Irriga- tion with cold water would, therefore, in this canal give rise to a downward movement of endolymph toward and through its ampulla. That cold irrigation in normal individuals is always followed by rotary nystagmus toward the opposite side is in exact accordance with Ewald’s experiments. Further corroboration of this theory is obtained from the fact that if, immediately after irrigation with cold water, the head is bent downward so that the top of the head is directly toward the floor,—a position in which the endolymph movement would be re- versed,—the direction of the nystagmus is also reversed,—i.e., is toward the ear irri- gated. Further, if the head, after irrigation with cold, is quickly bent forward to an angle of 90 degrees so that the face looks directly downward, the nystagmus is changed from the rotary to the horizontal type. The explanation of this is not far to seek, for in this position of the head the anterior vertical and posterior vertical canals assume positions somewhere between the vertical and horizontal planes, while the horizontal canals fall quite in the vertical plane. The chief endolymph move- ment is therefore in the horizontal canal, with resulting horizontal nystagmus. That the use of hot water, which would reduce endolymph specific gravity, should give rise to nystagmus in reverse directions tends further to support Barany’s theory as to the causation of these interesting phenomena. Vestibular Nystagmus.—Involuntary eye movements occur as an exceptional phenomenon with several conditions having no relation to disease of the labyrinth,—e.g., cerebellar lesions, certain ocular diseases, hereditary syphilis, neurasthenia. It is necessary, therefore, that a word be said as to certain characteristic features which distinguish vestibular nystagmus from other forms. To establish a claim to vestibular origin, Fig. 161.—Diagrammatic picture of inner tym- panic wall, showing (1) horizontal semicircular canal, and (2) anterior end of anterior vertical canal. VESTIBULAR NYSTAGMUS 283 (1) a nystagmus must be composed of a quick movement in one direction and a slow movement in the opposite direction; (2) it is increased, usually in rapidity and always in length of excursion, when the eyes are turned voluntarily in the direction of the quick movement; (3) it becomes weak, or may disappear wholly, when the eyes are turned in the direction of the slow nystagmic movement. The above are invariable characteristics of nystag- mus of vestibular origin, whether produced by experi- mental irritation or in the course of acute laby- rinthine disease. Vestibular nystagmus may be horizontal, oblique, vertical, or rotary. The nystagmus caused by acute labyrinthine disease is practically always rotary. Obviously all forms of vestibular nystagmus are rotary, since in all the eye movements take the form of to-and-fro rotation about some imaginary axis. The term “rotary,” however, is applied only to forms of nystagmus in which the eye movements as seen from in front do not seem to describe a straight line upon the cornea. We call all types of nystagmus “rotary,” therefore, in which our line of vision does not fall in the plane of the nystagmus. Thus, if our line of vision coincides with the axis of rotation,—i.e., is at right angles to the plane of rotation,—we have the most pronounced type of rotary nystagmus possible,—a veritable wheel nystagmus (Fig. 162). On the other hand, when our line of vision falls within the plane of rotation, there results a straight nystag- mus which may be horizontal (Fig. 163), vertical (Fig. 164), or oblique (Fig. 165), but can not be rotary. When our line of vision falls somewhere between the axis of rotation and the plane of rotation, we have a form of nystagmus falling somewhere between the straight and the wheel type, and partaking somewhat of the character ol each (Fig. 166). In such a nystagmus the excursion made by any giver point upon the cornea will, as seen from in front, represent the arc of a circle much larger than one whose radius is measured by the distance between the centre of rotation and the corneal point in question. Such a nystagmus is also called “rotary,” and is the type usually seen in acute labyrinthine disease. From the results of Ewald’s experiments, and from a clinical study of nystagmus as seen in suppurative lesions of the labyrinth, we may deduce the following,—viz.: That, since irritation of a single canal can produce nystagmus only in its own plane, and since the nystagmus accompanying acute labyrinthine disease rarely corresponds exactly to the plane of any single canal, we may assume that suppurative invasion of the labyrinth Fig 162. Fig. 163. Fig. 164. Fig. 165. Fig. 166. Figs. 162-166.—Types of vestibular nystagmus. 284 LESIONS OF THE LABYRINTH almost invariably involves all, and always more than one, of the three semicircular canals. A little practice may be required to detect the rotary character of the nystagmus usually accompanying acute labyrinthine disease. To the unpractised eye the ocular movements may at first seem quite in the hori- zontal plane. If, however, we fix our attention upon some dilated corneal vessel and note carefully its changing relation to the border of the lower lid, the rotary element becomes unmistakable. Lack of attention to this point has doubtless been responsible for some obviously incorrect clinical reports. Physiological Nystagmus.—This term has been applied by Barany to a form of nystagmus which is seen in many normal persons when the eyes are voluntarily placed in the extreme lateral position in either direction. It is mentioned in this place because it is of the greatest importance that the student should learn to recognize it as having no significance as an indication of suppurative labyrinthitis. The character of the eye move- ments is quite similar to that above described,—that is to say, it is usually rotary in character and is composed of a quick movement in one direction and a slow movement in the opposite direction. It is, however, easily differentiated from the nystagmus of labyrinthine disease by the following points: (a) Spontaneous vestibular nystagmus in its most active stage is constant, but is exaggerated when the eyes are voluntarily turned in the direction of the quick movement. Physiological nystagmus is present only when the eyes are turned strongly in one or the other lateral direction, and then usually lasts but a few seconds. (b) Vestibular nystagmus in its active stage is present whatever the position of the eyes. Later, however, as the strength of the nystagmus is gradually reduced, it may be wholly absent when the eyes are turned in the direction of the slow nystagmic movement. Physiological nystagmus changes its direction according to the position of the eyes,—the quick movement corresponding to the lateral direction in which the eyes are voluntarily turned. (c) Vestibular nystagmus in its most active stage is almost invariably accompanied by vertigo and ataxia, and these symptoms, even after the nystagmic movements have grown weaker, can usually be reinduced by sudden movements of the head. Physiological nystagmus is absolutely unaccompanied by any subjective symptoms. Barany’s estimate that this so-called physiological nystagmus occurs in 60 per cent, of normal persons seems to me exaggerated,—20 to 25 per cent, being, according to my observation, nearer the correct proportion. Rotation or Turning Experiment.—This is simply another method of inducing endolymph movements in the semicircular canals and thereby causing symptoms of vestibular irritation. When a normal person, seated, with head erect, upon a revolving chair (Fig. 167), is suddenly and forcibly rotated in one or other direction, —let us say to the right,—there occurs a horizontal nystagmus with the Fig. 167.—Revolving chair: patient and physician in position for rotation test. THE SEMICIRCULAR CANALS 285 quick eye movement in the direction in which he is turned,—i.e., to the right. When the rotations are suddenly stopped, the direction of the nystagmus is reversed,—i.e., it is now to the left. The average duration of this so-called “after nystagmus” is about 40 seconds. The rotation experiment is a useful aid in the study of vestibular phenomena in that, by placing the head during rotation in various posi- tions, one is able to induce at will almost any form of vestibular nystagmus. Obviously the various forms of nystagmus, vertigo, and ataxia can mean little to the student who has not a correct mental picture of the planes of the three semicircular canals, and also of the relative positions of their ampullar and small ends. These relations seem often to present such difficulties to the beginner that the writer is tempted to suggest a very simple device by which, with the aid of two visiting cards, one may easily fix them in memory. In Fig. 168, a-b represents a line throughout which the card is to be cut or divided by a sharp-pointed knife; c-d, a line at which the card is to be bent or folded upon itself. If now we bend the card at c-d, so that the Fig. 168. Fig. 169. Figs. 168 and 169.—Author’s scheme for remembering semicircular canal planes, two segments occupy planes at right angles to each other, and insert be- tween the cut edges, now also bent at right angles, the edge of a second card (Fig. 169), we have three planes, each at right angles to the other two. If we wish this little improvised model to represent the planes of the three canals of the right ear, we have only to hold it (mentally) to the side of the head, with the bisecting card in the horizontal plane, and its edge, d-e, parallel with the anteroposterior axis of the skull. In this position we have the upper half of the anterior segment of the vertical card (a) representing the plane and position of the anterior vertical canal, the middle part of the posterior segment (b) representing the posterior vertical canal, and the enclosed part of the inserted card (c) representing plane and position of the horizontal canal. If we wish this model to represent also the respective curves and the 286 LESIONS OF THE LABYRINTH ampullar and small ends of the three canals, we must outline these struc- tures upon the cards as indicated in Figs. 170 and 171, and with scissors cut away part of the card (Fig. 171), as indicated by the dotted lines. When these cards are cut, folded, and adjusted (Fig. 172), we have clearly before us the com- mon opening of the anterior and posterior vertical canals (a), the ampulla of the anterior vertical canal (b), the ampulla of the hori- zontal canal (c); and the ampulla of the posterior vertical canal (d). Explanation of Rotational Nys- tagmus.—When the head, held in the erect position, is suddenly turned in the horizontal plane either to the right or left, the endolymph in the two horizontal canals, by reason of its inertia, at first lags behind,—i.e., is dis- placed in the opposite direction. If, for example, the head is turned to the right, the initial endo- lymph movement will in the right horizontal canal be toward its ampulla, while in the left hoiizontal it will be toward the small end of the canal (see Fig. 173). Now, according to Ewald’s experiments, these are precisely the endolymph movements which in these canals should produce nystagmus to the right, and this phenomenon is always present during the rotations to the right. When the rotations are suddenly stopped, the endolymph, this time by reason of its momentum, is displaced in the opposite direc- tion, with the result that the direction of the nystagmus is re- versed,—i.e.} it is now to the left. Note.—When a normal individual is rotated about a vertical axis, the influence of the rotations upon any particular canal will depend upon the relation which the plane of this canal bears to the horizontal plane. If the canal in question lies quite in the Fig. 170. Fig. 171. Figs. 170, 171, and 172.—Author’s scheme for remem- bering exact relative positions of the three canals. Fig. 172. SYMPTOM COMPLEX OF VESTIBULAR IRRITATION 287 horizontal plane, the influence of rotation will reach its maximum, and will produce a maximum endolymph displacement. As the plane of the canal departs from the hori- zontal, the influence of rotation in the horizontal plane is diminished, and becomes progressively less in exact proportion as the angle of extension between the plane of the canal and the horizontal plane is increased. Finally, when the canal assumes the ver- tical plane, no displacement of endolymph results from rotation about a vertical axis. It is obvious, therefore, that with head erect, rotation in the horizontal plane influences only the two horizontal canals, the an- terior and posterior vertical canals being eliminated by their position. If, how- ever, the head during rotation is bent forward so that the face looks directly downward, the horizontal canals will be made to assume the vertical plane, while the posterior vertical canals will be brought more into the horizontal plane. Rotation with the head in this position will therefore be followed by rotary nystagmus. During rotation, then, we may, by changes in the position of the head, bring different canals under the influence of the experi- ment, and thus vary at will the form of nystagmus. In all cases, however, the direction of the nys- tagmus follows a definite rule, which may be briefly restated as follows: During rotation a person exhibits nystagmus in the direction in which he is turned. Arrest of rotation is immediately followed by nystagmus in the opposite direction. The diagnostic value of the rotation test and the method of applying it will be spoken of in con- nection with the latent stage of suppurative labyrinthitis. The Symptom Complex of Vestibular Irritation: Nystagmus, Vertigo, Ataxia.—Vestibular irritation, whether experimentally induced (e.g., by thermal, electrical, or mechanical stimuli) or resulting from acute labyrinthine disease, is almost invariably announced by three associated symptoms,—viz., spontaneous nystagmus, vertigo, and disturbance of equilibrium. These three phenomena are so constantly associated with the onset or acute stage of suppurative labyrinthitis that their absence during this period would of itself be sufficient to exclude the vestibule and static labyrinth as among the parts involved. Obviously, these symptoms, either singly or in association, may also be present in various conditions not dependent upon labyrinthine disease. Thus, nystagmus may occur with certain ocular lesions, with cerebellar abscess, with tumors occupying the posterior fossa of the skull, or may occur Fig. 173. — Diagrammatic picture of a horizontal section of skull, passing through horizontal semicircular canals, a, Large arrow indicating direction in which individual is rotated; b, small arrow = resulting en- dolymph displacement during rotation; c, medium arrow showing direction of quick eye movement dur- ing rotation. 288 LESIONS OF THE LABYRINTH as a physiological anomaly having no recognized pathological significance (“physiological nystagmus”). As with nystagmus, so may vertigo and ataxia result from many functional and organic disorders. It is very important, therefore, that we be able to recognize certain distinguishing features, either in the symptoms themselves or in their relation to each other, as they occur in acute labyrinthine disease. In the first place, vestibular vertigo is always rotary in character,— i.e., is always accompanied by a subjective impression of the rotation of surrounding objects, and this subjective rotation is always in a plane cor- responding to the plane of the nystagmus. There can be no doubt that the very closest relation exists between vestibular vertigo and vestibular ataxia, and that the character of each depends upon the type of nystagmus present. Barany was the first to observe certain seemingly constant rela- tions between vestibular vertigo and ataxia and vestibular nystagmus, which he formulated somewhat as follows: 1. Spontaneous vertigo of vestibular origin is always accompanied by some degree of spontaneous vestibular nystagmus, and is always increased when the eyes are voluntarily turned in the direction of the quick nystagmic movement. 2. Vestibular ataxia is always accompanied by nystagmus, and is always influenced by the position of the head. 3. A person exhibiting vestibular nystagmus tends to move within the plane of the nystagmus, and to fall in the direction opposite to the quick nys- tagmic movement. The writer believes that the above statements are in the main correct, and that what may seem to be occasional exceptions or contradictions will under more accurate methods of observation be recognized as apparent rather than real. The practical value of these hypotheses in furnishing us with criteria by which the value of single symptoms may be gauged must be apparent. Thus, vertigo which is not accompanied by nystagmus even when the eyes are turned strongly in one or other lateral direction, and ataxia which is not attended by nystagmus and is not influenced by changes in the position of the head, are certainly not suggestive of vestibular irritation. A word must also be said as to the reaction movement, or tendency which a person exhibiting vestibular nystagmus shows to fall in a certain direction. Barany’s law, it will be remembered, reads, “A person exhibit- ing vestibular nystagmus tends to move within the plane of the nystagmus, and to fall in the direction opposite to the quick nystagmic movement.” It seems to me that we shall obtain a better understanding of the principle involved if we say that a person exhibiting vestibular nystagmus tends to rotate within the plane of the nystagmus and in the direction opposite to the quick eye movement. This tendency to rotation is about an axis passing through his head, and he falls, or tends to fall, in the direction in which this rotation throws his body, and this, as we shall see, is not always in the opposite direction to the quick nystagmic movements. ATAXIA OF VESTIBULAR IRRITATION 289 Let us take for example a person who has been turned rapidly in a re- volving chair ten times to the right, and who as a result exhibits well- marked horizontal nystagmus to the left. He now experiences pronounced rotary vertigo in which surrounding objects seem to rotate about him in the horizontal plane,—and usually to the left. Immediately after the rotations of the revolving chair are stopped, let him stand and, with head erect and feet approximated, close his eyes. The nystagmus being in the horizontal plane, the reaction movement should be, not falling, but grad- ual turning in the horizontal plane to the right (Fig. 174). This, however, may not be demonstrated, or may be shown only by a tendency to turn the head to the right. Let us now test Barany’s proposition that vestibular ataxia is always influenced by the position of the head. Request him to incline the head forward to an angle of 90 degrees so that the face looks directly downward (Fig. 175). With this position of the head the plane of the nystagmus is changed from the horizontal to the vertical, and, the quick eye movement being to the left, the head tends to rotate to the right. This rotation of the head to the right results, however, in throwing his body in the opposite direction, and he falls to the left. In this case we seem at first glance to have a contradictory reaction, in that the subject falls in the direction of the quick eye movement. After a moment’s reflec- tion, however, and with Fig. 175 before us, it becomes clear that the rotation of the head in the direction opposite to that of the quick eye movement is precisely the factor which determines his falling to the left. If the head is inclined directly backward to an angle of 90 degrees so that the face looks directly upward, the rotation tendency will throw his body in the opposite direction,—i.e., he will fall to the right (Fig. 176). In acute suppurative labyrinthitis the nystagmus is of the same type as that induced by syringing the normal ear with cold water. The caloric test enables one, therefore, to investigate the ataxia accompanying the nystagmus seen in acute labyrinthine disease. Here, the nystagmus being rotary and falling therefore more nearly in the vertical plane, the patient, standing with head erect, tends to fall in the direction opposite to the quick eye movement (Fig. 177). In acute suppurative labyrinthitis, the nystagmus is practically always rotary and toward the sound ear, and hence the patient falls toward the diseased ear. Pointing Tests.