The Pressure Paralysis of Pott's Disease. BY GEORGE R. ELLIOTT, M. D. BBPKINTED FROM Weto Torfe ftlebical .journal for June 2, 18S8. Reprinted from the New York Medical Journal for June 2, 1888. THE PRESSURE PARALYSIS OF POTT'S DISEASE.* GEORGE R. ELLIOTT, M. D. The object of this paper is to determine the mechanism of the lesion which gives rise to pressure paralysis of the spinal cord, limited to that form of paralysis which com- plicates Pott's disease. Anatomical Considerations.-It may not be out of place to call attention to the following anatomical points: 1. The spinal cord reaches only to the lower border ot the first lumbar vertebra. 2. The cord only partially fills the vertebral canal. 3. The cord swings in the spinal canal, insulated by means.of the arachnoid fluid which surrounds it. 4. The cord is much nearer the anterior wall of the canal than the posterior, held in place by means of the anterior nerve-roots. 5. The tracts conducting motor impulses are more su- perficial than those transmitting sensory impulses. It further may not be out of place to state that paralysis in Pott's disease bears no relation to deformity. A spinal column may be bent at nearly a right angle without giving Read before the Section in Pathology of the Ninth International Congress, September, 1887. 2 THE PRESSURE PARALYSIS OF POTT'S DISEASE. rise to any paralytic symptoms, while in another case, manifesting no deformity, complete paraplegia may be present. Pathology.-Tn order to arrive at an intelligent under- standing of the pathology of the lesion to be considered in this paper, I cite briefly the carious process which is the ex- citing aetiological factor. It matters little whether we ac- cept the tubercular theory of caries or not. The process is one insidious in its onset and slow in its progress. Cornil and Ranvier, in comparatively recent investigations, seem to show rather conclusively that the disease begins not as an inflammatory process, but a fatty degeneration of the bone cells. The result-a destruction of the bone cells and con- sequent inability on their part to perform their function as agents of nutrition. The osseous trabeculae, killed by the death of their cellular elements, form so many small foreign bodies which determine suppurative inflammation about themselves. The medulla becomes vascular, adipose cells disappear and are replaced by embryonic cells, and sup- puration is established. The bone cells which have escaped fatty degeneration become active, the osseous substance surrounding them is dissolved, the necrosed trabeculae be- come free, and granulations or fungosities are formed from embryonic medulla. Islets of osseous tissue become ne- crosed oftentimes, and are dislodged by granulations and carried away by suppuration. In their place are left irregu- lar cavities. Here, then, we have a suppurative process in progress which is most frequently confined to the anterior portions -of the bodies of the vertebrae. These diseased portions, giving way, permit the vertebrae to fall together. The disease creeps dorsad and destroys, to a greater or less extent, the posterior common ligament. The latter, dissoci- ated, allows the pus to pass from the vertebrae. The dura mater and the peridural tissue are aroused to inflammatory THE PRESSURE PARALYSIS OF POTT'S DISEASE. 3 activity. The external surface of the dura mater becomes covered with granulations of a fungoid character, and infil- trated with caseous pus. This condition passes under the name of pachymeningitis externa caseosa. This process shows no tendency to extend beyond the site of the verte- bral disease. It is limited. In a cross-section we can see how the diseased condition abruptly gives way to the healthy membrane. Up to this point the pathology stands, I can safely say, undisputed. In the large majority of cases of caries of the spine the pathological chapter closes here. The products of inflammation remain imprisoned, ultimately to be ab- sorbed and replaced by reparative material. Frequently paralytic symptoms manifest themselves, and here the pa- thology is by no means settled. Ollivier * was among the first to describe at all carefully the changes which take place in the cord as a result of slow compression. He cites numerous cases where the mem- branes were found thickened and the cord softened without evidence of further disorganization. His findings were veri- fied and described later by Louis.f These writers, and many of their followers who have described this form of paralysis, have dwelt upon the mechanical lesion alone as the cause of the paralysis. From time to time cases were reported where the cord seemed harder than normal, a con- dition not dwelt upon by these writers, and consequently no explanation offered. That the cord should become injured as a result of crumbling and broken vertebral bodies suffi- cient to lead to the production of marked angular curva- tures, was considered but a natural sequence. This idea * " Ueber das Riickenmark und seine Krankheiten," uebersetzt von Dr. J. Radius, Leipsic, 1824, p. 202. f " Memoire sur 1'etat de la moelle dans la carie Paris, 1826. 4 THE PRESSURE PARALYSIS OF POTT'S DISEASE. became so thoroughly fixed that many books, even to this day, refer only to bone as the pressure cause of the paraly- sis. It was noticed, however, that very frequently no pa- ralysis followed in cases where the deformity was very marked. The spinal column might even be bent to a right angle as a result of the disease, and still no paralytic symp- toms become manifest. That marked deformity can occur without the cord becoming compressed is also observed in lateral curvature, where sometimes the deformity assumes a frightful aspect. In the words of Fagge,* " every patho- logical museum contains specimens which show that the spinal canal generally retains its full width, however much its direction may be altered." Further, paralysis was seen to complicate caries when careful examination of the spinal column gave no evidence of deformity. These observations naturally called for some explanation other than the current view. The middle of this century, which inaugurated an active interest in the physiology and pathology of the great nerve- centers, produced men who sought a solution of the prob- lem. Among others, Charcot f and his pupils made inves- tigations and published to the medical world their conclu- sions. To Michaud, J I think, can be credited the pioneer article upon this subject. These authors and investigators contended, and apparently demonstrated, that the cause of the paralysis in these cases is not directly due to a me- chanical lesion, but to a myelitis the result of the mechanic- al lesion. Michaud held that myelitis was invariably the lesion, and even went so far as to claim its existence in cases giving no evidence of paralysis. * Fagge, vol. i, p. 410. j- " De la compress, lente de la moelle 6p.," " Logons sur les mal. du syst. nerv.," 2me s£r., 2me fasc., 1873. | " Sur la meningite et la myelite dans le mal vertebral," Paris, 1871. THE PRESSURE PARALYSIS OF POTT'S DISEASE. 