—Closely related in origin or causation to the reaction movements (falling directions) are the phenomena brought out by the so- called pointing tests. The normal individual, with eyes closed and having located with a finger some fixed object by the sense of touch, can move his hand upward or downward in the horizontal plane and bring his finger again into contact with the object touched, or will miss it only by a fraction of an inch. This may be called normal accuracy. In an individual, on the other hand, who exhibits the symptom-complex of vestibular irritation (e.g., after rotation or the caloric test), pointing accuracy is lost, the hands in attempting without the aid of sight to move accurately in the vertical plane regularly diverging in the direction opposite to that of the nystagmus present. (For the theory and application of these important tests, see Chapter XIY.) 290 LESIONS OF THE LABYRINTH From this short preliminary discussion of vestibular phenomena we must pass to a consideration of the lesions upon which they throw light. The subject of vestibular irritation is so many-sided and presents so many phases which are of practical or academic interest to the otologist, that it is no easy matter to condense one’s discussion into the narrow space limits Fig. 174. Fig. 175. Figs. 174, 175, 176 and 177.—Diagrams showing falling directions in relation to vestibular nystagmus. N arrow, direction of nystagmus; DR arrow, direction of rotation or falling. Fig. 176. Fig. 177. of a manual of this character. Naturally, this is possible only by the elim- ination of much which one would like to include were more ample space at his command. The student who wishes to study for himself the variations in vertigo and ataxia in response to different forms of vestibular nystagmus, may do so by observing a person who has just been rotated upon a TYPES OF ROTATION NYSTAGMUS. 291 revolving chair. In order to facilitate such studies, we append below a synopsis of Barany’s3 rules for determining in advance the form of nystagmus which shall follow rotation. “Sitting erect upon a revolving chair a person revolves about a vertical axis. If we now imagine his eye cut through in a horizontal plane,—i.e., by a plane at right angles to the axis about which he revolves,—it is evident that this section will describe a line upon the cornea which will vary according to the position of the head. This line will indicate the form of the nystagmus (Fig. 178). Thus, with head erect, the horizontal plane in bisecting the eye will form a line passing horizontally across the cornea, and produce a horizontal nystagmus (Fig. 178, A). With head bent laterally toward the Fig. 178.—Diagrams showing different forms of rotation nystagmus. shoulder so as to form an angle of 45° with the vertical, a horizontal section will be indicated by a line passing obliquely across the cornea, and produce an oblique nystag- mus (Fig. 178, B). If the head is bent fully toward the shoulder so as to form an angle of 90° with the vertical, the eye will be bisected in a plane at right angles to its trans- verse diameter, and give rise to a vertical nystagmus (Fig. 178, C). With the head bent forward so that the face looks directly downward, the horizontal plane would divide the orbit so as to remove a segment which would include the iris. It should, therefore, be indicated by a circular line about the iris. The character of the nystag- mus, howrever, is indicated by the points of contact at which the horizontal plane enters the orbit, and not by those at which it cuts its way out. With the head bent directly forward, therefore, a horizontal section is indicated by a curved line above the iris, and turning to the right will be followed by rotary nystagmus to the left (Fig. 178, D). With head bent directly backward so that the face looks upward, a horizontal section describes a curved line below the iris. With head in this position, rotation to the right is followed by rotary nystagmus to the left. But in this case the concavity of the nystag- mic curve is directed upward (Fig. 178, E).”4 3 Barany: Physiologie u. Pathologie des Bogengang-Apparates beim Menschen, 12-13. 4Kerrison: Phenomena of Vestibular Irritation, Annals of Otology, Rhinology, and Laryngology, Sept., 1909. 292 LESIONS OF THE LABYRINTH SUPPURATIVE LABYRINTHITIS. Under this head are grouped such lesions of the labyrinth as are sec- ondary to suppurative disease of the middle ear or mastoid. In the order of their importance and frequency, they may be mentioned as follows: Diffuse suppurative labyrinthitis, circumscribed suppurative labyrinthitis, diffuse serous labyrinthitis, perilabyrinthitis. Diffuse Suppurative Labyrinthitis.—Etiology.—Suppurative iaby- rinthitis is always secondary to a suppurative lesion originating elsewhere in the body,—usually within the middle-ear cavity. While it may be argued upon theoretic grounds that an infective process may reach the labyrinth by other pathways,—e.g., by the blood-vessels from a focus of infection within the tonsil or parotid gland, or by way of the vestibular or cochlear aqueducts from a suppurative lesion within the cranium,—it is exceedingly doubtful if such modes of infection have been definitely estab- lished in any case in which tympanic suppuration was absent. For practical purposes, therefore, we may say that suppurative laby- rinthitis is always secondary to a suppurative process within the middle ear. The spread of an infection from the tympanum to the labyrinth may occur by any one of several routes, viz.: 1. By erosion of the bone at some point upon the labyrinthine wall giving rise to a so-called labyrinthine fistula. The points at which such fistulse are seen may be mentioned in accordance with the frequency of their occurrence in the following order,—(a) horizontal semicircular canal, (b) oval window, involving necrosis of the stapedial foot-plate or mem- branes, and (c) some point upon the promontory. 2. By extension of the inflammatory process through the bone, or by way of the minute anastomotic vessels without the production of a demon- strable fistula. 3. Through invasion of the labyrinth from a deep-seated extra-dural abscess on the posterior surface of the petrous pyramid (Hinsberg). This pathway of infection is considered here because an extra-dural abscess at this point is usually of otitic origin. 4. Infection of the labyrinth as a result of injury to the labyrinth wall during operation. Mygind5 states that he has seen a considerable number of such cases, and records his belief that labyrinthine suppuration occurs more frequently as a result of traumatism incident to the radical operation than is generally recognized. That such a mode of infection must be con- sidered seriously is emphasized by the statement of Jansen6 that in his own operative experience suppurative labyrinthitis has occurred in 16 cases as a direct result of injuries inflicted during the radical operation, or subsequent curettage. Hinsberg7 collected from the reports of other aural surgeons 25 cases of injury to the stapes during operation, two of which BMygind: Trans. Am. Med. Assoc., Otological Section, 1910, p. 189. 6 Jansen: Trans. Am. Laryn., Rhin., and Otol. Society, 1908, p. 115. 7Hinsberg: Uber Labyrintheilerungen, p. 4. T Y M PANIC SUP P UP AT 10 N 293 ended fatally. To these he added a fatal case of his own. It is obviously incumbent upon us to give greater prominence to this possible source of infection than is accorded it in most text-books. Frequency of Labyrinthine Suppuration as a Complication of Suppurative Otitis Media.—This is a question almost impossible of exact solution. Undoubtedly many deaths have occurred as a result of intracranial com- plications in which an intermediate lesion of the labyrinth has been un- recognized and therefore ignored. Presumably the discrepancy in the percentages of cases developing suppurative labyrinthitis reported in different clinics has been due in part to the closer study, and therefore more exact knowledge, of the disease in certain clinics as compared with others. Thus, in Prof; Urbantschitsch’s clinic in Vienna, and in the Uni- versity-Polyclinic presided over by Prof. Hinsberg in Breslau, where the disease has been made the subject of special study, the number of cases reported has been larger than elsewhere in Austria and Germany. According to Hinsberg,8 one in every 100 cases of middle-ear suppura- tion develops suppurative labyrinthitis. Von Stein,9 of Moscow, in 420 cases of middle-ear suppuration operated on, found suppurative labyrin- thitis in 10 cases; he therefore places the percentage as high as 2.2 per cent. Hinsberg states his belief that infection of the labyrinth is a more frequent complication of tympanic suppuration than all the intracranial complica- tions (meningitis, brain abscess, sinus thrombosis) combined; and further that a very large percentage of all cases of meningitis and brain abscess following middle-ear disease are in reality secondary to an intermediate suppurative process involving the labyrinth. These statements are based partly upon his own observations and partly upon an analysis of the pub- lished reports of others. Of conditions within the middle ear rendering invasion of the labyrinth probable, all writers agree that the presence of cholesteatoma is the most potent factor. Jansen some years ago reported a series of 121 cases of suppurative labyrinthitis in which cholesteatoma was the apparent cause in 71 cases. Holinger,10 after examining the literature bearing upon this question, concludes that a majority of cases of suppurative labyrinthitis are traceable to the influence of cholesteatoma. Tubercular lesions of the middle ear are also said to be responsible for many cases of labyrinthine disease (Siebenmann, Nager, Hinsberg). Aural tuberculosis, however, is more likely to cause widespread necrosis of the labyrinthine capsule without early signs of vestibular irritation. While either an acute or a chronic middle-ear suppuration may lead to labyrinthine infection, by far the greater number of cases are caused by the chronic form of suppurative otitis media. On the other hand, infec- tions of the labyrinth secondary to acute purulent otitis media seem to exhibit a greater tendency to spread rapidly to the meninges, and there- 8 Hinsberg: ibid., p. 1. 9 Von Stein: Annales des maladies de l’oreille, 1896, p. 30. 10Holinger: Trans. Section Laryng. and Otol., Am. Med. Assoc., 1910, p. 155. 294 LESIONS OF THE LABYIUNTII fore to end fatally. This difference is presumably due in part to the greater average virulence of the acute tympanic infections. As to the comparative significance of different points of attack as in- fluencing the subsequent course of the disease, experienced observers very generally agree that infection of the labyrinth through necrosis (fistula) of the external semicircular canal offers a much more favorable prognosis than do lesions in which the pathway of infection is through the oval or round window, or even through a necrotic defect in the promontory. As far back as 1907, Panse11 emphasized his belief that fistulse of the semi- circular canals constitute a condition prognostically favorable so far as life is concerned. Somewhat in accord with this view is the statement of Hinsberg that in nearly all the fatal cases coming under his observation, one or both windows were perforated or “broken down” (“so ist in der Tat kein Zweifel dariiber moglich dass bei den todlich verlaufenden Fallen fast stets eins oder beide Fenster durchbrochen sind, wahrend Bogen- gangsfisteln bei ihnen sehr selter sind”). If these facts have any practical significance, they should teach us the danger of careless surgery in the neighborhood of the stapes and oval window. These are points which the student of practical otology will do well to think over and bear in mind. Symptoms.—As the labyrinth is composed of two distinct mechanisms, —viz., the cochlea and the static or vestibular apparatus,—so the symptoms of diffuse labyrinthitis must fall under two heads,—(1) those due to impair- ment or loss of the cochlear function—(i.e., deafness), and (2) those due to disturbance of the static or vestibular function. Undoubtedly the most striking and characteristic phenomena of the disease are those referable to the disordered vestibule, and these will chiefly occupy our attention in the following pages. To appreciate properly these phenomena, it is necessary to recognize two distinct and clearly differentiated stages of vestibular disturbance,—viz., (a) an acute stage, characterized by symptoms of vestibular irritation; and (b) a latent or quiescent stage, characterized by vestibular paralysis. Clinical Features of the Onset and Acute Stage.—Since suppurative labyrinthitis is practically always secondary to purulent otitis media, there may be pre-existing symptoms referable to that disease, upon which those of the labyrinthine lesion are engrafted. The invasion of the labyrinth is usually announced by sudden and very distressing vertigo. If the patient has been previously confined to bed, as when the labyrinth is invaded during an attack of acute mastoiditis, the onset is less spectacular, and possibly somewhat less severe subjectively, than may be the case when the patient is up and about, under which cir- cumstances he may be overwhelmed by the suddenness and severity of the attack. If the patient does not fall, he usually requires support, and, as a rule, is obliged by the severity of the symptoms to go to bed. Following quickly upon the appearance of vertigo, nausea and vomiting frequently 11 Panse: Arch, of Otol., Amer. edition, April, 1907, p. 87. SYMPTOMS: NYSTAGMUS, VERTIGO, ATAXIA 295 add to the patient’s distress. Vomiting is often a persistent and frequently recurring disturbance during the first day or two of the attack. Nystagmus.—If the eyes are observed at this time, there will invariably be seen an active rotary nystagmus with the quick eye movements toward the sound ear. The eye movements are increased in rapidity and extent when the eyes are voluntarily turned in the direction of the quick nystagmic movement, and are noticeably diminished when they are turned in the opposite direction. The nystagmus is noticeable, however, and the direc- tion of the quick movement is unchanged, whatever the position of the eyes. The nystagmus accompanying suppurative labyrinthitis, while usually described as rotary, is really in most cases a combination of the horizontal and the wheel types (see Fig. 166 on page 282). Vertigo.—The vertigo also is of the rotary type, i.e., the patient has the impression that surrounding objects are rotating about him, sometimes in such bewildering fashion that he is unable to analyze and correctly de- scribe his sensations. When he is able to do so, it is found that the plane in which objects seem to rotate always corresponds to the plane of the nystagmus. When, therefore, he stands or is supported with head erect, objects seem to rotate about him in a plane approaching the vertical, but when he lies upon his back (i.e., with face turned upward), the plane of the nystagmus falls more into the horizontal plane, and his sensation is of the rotation of objects in the horizontal plane about him. The direction of seeming rotation varies; most usually it is from the side of the slow nystagmus movement. Thus, with head erect, objects seem to rise from the floor on the side corresponding to the diseased ear, and to fall or sink on the other side of his body. In some cases, however, the direction is reversed. If he closes his eyes, he has the sensation of himself rotating. If his eyes are voluntarily turned in the direction of the quick nystagmic movement, not only is the nystagmus more marked, but the severity of the vertigo and the sense of rotation are greatly increased. It has been noted (Jansen, Barany, and others) that the patient frequently assumes a characteristic position in bed,—i.e., he lies with the sound ear buried in the pillow, so that, when tempted to look about the room, the movement of the eyes will be in the direction of the slow eye motion, which position tends to lessen not only the nystagmus but also the distressing subjective symptoms. Ataxia.—If the patient stands or is supported in the upright position with head erect, he exhibits marked disturbance of equilibrium, and falls or tends to fall toward the diseased ear. Supposing, for example, that the lesion is an acute suppurative invasion of the right ear, the nystagmus will be to the left and the patient will fall to the right. If he turns his face toward the right shoulder, thus changing the plane of the nystagmus, he will fall backward. If his face is turned toward the left shoulder, he will fall forward. The pointing reactions in the acute stage of a diffuse suppurative labyrinthitis are those invariably present during active vestibular irri- tation from any cause. (See Chapter XIV.) 296 LESIONS OF THE LABYRINTH While the patient lies quietly in bed, the subj ecti ve symptoms are minimized, and, since any sudden movement of the head tends to increase their severity, he soon learns to remain quiet and to resist any unnecessary movement. The syndrome above described—i.e., the nystagmus and associated vertigo and ataxia—is present at the onset and to some extent throughout the acute stage of practically every case of suppurative labyrinthitis. Com- plete absence of this triad is, therefore, a valid reason for excluding acute suppurative labyrinthitis. Of other symptoms probably the most constant at the onset is headache in some form. Often this takes the form of severe deep-seated earache. In other cases the pain is not so localized, but is referred to other parts of the head,—e.g., the vertex or occiput. The temperature is probably always elevated at the onset, and may rise to 103° or 104° F. On the other hand, the writer has seen cases of extensive labyrinthine suppura- tion in which the temperature at no time exceeded 101° or 102° F. When in addition to the characteristic vestibular phenomena there are frequent vomiting, high temperature, and severe headache, and these symptoms do not show early tendency to amelioration, one is forced to consider the possibility of meningeal infection. It must not be forgotten, howrever, that any or all of these symptoms may be present at the onset as a result of the labyrinthine lesion alone. Cochlear Disturbance; Deafness.—A very brief statement will suffice as to the deafness of the acute stage of diffuse suppurative labyrinthitis. Usually the deafness is such as to force itself upon the physician’s attention. In a case which I had an opportunity of watching from the onset to the final recovery, one of the earliest symptoms—apparently synchronous with the vestibular phenomena—was the profound deafness of the diseased ear. As the patient lay with the sound ear buried in the pillow, her failure to notice questions or even sounds originating quite near the diseased ear proclaimed its practical loss of hearing power. There was never in this case any return of cochlear function. Personally, I have never seen an indubitable case of diffuse suppurative labyrinthitis in which very marked deafness was absent. Sudden and profound deafness is, therefore, an important sign of labyrinthine suppura- tion, and the retention of a demonstrably useful degree of hearing power should in my opinion be given very considerable weight as an indication that the labyrinth is not involved in a severe suppurative process. When in a case of unilateral labyrinthine disease the deafness is in doubt, the most convenient and also the most useful and reliable test is by means of words and numbers spoken in rather loud voice close to the diseased ear, the function of the sound ear being excluded by means of the Barany noise instrument (see Fig. 79 on page 95). Caloric Test in Relation to the Acute Stage.—In a typical case of diffuse suppurative labyrinthitis, the nystagmus toward the sound ear is due not to irritation of the diseased vestibular apparatus, but to sudden annulment of its function,—this being equivalent in effect to a direct irritation of the sound and nowr unopposed, vestibular mechanism. Irri- CALORIC TEST IN RELATION TO ACUTE STAGE 297 gation of the diseased ear with hot or cold water would, therefore, be abso- lutely without effect upon the spontaneous nystagmus present. Irrigation of the sound ear with cold water would temporarily check the nystagmus or possibly reverse its direction for a few moments. Irrigation of the sound ear with hot water would cause great exaggeration of the nystagmus and subjective symptoms present, possibly inducing a paroxysm of nausea and vomiting. All or any of these phenomena would be more or less cor- roborative. The author can not see, however, that this test in the average run of cases is in any way essential to a correct diagnosis during the acute stage, and its influence upon the course of an acute inflammatory process within the labyrinth can not be regarded as free from possibilities of harm to the patient. With characteristic signs of vestibular irritation and profound deafness, the diagnosis of diffuse suppurative labyrinthitis would seem to be clear without recourse to the caloric test. On the other hand, with symptoms of vestibular irritation and retention of hearing, it would seem obviously unwise to subject the diseased ear to any shock which might possibly convert a circumscribed infection into a diffuse suppurative labyrinthitis. Unless, therefore, there are atypical or contradictory symp- toms leaving the diagnosis in doubt, the caloric test is to be advised against until the symptoms of vestibular irritation have completely subsided. Subsidence of Vestibular Symptoms.—In cases in which no intracranial complications occur, the disease runs a fairly characteristic course. The symptoms of vestibular irritation usually show rather rapid amelioration, and in their abatement follow a fairly definite order. That is to say, the vertigo and ataxia regularly subside before the nystagmus. Usually from the second to the fourth day the nausea and vomiting are relieved. From the third to the fifth day of the attack the vertigo is in many cases so much less pronounced that the patient is comparatively comfortable as he lies quietly in bed. The nystagmus, however, is still present, and turning the eyes voluntarily in the direction of the quick nystagmic movements brings a return of the vertigo. Sudden or violent movements of the head also induce recurrence. The temperature, which may be rather high at the onset,—i.e., 102° or 103° F.,—usually subsides with the recession of the vestibular phenomena. At least this is the usual course in an uncompli- cated case. Usually by the middle or end of the second week, and in some cases sooner, the vertigo is so far relieved that the patient—in the absence of course of contra-indicating constitutional symptoms—is able to stand without discomfort. Even now, however, sudden or exaggerated head movements are apt to induce vertigo and ataxia. Finally, during, or by the end of, the third week the spontaneous nystagmus usually completely disappears. This describes the average, with of course very considerable variations in individual cases. The writer recalls one case of Very severe and rapidly fatal labyrinthine infection in which the vertigo and nystagmus seemed completely to have disappeared within a week of the onset. In another case of extensive labyrinthine suppuration, which recovered only after 298 LESIONS OF THE LABYRINTH surgical removal of the labyrinth, the spontaneous nystagmus persisted until well into the fifth week. The Use of Covered Glasses.—It has been found that vestibular nystag- mus is more or less controlled, or lessened, when the gaze is fixed upon some object within easy visual range. The inhibitory influence of this focusing of the vision upon one object is not appreciable during the most active stage of the nystagmus, but becomes progressively more noticeable as the strength of the eye movements is reduced. Barany, following a suggestion of Dr. Hans Abels, makes use of this fact by placing before the patient’s eyes a pair of opaque, or covered, spectacles, the surfaces of which are so near the eye that the vision can not be focused thereon. By thus removing the visual resting point, the nystagmus in many cases becomes much more marked. In this way the character of a very slight or rapidly diminishing nystagmus may be determined, or one that has apparently ceased may again become noticeable. It is well, therefore, in doubtful cases,—i.e., in cases in which the presence of spontaneous nystagmus is in doubt,—to make use of this device. When finally the nystagmus has completely disappeared, the patient no longer exhibits any demonstrable symptoms of vestibular irritation. We have now to determine whether he has suffered from (a) some form of transitory inflammation of the labyrinth which has undergone resolution, leaving an intact and functionating organ; or (b) from a suppurative laby- rinthitis by which the vestibular function has been abolished. It is at this stage that the caloric test is of paramount importance. Symptoms of Labyrinthine Fistula.—Before leaving the discussion of the acute stage, a word should be said about the so-called “fistula test.” It is a recognized fact that suppurative labyrinthitis may be established with or without the demonstrable presence of a gross defect—i.e., fistula— in the labyrinthine wall. It is also conceivable that defects in the bony capsule of the labyrinth may exist, as a congenital condition or even as a result of tympanic disease, without giving rise to a suppurative process within the vestibule. In any case in which vestibular irritability is retained, the presence of a fistula leading into the labyrinth may be demonstrated by means of any instrument by which the air in the external auditory canal can be alternately compressed and rarefied. The best instrument for this purpose is one embodying the principle of the Politzer inflating apparatus, but having a smaller end piece to fit the orifice of the auditory canal. When this is moistened and pressed into the meatus, compression of the bulb condenses the air in the auditory canal and tympanum and, if a fistula is present, forces air into the labyrinth. When the static labyrinth is still functionat- ing (i.e., susceptible of irritation), this is regularly followed by nystagmus which varies in direction in accordance with the location of the fistula and the direction of the resulting endolymph displacement. The nystagmus thus induced is usually preceded by a slow movement of the eyes in one or the other direction, and this slow movement corresponds to the slow FISTULA TEST: ITS DIAGNOSTIC VALUE 299 component of the nystagmus. Compression may result in a single slow movement of the eyes and their quick return when pressure is relieved, or the preliminary slow excursion may be followed by several characteristic vestibular movements lasting some seconds. In the presence of a fistula, nystagmus can be induced either by compression or aspiration, which, however, give rise to nystagmus in opposite directions. That is to say, if compression causes nystagmus to the left, aspiration will reverse this direction, giving rise to nystagmus to the right. When no fistula exists, this experiment is either negative, or gives rise to very slight, almost imperceptible eye movements due presumably to pressure upon the struc- tures closing the labyrinthine windows. Obviously if the vestibular irrita- bility is completely lost, this test will give negative results even in the presence of a fistula. The conditions upon which the compression and aspiration test may throwT light may be stated as follows: 1. Chronic suppurative otitis media without labyrinthine infection and with intact bony capsule: compression test negative. 2. Defect (fistula) in bony capsule of the labyrinth, but without infec- tion of membranous labyrinth; shown by absence of spontaneous symp- toms of vestibular irritation, plus strong reactions to compression and aspiration (caloric irritability normal). 3. Acute stage of suppurative labyrinthitis with fistula; spontaneous nystagmus modified by compression and aspiration experiment. 4. Presence of fistula in the latent stage of suppurative labyrinthitis: shown by negative caloric reaction and very slight, but typical, response to compression. In this case one might infer that the vestibular mechanism had retained a vestige of functional activit}' which can no longer be stim- ulated by heat or cold, but can still react to the stronger mechanical irrita- tion produced by compression. Obviously when the caloric reactions are absolutely negative, the absence of response to compression or aspiration can not be regarded as disproof of the presence of a fistula, since vestibular irritability may be completely abolished. Since it is easily conceivable that infective matter may be forced by air under pressure from an infected tympanum into an uninfected vestibule, it is clear that this test should be used with moderation and care. Latent, or Quiescent, Stage of Suppurative Labyrinthitis.—This stage is sometimes spoken of as “chronic suppurative labyrinthitis,” a term which is distinctly misleading, since it seems to imply two varieties of the disease, just as in acute and chronic purulent otitis media we have different types of tympanic inflammation. But whereas acute purulent otitis media may run its course from onset to resolution without having passed through any of the phases characteristic of chronic middle-ear suppuration, every case of diffuse suppurative labyrinthitis must inevitably progress — and usually quite rapidly — to the latent stage. The disease is said to have reached the latent stage as soon as the symptoms of vestibular 300 LESIONS OF THE LABYIHNTH irritation—i.e., spontaneous nystagmus, vertigo, etc.—have completely disappeared. In the latent stage of the disease, the patient may be up and about, and may apparently regain his normal standard of health and strength. He may now experience no subjective symptoms referable to the labyrinth beyond the deafness and certain defects of orientation to be referred to presently. For the time being—though this is by no means invariable— the aural disease may have resumed the role of a circumscribed lesion having no appreciable influence over his general constitutional state. It is now of the greatest importance to apply some test by which loss or retention of vestibular irritability may be determined. The tests which have been proposed for this purpose are: (a) the caloric test, (b) the rotation test, and (c) the galvanic test. The Caloric Test.—To those who have not made use of this test, a word as to the method of applying it may be of service. Since the reaction depends wholly upon the temperature of the water, and not in any degree upon the force employed, a slow continuous current gives better results than a stronger intermittent stream. The fountain syringe is, therefore, preferable to any form of hand syringe. Barany takes care that the water shall be at 30° C. (86° F.), having found that this temperature gives a positive reaction in the great majority of cases. There are some cases, however, in which no satisfactory reaction follows irrigation with water at this temperature. In such cases, reducing the temperature to 75° or 65° F. may induce a quick and positive reaction. The disadvantage of using very cold water is the greater likelihood of causing nausea and vomiting. We should watch carefully for the first appearance of nystagmus. To con- tinue the irrigation after the nystagmus is clearly established adds nothing to our knowledge of the condition and will be likely to cause nausea and vomiting. Using water at about 86° F., the average time required to pro- duce nystagmus is about 40 seconds. There are, however, great variations within the physiological limits,—i.e., from 10 seconds to as much as 3 minutes. The slowest reaction in a presumably normal labyrinth which has come under the writer’s personal observation was a case in which the nystagmus appeared after two minutes and fifty seconds of continuous irrigation. As with all forms of vestibular nystagmus, the eye movements are most marked, and therefore first become noticeable, when the eyes are turned in the direction of the quick nystagmic movement. It is, therefore, well to direct the patient to keep the eyes turned in the direction of the ear not irrigated when cold water is used and to look toward the ear irrigated when hot water is employed. In a case of normal caloric reaction, the nystagmus has an average duration of 2 minutes,—differing in this respect from the nystagmus following the so-called rotation experiment, the average dura- tion of which is about 40 seconds. Instruments which facilitate the experiment—especially when one is working without an assistant—are Barany’s “fixator” for holding the CALORIC TEST: ITS DIAGNOSTIC VALUE 301 gaze in the desired direction, and a self-retaining basin for receiving the return flow of water (see Fig. 179). An ordinary stop watch is convenient, and, if one would be exact, almost essential for determining the quickness of the reaction and its subsequent duration. It is in the latent or quiescent stage of the disease that this test is of the greatest value, leading logically to one or other of two conclusions: 1. If the caloric test is fol- lowed by a normal reaction, one may infer quite confidently that the labyrinth has been in- volved in a comparatively simple process, which, while sufficiently severe to have annulled tem- porarily vestibular irritability, has undergone resolution, leaving the vestibular apparatus intact. Prognosis favorable. 2. If, on the other hand, the caloric test evokes absolutely no response, one may conclude with equal certainty that the labyrinth has been involved in a suppura- tive process which has either (a) actually destroyed the essential structures of the membranous vestibule, or (b) has inflicted upon them such injury as to have abolished the vestibular function. While this describes a condition in which the patient may go for long periods or even indefinitely without alarming symptoms, there is no possible assurance of such immunity, and the prognosis as to the ultimate outcome can not be regarded other- wise than with anxiety. Rotation Test.—We have seen that wncz a normal person seated with head erect upon a revolving chair fe turned rapidly in either direction, there results when the rotations are suddenly stopped a horizontal nys- tagmus in the direction opposite to that in which he was turned. The average duration of this “after-nystagmus” is about 40 seconds. While this duration varies considerably within physiological limits, the duration of the nystagmus resulting from rotation in opposite directions is usually about the same,—i.e., shows a difference of not more than 3 or 4 seconds. The diagnostic value of this experiment depends, therefore, entirely upon a comparison of the duration of the “after-nystagmus” in opposite direc- tions. If, for example, an individual is turned ten times to the left and exhibits an “after-nystagmus” to right lasting 30 seconds, while ten rota- tions to the right result in a nystagmus to the left lasting but 15 seconds, the inference, so far as we may draw one from this experiment, is that his Fig. 179.—Barany’s fixator and self-retaining basin. 302 LESIONS OF THE LABYRINTH left vestibular apparatus is non-irritable,—i.e., that its function is destroyed or abolished. Reducing this to a formula, we may say that great shortening of the rotation after-nystagmus in one direction as compared with that in the opposite direction points to a non-functionating labyrinth on the side toward which the shortened nystagmus is directed. One can understand the rationale Gf this test only by reverting to Ewald’s experiments. Ewald found by his experiments on pigeons that in either horizontal canal an endolymph movement toward its ampulla induced head and eye movements (nystagmus) much stronger than those caused by endolymph movement toward the small end of the canal. Barany believes that the same is true of human beings, and that the horizontal nystagmus to the right following rotation to the left is due in the proportion of two- thirds to the endolymph movement in the right canal toward its ampulla, and one-third to the endolymph displacement in the left canal toward its small end. It is clear, therefore, that if the right vestibule be destroyed, the nystagmus to the right following rotation to the left will be reduced by two-thirds, while' the nystagmus to the left following rotation to the right will be reduced only by one-third. Therefore the duration of the nystag- mus toward the destroyed labyrinth will be only half that toward the sound ear. Careful examination of the accompanying diagrams with the explana- tory notes will, it is believed, make these points and their diagnostic signifi- cance clear. Fig. 180.—Horizontal section of skull passing through both horizontal semicircular canals. Ny- stagmus during rotation to right. (x) axis of rotation. Large arrow (a), direction of rotation; small arrow (c), direction of endolymph displace- ment caused by rotation to right; medium arrow (6), direction of nystagmus during rotation. Dur- ing rotation to right there is horizontal nystag- mus to right. Fig. 181.—Nystagmus during rotation to left, (x) axis of rotation. Large arrow (a), direction of rotation; small arrow (c), direction of endo- lymph displacement caused by rotation to left; medium arrow (6), direction of nystagmus ddring rotation. During rotation to left there is horiion- tal nystagmus to left. Fig. 182.—After-nystagmus (i.e., immediately following rotation to right), both labyrinths being sound. (x) axis of rotation. Large arrow (a), direction of rotation suddenly checked at A; small arrow (c), reversed direction of endolymph displacement when rotations are suddenly checked; medium arrow (b), direction of reversed or after- nystagmus. Force and duration of this after- nystagmus are due to endolymph displacement in the two canals in the following proportion: by two-thirds to the endolymph displacement in the left canal toward its ampulla, and by one-third to the displacement in the right canal toward its small end. Fig. 183.—After-nystagmus (i.e., immediately following rotation to left), both labyrinths be- ing sound. (x) axis of rotation. Large arrow (a), direction of rotation suddenly checked at A ; small arrow (c), reversed direction of endolymph displacement when the rotations are suddenly checked; medium arrow (6), direction of reversed or after-nystagmus. Force and duration of this after-nystagmus are due to endolymph displace- ment in the two canals in the following proportion: by two-thirds to the endolymph displacement in the right canal toward its ampulla, and by one- third to the displacement in the left canal toward its small end. Fig. 184.—After-nystagmus (i.e., immediately following rotation to right), right membranous canal having been destroyed by disease. (x) axis of rotation. Right canal (solid black) destroyed by disease. Large arrow (o), direction of rotation suddenly checked at A; small arrow (q), direction of endolymph displacement when rotations are suddenly checked; medium arrow (6), direction of after-nystagmus. Force and duration of after- nystagmus are due to endolymph displacement in left canal toward its ampulla, and represent two- thirds of the normal force; right canal, usually supplying one-third, having been eliminated by disease. Fig. 185.—After-nystagmus (i.e., immediately following rotation to left), right membranous canal having been destroyed by disease. (x) axis of rotation. Right canal (solid black) destroyed by disease. Large arrow (a), direction of rotation suddenly checked at A; small arrow (c), direction of endolymph displacement in left canal when rotations are suddenly checked; medium arrow (6), direction of after-nystagmus. Force and dura- tion of after-nystagmus are due to endolymph displacement in left canal toward its small end, and represent therefore only one-third of the nor- mal force; right canal, usually supplying two- thirds, having been eliminated by disease. Therefore, the after-nystagmus toward the right is of only half the duration of that toward the left, showing loss of function in the right vestibular apparatus. DEMONSTRATION OF ROTATION TEST 303 The key to the diagnostic significance of the rotation test is found in Ewald’s theorem that in either horizontal canal endolymph displacement toward the ampulla causes much more forcible movements (nystagmus) than a similar displacement toward the small end. Barany accepts this fact and assumes that in man the influence of an endolymph movement toward the ampulla as compared with a displacement in the opposite direction is as 2 to 1. The diagnostic value of the rotation test is greatest just after the symptoms of vestibular irritation have disappeared,—i.e. in the very early period of the latent stage. In suppurative labyrinthitis of long standing its significance and value are lessened by the fact—now rapidly gaining recognition—that as the organism gradually becomes accustomed to dependence upon one vestibular apparatus, the after-rotation nystag- mus toward the destroyed or paralyzed labyrinth gradually approaches and finally equals that toward the sound labyrinth. In the writer’s opinion, the rotation test is altogether secondary in diagnostic importance to the caloric test, but it is nevertheless of some value as a corroborative test. It can be applied much more quickly than the caloric experiment, and its effects, so far as the patient’s discomfort is concerned, wear off much more rapidly. The galvanic test differs from the caloric and rotation tests in the follow- ing particulars,—viz., that, while the latter two give rise to vestibular phenomena as a result of endolymph displacement in one or other set of co-active semicircular canals, the nature of galvanic irritation is unknown, or at best conjectural. It is applied in the follbwing way: One electrode being held in the patient’s hand, the other is applied against the mastoid, or in front of the tragus, of the ear to be examined. With the cathode in contact with the ear, there results a rotary nystagmus in its own direction, —i.e., toward the ear experimented upon. When the anode, or positive electrode, is held against the ear, a rotary nystagmus in the direction of the opposite ear results. These are the normal reactions, and it has been com- puted (MacKenzie) that a current strength of 4 ma. should induce the reaction when the labyrinth is intact and normal. Taking this as a stand- ard of normality, the advocates of this test (MacKenzie, Alexander) claim that the requirement of a current strength of more than 4 ma. is to be regarded as an evidence of diminished vestibular irritability. This standard has not, however, been generally accepted by students of vesti- bular disease, and the reports of different observers as to the results of galvanic irritation both in health and disease have been so contradictory as to leave its practical diagnostic value in considerable doubt. Vertigo of Vestibular Paralysis.12—I have described the latent stage of suppurative labyrinthitis as that in which all symptoms of vestibular irritation are absent. Even after the vertigo of vestibular irritation has 12 So far as the writer knows, he was the first to describe this phase of suppurative labyrinthitis and to include it among the regular manifestations of the latent stage of the disease. Vertigo of Vestibular Paralysis: Transactions Am. Otolog. Society, 1911. 