5 This explanation of the cause of this form of paralysis, first described by Michaud and Charcot, and subsequently supported by Bouchard * and Courjon,f was accepted and apparently verified by Leyden J in his microscopical exami- nations of compressed cords. Great controversy has now long been in vogue regarding the exact nature of inflammatory processes of the cord. So loosely has the term myelitis been employed that various affections of the cord have been called myelitis-polio-mye- litis, ascending and descending degeneration, various kinds of softening; all these have been described by observers under the head of inflammatory lesions. Recent pathologists have come to look upon the disease myelitis as one giving rise to certain unmistakable and ever- present findings. Stricker, Leyden, Joffroy, Schultze,* Strumpell, || and others have found the following patho- logical findings which they regard as pathognomonic of the inflammatory lesion: 1. Increased size of nerve-elements, axis-cylinders en- larged, or without the sheath of Schwann. 2. Swelling of the interstitial tissue and increase of same, according to age of process. 3. Increased number of round cells in the connective tissue and around the blood-vessels. 4. Enlargement of Deiter's cells. The later stages characterized by hyperplasia of the connective tissue. * " Compress, lente de la moelle," " Diction, ency. des sc. medic.," 2me s6r., vol. viii, p. 664, 1874. f " fitude sur la paraplegic dans le mal de Pott," Paris, 1875. £ " Klinik der Riickenmarks-Krankheiten," vol. ii, first part, p. 149. * " Arch. f. klin. Med.," vol. xxv, p. 297 ; Virch. " Archiv," vol. Ixviii, p. 111. || " Archiv f. klin. Med.," vol. xxx, p. 526. 6 THE PRESSURE PARALYSIS OF POTT'S DISEASE. Erb practically coincides with the view of these authors, and their observations have been verified by numerous com- petent and careful observers both here and abroad. The progress of the lesion in cases of slow compression is, as a rule, insidious, and, to reconcile the clinical symp- toms with the lesion, the interstitial form of myelitis is be- lieved to predominate. This is characterized by an increase of the neuroglia or connective tissue, similar to that occur- ring in other organs, the parenchyma becoming second- arily implicated. The interstitial tissue becomes increased, together with proliferation of the nuclei, great thickening of the walls of the blood-vessels, and distinct atrophy of the nerve-fibers. A later stage is characterized almost exclu- sively by the presence of connective tissue. In support of the inflammatory theory are usually found post-mortem findings, showing the cord at the site of com- pression converted largely into connective tissue with thick- ened blood-vessels and sparsely distributed changed nerve- fibers and granular bodies. Further, in one case examined by Michaud, when the compression had not as yet produced paralysis, but where sensory disturbances in the form of fulgurating pains were complained of by the patient, the microscope revealed in- crease of the connective tissue throughout the posterior root zone. This explanation, then, of this form of pressure paraly- sis, which was so ably treated by Michaud and Charcot, supplemented by the studies of Courjon and Echeverria,* became as thoroughly implanted and accepted as had the explanation of Ollivier and Louis a quarter of a century before. Let us proceed now to a closer study of the subject in * " Sur la nature des affections dites tuberculeuses des vertebres," These, Paris, 1860. THE PRESSURE PARALYSIS OF POTT'S DISEASE. 7 hand, and to that end we ask, Can a mechanical lesion satisfy the demands of pathology and symptomatology ? Let us see. A mechanical cause is present. We have seen how the bodies of the vertebrae become destroyed by the carious process going on in the bone, leading to the formation of an abscess the walls of which are composed of bone and of the thickened surrounding soft tissues. We have further seen how the dura mater becomes involved, the process which goes on being called pachymeningitis externa caseosa. The abscess-cavity is not a simple one, but in it are devel- oped fungoid granulations, and the abscess products tend to accumulate. Nature tends to fortify the walls as far as pos- sible. It is not common for the pus to perforate the walls and escape into the surrounding tissues. The site of least resistance is toward the spinal cord, which swings insulated in the spinal canal. The membrane bulges into the canal and the cord recedes. The canal offers escape for the cord up to a certain limit, when, if bulging still goes on, the medullary substance is destined to suffer. Here, then, is practically a fluid sac, its pressure force commensurate with its fluid tension, mechanically an elastic ball. Clinically, the appearance of a psoas or gluteal ab- scess in a case of paralysis is often attended with the disap- pearance of paralytic symptoms. No one who has seen many of these cases has failed to note this clinical symp- tom. It is unnecessary to dwell upon the mechanism of this relief further than this allusion to it. I may add that bone is sometimes found pressing upon the spinal cord post mortem in cases which have had paralytic symp- toms. What does the gross lesion tend to show ? At the com- pressed site the spinal cord is often reduced in size to such an extent as to appear simply like a band of connective 8 THE PRESSURE PARALYSIS OF POTT'S DISEASE. tissue. It is a striking fact that the diseased dura mater is limited to the site of the diseased vertebrae. The change from " pachymeningite externe " to normal dura mater is abrupt. This has been noted by numerous ob- servers. Cornil and Ranvier * say : " Inflammation of the dura mater is limited exactly to the parts of the vertebrae diseased." This change in the dura mater is invariably in the anterior part of the membrane, and only in grave cases of caries does it encircle more than half of the cord. Does not this limitation of the diseased dura to the exact site of vertebral disease argue the non-tendency of the inflamma- tory process to extend in the membrane beyond what is ne- cessary to protect the cord from the abscess cavity itself- beyond nature's necessary protective area ? Medullary Surface of the Dura Mater.