304 LESIONS OF THE LABYRINTH subsided, however, the patient may experience considerable inconvenience as a result of the loss of orientation sense, or knowledge of the position of his body in space, which the intact vestibular organs confer. Orientation.—It is clear that the power of maintaining one’s equilibrium in all customary positions of the body depends upon what is called orienta- tion, or the subconscious knowledge of the position of the body in space. If through accident, or attempting the unusual, the body is thrown into positions in which its usual relations to the three planes of space are re- versed, orientation becomes defective or insufficient, and the subjective disturbance known as vertigo results. Again, if the faculty of orientation is suddenly disturbed or ablated, the individual at once loses his sense of stability in space, or in other words experiences vertigo. Obviously the vertigo of vestibular paralysis is the vertigo of defective orientation. That the vestibular organs can not be regarded as the essential organs of orientation is shown by the fact that after removal of one or both laby- rinths, the individual regains in time his equilibrium. There must be, therefore, other contributory factors, and these are found in the muscular and arthrodial senses, the tactile sense, and the sense of sight. It. T. Slinger and Sir Victor Horsley13 published in 1906 the results of some very interesting investigations, the purpose of which was to measure the approximate accuracy of the muscular and arthrodial senses in what they called topognosis, or “the orientation of points of space.” These experiments were carried out in the following manner: The person ex- perimented upon is blindfolded, and before him is held a glass plate gradu- ated in squares of a half centimetre each. The plate being placed in one of the three planes of space,—let us say the sagittal-vertical,—i.e., a vertical plane bisecting his body anteroposteriorly,—the left hand is passively moved in different directions and the tip of its forefinger then brought in contact with some point upon the plate. He is then directed to bring the tip of the right forefinger to a corresponding point upon the opposite surface of the plate. It is obvious that in this test no information is gained through his tactile sense, which would convey the same impression wherever the finger might rest. Sight is eliminated by the blindfolding of the individ- ual. Orientation must, therefore, be chiefly attributed to the muscular and arthrodial senses. This experiment was repeated with a large number of normal persons. It was found that there is a physiological or normal variation, or error, which varied greatly according to the position of the plate in relation to the body. Thus, with the plate held immediately in front of him in the vertical anteroposterior plane of the body and at a height about on a level with the lower end of the sternum, the average physiological variation or error was found to be lM to centimetres. As the plate, still in the same vertical plane, is gradually elevated,—e.g., first to a level opposite the neck, then opposite the head, and lastly above it,—the average error of orientation shows progressive and very rapid 13 It. T. Slinger and Sir Victor Horsley: Orientation of Points of Space, Brain, April, 1906. COMPLEX MECHANISM OF ORIENTATION 305 increase. From these variations the investigators concluded that “there is a progressive diminution of knowledge of space as we pass outward from the central axis of the body.” These experiments were repeated with 22 adolescent or young adults who had become totally and permanently blind in early childhood, and with this interesting result,—viz., that the blind subjects exhibited similar errors, which also varied in accordance with the level or height at which the plate is held; but the errors were distinctly smaller, the average error being less by one-fourth than the average error of people with normal eyes. From this they concluded, that, “if the information gained by sight is permanently blotted out, the muscular sense under necessity can by education be brought to a point at least one-fourth better than that learned by the normal person.” The above experiments have an important bearing upon the compen- satory power of one part of the mechanism of orientation to assume the work of another part whose function is annulled. We have seen that in the normal man orientation is a complex function in which the vestibular apparatus, the muscular, arthrodial, and tactile senses, and sight, all take part. When sight is lost, muscular and arthrodial impressions become more sensitive and accurate. When one vestibular apparatus is destroyed, the opposite labyrinth must become accustomed to unopposed, unilateral ac- tivity, and the muscular, arthrodial, and tactile impressions of space and position must be immensely increased. Until this process of involuntary education is well advanced, it is not surprising that the individual experi- ences occasional vertigo and ataxia, though he does not exhibit nystagmus and may show no constant tendency to fall in any given direction. Clinical Manifestations of Vestibular Paralysis.—We know that the onset of diffuse suppurative labyrinthitis or the removal of one labyrinth is invariably followed by very severe vertigo and disturbances of equilib- rium—these symptoms being the result of hyperactivity of the sound, unopposed labyrinth. After these symptoms of vestibular irritation have completely subsided, the patient is comparatively comfortable. He has now passed the stage when sudden movements of the head cause nystag- mus and its attendant phenomena, and may be up and walking about his room. On getting out of bed in the moruing, however, and on making any sudden and pronounced changes in the position of his body,—e.g., as in stooping over to pick up something from the floor, or even on suddenly rising from the sitting posture,—he becomes momentarily dizzy, and may even require support to prevent his falling. These symptoms are due solely to defective orientation, and, though at first occurring frequently, are very slight as compared with the constant and distressing rotary vertigo of the acute stages. The attacks rapidly grow less pronounced, and may appar- ently cease within a few days, so that the patient is led to believe himself cured. He is likely, however, to experience a severe recurrence on attempt- ing any physical act to which he has not reaccustomed himself. For ex- ample, when he first attempts to walk down an inclined plane,—e.g., in 306 LESIONS OF THE LABYRINTH going down stairs,—he may experience sudden and severe vertigo, due to the sudden call upon his still defective faculty of orientation by this new situation; and this may cause him to fall. Having had this experience, he calls into compensatory activity certain other senses,—chiefly the muscular and arthrodial senses and the sense of sight,—and soon learns to go up and down stairs without fear or danger. Again, when he first attempts to walk in the dark,—e.g., in getting out of bed at night,—he may lose all sense of direction and may fall, and now must relearn to maintain his equilibrium without the aid of sight. All the above manifestations of impaired orientation in the latent stage of suppurative labyrinthitis were demonstrated in the single case of a young physician who was under the care of Dr. A. B. Duel. The same patient, having relearned many of the common acts, such as stooping over, going up and down stairs, etc., was strolling along the street, and suddenly looked up at a tall building then in the process of erection. This deprived him of his sense of position or balance and he fell backward. Even more typical of the vertigo of vestibular paralysis was a case which came under my care at the Manhattan Eye and Ear Hospital some years ago. The patient, a man of 28 years, had contracted syphilis seven or eight months previously, and some five weeks before I first saw him had become suddenly and absolutely deaf, first in the left and then in the right ear. Examination revealed the following conditions: Both drum membranes practically normal; absolute deafness of both ears, both by aerial and by bone conduction. Caloric reactions absolutely negative. The patient, seated upon a revolving chair, was rotated rapidly first in one direction and then in the other, with perfectly negative results,—i.e., there "was no nystagmus, and the patient experienced absolutely no vertigo or discom- fort. Clearly we had to deal with a patient both of whose labyrinths were absolutely non-functioning and non-irritable. Yet this patient complained as much of vertigo as of the deafness. Tests of his equilibrium demon- strated a type of ataxia presenting the following interesting contrasts with the ataxia of vestibular irritation: He walked with marked unstead- iness,—i.e., with a somewhat tottering gait, keeping his eyes persistently on the ground before him. Asked why he looked on the ground he said, ‘to keep from falling.” Yet he was able to keep a straight course and walked wdierever his will directed. With eyes closed and feet approximated (Romberg), he able to stand steadily. In walking w-ith eyes closed, his unsteadiness was greatly exaggerated, but he still contrived to main- tain a fairly straight course. As differentiating the ataxia in this case from that characteristic of vestibular irritation, this patient exhibited no nystagmus, complained of no sense of rotation, showed no tendency to fall in any given direction. He wralked laboriously and with some difficulty, compelling his muscles to carry him where his will and sight directed. The patient was admitted as a ward patient, where his symptoms wrer9 MANIFESTATIONS OF VEST1BULAE PAPALYSIS 307 studied by some of my colleagues as well as myself. He never showed any signs of returning hearing, but his improvment. in orientation was progressive and marked, so that when I last saw him, his gait presented no peculiarities which would attract the casual observer. In this he illustrated the rapid development of the muscular and arthrodial senses under the spur of necessity. It sometimes happens that a case studied carefully at the time presents symptoms which are correctly interpreted only in the light of later expe- rience. I mention by name such a patient, because her case was carefull}' studied by some of my hospital associates. Selena Miller, a girl then of 14 years, was admitted to the Manhattan Eye and Ear Hospital in Novem- ber, 1908, with the following history. Four months previously a radical operation was performed on the right ear by a competent surgeon. The suppurative process had not been relieved thereby, and she had been re- admitted to the hospital on account of failing health and atypical symp- toms of disturbed equilibrium. In the hospital she rapidly lost strength and flesh, and soon became rather apathetic and practically bed-ridden. When induced to get out of bed, she could not walk without support. Support being withdrawn, she was apparently unable to maintain her equilibrium and would fall. There was no constancy in the direction of her falling, and the character of her ataxia seemed so atypical that she was suspected of being a quasi-malingerer. On careful re-examination of the ears, it was found that the right ear was absolutely deaf and gave no response to the caloric test. Operative exposure of the old wound revealed a fistula leading into the horizontal canal and granulations pro- truding from the open oval window. Following an operation providing free drainage from the labyrinth, she made a fairly rapid recovery with relief of all ataxic symptoms. The interesting feature in this case was the peculiar and excessive form of ataxia, which can be satisfactorily explained only on one hypothe- sis: She had suffered suppurative destruction of one labyrinth; she was a delicate girl, and the effect of a rather prolonged illness had been to reduce to an unusual and remarkable degree her muscular force and control. In the latter condition, her muscular and arthrodial senses were so far below par as to have failed utterly in compensating for the disturbed labyrinthine balance. Hence the patient’s inability to stand or walk, and her liability to fall in any direction according to the chance position of the body. The disappearance of the ataxia can not in this case be logically ascribed to the removal of the diseased and already non-functionating labyrinth, but rather to the relief of an extensive suppurative process, elimination of which enabled the patient to regain her muscular strength and tone, and her muscular and arthrodial senses to resume their role in the complex function of orientation. The following case, which is the last I shall refer to in this connection, was in no wise unusual clinically. It will, therefore, serve the better to illustrate the point I wish to make,—viz., the great importance of recog- 308 LESIONS OF THE LABYRINTH nizing these defects of orientation and their resulting phenomena as be- longing logically among the late clinical manifestations of the disease. L. M., 34 years of age, a carpenter, was admitted to the Manhattan Eye and Ear Hospital in May, 1910, suffering from chronic middle-ear suppura- tion plus chronic suppurative labyrinthitis of the left ear. The labyrinth lesion wras of long standing and the ear absolutely deaf and quite irrespon- sive to the caloric test. For this a combined radical and labyrinth exente- ration was performed. The immediate result of the operation proved that the static labyrinth was not wholly non-functionating, for he suffered a few days of characteristic vestibular symptoms,—i.e., rotary nystagmus, vertigo, etc. These quickly subsided, and the patient was soon up and about, and left the hospital to continue treatment in the dispensary. Some two months after the operation, while still under treatment for a slight discharge, the patient stated that he was in need of money and asked if he could take up his work as a carpenter, stating that he felt perfectly fit. I told him to do so, only cautioning him to make no arrangements which would prevent him coming regularly for treatment. The patient was a light-hearted, optimistic Italian, but when I next saw him he was deeply despondent. He told me that he had arranged to take up his work, but had been obliged to surrender it by the frequent attacks of dizziness which overcame him. I had little difficulty in assuring him that his trouble was only tempo- rary and would assuredly wear off in time. But While reassuring him, I had time to consider the rather serious possibilities of such a case. Suppose that this man had been a builder’s employee whose occupation required him to perform his work while standing upon a scaffold suspended high in the air. It is not difficult to imagine what might have resulted from an attack of vertigo for which he would have been wholly unprepared. Suppose that we are called upon to operate for diffuse labyrinthine suppuration upon a boy, and, after all spontaneous symptoms have passed, allow him to resume the practice, dear to most boys, of diving into the river or swim- ming pool. May he not drown before he can recover from the ataxia dependent upon a sudden disturbance of orientation? The type of vertigo which I have endeavored to describe naturally shows some variation in different individuals. Ordinarily induced only by unusual demands upon the disabled mechanism of orientation, there are undoubtedly individuals whose muscular and arthrodial senses are far below the normal average of efficiency and who after destructive labyrin- thitis logically experience for a considerable period a mild grade of vertigo and ataxia of more or less constant type. To recapitulate: The point I wish to emphasize is that there are two distinct forms of labyrinthine vertigo and associated ataxia,—one the familiar spontaneous type, due to vestibular irritation and occurring only during the acute stage of suppurative labyrinthitis; and the other not spontaneous, not constant, not necessarily accompanied by nystagmus, characteristic only of the latent, or quiescent, stage of the disease, and MANIFESTATIONS OF VESTIBULAK P ANALYSIS 309 induced solely by sudden and unexpected calls upon the lost or defective orientation sense, in the maintenance of which the intact vestibular organs are normally so important a factor. This type of vertigo is usually wholly relieved in time as other senses are trained to compensate completely for the lost or impaired vestibular function. Terminations; Prognosis.—Diffuse suppurative labyrinthitis may become quiescent and, having permanently destroyed the hearing and the vestibular function, may in some cases undergo gradual resolution,— possibly by obliteration of the infected labyrinthine cavities by deposition of new connective tissue. On the other hand, the suppurative process may remain quiescent during many years and then give rise to a rapidly fatal intracranial infection. Complications.—The pathways of intracranial infection are (a) from the cochlea by way of the cochlear nerve channels into the internal auditory meatus; (b) by w'ay of the aquseductus cochleae to the subarachnoid space; and (c) from the vestibular cavity by the aquaeductus vestibuli. By far the most frequent intracranial complication of suppurative labyrinthitis is meningitis; then come cerebellar abscess, sigmoid sinus infection, and lastly cerebral abscess. A certain percentage of cases of diffuse suppurative laby- rinthitis give rise, even before the acute stage is passed, to fatal meningitis. Probably the majority of recognized cases reaching the latent stage are now operated upon. There are at present, therefore, no available statistics by which we may determine what percentage of cases of latent suppurative labyrinthitis, not subjected to operation, give rise to intracranial disease. Of this, however, there can be no doubt,—viz., that a patient who presents symptoms of chronic suppurative otitis media plus symptoms of past suppurative invasion of the labyrinth, harbors a lesion which places his life in more or less constant danger. Circumscribed Suppurative Labyrinthitis. — Circumscribed infection of the labyrinth can be said to exist only when one or other main division of the labyrinth can be shown to have escaped serious involvement. Thus a suppurative process confined either to the cochlear or to the vestibular portion would come under this head. Theoretically, an infection of the cochlea, not reaching the vestibule, should provide an occasional example of circumscribed labyrinthitis, but it is a fact, abundantly established by clinical experience, that primary invasion of the cochlea rarely remains localized, but tends rather to rapid infection of the entire labyrinth (diffuse suppurative labyrinthitis). The static labyrinth, on the other hand, is sometimes invaded by a suppurative process which does not spread to the cochlea. Just why a suppurative lesion in this portion of the labyrinth more frequently remains localized is not easily determined. Probably these circumscribed lesions have their inception in a gradual destruction of the bony wall of one or other semicircular canal,—most frequently the horizontal,—resulting in a fistula at this point; it is possible that the grad- ual progress of this process is accompanied by a surrounding subacute inflammation, by which adhesions are formed, and it may be that such 310 LESIONS OF THE LABYRINTH adhesions act as a limiting barrier to the spread of the destructive lesion to the labyrinthine spaces beyond. However this may be, I believe that circumscribed suppurative labyrinthitis may in almost every case be de- fined as a suppurative lesion confined to the vestibular apparatus. Symptoms.—The most typical examples of circumscribed suppurative labyrinthitis are probably found in cases in which infection has taken place through a necrotic defect in the outer wall of the horizontal semi- circular canal. The symptoms of the onset and acute stage are precisely similar to those characterizing the acute stage of diffuse suppurative laby- rinthitis. That is to say, the onset is announced by spontaneous nystagmus, usually rotary and toward the sound ear, and by vertigo and ataxia, cor- responding in type to the form of nystagmus present. The hearing, how- ever, remains fairly good or is only moderately impaired. This preserva- tion of cochlear function is in reality the differential point between the circumscribed and diffuse lesions. The manifest symptoms of vestibular irritation undergo progressive amelioration and may completely subside within ten days to two or three weeks. The patient now presents no conspicuous vestibular symptoms, having reached the latent stage, corresponding to the latent or quiescent stage of diffuse suppurative labyrinthitis. The acute symptoms having subsided, it becomes necessary to investi- gate the condition of the static labyrinth. Usually the caloric reactions are quite negative. In this case the rotation test usually shows greatly shortened after-nystagmus in the direction of the diseased ear. In certain cases, however, there is a partial recovery of vestibular irritability, the caloric tests being followed by reactions of diminished force and short- ened duration. When vestibular irritability is completely absent, there is usually no return of vestibular symptoms; whereas with partial restora- tion of caloric irritability, the patient is not infrequently subject to very distressing attacks of recurrent vertigo. There is always a possibility in these cases that the hearing, though not profoundly affected at the time of the acute symptoms, may later undergo gradual and very pro- nounced impairment. It must not be implied from the brevity of this discussion that a sup- purative process confined to the vestibular apparatus is not a very serious lesion. Obviously, such a lesion may at any time spread to the cochlea. It may also give rise to meningeal infection. There can be no question, however, that so long as the cochlea escapes infection, the danger of serious intracranial involvement is distinctly less imminent than when the cochlea is also diseased. For this reason, and in order that every rational effort may be made to prevent its conversion into a diffuse suppurative laby- rinthitis, it is of great importance that the circumscribed nature of the lesion should be determined as early as possible. Diffuse Serous Labyrinthitis.—As compared with the suppurative form, serous labyrinthitis is a rare lesion. As with the former, it occurs during the course of a suppurative middle-ear lesion. With serous as with diffuse DIFFUSE SEROUS LABYRINTHITIS 311 suppurative labyrinthitis, the symptoms are dependent upon ablation or suppression of the vestibular and cochlear functions. During the acute stage the symptoms of the two lesions are practically identical, and the diagnosis of serous labyrinthitis can not therefore at this time be positively made. In the latent, or quiescent, stage, the symptoms diverge, from the fact that in suppurative labyrinthitis the loss of vesti- bular and cochlear function is practically always permanent, while in the serous form of the disease resolution is followed by partial or complete restoration of function. The symptoms of the onset and acute stage are characterized by sudden and intense vertigo, with rotary nystagmus, which may at the very start be toward the diseased ear, but quickly changes its direction toward the sound ear. Nausea and vomiting are also commonl}', though not invariably, present. Deep-seated earache and headache may be more or less distress- ing additions to the patient’s discomfort. From this short description it will be seen that the difficulties of differ- ential diagnosis between the serous and suppurative lesions are at this stage practically insuperable. It has been claimed (MacKenzie) that severe headache, usually present in suppurative labyrinthitis, is commonly absent in serous labyrinthitis. The writer has seen, however, cases of destructive labyrinthine suppuration in which headache did not at any time appear to be an urgent symptom. On the other hand, a sufficient number of authenticated cases of serous diffuse labyrinthitis has not yet been observed and recorded to enable one with safety to exclude such common and easily induced phenomena as headache. The severe form of headache occurring during the acute stage of many cases of suppurative labyrinthitis which progress favorably—i.e., without serious complica- tions—is presumably due to hyperaemia or slight serous inflammation of the meninges, and there is no reason to believe that the same may not occur in the acute stage of a serous labyrinthitis. With the subsidence of vestibular symptoms, the disease lapses into a latent or quiescent stage quite similar to that described in suppurative labyrinthitis. It now becomes possible for us to make a more positive diagnosis by means of the usual tests of vestibular function. If the caloric tests induce absolutely no response, and a shortened nystagmus toward the diseased ear follows rotation, and the negative reaction to these tests is repeated after twro or three weeks, the diagnosis of suppurative laby- rinthitis would seem to be positive. If, on the other hand, the caloric test shows returning vestibular irritability, the serous character of the inflammation may be assumed. As before stated, diffuse serous labyrinthitis is, in the light of our present knowledge, a comparatively rare disease. The importance of distinguishing such a lesion from a suppurative labyrinthitis depends in great part upon two facts: (1) Serous labyrinthitis offers a comparatively favorable prognosis, both as to life and the aural function; and (2) operation upon the labyrinth is therefore clearly contraindicated. 312 LESIONS OF TIIE LABYRINTH Perilabyrinthitis.—This term is used to describe the condition in which the cellular bone surrounding the labyrinthine capsule is acutely inflamed. It may occur either in acute mastoiditis, or during acute exacerbations of chronic otitis media. Presumably the inflammatory process involving the cellular bone surrounding the labyrinth involves also to some extent the labyrinthine capsule itself. On this hypothesis, the vestibular symp- toms may be attributed to intralabyrinthine congestion secondary to the inflammatory changes in the bone. The occasional presence with perilaby- rinthitis of facial paresis or paralysis is presumably due to pressure upon the nerve by inflammatory exudates within the facial canal. The lesion may undergo resolution after the mastoid or tympanic disease is controlled, or may give rise to serous labyrinthitis or even to diffuse suppurative labyrinthitis. Symptoms.—In typical cases, the disease is announced by sudden attacks of characteristic vestibular vertigo, which may last but a few minutes or an hour or more, but which show a marked tendency to recur- rence. The first attack may be induced by some sudden movement of the head, as in stooping low, sudden rising from the recumbent position, etc., or it may occur spontaneously,—e.g., during the night, awakening the patient from a sound sleep. The accompanying nystagmus is usually of rotary character and is commonly directed toward the diseased ear. Hear- ing during the attack may be moderately or very markedly impaired. As the attack wears off, the hearing powder improves, and may reach the aver- age acuteness for the patient. Between the attacks Weber’s test is usually referred to the diseased ear (Neumann). During the intervals between the attacks the caloric reactions and the reactions to the tuning experiment are normal. With the recurrence of the attacks, their character may change in that the direction of the nystagmus may be reversed—i.e., may be directed toward the sound ear—and the loss of hearing may be much more pronounced. Such changes, however, suggest the conversion of the lesion into a diffuse labyrinthitis, serous or purulent. According to Fletcher, the labyrinthine symptoms in perilabyrinthitis clear up after the tympano- mastoid lesion has been corrected,—i.e., after a simple mastoidectomy or a careful radical operation according to the indications present. In reviewing the foregoing pages, it may seem to the reader that the dividing line between these lesions is in many cases so indefinite as to be of academic interest rather than of practical importance. Thus, a circum- scribed labyrinthitis may easily become diffuse, a serous labyrinthitis may become purulent, and a perilabyrinthitis may give place either to serous or to purulent inflammation of the labyrinth. This narrow boundary line between the different lesions renders their clinical recognition the more important, since the indications for treatment are quite different, and the correct diagnosis and management of a comparatively simple lesion may preclude the development of one in the highest degree dangerous as to life. The more important clinical differences between the four lesions above described are given in the following table: ■ Diffuse Suppurative Labyrinthitis. Diffuse Serous Labyrinthitis. Circumscribed Suppurative Labyrinthitis. Perilabyrinthitis. Onset and acute stage.... Onset and acute stage.... Onset sudden,—u s u a 1 1 y during acute mastoiditis or chronic suppurative otitis media,—or may re- sult from injury to laby- rinth wall during radical operation. Onset sudden, but often preceded by short recur- rent attacks of vestibular vertigo (i.e., often pre- ceded by perilabyrinth- itis). Deafness usually profound.. Sudden onset, secondary usually to chronic suppu- rative otitis media. Hearing only moderately Gradual development, char- acterized by recurrent at- tacks of vestibular vertigo and ataxia, of short dura- tion. Occurs during acute mastoiditis or exacerba- tion of chronic suppura- tive otitis media. Hearing during attacks im- paired. Between attacks may regain normal stand- ard. Nystagmus rotary and to- ward diseased ear. impaired. Onset and acute stage. . . Nystagmus, sometimes horizontal at onset, soon changing to combined horizontal and rotary type; directed toward Nystagmus rotary, or com- bined horizontal and ro- tary type, toward dis- eased ear. Nystagmus, sometimes hor- izontal at onset, soon changing to combined hor- izontal and rotary type; directed toward sound ear. Onset and acute stage.... Onset and acute stage.... Quiescent or latent stage *. Quiescent or latent stage * Quiescent or latent stage * sound ear. Fistula symptom very com- mon. Fistula symptom not com- mon. Caloric reactions absent.... Fistula symptom very com- mon. Caloric reactions absent.... Fistula symptom not com- mon. Caloric and rotation reac- tions normal between the attacks. Caloric reactions normal. Hearing power normal (i.e., the individual’s average acuteness). Prognosis, under proper treatment, favorable. Caloric irritability perma- nently lost. Deafness complete and per- manent. Caloric tests show return- ing vestibular irritability. Gradual return of hearing power. Prognosis comparatively Caloric reactions usually absent. Hearing power may be sta- tionary, or show gradual improvement or loss. (Sudden absolute deafness would indicate conversion of lesion into diffuse sup- purative labyrinthitis.) Prognosis doubtful as to favorable. final outcome. —- *Aftei complete subsidence of symptoms of vestibular irritation ACUTE LABYRINTHINE HYPERiEMIA 313 Acute Hyperaemia of the Labyrinth. — Before leaving the subject of acute vestibular disease, a word should be said as to the condition de- scribed as labyrinthine hyperaemia. Since a direct anastomosis between the vessels of the tympanum and those of the labyrinth has not been de- termined, it is somewhat difficult to explain this condition as secondary to tympanic congestion. There are, however, occasional cases of severe vestibular vertigo, usually accompanied by loud tinnitus and lasting but a few minutes, which are difficult to explain upon any other hypothesis than as depending upon temporary changes in the local blood supply or pressure. A personal experience of the writer may provide an illustration. Hav- ing suffered for twenty or more years with bilateral catarrhal otitis media, I have never experienced an acute middle-ear lesion. Some fifteen years ago, I awoke one morning with what seemed to me the severest form of vertigo. Everything in the room swam in circles about me in the hori- zontal plane. There was a loud roaring sound in my right ear. Whether the hearing was temporarily involved I do not know. The severity cf the vertigo was such that it would have been quite impossible for me to have stood without support. This vertigo lasted probably ten or fifteen min- utes,—it seemed much longer,—and then gradually wore off, leaving my ears apparently in statu quo. There has never been the slightest recurrence. The transitory character of the attack apparently negatives the possibility of the smallest hemorrhage or effusion into the labyrinth, and leaves sud- den temporary hyperaemia as the most plausible theory as to its causation. As to the causes of the hyperaemia in such cases, we are very much in the dark, unless it be due to disturbances of the general circulation combined with local changes in the minute labyrinthine vessels. While attempts have been made to describe in detail the symptoms of acute labyrinthine hyperaemia, I know of no recorded series of cases upon which data are based. Probably, were-a sufficient number of cases brought under the care of a competent observer, it would be found that the vesti- bular phenomena of nystagmus, vertigo, and ataxia are invariably present and are co-ordinated according to Barany’s laws, and that when the aural disorder is unilateral, the nystagmus is usually directed toward the in- volved ear. Prognosis and Treatment of Diffuse Suppurative Labyrinthi- tis.—Before taking up in detail the management of infective diseases of the labyrinth, there are one or two general facts which deserve brief consideration. Suppurative labyrinthitis per se is not a fatal malady. If resulting fatally, death is caused not by the labyrinthine disease itself, but by some intracranial lesion to which it gives rise. The necessity in any case for immediate operation must be determined, therefore, not by the evidences of vestibular involvement, but by the danger of intracranial infection. If our experience, judgment, and diagnostic skill enable us to foretell from the physical character of the lesion and its clinical phenomena that menin- geal infection is threatened or imminent, prompt surgical drainage of the 314 LESIONS OF THE LABYRINTH labyrinth is clearly the rational and conservative method of treatment. On the other hand, if we are able to deduce from the character and course of the symptoms a comparative freedom from such danger, early operative intervention is often distinctly contra-indicated. We now know that in any series of correctly diagnosticated cases of labyrinthine suppuration a certain percentage of the patients will survive the attack without surgical intervention; that others of the same series will prove fatal through extension of the disease to the brain or meninges. Hinsberg,. from his own personal experience and from an analysis of the published records of other surgeons, believes that, of uncomplicated cases correctly diagnosticated and operated upon by competent surgeons, the mortality will not exceed 2 per cent., while of such cases not operated upon the ultimate mortality will reach 10 per cent. A consideration of such estimated percentages, and probably the observation of certain cases of rapidly fatal meningitis, have led some surgeons to the statement of rather hasty conclusions as to the necessity of early operation upon the labyrinth in all cases of suppurative labyrinthitis. Thus, Jansen14 says, “If we appreciate the freedom from danger of opening the vestibule, . . . w7e should be able to set up the principle that as soon as labyrinth disease has been diagnosticated in one of its principal parts, the (labyrinth) opera- tion is admissible in every case.” The writer believes that such a dogma is not only incorrect in theory, but is likely in practice to lead to operations which are in many cases uncalled for, and in others actually dangerous to life. The author would emphasize the statement of Neumann,15 that “not every circumscribed labyrinthine suppuration must become a diffuse one, for the intact portion of the labyrinth may be protected by firm adhesions until the diseased part of the labyrinth shall have entirely and spontane- ously healed.” Clearly the management of these cases calls for careful and skilful surgery when surgical aid is indicated; but in even greater degree may the patient’s life depend upon the physician’s ability correctly to interpret symptoms and to deduce therefrom a correct plan of treatment. Diffuse Suppurative Labyrinthitis. — The treatment of this disease varies with the stage and also with the type of the attack. It is best con- sidered, therefore, under different headings. I. Typical Uncomplicated Case; Acute Stage.—Symptoms: Nystag- mus, vertigo, and disturbance of equilibrium; nausea and vomiting; ear- ache, headache, moderate fever, absolute deafness of involved ear. Treatment: The symptoms at this stage usually confine the patient to bed, where he should be kept until all signs of vestibular irritation have completely disappeared. The bowels should be evacuated by cathartic drugs or by enema. The patient should be placed upon fluid diet, this to be replaced by light diet as soon as the condition of the stomach will 14 Jansen: Trans. Amer. Laryn., Rhin., and Otol. Soc., 1908, p. 136. 15 Neumann: Infectious Diseases of the Labyrinth, Laryngoscope, November, 1910, p. 1032. SUPPURATIVE LABYRINTHITIS 315 permit. He should be advised and guarded against any unnecessary movements. He should not be allowed to get out of bed in order to go to the closet or for any other purpose. No attempt should be made at this time to investigate his control of static equilibrium. In the author’s opinion, the caloric test should not at this time be applied except in certain obscure cases in which it may aid in the differentiation between a possible brain or labyrinthine lesion. In t}Tpical cases the caloric test adds little to our practical knowledge of the condition during the acute stage, and may influence the progress of the lesion unfavorably. The cleansing of the ear at intervals should be accomplished with the least possible dis- turbance of the patient. In a word, he should be subjected to no measures of examination or treatment calling for unnecessary movements of the head, which invariably add to the severity of the vestibular symptoms. The question of operating upon the labyrinth during the acute stage of suppurative labyrinthitis should be decided solely by the presence or absence of symptoms pointing to danger of intracranial infection. If excessive and continuous headache, high fever, mounting rather than receding from day to day, frequent and persistent vomiting,—if these symptoms by their severity and particularly by their continuance point to dangerous meningeal congestion, we may be forced to drain the laby- rinth in the hope of checking the spread of the disease. On the other hand, if the clinical picture does not indicate impending intracranial infection,—e.g., if the temperature is normal, or, having been elevated, shows progressive, though gradual, recession toward the normal line; if the patient is reasonably comfortable, and from day to day becom- ing more so; and if the symptoms of vestibular irritation are gradually subsiding, the writer believes that surgical intervention, for the time being, is distinctly contra-indicated, and should not be thought of until all symp- toms of vestibular irritation have completely subsided. II. Diffuse Suppurative Labyrinthitis with Fistula; Acute Stage.