-This is usually intact and perfectly normal in appearance, the inflammatory process seeming to have spent its force in the external lay- ers. Microscopical examination of the diseased membrane rarely shows even infiltration of the internal layers. Can we not draw from this a further inference of the non-tend- ency of the process to extend ? Here, then, is a slow form of inflammation which does not seem active enough to ex- tend beyond the limits of the diseased vertebrae, not active enough to involve, as a rule, the internal layers of the mem- brane in which it originates. Is it possible, then, a priori, that it will extend to the cord ? It is proved, then, I think, that the irritation force is simply that of the pressure of a bland mechanical body. Is there anything in the pathological findings to militate against the lesion being a mechanical one ? Examination of compressed cords in the recent state show : 1. Granule cells, many or few, according to the mass of destroyed nerve-fibers. * Ed. 1882, vol. i, p. 606. THE PRESSURE PARALYSIS OF POTT'S DISEASE. 9 2. Debris of broken-down nerve-tissue. 3. Swollen axis-cylinders, or absence of the same. If examined at a later stage : 1. Nothing indicating changes in the blood-vessels. 2. No increase of cells about the vessels. 3. Occasionally traumatic haemorrhage. 4. Nerve-fibers in course of destruction and others which have been destroyed. 5. Swollen axis-cylinders or empty spaces, the former site of nerve-fibers. Then follows, as in all other analogous conditions, a sec- ondary increase of the neuroglia. Experimental Physiology.-It is a settled fact that press- ure upon nerve-trunks interferes with nerve conductivity. It has been demonstrated over and over again that a very moderate constrictive force about a nerve separates the mye- ]ine within the sheath, and, if severe enough, leads to sec- ondary degeneration, accompanied by all its pathological findings, rendering the nerve incapable of transmitting nerve impulses-e. g., the injury to the musculo-spiral nerve from pressure. Has it been demonstrated in these cases that the pressure invariably leads to a neuritis in the sense of an in- flammatory lesion ? Vulpian has shown experimentally that paralysis fol- lows the introduction of a wooden match so placed as to press upon the spinal cord of a guinea-pig. The pressure was continued a quarter of an hour, and the paralysis disappeared one hour after the pressure was re- moved. Attention is directed to what occurs after a nerve has been tied : 1. Segmentation of the myeline and disintegration of the same. 2. Disintegration of the axis-cylinders. 10 THE PRESSURE PARALYSIS OF POTT'S DISEASE. 3. Complete absorption of the mass, leaving the nerve- sheath empty or containing only debris and nuclei. The nuclei of the perineurium and endoneurium aid in the transformation of the nerve into a band of connective tissue. Here, then, is a process the result of which is prac- tically identical with that following compression of the cord -changes, degenerative in character, the result of the me- chanical interference, followed by increase of the connective- tissue elements. Pathological views characterizing degen- erative changes as inflammatory are by no means estab- lished. In the endeavor to settle this point, Dr. O. Kahler * made certain experiments upon dogs. He injected bee's- wax about the spinal cord; motor and sensory paralytic symptoms followed in the lower extremities. At varying periods the cords were carefully examined. After the com- pression had lasted from six to thirteen hours he found slight nodular foci located in the posterior and lateral col- umns. Microscopical examination of the same revealed marked swelling of the axis-cylinders, disappearance of the myeline sheath-no interstitial changes. Two to Ten Days.-Microscopical examination showed greater swelling of the axis-cylinders and destruction of the same, granular cells, slight increase of Deiter's cells. Later, five weeks to six months, there were found nodules of sclerosis with marked thickening of the connective tissue. He claims to have found none of the characteristics consid- ered by Leyden, Joffroy, Stricker, and Schultze as pathog- nomonic of myelitis, and concluded that the results were purely those of a mechanical lesion. Kahler states, as in peripheral nerves so in the spinal cord a moderate pressure is enough to excite a break in con- * " Zeitschrift fur Heilkunde," vol. iii, 1882, p. 18*7. THE PRESSURE PARALYSIS OF POTT'S DISEASE. 11 duction. A few fibers are destroyed in such cords, and we find lacunar changes distributed in the form of nodules. Do the connective-tissue-growth changes which are usually found at the site of the compression lesion necessarily signify the inflammatory character of the lesion? It is not denied that we usually find a sclerotic condition of the cord at the compression site when paralysis has ex- isted for any length of time. A glance at the observations will make this conclusive. That such is the outcome of the lesion is beyond dispute. We contend, however, that the presence of sclerotic tissue in the cord is no proof that the initial lesion was inflammatory. We have seen that this fol- lows various processes. Ziegler says the increase of connective tissue is a result of every process of softening. The connective-tissue increase characterizes every process of degeneration. Throughout the nerve-centers destruction of nerve-tissue by processes degenerative or otherwise is invariably followed by increase of the neuroglia. The examination in the great majority of these cases is made long after the onset of the lesion. We find only the result of the process which has produced de- struction. Leyden,* who came to look upon the lesion as identical with transverse myelitis, drew his conclusions al- most exclusively from old findings, and these are identical with those following myelitis. Charcot's f case-where the disease was cured after one year's standing, and where, two years subsequently, death occurred, the cord at the com- pressed site being found smaller and presenting a sclerotic condition-does not seem to offer any great support to the theory that the difficulty had been inflammatory. Michaud himself offers but one case as the strong pillar of his argu- * " Klinik der Riickenmarks-Krankheiten," vol. ii, part 1st, p. 149. f " Communication de M. Charcot la Societe de biologie," Sept., 1871. 12 TIIE PRESSURE PARALYSIS OF POTT'S DISEASE. in ent, where interstitial changes were found at an early stage, and this case had not as yet given evidence of paralysis. Erb * says the fact that in not a few cases of compres- sion of the cord the microscope reveals in the softened mass no granule cells, no hyperplasia of the connective tissue, no proliferation of the nuclei, but only swollen and disinte- grated nerve-elements, speaks unmistakably in favor of the view that the process is sometimes one of simple softening. Strumpell f contends that in repeated examination of cords compressed through spinal caries he has never found signs of inflammatory change. He refuses it upon patho- logical grounds, and believes that there is nothing found his- tologically that can not be accounted for as a result of a mechanical lesion. He says : " We must maintain, against the theory generally received at present, on the ground of many of our own investigations, that we have not the slight- est reason to refer the occurrence of paralysis in spondylitis to a secondary myelitis. Such a ' compression myelitis '- that is, an inflammation of the spinal cord arising from the pressure as such-is to be rejected from general pathological reasons, and the microscopical examination of the cord also shows nothing which points to an inflammation or what may not be entirely the result of mechanical compression. If we make stained cross-sections of the hardened cord, we see under the microscope no signs of vascular changes, of hyperaemia, of accumulation of cells about the vessels, and only exceptionally a little traumatic haemorrhage ; but we do find, in addition to many still preserved nerve-fibers, other fibers which are involved in the disintegration, and evidence of those already destroyed. If the destruction of nervous * " Ziemssen," vol. xiii, p. 469. f " Lehrbuch der sp. Pathologie und Therapie der inneren Krank- heiten," vol. ii, part 1st, p. 167. THE PRESSURE PARALYSIS OF POTT'S DISEASE. 13 tissue has advanced to a certain degree, there is in the later stages, as in all analogous processes, a secondary implication of the neuroglia. Now follows an increase of the interstitial connective tissue. Its proliferations, which take the place of the destroyed nervous tissue, seem diffuse at first, but later firm and fibrillary. Thus it happens that in old cases we find nothing at the point of compression but a loss of nerve- fibers in the cord, and in their place a firm fibrous tissue." What inferences can be drawn from a study of post-mor- tem findings ? In the light of the present well-recognized value of post-mortem findings in settling pathological ques- tions it would be a superficial study, indeed, in the present instance that neglected to consider them. From the literature of the subject those cases only are selected which have been reported with some attention to detail, for from such cases only is it possible to draw any reliable inferences. The cases are first cited and then analyzed. Observation I.-Male, aged six years, with marked angu- lar spinal curvature of eighteen months' duration, complicated with paraplegia which had existed for four months. Exami- nation showed complete loss of voluntary power of both lower extremities; very little muscular atrophy ; exaggerated reflexes even to the exhibition of spinal epilepsy. Died, seventeen months after the beginning of the paraplegia, from pulmonary complications. Autopsy.-Partial carious destruction of the sixth, seventh, and ninth dorsal vertebrae, and complete destruction of the eighth. An abscess, the contents of which had degenerated into a white, cheesy mass, occupied the site. Pultaceous mat- ter occupied the body of the eighth dorsal vertebra, and pressed upon the spinal cord. Microscopical examination by Dr. E. C. Seguin showed cord converted into connective tissue at the site of compression, also above and below, the usual lesion of secondary degeneration.- G-ibney, "The Illustrated Quarterly of Medicine and Surgery," April, 1882, p. 43. 14 THE PRESSURE PARALYSIS OF POTT'S DISEASE. Observation II.-Male, aged twenty-three years, com- plained for a short period of lancinating pains in the lower ex- tremities, preceded by malaise and fever, and soon followed by complete paraplegia. The legs were flexed upon the thighs, and the latter upon the abdomen. Reflexes markedly exag- gerated. Death occurred five weeks after the onset of the paralysis. Autopsy.-Body of fifth dorsal vertebra completely destroyed by caries. The spinal cord was found compressed at the level of the fifth dorsal vertebra by a purulent mass which existed in the vertebral canal. Spinal cord showed sclerotic changes at site of compression ; inflammation of pia mater involving spinal portion.-Mathieu, "Le progres medical," No. 35, September 2, 1882. Observation III.-Male, aged thirty-one years, complained for three months of a fixed pain in the region of the inferior angle of the left scapula. This was soon followed by a painful stiffness of the neck, together with marked atrophy of the infra-spinatus and deltoid muscles of the right side; later by atrophy and paralysis of muscles of both upper extremi- ties. Died, five months after the onset of the lesion, from asphyxia. Autopsy.