—Symp- toms : Phenomena of vestibular irritation (nystagmus, vertigo, etc.) plus fistula symptom (nystagmus modified by compression and aspiration test); temperature normal or only slightly elevated; absolute deafness of diseased ear. , The treatment is practically the same as for Group I. The presence of a fistula of spontaneous deve]opment and presumably leading into one of the semicircular canals is generally regarded as influencing the prognosis favorably (Hinsberg, Panse, Jansen). The labyrinthine operation is, therefore, contra-indicated during the acute stage except in the presence of symptoms of threatened intracranial disease. III. Suppurative Labyrinthitis following Stapedial Injury.—Character- ized by symptoms of vestibular irritation and profound deafness following quickly upon accidental injury to the stapes during a radical or other tympanic operation,—e.g., subluxation of stapes, rupture of annular ligament, etc. Most observers agree that infection of the labyrinth resulting from 316 LESIONS OF THE LABYRINTH surgical injury in the region of the oval window is particularly prone to spread rapidly to the brain or meninges. Pus thus admitted reaches the vestibule and cochlea before any inflammatory products are formed to bar its passage along the minute channels uniting the labyrinthine and brain cavities. Such lesions also almost invariably cause absolute and permanent deafness. The author, therefore, believes that they constitute an exceptional group in which the labyrinth should be opened and drained as soon as the diagnosis of labyrinth infection is made. As bearing upon the importance of early operation in these cases, the statistics of Jansen are of interest. His report16 included 19 cases of acci- dental injuries, made during the radical operation, subsequent curette- ment, etc. Of these the labyrinth was subsequently opened and drained in 13 cases, of which 9 recovered. Of 5 cases in which the labyrinth was not operated upon, all died. The extreme gravity of infections of the labyrinth resulting from accidental injuries during operation is indicated by the total mortality,—viz., 9. out of 19. Jansen’s report is also impres- sive as showing the importance of care to avoid such surgical mishaps. Note.—It should be understood that under Group III the writer includes only those cases of traumatic labyrinthitis which result from injuries involving the stapes. The accidental opening of the horizontal semicircular canal may not give rise to diffuse suppurative labyrinthitis, in which case it belongs to a quite different class. IV. Suppurative Labyrinthitis with Meningeal Irritation; Acute Stage.— Symptoms of vestibular irritation plus continued high temperature, per- sistent headache, frontal or occipital, and vomiting. These latter symp- toms, wrhile not very uncommon at the onset, usually show progressive diminution even during the first days of the attack in uncomplicated cases. When they persist undiminished, or are increased from day to day, one is forced to infer at least meningeal congestion of rather high grade. In such cases the labyrinth should be opened and drained and the meninges should be exposed in the posterior fossa, i.e., by removing the bony plate covering the cerebellar dura from the anterior border of the sigmoid sinus forward toward the petrous bone. It has frequently been argued that intracranial complications might be forestalled by routine early operation,—i.e., early drainage of the laby- rinth,—as soon as suppurative labyrinthitis has been diagnosticated. This argument is invalidated by the fact that the labyrinth operation itself may precipitate a spread of infection beyond the confines of the labyrinth,—i.e., to the brain or meninges. There can be no doubt that this is far more likely to occur when the operation is performed in the early days of a labyrinthine attack than when it can be postponed until the disease has reached the latent or quiescent stage. Latent Stage of Diffuse Suppurative Labyrinthitis.—Symptoms: Abso- lute deafness; absence of caloric irritability; after-rotation-nystagmus toward diseased ear only half the duration of that toward the sound ear. 16 Jansen: Trans. Amer. Laryn., Rhin., and Otol. Soc., 1908. TREATMENT OF DIFFUSE LABYRINTHITIS 317 Occasional disturbance of equilibrium due to loss of orientation sense. Usually persistent aural discharge. Treatment : In this condition we have to deal with a lesion which has already destroyed the cochlear and vestibular functions. It is a condition which imposes a very considerable responsibility upon the physician. If he could satisfy himself that the disease had run its course, setting up barriers against the further invasion of surrounding structures, it might be justifiable to treat such cases expectantly. There are, however, no means of determining that such a lesion is, or will remain, so limited. The middle- ear disease is still subject to exacerbations, and in any one of these recur- rent attacks, the already exposed labyrinth may have to bear the brunt. I believe, therefore, that the safest method of treatment, and the only one which effectually removes a very positive menace to life is by the combined radical-labyrinth operation. In many cases, aside from the dangers above referred to, the continued discharge and the dread engendered by the recent vestibular attack con- stitute a rather urgent reason for the adoption of some plan offering reason- able promise of a complete cure. Again the radical-labyrinth operation affords the only means to this end. Over this question—i.e., whether in a case of diffuse suppurative laby- rinthitis which seemingly has run its course, leaving a functionally dead labyrinth, a radical mastoid operation, if indicated, should always be sup- plemented by surgical drainage of the labyrinth—there has been a growing diversity of opinion. The old dogma of the Vienna School, that in such a case any operation upon the mastoid which does not include surgical drainage of the labyrinth subjects the patient to increased danger, now finds many dissenters. Many New York surgeons of reputation now hold that there are cases in which in the presense of a functionally dead laby- rinth, with sufficient time having elapsed for the labyrinthine lesion to have undergone resolution, and with no physical evidences of a labyrinthine fistula, one is justified in doing simply a careful radical operation, without opening the labyrinth. In support of this view, the fact is adduced that certain competent surgeons have opened the labyrinth in such cases with- out noting any macroscopic evidences of labyrinth infection; and the further fact that many cases have now been treated surgically without opening the labyrinth with apparently perfectly satisfactory results. These views and the clinical reports on which they are based are certainly worthy of careful consideration. Personally I have not up to the present time been able to accept in principle the hypothesis on which the above treatment is based for the following reasons:— (1) To withhold operation in the labyrinth because of the absence of a visible defect in the labyrinthine capsule is possibly to overlook the most dangerous type of case,—i.e., one in which a latent focus of intra-laby- rinthine infection persists and in which no natural pathway of escape to the tympanum is present. (2) To operate on the labyrinth only in those cases in which a fistula, or 318 LESIONS OF THE LABYRINTH necrotic defect, is disclosed during a radical operation, seems illogical from the fact that the commonest cases of demonstrable fistulae—i.e., in the horizontal semicircular canal—are precisely those which are regarded by many competent observers (Hinsberg, Panse) as offering the least danger to the patient’s life. (3) Assuming in a given case that a radical operation without surgical drainage of the labyrinth is quite satisfactory in its im- mediate results: is the future safety of the patient so well provided for or assured? (4) There can be no doubt that the latent stage of a diffuse suppurative labyrinthitis is the stage in which operative intervention is attended with least risk. Is not this risk very small as compared with the possibility of a latent focus of intralabvrinthine infection which may be rekindled either by the radical operation itself or by other causes later in life? (5) Personal Experience,—I have operated on a fair number of cases of diffuse suppurative labyrinthitis in the “chronic”, or latent stage, with- out a single mishap or fatality. Conversely, in a case of chronic suppurative otitis media, with a functionally dead labyrinth, in which I performed a radical operation without opening the labyrinth, the patient redeveloped an active suppurative labyrinthitis which led to the formation of a cerebellar abscess, this causing the patient’s death. This patient was 60 years old, the original invasion of the labyrinth had occurred many years previously, and the labyrinth walls showed no macroscopic defect during the radical operation. The whole question of labyrinthine surgery is one in which dogmatic statement should be avoided, since what is safe in one man’s hands is not so in another. Any labyrinthine operation by a man who is not sure of his anatomy, who has not a clear conception of the mechanical result he wishes to accomplish, and who has not been at some pains to develop his technic, is necessarily extremely dangerous. There is also a choice of operations as involving different degrees of risk. The use of the chisel in the region of the labyrinth is surely dangerous. I believe that I have evolved, not a new operation, but a simple surgical method of opening an infected labyrinth, which in the latent stage involves little or no risk to the patient’s life. On the other hand, any operation in the acute stage is attended with danger which the methozl employed cannot eliminate. If we act on a hypothesis of supposedly greater conservatism, and operate in a case of latent sup- purative labyrinthitis without draining the labyrinth, the patient may le- cover perfectly. But, if an active labyrinthitis is rekindled, the danger to life is many times increased, and operative intervention, if called for, offers a much less favorable prognosis. Treatment of Circumscribed Suppurative Labyrinthitis.—Acute stage characterized by vestibular nystagmus, vertigo, and ataxia, earache, normal or moderately elevated temperature, nausea and vomiting at onset. Hearing only moderately impaired. TREATMENT OF CIRCUMSCRIBED LABYRINTHITIS 319 The treatment is the same as for the acute stage of diffuse suppurative labyrinthitis,—i.e., absolute rest in bed, fluid or light diet, regulation of bowels, local cleansing treatment of diseased ear. Operation upon the labyrinth is positively contra-indicated except in the presence of rather pronounced and persistent symptoms of meningeal irritation. Latent Stage.—Circumscribed suppurative labyrinthitis may in the quiescent, or latent, stage show clinical differences justifying a division of cases into two groups. Group I, characterized by total, permanent loss of vestibular irritability (absence of caloric reactions) plus retention of a useful degree of hearing power. The conservative treatment of such a case calls for a very careful radical operation. The region of the horizontal canal should be closely scrutinized for evidences of localized necrosis (fistula). Finding a necrotic tract leading toward the vestibule or canals, the diseased bone should be carefully removed, an effort being made to avoid injury to the membranous labyrinth beyond the area of osseous necrosis. The posterior wound should not be closed at the time of the bone operation, the plastic work upon the membranous canal being postponed until the site of the fistula has been closed or filled in by healthy granulations. Should absolute deafness follow quickly upon the bone operation, and particularly should symptoms of meningeal irritation supervene, the safety of the patient might call for prompt surgical drainage of the labyrinthine cavities. Should close scrutiny reveal no area of necrosis leading toward the labyrinth, the operation should be completed as a very careful “radical.” While this does not cover all possible sources of danger, it contemplates a reasonable division of risk, and avoids possible harm to the patient through what is sometimes not inappropriately called “meddlesome surgery.” Group II.—Symptoms: Vestibular irritability diminished but not lost; useful hearing power retained. Periods of comparative comfort alternat- ing with recurrent attacks of vertigo. Presumably the lesion is of the nature of a necrotic process which has destroyed a limited portion of the membranous vestibular mechanism. The patient experiences periods of comparative freedom from vestibular symptoms, and again recurrent attacks of vestibular vertigo. The ves- tibular attacks probably correspond with peiiods in which the vestibular lesion is rekindled into fresh activity or into actual advance. Only in this way can be explained a class of cases examples of which have come under the writer’s observation both in this country and in clinics and hospitals abroad. These patients are much more miserable than those in whom the vestibular mechanism has been destroyed and its function permanently annulled. Treatment: Considering the distress and suffering which this condi- tion imposes upon its victims, and also the dangers which are inseparable from the recurrent attacks, the writer believes that the only adequate 320 LESIONS OF THE LABYRINTH treatment is one which, unfortunately, sacrifices the hearing of the dis- eased ear,—viz., the radical operation combined with surgical drainage of the labyrinth. Treatment of Diffuse Serous Labyrinthitis.—The treatment of serous labyrinthitis can be dealt with very briefly. During the acute stage—i.e., while active symptoms of vestibular irritation are present— the disease cannot with certainty be differentiated from suppurative labyrinthitis, and the treatment is the same as for an uncomplicated case of that disease. After the vestibular symptoms have completely subsided (quiescent stage) the simpler character of the lesion is made known by returning ves- tibular irritability. Obviously labyrinthine operation is not only uncalled for but contra-indicated. It is equally clear that the pre-existing tympanic or mastoid disease should be corrected, and for this reason a radical opera- tion or simple mastoidectomy may be necessary. Treatment of Perilabyrinthitis.—Since the symptoms of this disorder are dependent chiefly upon acute inflammatory changes in the cellular bone surrounding the bony capsule of the labyrinth, the logical treatment should be the correction of this underlying cause. In a majority of cases the attack is secondary to acute mastoiditis, less frequently to an acute exacerbation of chronic suppurative otitis media. Quite recently the writer had under his care a typical case, with nystagmus, pronounced vertigo, nausea and vomiting, in a patient suffering from acute purulent otitis media. This patient made a perfect recovery with no other treat- ment than incision of the drum membrane and the usual treatment for acute middle-ear suppuration. When perilabyrinthitis occurs as a com- plication of acute mastoiditis, the treatment involves a dual problem,— (a) relief of the mastoid lesion, and (b) avoidance of any unnecessary jar, or concussion, which might convert a simple labyrinthine congestion into an acute inflammatory process leading quickly to diffuse suppurative labyrinthitis. If the mastoid symptoms are of moderate grade, it is much safer to depend for the time upon free incision of the drum membrane and the so- called abortive method of treatment described under acute catarrhal otitis media, leaving the question of mastoid operation to be decided later. Under this expectant plan, it will be found that many cases will make very rapid progress toward recovery. It is of course important, however, that the physician keep the patient under close observation and be prepared promptly to open the mastoid should the symptoms either of labyrinthine disturbance or of the lesion within the mastoid become more marked. If the mastoid disease itselt is of such a character as to demand prompt surgical relief, the greatest care should be observed to avoid any concus- sion or jar of the temporal bone. It is clearly desirable, therefore, that the mallet and chisel should not be used. The best operative method for these cases is that described by Dr. W. S. Bryant, by which the mastoid tip is first removed by means of a suitable rongeur, the same instrument TREATMENT OF PERILABYRINTHITIS 321 being used to remove the entire cortex. Entering the mastoid by this route, it is perfectly practicable to complete the operation with no other bone-cutting instruments than the usual mastoid curettes and rongeurs. In America this method of opening the mastoid has become the routine practice of many surgeons of note, among whom may be mentioned Drs. T. Passmore Berens and Arthur B. Duel, of New York. Bryant’s description of this operation is short, clear, and contains a convincing statement of its advantages over other methods in certain cases.17 To epitomize: While the logical treatment of perilabyrinthitis is directed against the surrounding zone of inflammation, the time of prefer- ence for surgical intervention is the period between labyrinthine attacks. There are cases in which the attack may be aborted, or the lesion con- trolled, by non-operative measures. When surgical intervention during, or closely following, the labyrinthine attack is clearly indicated by the urgency of the symptoms it is important that some operative method be adopted by which surgical or bone concussion can be as far as possible eliminated. Differential Diagnosis.—There are few conditions not direotly depen- dent upon aural disease for which suppurative labyrinthitis is likely to be mistaken. Cerebellar abscess in certain cases gives rise to rotary nystag- mus, vertigo, and ataxia, but usually there are differences in the relation of these phenomena to each other and to other symptoms present which should enable a trained and careful observer to recognize their origin. On the other hand, the physician or aurist who has only a superficial knowledge of labyrinthine phenomena might easily be led into a mistaken diagnosis, and from this to an unfortunate, and perhaps disastrous, error in treatment. It is hoped that a careful reading of the foregoing pages may be of value not only to students and practitioners of medicine, but also to special students of otology, in placing before them a sufficiently comprehensive picture of labyrinthine reactions, both in health and dis- ease, to render such errors unlikely. The more important clinical differences between diffuse suppurative and other inflammatory lesions of the labyrinth are given in tabular form facing page 312. The differential diagnosis between diffuse suppurative labyrinthitis and cerebellar abscess is of special importance to the student of aural and brain surgery. It will be considered in connection with the symptoms of cerebellar abscess. 17 Bryant: The Technic of the Complete Mastoid Operation, Improved, Shortened, and Simplified through the Digastric Route, Transactions Am. Otol. Society, 1907. CHAPTER XII. SYMPTOMS OF INTRACRANIAL DISEASE SECONDARY TO AURAL SUPPURATION. It is not to be expected that the otologist should bring to the consid- eration of brain lesions the broad and comprehensive knowledge of the trained neurologist. Necessarily, there may be aspects of a given case, patent enough to the latter, which escape the former. Yet it is probably true that any otologist in large hospital practice is obliged to assume responsibilities in the treatment of suppurative brain lesions quite as heavy as fall to the lot of the average neurologist. Cases are not unknown in which a competent neurologist called to such a case has been able to provide theories,—correct so far as they have gone.—but has not felt justified in advising the prompt and active intervention necessary to save the patient’s life. On the other hand, there have been cases in which the surgeon, acting upon his own judgment, has performed exploratory opera- tions on account of supposed brain lesions which have not been found on opening the skull. It is a pity, therefore, that all such cases should not come under the careful joint study of specialists in both branches of med- icine. Unfortunately, the aural surgeon is frequently called upon to act in cases in which the patient’s only chance lies in prompt intervention. There are then certain suppurative lesions of the brain or meninges which will inevitably form part of the aurist’s experience. Mentioned in the order of their frequency they would probably come somewhat in the following order: (1) extradural abscess, (2) infective sigmoid sinus throm- bosis or phlebitis, (3) cerebral abscess, (4) leptomeningitis, (5) cerebellar abscess. In any large series of cases of middle-ear suppuration, these brain lesions recur with sufficient frequency to impose a rather heavy responsi- bility upon the aurist. It may be well, therefore, to devote a few pages to a brief preliminary discussion of certain more or less common phenomena— including headache, vomiting, pulse changes, temperature changes, local- ized convulsions, localized paralyses, mental changes, and the different forms of aphasia—one or more of which are usually present in every case of meningeal or brain infection. Headache.