-Oheesy osteitis, third, fourth, and fifth cervical vertebrae; "pacby. externe" limited to site of lesion, com- pressing same at height of fourth pair of cervical nerves through a cheesy proliferation which had broken through the dura mater.-Chantemesse, " Le progres medical," No. 8, 1883. Observation IV.-Male, aged forty-eight years, complained of occasional sharp pains in left arm, followed by weakness of both upper extremities and contraction of same. Lower ex- tremities subsequently became weak, accompanied by a spastic condition of same. After ten weeks the lower extremities became completely paralyzed, with marked contracture. The upper extremities remained only partially paralyzed, with a high grade of atrophy of the thenar eminence of both hands; partial degenerative reaction of the atrophied muscles; otherwise nor- mal electrical excitability, no fibrillary contractions, tendon re- flexes increased only in lower extremities. The only disturb- THE PRESSURE PARALYSIS OF POTT'S DISEASE. 15 ances of sensibility were slight pains and paraesthesia in the arms. Death occurred, seven months after the beginning of the disease, from sepsis. Autopsy.-Beginning caries, fourth, fifth, and seventh cer- vical vertebrae, without deformity of same. External surface of dura mater presented the condition of " pachy. externe" lim- ited to the site of the bony lesion, the medullary surface of the dura mater remaining smooth and intact. The spinal cord at the site of compression was found soft- ened in a marked degree and unfit for microscopical examina- tion.-Kahler, "Prager medicinische Wochenschr.," No. 49, p. 480, 1883. Observation V.-Female, aged six years, with a history of paraplegia of four years' duration ; reflexes markedly exag- gerated ; no sensory disturbances. Under treatment the pa- ralysis disappeared to a considerable extent, so that the patient could bear considerable weight upon the feet. Death occurred from embolic pneumonia. Autopsy.-Caries of the seventh cervical and first five dor- sal vertebras, the bodies of same being hollowed out and filled with cheesy pus. The spinal cord included between the second and seventh dorsal segments, measuring about 7 ctm., is trans- versely flattened, and has an increased consistency. In this portion of the cord there is destruction of both the gray and white matter. The walls of the blood-vessels are thickened, and the anterior portion of the dura mater is thickened and contains calcareous deposits. The cord above and below the compressed portion shows the usual lesion of secondary degen- eration.-Ridlon, "N. Y. Path. Soc. Rep.," "Medical Record," March 26, 1887, p. 361, and July 16, 1887, p. 84. Observation VI.-The patient, a male, complained for some months of pain in the back, followed by paresis of the lower extremities, which soon became completely paralyzed; reflex movements exaggerated; no marked sensory disturbances in same. Autopsy.-Partial destruction of the four upper dorsal ver- tebrae. The spinal cord was found compressed at the point opposite the second dorsal vertebra. At this point careful ex- 16 the PRESSURE PARALYSIS OF POTT'S DISEASE. amination failed to detect any inflammatory evidence.-Kadner, " Archiv d. Heilk.," xvii, 6, p. 481, 1876. Observation VII.-Male, aged forty-four years, November 10, 1875, seized with pain in chest, neck, and shoulders, accom- panied by cough and dyspnoea. These symptoms were soon followed by paralysis of the lower extremities, rectum, and bladder; sensibility of lower extremities diminished and reflex movements increased. Died February 17, 1876. Autopsy.-Caries of the seventh cervical and four upper dor- sal vertebrae. Examination of the spinal cord negative. There was a marked purulent infiltration beneath the periosteum, some pus having found its way into the spinal cord. This was the only lesion to account for the paralytic symptoms.-Kad- ner, loo. cit. Observation VIII.-Patient gave a history of stiffness of the neck, followed soon by a numb feeling in the arms, which extended up the arms over the trunk. Head, neck, and legs remained unaffected. Examination upon admission into the hospital at Stockholm elicited partial anaesthesia, most marked upon the right side in hands and fingers. There was also pare- sis of the lower extremities. The right side of the body became completely paralyzed. Patient died from failure of respiration. Autopsy.-Caries second, third, and fourth cervical verte- brae, with subperiosteal blood effusion. At a point opposite the second cervical vertebra the spinal cord was found com- pressed by a portion of bone. The pia mater at point opposite second and fourth cervical vertebrae was injected, but there was no exudation. The spinal cord at same height was softened exactly where the piece of bone pressed. Small haemorrhagic foci were found in the cord substance at the site of compression. -Malmsten, Schmidt's " Jahrb.," Bd. 171, S. 65. Observation IX.-Patient, aged sixteen years, upon admis- sion into hospital was found to have complete paralysis below the upper extremities, with marked anaesthesia of same; reflexes markedly increased. Died four months after admission. Autopsy.-Body of sixth cervical vertebra almost totally destroyed by caries. A rough protuberance projected into the anterior part of the spinal canal at this point, narrowing it con- THE PRESSURE PARALYSIS OF POTT'S DISEASE. 17 siderably. Dura mater shows the lesion " pachy. externe." Spinal cord at this point was found compressed and flattened. Microscopical examination not given.-Savory, " St. Barthol. Hosp. Reports," v, p. 45, 1869. Observation X.-Male, aged sixteen years; voluntary move- ments of lower extremities completely abolished; no anaesthe- sia; electrical contractility normal; reflexes markedly exag- gerated ; absence of pain in the beginning of the disease, but later some pains of a lancinating character; pupils dilated, but they react slowly to light; function of bladder and rectum normal. Autopsy.-Caries of the first four dorsal vertebrae. The an- terior columns of the spinal cord were compressed at the site of the lesion, and found softened and markedly anaemic; the re- maining portions of the cord are normal.-E. Rallett, " Wien, med. Wochenschr.," iv, p. 24, 1864. Observation XI.- Patient, aged five years and a half, brought to the hospital with measles, complicated with capillary bronchitis. Examination of the spinal column showed an angu- lar curvature at point of ninth and tenth dorsal vertebrae; no paralysis. Death occurred from the pulmonary disease. Autopsy.-At the posterior surface of the diseased vertebrae a small pocket was found formed by the prevertebral cellular tissue, and filled with cheesy pus; the posterior ligament was found perforated at this point, and the contents were in contact with the anterior surface of the dura mater. The membranes appeared as though sprinkled with vegetations, forming plaques 4 to 5 ctm. square. Hardened sections of the cord showed begin- ning myelitis.-Michaud, " Sur la meningite et la my&lite dans le mal vertebral," Paris, 1871, p. 66. Observation XII.-Patient, aged two years, admitted to hospital November 9, 1869, with left hemiplegia, with rigidity. Later, the right inferior limb became paralyzed. The thighs were flexed upon the abdomen, and the legs upon the thighs. Nothing was observed abnormal with the right superior ex- tremity, which alone could execute movements. Died April 2, 1870. Autopsy.-Spinal cord at the site of the compression lesion 18 THE PRESSURE PARALYSIS OF POTT'S DISEASE. due to caries showed marked evidence of sclerosis.-Michaud, ibid., p. 68. Observation XIII.-Female, aged thirty-four years, noticed, after birth of first child, at the age of twenty-five years, slight deformity of the spinal column, followed three months later by numbness in the lower extremities. Entered the Hotel Dieu with complete paraplegia of the lower extremities, accompanied by contracture of same. The paraplegia continued for more than four years. Patient died from a complicating morbus cox- arius, September, 1869. Autopsy.-Upon opening the rhachidian canal, the dura mater was found covered with a grayish exudation, which caused it to adhere to the posterior face of the changed vertebral bodies. An osteoform projection compressed the spinal cord at the level of the third dorsal vertebra. The spinal cord at this point was found extremely diminished in size and of about the size of a goose-quill. Above and below, the cord regained gradually its normal dimensions. Microscopical examination showed sclero- sis of cord, with ascending and descending degeneration.- Michaud, ibid., p. 70. Observation XIV.-Male, aged thirteen years, entered hos- pital Sainte-Eugenie, September 16, 1869, with dorsal angular curvature and complete paraplegia; moderate contracture of legs and thighs; sensibility to touch, temperature, and pain completely abolished ; reflex movements exaggerated ; function of bladder and rectum normal. Died January 29, 1870. Autopsy.-Caries of the five lower dorsal vertebrae, the apex of the angular deformity being found by the tenth. Two of the vertebrae are completely destroyed; the osseous tissue is infiltrated with tubercle. The dura mater is thickened at the site of the disease, showing the lesion "pachy. externe." The spinal cord at the site of the lesion shows well-marked evidence of sclerosis, with dislocation of one of the anterior horns.- Michaud, ibid., p. 73. Observation XV.-Male, aged forty-two years, admitted into the service of M. Vulpian at hospital La Piti6, March 31, 1870, complaining of severe neuralgic pains in the lumbar and epigastric regions. Examination revealed angular curvature of THE PRESSURE PARALYSIS OF POTT'S DISEASE. 19 the spinal column at the junction of the upper and middle thirds of the dorsal region; analgesia of the lower extremities most marked upon the left side; sensibility to temperature very well preserved. Died January 18, 1870. Autopsy.-The dura mater is considerably thickened at a point corresponding to the eighth and ninth dorsal vertebrae, and the latter present a condition of extreme friability as a re- sult of caries; the posterior ligament is destroyed opposite the diseased vertebrae. The spinal cord at the site of the lesion does not offer a uniform alteration. Toward the superior part of the compressed segment are found tracts of sclerosis in the posterior columns following the course of the internal radical filaments. The corresponding nerve-roots present evidence of neuritis, with granulo-fatty change. At the lower part of the compressed segment is found a peripheral sclerosis, presenting a tendency to assume the annular form, most marked upon the lateral columns; the left lateral half of the gray substance is deeply changed. Above the site of the lesion is found sclerosis, which continues in the lateral columns up to the cervical region. -Michaud, ibid., p. 74. Observation XVI.- Infant, aged eight months, began gradually to lose power of the right arm, and subsequently of the left. After two months and a half, partial paralysis of the lower extremities. Died at the end of seven months after the onset of the disease. Autopsy.-Caries of the sixth and seventh cervical vertebrae, opposite which point the cord seemed enlarged. This enlarge- ment was due to tubercular infiltration, which at this point had caused complete absorption of the proper tissue of the cord. The tubercular mass seemed to have had its origin in the right postero and postero-lateral columns; then extended until the cord was gradually destroyed, only slight traces of the anterior columns remaining.-Gull, " Guy's Hosp. Reports," 1858, 3d series, vol. iv, p. 206. Observation XVII.- Male, aged fifty-eight years, com- plained of backache for thirteen years, the pain being most severe in the lumbar region, thence radiating toward both sides; loss of power slowly developed in the lower extremities, which 20 THE PRESSURE PARALYSIS OF POTT'S DISEASE. soon became completely paralyzed ; reflex movements markedly exaggerated ; severe muscular cramps. Autopsy.-Caries of the sixth, seventh, and eighth dorsal vertebrae. At a point opposite the posterior surface of the body of the eighth dorsal vertebra the dura mater is thickened and adherent to the bone ; the vertebral canal is narrowed at this point; the intercostal nerves in the vicinity of the diseased vertebrae are imbedded in thickened callous tissue. Above and below the site of the lesion the dura mater is normal. The spinal cord at the site of the lesion was compressed, and smaller than that above and below. Alicroscopical examination of the same revealed absence of a portion of the nerve-fibers; medul- lary sheaths destroyed in places ; connective tissue increased ; the nuclei were but slightly increased, in no place more than two or three being found together ; little fat droplets and amy- loid bodies also found.