—With the exception of infective sinus thrombosis or phlebitis, headache in some form is present at some stage of every sup- purative lesion within the cranial cavity. On the other hand, if we except purulent leptomeningitis, in which headache is usually both severe and constant, there is no intracranial lesion secondary to middle-ear suppura- tion in which it may not be absent during very considerable periods. Macewen mentions severe headache as a characteristic and invariable symptom of the onset, or acute stage, of cerebral abscess. This, however, 322 HEADACHE; VOMITING 323 is just the stage of intracranial disease which the surgeon most rarely has the opportunity to observe. After the abscess is fully formed,—i.e., after it has taken the form of a circumscribed subcortical collection of pus,—• the excruciating character of the pain usually subsides, giving place to dull, indefinite, and in most cases intermittent head pains. The writer has seen fatal cases of brain abscess in which for days the patient complained of little pain. To this extent, then, headache may approach the dignity of a differ- ential sign,—i.e., in that it is quite often of dull, indefinite, or intermittent character in fully developed cerebral abscess, while in leptomeningitis it is usually constant and tends to increasing severity up to the time when the patient becomes stuporous or enters upon convalescence (rare). Complete absence of headache extending over considerable periods would justify the physician in positively excluding leptomeningitis. In cases seen by the author, the headache of cerebellar abscess has been of distinctly severer and more persistent type than that accompanying cerebral abscess. In cases presenting the characteristic features of brain abscess, the sudden development of very severe and persistent headache would render the prognosis more grave in pointing to probable extension of the disease to the meninges. To whatever lesion the headache may be due, the part of the head to which the pain is referred furnishes no reliable indication of the site of the lesion; for either in cerebral or cerebellar abscess or in meningitis, the pain may be referred either to the frontal or to the occipital region, or less frequently to the vertex, or it may migrate from one to the other. Vomiting.—Aside from that due to digestive disorders, vomiting may be induced reflexly by so many peripheral disorders that one should be in no haste to refer its origin to a supposed lesion within the skull. Neverthe- less, it is an accepted fact that the act of vomiting is under the control of a “centre,” possibly in the medulla, and excited through the medium of the vagus; and it is a reasonable hypothesis that this centre may be irritated, either directly or through association fibres, by various intracranial lesions. Starr says that vomiting may be induced by apoplexy (initial stage), by brain tumor or abscess, or by meningitis. Gowers states that “organic disease in any part of the brain may cause vomiting.” According to Mac- ewen, “vomiting occurs in the initial stage of brain abscess,” but rarely after the abscess is fully formed. Vomiting, then, may be caused by any lesion so situated as to irritate or press upon certain nerve centres at the base of the brain. In its most typical form, central vomiting presents the following characteristics: It is projectile, is not accompanied by nausea or the usual signs of disturbed digestion, and is not influenced by remedies usually corrective of gastric disorder. While this describes the type, it is not safe to assume that vomiting is not of central origin simply because symptoms of digestive disturbance are present. The central irritation may be suffi- 324 SYMPTOMS OF INTRACRANIAL DISEASE ciently pronounced to induce independent contraction of the stomach with projection of its contents, or may fall short of this result, leaving the ner- vous control mechanism of the stomach in a state of irritable unbalance easily acted upon by slight peripheral causes. Vomiting, with or without nausea, occurs so much more frequently with meningitis than with other intracranial lesions that, taken alone, it must be regarded as pointing rather strongly to meningeal disease. Next to meningitis there can be no doubt that vomiting is more fre- quently present with cerebellar abscess than with any other brain lesion. While it rarely occurs after the onset, or formative stage, of cerebral abscess (Macewen), the author has observed several cases of cerebellar abscess in which it was a rather prominent symptom not only at the onset but recurred at intervals throughout the entire course of the disease. Aside from its frequent association with meningitis, vomiting is a general rather than a focal symptom. In association with other symptoms, however, it may be of considerable value in determining the site or charac- ter of an intracranial lesion. Among such combinations may be mentioned the following: 1. Recurrent vomiting with nausea, accompanied by rotary nystag- mus, vertigo, and ataxia, showing rapid and progressive diminution in severity, suggests suppurative labyrinthitis. 2. Recurrent vomiting without nausea, accompanied by rotary nys- tagmus, vertigo, and ataxia, persistent or tending to increased severity, strongty suggests cerebellar abscess. 3. Recurrent vomiting with incoordination ataxia of one or both hands, high temperature and tendency to delirium being persistently absent, suggests cerebellar abscess. 4. Recurrent vomiting with headache, fever, and tendency to delirium points almost with certainty to meningitis. Gowers’s Syndrome.—Gowers believes that persistent headache coupled with persistent vomiting, for which no discernible cause is present, and which is not relieved by any of the usual remedies, constitutes an important syndrome which in itself is very strongly diagnostic of intracranial disease. Temperature Changes.—Moderate temperature variation may be excited by causes too various for it to be of great diagnostic value except in association with other symptoms. There are, however, certain facts which may well be borne in mind in examining the temperature chart in a case of suspected brain disease. It is probable that most suppurative brain lesions are ushered in by a rise of temperature. If, however, it be situated well beneath the cortex in the cerebral substance,—e.g., a cerebral abscess,—the temperature after the lesion is fully developed may return to normal and remain so for considerable periods. In deep-seated cerebral lesions, therefore, the temperature may furnish absolutely no evidence of the actual condition. On the other hand, any form of inflammation in- volving the meninges or the cerebral cortex is commonly announced by an elevation of temperature which, though varying in degree, is usually more TEMPEEAT'UHE AND PULSE CHANGES 325 or less continuous. A continuously normal temperature is usually suffi- cient, therefore, to exclude meningeal involvement; and, per contra, in suspected intracranial disease constant elevation of temperature is rather strongly suggestive of a cortical lesion,—i.e., meningitis or peripheral encephalitis. The only intracranial disease to which, after exclusion of other causes, the temperature may furnish the positive clue is infective sinus thrombo- sis. Naturally an infected clot, situated within a large venous channel, and from which infected particles may be periodically discharged directly into the general circulation, might be expected to give rise to a very charac- teristic type of temperature variation,—the intermittent type character- istic of periodic septic absorption. Changes in Pulse-rate.—Within certain limits the pulse-rate varies in acute intracranial disease in accordance with the same laws which regulate its changes in acute disease originating in other parts of the body. That is to say, it is probable that the temperature is elevated and the pulse quickened at the onset of every acute suppurative lesion involving either brain or meninges. It is also an established clinical fact that in nearly every fatal case of acute intracranial disease the pulse is greatly accele- rated shortly before the end. Between the initial and terminal stages, how- ever, the pulse-rate may show changes of the greatest diagnostic importance. It has been noted in many cases of brain abscess that the pulse-rate at some stage of the disease has been markedly reduced in frequency. This occurs quite as often with abscesses of the cerebrum as with those of the cerebellum. The same lowering of the pulse-rate has been frequently observed also in connection with rapidly growing brain tumors. It has also been noted in certain cases of purulent leptomeningitis. The phe- nomenon seems, therefore, to be due largely, but not always solely, to increased intracranial pressure. The relation between reduced pulse-rate and such lesions has frequently been demonstrated by post-mortem findings and by surgical intervention. Furthermore, in many cases of brain abscess, the slow pulse-rate has been immediately corrected by surgical evacuation of the pus (Macewen). When, therefore, a patient suffering from suppurative middle-ear or mas- toid disease suddenly exhibits a markedly reduced pulse-rate,—e.g., 60, 50, or 40 beats per minute,—this symptom alone is rightly regarded as rather strongly suggestive of brain abscess. Somewhat puzzling are certain cases of meningitis in which a reduced pulse-rate has been observed. While increased intracranial pressure is, of course, common in some forms of meningitis, it seems probable that there may be other causative factors at work in the bradycardia of such cases,—e.g., an accompanying encephalitis causing perhaps irritation or excitation of some centre exerting an inhibitory influence over the heart- beats. This is apparently the view held by Gowers. Such cases, however, are somewhat exceptional. As a rule, all forms of meningitis are accom- panied by an acceleration of the pulse-rate. 326 SYMPTOMS OF INTRACRANIAL DISEASE The slow pulse resulting from the formation of a brain abscess is usually a changing symptom, having some relation to the increasing pressure. The reduction of the pulse-rate is not, however, in direct proportion to the size of the abscess,—a very small abscess sometimes causing very appreciable slowing of the pulse. If the abscess becomes encapsulated,— i.e., enters upon a latent stage of indefinite duration,—it is probable that the intracranial pressure undergoes gradual readjustment with restora- tion of the normal pulse frequency. On the other hand, rupture of a brain abscess with escape of pus either into the ventricles or subarachnoid space, is invariably announced by a train of alarming symptoms, among which an exceedingly rapid pulse is always prominent. Macewen’s Syndrome.—Mace wen has called attention to the combina- tion of two symptoms,—viz., high temperature associated with subnormal pulse-rate,—as strongly diagnostic of intracranial disease. The author believes that this association—even when the fever is not high and the pulse retardation is of moderate degree—is most important. It is so diffi- cult to think of any lesion outside of the skull cavity which could give rise to this phenomenon, that he is inclined to regard it as pathognomonic, not of any particular lesion, but of intracranial disease. Unilateral Muscular Spasm as a Symptom of Cerebral Disease. —General convulsions—i.e., of both sides of the body—rarely occur as the result of a cerebral lesion of otitic origin. On the other hand, unilateral spasms confined to certain groups of muscles may point quite clearly to irritation by such a lesion of the motor centres of the muscles involved. The condition may consist merely of twitching of a single muscle or muscle group, or may be so severe as to justify the term localized convulsion, which condition is known as Jacksonian epilepsy, after the man who first described it.1 In a typical case the symptoms occur somewhat in the following order: First a sensation of tingling in the limb or region involved, then there is ail involuntary contraction of a single muscle or muscle group, this being fol- lowed by clonic spasms or convulsions, other related muscle groups being successively involved. Thus, the contractions may begin at the shoulder and gradually extend down the arm so as to include the wrist and fingers, or they may commence in the finger s and extend in the opposite direction tow- ard the shoulder. In either case the spasms of these muscles would point to irritation of the middle third of the precentral or ascending frontal gyrus. Or the convulsion may in a similar way involve the muscles of the lower limb, which would point to irritation of the paracentral or upper third of 1 Hughlings Jackson, of London, published in 1861 the first recorded series of cases in which the patients, having suffered from a peculiar form of unilateral spasm confined to certain muscle groups (“Jacksonian epilepsy”), were subjected post mortem to care- ful examination in the dead-house. The post-mortems showed uniformly lesions involv- ing certain cortical areas of the opposite cerebral hemisphere, which he therefore assumed to be the motor centres of the muscles in which contractions had occurred. These records provided the starting-point and foundation upon which our knowledge of cere- bral motor localization has been built up. MUSCULAR SPASMS; PARALYSIS 327 the precentral convolution. Another typical Jacksonian attack is charac- terized by convulsive lateral movements of the head and eyes to one or the other side,—i e., there are coincident lateral nystagmus and successive jerky movements of the head in the horizontal plane in one direction until the face looks over one or the other shoulder. This phenomenon is caused by irritation of the motor centre for the head and eyes, which is located in the posterior end of the second or middle frontal convolution. The move- ments are toward the shoulder opposite to the side of the lesion. In these attacks there is no loss of consciousness. The convulsion may last several minutes, and, in accordance with its severity and duration, leaves the mus- cles in a condition of flaccid weakness or actual paralysis, which, however, is only temporary. If such an attack has been carefully observed, much may be learned from the order in which it occurs. Thus, the premonitory tingling, which may precede the convulsion by several minutes, is usually referred to the region of the initial contraction; and the initial contraction will throw light on the initial centre of irritation in the cerebral cortex. The subsequent muscular paralysis, or weakness, will be most marked in the muscle group in which the spasms first occurred, and these muscles will be the last to recover their tone and power. It is generally conceded that a cerebral lesion can cause muscular spasms only when so placed as to be capable of causing, either directly or indirectly, irritation of the cortical motor area. For this reason many cases of intracranial disease end fatally, or are relieved by surgical intervention, without ever having produced motor disturbances of any kind. Never- theless, it is known that a cortical lesion primarily outside of the Rolandic area may by cortical extension involve the motor area, and it is clear that a subcortical lesion may by peripheral extension also involve the cortex. It seems evident that irritation from a subcortical lesion, acting by pres- sure or through its proximity to the cortex, would give rise to but slight muscular contractions as compared with an irritative lesion of the cortex itself. Nevertheless, such slighter phenomena might throw much light upon an otherwise obscure lesion. The symptoms should therefore be borne in mind in every case of suspected intracranial disease of otitic origin. When localized muscular spasms do occur in the course of a brain lesion, they point clearly to the following facts,—viz.: (a) that the lesion, if subcortical, is sufficiently peripheral to cause cortical irritation; (b) that, if cortical, it must be so situated as to involve either directly or by lateral extension the precentral, or motor, area; and (c) if the sequences of the attack have been carefully observed, they may supply further data as to its exact localization. Unilateral Muscular Paralysis or Paresis.—The results of cor- tical lesions in the motor area of the brain are so generally understood as hardly to require more than passing mention here. Destructive lesions in any part of the motor area of either cerebral hemisphere are followed regularly by volitional paralysis, partial or complete, of the corresponding muscle-groups of the opposite side of the body. Thus, a paralysis of cere- 328 SYMPTOMS OF INTRACRANIAL DISEASE bral origin confined to the wrist or elbow muscles of either side would suggest a cortical lesion of the middle third of the ascending frontal con- volution of the opposite cerebral hemisphere; while paralysis of the foot or leg muscles would point to a lesion in the upper third of the same convolu- tion. But paralysis of the same muscle-groups may also result from any subcortical lesion within the motor tract, which includes the projectional fibres of the appropriate cortical centres. A brief reference, therefore, to the common paralytic effects of such subcortical lesions, as compared with those usually resulting from a cortical lesion of equal size, may be permis- sible here. From the under surface of the motor (precentral) area, the projectional fibres converge to meet in the internal capsule and there form the densely arranged motor tract which from this point is continued downward through the crus cerebri, pons varolii, and medulla to the opposite side of the cord. It is obvious that, in their passage from the cortex to the internal capsule, the fibres from the lower third of the precentral, or ascending frontal, convolution pass more or less horizontally inward, while the fibres of the middle third must assume more oblique directions gradually approaching the vertical plane. Finally the motor fibres of the upper third pass down- ward and somewhat outward around the lateral ventricle to join those of the lower and middle thirds in the internal capsule. This arrangement is shown in the diagrammatic figure (Fig. 186), which also shows very graph- ically the varying results of lesions in the cortex and in the motor tract. The darkened areas represent destructive lesions in the cortex, internal capsule, and crus cerebri. Numbers 1, 2, and 3 represent cortical lesions in the motor areas of the leg, arm, and face respectively. It is obvious that any one of these, occurring singly, could give rise to paralysis of but one set of muscles,—i.e., those of the leg, arm, or face; and that similar monoplegias might result from subcortical lesions in the centrum ovale involving the projectional fibres from single motor centres (4 and 5). If, however, we follow these projectional fibres from the various motor centres into the internal capsule, it becomes clear that a comparatively small lesion in this situation (6) would be likely to result in more widespread paralysis (hemiplegia). While it is perhaps theoretically possible for a small lesion situated in the internal capsule to involve the projectional fibres of one motor centre only, with consequent monoplegia, this is exceedingly unlikely to occur. A comparison of the autopsy finding with the clinical records in fatal cases of paralysis due to cerebral lesions would seem to show that in the great majority of cases, lesions of the internal capsule, if sufficiently severe to intercept motor impulses, give rise to rather widespread paralysis; and conversely, that a majority of all cases of hemiplegia resulting from suppurative brain lesions are due to lesions involving the internal capsule. On the other hand, only the most extensive cortical lesion could give rise to widespread paralysis. While an abscess confined to the temporosphe- noidal lobe—the usual seat of an otitic abscess—might through transmitted MUSCULAR PARALYSIS 329 pressure give rise to extensive paresis, complete hemiplegia—i.e., involving equally upper and lower limbs—is rarely or never so produced. As in the internal capsule, so in the crus cerebri, pons and medulla oblongata, lesions of the motor tract give rise to paralysis coextensive with the cortical area whose motor fibres are interrupted. From the fact that the motor oculi nerve arises from the inner side of the crus cerebri and supplies the ocular muscles on the same side as the crus from which it springs, a lesion in this situation (7) is apt to produce a Fig. 186.