-Frommann, Virchow's " Archiv," Bd. 54, S. 42. Observation XVIII.-Male, aged thirty-seven years, fell on the 10th of October, 1885, spraining his right hand ; three weeks later complained of some pain in his right shoulder, and gradu- ally his right arm became paralyzed. Examination showed paralysis of deltoid, brachialis anticus, and biceps muscles; sen- sibility of arm slightly diminished ; hypenesthesia over the re- gion of the superior cervical nerve; pupils dilated. One year after beginning of the disease general emaciation, with very pronounced atrophy of the muscles of the right arm; less ot the left. Finally, complete paralysis of both upper extremities and of the muscles of the neck, with moderate anaesthesia; paresis of legs, with increased tendon reflexes. Died Novem- ber 14, 1886. Autopsy.-Bodies of the third and fourth cervical vertebrae carious; intevertebral substance destroyed ; the posterior liga- ment is bowed with the convexity toward the spinal cord, com- pressing same. Spinal cord: 4 to 5 ctm. of the cervical enlarge- ment softened into a reddish pulp; the meninges are intact; fourth cervical nerve surrounded by pus.-Grasset and Estor, "Revue de m6d.," viii, 2, p. 113, 1887. Observation XIX.-Female, aged sixty years, admitted THE PRESSURE PARALYSIS OF POTT'S DISEASE. 21 into Guy's Hospital, November 6, 1867, with complete para- plegia, which had been progressive from time of onset, three months previous; partial anaesthesia, but no pain. Died sud- denly, ten days after admission, with symptoms of heart- failure. Autopsy.-Third and fourth dorsal vertebrae partially de- stroyed by caries, with complete destruction of the interverte- bral substance. At the site of the lesion a mass of softened material projected into the spinal canal, causing pressure upon the cord. Spinal membranes intact. Spinal cord diminished in size at site of compression and somewhat softened.-Ogle, "Trans, of the Path. Soc. of London," vol. xix, p. 16, 1868. Observation XX.-Male, aged forty-one years, afflicted with caries of the middle dorsal region of the spine, complicated with paresis of both lower extremities; reflex movements markedly exaggerated. Died from phthisis complicating the carious disease. Autopsy.-Caries of the fifth and sixth dorsal vertebrae and complete destruction of the intervertebral substance. At the site of lesion an abscess pressed upon the spinal cord. The spinal membranes were found intact, and the spinal cord presented no evidence of inflammatory change.-Ogle, loc. cit. Observation XXL - Male, aged forty-five years, com- plained, during year 1878, of stiffness of his neck which ren- dered rotation of same impossible. During the year a retro- pharyngeal abscess formed, which broke externally. Examina- tion, January 1, 1879, showed rigidity of the upper part of the vertebral column, but no paralysis of upper or lower extremities. The only marked symptom aside from the rigidity of the muscles of the neck was profound atrophy of the thenar eminence and interossei of both hands. Autopsy.-Posterior ligament in great part destroyed from the third dorsal to the superior cervical vertebrae; body of first dorsal and all the cervical vertebrae carious. Dura mater oppo- site diseased site shows the condition of " pachy. externe," the internal surface, however, remaining intact. The condition of " pachy. externe " extends laterally in the dura mater far enough THE PRESSURE PARALYSIS OF POTT'S DISEASE. 22 to include the anterior and posterior spinal nerve-roots travers- ing same. Microscopical Examination. - The anterior nerve-roots which form the brachial plexus show the degenerative lesion- proliferation of the nuclei, atrophy, and crowding together of the myeline and axis-cylinders. This same lesion is found in the nerves which supply the atrophied muscles. The posterior spinal roots appear normal. Spinal Cord.-Several ctm. of the middle and inferior cervi- cal segments show : a. Slight sclerosis of the direct cerebellar tract. J. The internal root-zones of the posterior columns show a sclerotic lesion similar to that of locomotor ataxia, which lesion is prolonged into the gray substance. The motor cells of the anterior horns are also somewhat atrophied, and the cells fewer than normal. No evidence of ascending or descending degeneration in the white columns usually found consequent to lesions of the cord.-Proust and Ballet, "Revue mensuelle," vol. iv, p. 425,1880. Analysis of the Findings. - In examining the cases which have just been cited, we are struck with the super- ficial manner in which some have been reported-so im- perfectly reported in some instances, even by competent observers, as to render them almost worthless beyond giv- ing a rough description of the gross findings. Yet, in- asmuch as these are valuable to us, they have been , in- cluded with those where the microscopical findings are also given. Dura Mater.-The medullary surface is found intact in all observations excepting III and VII, which showed per- foration of the dura. Pia Mater.-In Observation VIII found injected, but unaccompanied by exudation; in the remaining cases normal. Spinal Cord.-Observations I, II, V, IX, XII, XIII, XIV, and XVII show the spinal cord converted into con- THE PRESSURE PARALYSIS OF POTT'S DISEASE. 