—Diagrammatic picture of a transverse section of the brain. (Modified from Starr.) characteristic form of paralysis,—i.e., to involve the motor tract supply- ing the muscles of the opposite side of the body (hemiplegia), and the third nerve (ocular paralysis) on the same side as the lesion. So far as we may formulate deductions from the above, they may be stated as follows: (a) In suppurative intracranial disease, however originating, paralysis of a single group of muscles suggests a cortical lesion, or a lesion so placed in the centrum ovale as to intercept only the projectional fibres of the motor centre involved. (b) Hemiplegia, or widespread unilateral paralysis, points with greater probability to a lesion involving the internal capsule. (c) Unilateral ptosis with external squint and inability to rotate the 330 SYMPTOMS OF INTI!ACRANIAL DISEASE eyeball upward, inward, and downward, accompanied by paralysis of the leg, arm, and face muscles of the opposite side, points to a lesion of the crus cerebri on the side corresponding to the ocular symptoms. Mental Disturbances.—The relation of mental disturbances to intra- cranial disease is hardly within the scope of a manual of otology. The author wishes merely to refer briefly to certain forms of mental disorder as having a practical bearing upon the diagnosis and prognosis of brain lesions of otitic origin. So far as he has been able to observe, the mental symptoms occasionally characterizing these lesions conform almost inva- riably to one or other of three main types,—viz.: (1) Depressed or retarded cerebration, due usually to a lesion producing great increase in intracranial pressure; (2) loss of cerebral control, leading first to mental excitement and finally to delirium, due usually to an irritative lesion of the cortex or the meninges; and (3) apraxia, or inability to think coherently, this being due to a loss of the concepts of familiar things. 1. Depressed or Retarded Cerebration.—In this condition cerebration may be obscured almost to the point of cessation. It is a condition of extreme mental lethargy. As a consequence, there is more or less difficulty in commanding the patient’s attention even to simple questions. Having gained his attention, he answers, if at all, correctly. Sometimes there is distinct evidence of retardation of the mental process. Having asked him a question and waited for a reply, the answer comes after a long delay, just when you have concluded that he has either not heard or not under- stood. The condition is frequently accompanied b}'' a tendency to lethargic somnolence. He may ask for something, and doze off, forgetting his request, before it can be brought. Evidently, the mental processes are obscured, retarded, minimized, but neither ablated nor perverted. This form of mental disturbance is usually the result of great increase in intracranial pressure, as in the case of a large and rapidly formed brain abscess. It is not of itself an evil prognostic sign, since it usually charac- terizes a lesion which may respond favorably to surgical treatment,— e.g., the successful evacuation of a brain abscess. 2. Delirium may be of low, muttering form or of the violent type, in which the patient screams, uses wild or abusive language, and can with difficulty be kept in bed. In either case the condition is equivalent to mental oblivion, since the patient, if he regains his mental balance, never has any knowledge or memory of what has occurred. Delirium resulting from intracranial infection usually points to a cor- tical lesion,—i.e., peripheral encephalitis or meningitis. It is of unfavor- able prognostic significance, in that it points to a type of lesion which ends oftener in death than in recovery. 3. Apraxia describes a condition in which the patient, though con- scious and perhaps striving to think coherently, is unable to do so because he can not command clear and complete mental pictures of familiar objects. It is demonstrated when a person by the incoherence of his speech shows that he is unable to recognize or appreciate the nature or uses of things APHASIA 331 about him. Etiologically it bears a strong analogy to the various forms of aphasia (next to be described), with some of which it coexists. In right- handed individuals it indicates a lesion in the left cerebral hemisphere and vice versa. It is not necessarily an unfavorable prognostic sign, pro- vided the site and character of the lesion can be determined. APHASIA. The subject of aphasia is so large, and its causes so deeply rooted in neurology, that we can attempt here only a brief description of such speech defects as may occasionally occur in brain lesions of otitic origin. By aphasia we mean loss of the power of expressing one’s thoughts intelligibly in spoken words. This definition is elastic, as it should be, for the aphasic individual may be practically or nearly speechless (motor aphasia); or his words may come in disordered and meaningless sequence (paraphasia); or he may be unable to recall a familiar object from the sound of its name, and, since all name-sounds have ceased to have any mental associations, he is also unable to command the name of a familiar object seen (word-deafness). Any of these defects may result from a cerebral abscess of otitic origin. Inability to convey one’s thoughts correctly in spoken words is not infrequently associated with inability to recognize written words or sym- bols (word-blindness), in which case the individual would naturally be unable to write at will,—or, rather, to express his thoughts in writing (agraphia). Again, either aphasia or agraphia may be of two main types.—i.e., either sensory or motor. The cortical centres, the integrity of which is essential to intelligible speech, are in the left side of the brain in right-handed persons, and vice versa. Before attempting to trace these commoner forms of aphasia to their appropriate lesions, it may be well to recall briefly the physiological basis of coordinate speech. It will be remembered that, as with the convolutions of the brain, so the smallest cortical “centres” are brought into relation with each other and with other parts of the cerebrospinal system by three sets of fibres,—viz., (a) association fibres which pass from one centre to another, and by virtue of which the smallest cortical area is said in some degree to be associated with every other; (b) commissural fibres which pass, as in the corpus callosum and anterior commissure, from one hemisphere to the other, and by virtue of which the two hemispheres act as one organ; and (c) the projectional fibres which pass from each cortical centre to the base of the brain and spinal cord. The time intervening between a baby’s birth and its first efforts at intelligible speech is consumed not so much in acquiring the physical power of articulation, as in storing the mind with certain impressions, or “memory pictures,” which are essential to coordinated thought,—this being prerequisite for coordinated speech. The lowest type of idiot can not acquire language because coordinated thought is to him impossible. 332 SYMPTOMS OF INTRACRANIAL DISEASE “The basis of language,” Starr tells us, “is a series of memory pictures,” and these memory pictures are stored in various special centres for the Fig. 187.—Chart showing important aphasia centres. reception and retention of such impressions. Thus, before the child can make intelligent use of the simplest noun, he or she must have a series of memory pictures relating to it stored in various memory centres in differ- THE APHASIC CENTRES 333 ent parts of the cerebral cortex. Taking, for example, the word “doll,” the child must have, first, a definite memory picture of the sound of this word, and this is stored in a special cortical centre for the memory of various sounds. This centre is located in the middle of the first and second temporal convolutions (Fig. 187, a). Next, she must have also a definite memory picture of the shape, general color scheme, and common sizes of dolls,—i.e., a visual impression based upon the dolls she has seen. The special memory centre for visual impressions of various objects is located in the second occipital convolution (Fig. 187, b). And, third, she must have a definite impression of the texture or solidity of the various parts of the doll, this memory picture being stored in a special area for the reten- tion of tactile impressions of various objects. This centre probably in- cludes adjacent portions of the posterior central and superior and inferior parietal convolutions (Fig. 187, c). To these memory pictures—i.e., of the sound of the name, the visual impression of the image, and the tactile impression of its texture and consistency—-must be added a memory picture of the motor effort required to produce the articulate sound, this being stored in a special centre located in Broca’s convolution (Fig. 187, d). It is now quite intelligible that these four memory impressions, brought into relation and coordinated through the association fibres passing between the various memory centres involved, should produce a concept, or complex mental image, and that this concept is essential to the intelligent use of the word. It is also a logical deduction that destruction by injury or disease of any of these memory centres, or of the association fibres through which their impressions are combined and coordinated, might easily pro- duce defects of speech,—i.e., some form of aphasia. It is clear that in addition to the four “memory pictures” above de- scribed, and which probably constitute the essentials of the earliest and simplest conception of the child’s mind, there are also innumerable other memory impressions relating to the object named,—i.e., its uses, advant- ages and disadvantages of certain kinds, its associations by analogy or contrast with similar or dissimilar objects, etc.,—which come with in- creasing experience and advancing mental development. With the edu- cated adult, for example, the concept of each object must include at least two additional centres for the special memory pictures which enable him to read and to write, respectively:—i.e., he must have memory pictures of the appearance of written words and letters, the special centre for such impressions being located in the angular gyrus (Fig. 187, e); and he must have a memory picture of the motor acts required to form the letters and particular words. Destruction of the first of these—i.e., the visual word centre—would render the individual unable to read. Destruction of the centre for the motor or effort memories of writing would render him unable to write, though he might still be able to read with understanding. Obviously, with normal individuals the special senses—particularly of hearing, sight, and touch—are essential factors in the development of every complete concept. The cortical centres for the special senses of sight, 334 SYMPTOMS OF INTKACKANIAL DISEASE hearing, touch, etc., therefore play an essential part in the normal auto- matic development of speech. The congenitally blind are slow in learning to talk. The child absolutely deaf from birth never acquires language except through artificial methods of instruction. With the above facts in mind, the various speech defects become more intelligible to us; for it is clear that we can interfere with the processes of coordinated thought and speech either by destruction or injury of one or more of the special memory centres involved, or by destroying the associa- tion fibres by which they are connected. We are now better equipped to study the different forms of aphasia as aids to diagnosis. Suppose, for example, that we are examining a right-handed individual suspected of having an abscess in the left cerebral hemisphere. We begin by asking him very simple questions requiring chiefly affirmation or nega- tion,—e.g., if he feels any pain; if he is married; if he has children, etc., etc., receiving intelligent replies which indicate that up to a certain point his cerebration is normal. Sensory Aphasia.—Partial Word-deafness.—We now show him some familiar object, as, for example, a penknife, and ask him to name it. He can not do so, and may call it a “key” or a “pencil.” Ask him what it is used for, and he answers correctly,—e.g., “to cut with.” Ask him if it is a key, a pencil, or a penknife, and he corrects his former statement and says that it is a penknife. Now ask him the uses of articles not exposed to his view,—e.g., “what is a pencil used for?” “What is a watch used for?” etc. He may be unable to answer correctly. This condition is one of sensory aphasia due to partial word-deafness,—partial because, though unable to name a familiar object shown him, he can, when several names are spoken for him, select the correct one. Though he may be unable to recall the uses of an object from the sound of its name alone, he can, if both the name be sounded and the object shown him, recall their relation. In other words, both the auditory and the visual memory pictures are intact, but there is a break in their association through a lesion involving the association fibres by which the auditory memory centre is brought into relation with others. In such a case, the lesion is subcortical and one which has to a great extent cut off the special centre for sound memories from its associa- tion with the other memory centres essential to intelligent speech. One would expect in such a case a subcortical lesion in the neighborhood of the first and second temporal convolutions. This, in the writer’s experience, is the commonest form of aphasia in cases of brain abscess of otitic origin. Total Word-deafness.—If the patient is unable to call the name of a familiar object shown him, though recognizing its character and uses, and, when its name with several others is spoken for him, is still unable to call the correct one, the condition is one of total word-deafness and presum- ably due to a cortical lesion involving the special centre for sound memories. Such a lesion usually produces great confusion of speech, and also renders his mother tongue almost incomprehensible to him. It is exceedingly rare as a result of suppurative brain lesions. APHASIA 335 Intercortical Motor Aphasia.—This condition is produced by a sub- cortical lesion which injures, or presses directly upon, the association fibres connecting Broca’s convolutions (motor speech memories) with the other memory centres. The other memory centres essential to coordinated thought being intact, and their interassociation not disturbed, the patient’s cerebration is not necessarily disturbed. He understands what is said to him, and can express his thoughts in writing. He therefore makes con- scious and strenuous efforts to express himself coherently in speech, but without success, the words and even syllables being transposed, and fol- lowing each other without intelligible sequence. According to Starr, this variety of speech defect is produced by lesions involving the association tract between Broca’s centre and the temporal auditory memory area, which tract passes beneath the island of Reil. Word-blindness (causing Sensory Agraphia).—The special centre in which are stored visual memory pictures of objects seen and visual centre for written symbols,—i.e., written or printed letters, words, etc.,—are not identical,—the former being located in the second occipital convolution, and the latter in the angular gyrus (Fig. 187, e). It is possible that an individual with a brain lesion—e.g., abscess—- may be able to answer all questions intelligently, and to recognize the character and uses of any familiar object shown him and to give its name correctly, yet may be quite unable to read a single word of written or printed matter. He may be unable to recognize even the letters of the alphabet. This condition is called word-blindness (alexia), and is caused by a subcortical lesion which cuts off the centre for the memory pictures of written symbols from the other memory centres essential to coordinated speech. And, since the patient can not recall the form and appearance of the letters and written words, he is also unable to write. He may, however, be able to copy written matter, but does so with little or no understanding of the sense, or meaning, conveyed. This form of agraphia is called sensory, in contradistinction from the condition in which the patient recalls the forms of letters and written words, and can therefore read but is quite unable to inaugurate the finger movements necessary in writ- ing (motor agraphia). Word-blindness and consequent sensory agraphia are determined by testing the patient’s ability to read and write simple sentences in his mother tongue. The condition may occur independently or coexist with word-deafness. Sensory Visual Aphasia (Psychical Blindness).—Again, if we suppose or find that our patient is unable either to name a familiar object shown him or to bring to mind its uses, but that he can recall its name when this, with others, is spoken for him, and from its sound can also recall its uses,— we have another variety of sensory aphasia dependent upon what is some- times called psychical blindness. It is due to a subcortical lesion which practically isolates the special memory centre for visual impressions of objects seen. The “centre” is not actually destroyed, for the visual 336 SYMPTOMS OF INTRACRANIAL DISEASE memory pictures can be recalled by the sound of the name acting through certain indirect associational tracts. In such a case, we should not be surprised at finding the lesion rather far back,—i.e., in the region of the second occipital convolution. Motor Aphasia.—A somewhat kindred lesion, but producing quite different functional defects, is known as motor aphasia. This is due to a lesion directly involving the centre in which are stored the motor effort- memories necessary to the production of articulated speech (Broca’s centre,—posterior part of third frontal gyrus). The patient can not talk, can not even repeat sentences word for word after another. He may, however, retain the use of a few monosyllabic words,—e.g., yes, no, etc. This incapacity for speech may coincide with intelligent understanding of what is said,—this apparent anomaly being indicated by his gestures in response to questions, and possibly in some cases by the ability to convey his meaning in writing. Motor agraphia, occurring alone,—i.e., without disturbances of co- ordinated thought or speech,—is probably an exceedingly rare condition. For a typical case, we would have to suppose a lesion, cortical or sub- cortical, which had involved directly and solely, or at least cut off from association with other memory centres, the special centre for the motor effort-memories essential to the act of writing. The patient, while able to read printed or written matter with understanding, and while showing no evidences of apraxia,2 is unable to write a single word. He can neither express his thoughts in writing, write at dictation, nor even copy the sim- plest sentence. Motor agraphia and motor aphasia not infrequently coexist,—-the effort-memory centre for writing being supposed to be not distant from the centre in which are stored the motor speech memories. The differential points between motor agraphia (without motor apha- sia) and sensory agraphia are repeated below: Motor Agraphia. Due to a lesion which inhibits solely the mechanical act of writing; patient can therefore read with understanding. Patient cannot write either at will or from a copy. Sensory Agraphia. Sensory agraphia is part of the con- dition known as word-blindness; patient cannot therefore either read or write. Patient cannot write at will, but usu- ally can write from copy. 2 Apraxia is a term used to describe the inability to think coherently which results from a loss of the concepts of familiar things. CHAPTER XIII. INTRACRANIAL LESIONS OF OTITIC ORIGIN: EXTRADURAL ABSCESS; PERISINOUS ABSCESS; SEPTIC SINUS THROMBOSIS OR phlebitis; purulent leptomeningitis; cerebral abscess; cerebellar abscess. Avenues of Infection (Fig. 188).—Aside from the more favorable avenues of escape through the external cortex, it is clear that pus within the mastoid may travel in various directions, and in accordance with its Fig. 188.—(Diagrammatic.) Otitic pathways of pus to brain or meninges, (a) Epidural abscesses; (f>) temporosphenoidal abscess; (c) perisinous abscess; (