23 nective tissue at the site of compression. This gives no clew to the pathology of the original lesion, since we have seen that connective-tissue growth is a result of a variety of lesions affecting nerve-tissue. Softening of the cord at the compression site is found in Observations IV, VIII, X, XVIII, and XIX. In Observa- tion VIII the cord was softened exactly where it was pressed upon by bone, and small haemorrhagic foci were found in the cord substance-changes non-inflammatory, similar to changes already described, which experimental physiology tends to show take place in the cord as a result of com- pression. In Observation X the lesion was limited exactly to the anterior columns of the cord, and these were found softened and anaemic, the presence of the latter condition, as held by the observer, pointing to a non-inflammatory lesion. In Observation XIX, Ogle adds, with some em- phasis, that the lesion at the site of compression was purely a mechanical one, as nothing indicative of inflammation was found. In Observations IV and XVIII the lesion may or may not have been inflammatory. A compression cause existed in the form of abscess products which compressed the cord. In both cases it is to be noted that the meninges were found normal. Observations VI, VII, and XX give no evidence of inflammatory destruction reported by such observers as Kadner and Ogle. In Observation XVI the cord tissue proper was found absorbed by the tubercular neoplasm. In Observation XI Michaud sums up the histo- logical findings under the head of beginning myelitis, with- out detailing the formr. If we carefully compare the findings in Observations XV and XXI, we will notice a marked resemblance and at once see that they differ materially from those histological changes usually met with at the site of compression. While no paralysis existed in either case, it is deemed best to refer THE PRESSURE PARALYSIS OF POTT'S DISEASE. 24 to them here, inasmuch as they have been thought by some authors to indicate the early lesion of so-called " compression myelitis." In Observation XXI, especially, we notice that the lesion is confined to definite tracts in the spinal cord-viz.: the posterior root-zones or columns of Burdach and gray matter adjoining, the direct cerebellar tracts, the anterior horns and nerves originating from the latter. How is such a lesion to be explained ? Proust and Ballet were inclined to accept the following hypothesis: Irritation of the pos- terior nerve-roots excited inflammation of the posterior root- zones, which inflammation extended from thence to the parts of the cord found implicated-in other words, an ascending neuritis. Kahler,* in commenting on this case, calls at- tention to a fact which we have also observed, that usu- ally in cases of lower cervical caries giving rise to symp- toms similar to those enumerated, the reflexes of the upper extremities are preserved even when the atrophy is quite profound, and correctly infers that such phenomena are quite inconsistent with a neuritic disease of the cervical nerve-roots. The distribution of the pathological findings to rather definite tracts of the cord argues a lesion having a definite cause and progressing in a definite order. The following hypothesis would seem to offer a satisfactory explanation : The lesion is twofold in character: 1. Alteration of the posterior root-zones and direct cerebellar tracts due to a degenerative lesion, the result of implication of the sensory roots at the site of pachy. externe. 2. The changes in the anterior horns are believed to be the direct result of moder- ate compression of the cord, and the degeneration of certain of the anterior nerve-roots necessarily secondary. The preservation of the reflexes in these cases renders it con- clusive that the spinal-cord substance itself is primarily in- * Kahler, "Prag. med. Woch.," viii, No. 49, p. 480. THE PRESSURE PARALYSIS OF POTT'S DISEASE. 25 volved. Even here, then, there seems to be nothing which a mechanical lesion will not readily explain. We may add, Is there, even in those cases where the sclerosis is said to have an irregular distribution at the compressed site, anything especially incompatible with the theory that such changes are but later stages of non-inflam- matory foci, induced by moderate compression of the cord ? That such is the case is rather corroborated by Kahler's experiments, already dwelt upon in an earlier part of this paper. To briefly summarize, then, we have shown: 1. That we have present a simple mechanical press- ure in the form of abscess products, thickened dura, or bone. 2. That the inflammatory process is invariably a limited one, the inflammation of the dura mater being limited ex- actly to the site of the diseased vertebrae, exhibiting no tendency to extend in the membrane-nature's medullary protection. 3. That the medullary surface of the dura mater is al- most invariably normal. 4. It follows, then, that the pressure lesion is simply mechanical, possessing no tendency to involve the spinal cord through any inherent specific characters of the carious process-a bland mechanical lesion-and the damage it in- flicts commensurate with the pressure exerted. 5. That examinations of the pathological findings have, in the vast majority of cases, necessarily been confined to old cases where the lesion had existed for a very considera- ble period, and that such examinations usually revealed the cord largely converted into connective tissue at the site of compression. 6. The presence of sclerotic tissue at the site of com- pression is no evidence that the original lesion was of an 26 THE PRESSURE PARALYSIS OF POTT'S DISEASE. inflammatory character, since it is a well-established patho- logical law, to which we have alluded, that throughout the nerve-centers destruction of nerve-tissue, by processes de- generative or otherwise, is invariably followed by increase of the connective tissue. Experimental physiology gives no evidence of an in- flammatory lesion following experimental compression of the cord, microscopical examination of the same showing a few granular cells, swollen axis-cylinders and evidence of de- struction of the same, foci of traumatic haemorrhage- changes identical with those observed by Strumpell, Kahler, and others, at the site of recent compression of the human spinal cord. We do not find signs of vascular changes, of hyperaemia, of accumulation of cells about the vessels, and in the connective tissue ; in other words, no evidence of those pathological changes which are considered by Leyden, JofTroy, Stricker, Schultze, and others as pathognomonic of inflammatory change. 8. A careful examination of the pathological findings of reported cases reveals to us, in the light of recent patho- logical knowledge, but few instances where we have reason to believe the original lesion to have been inflammatory. These were cases where the process was virulent, leading to a perforation of the dura mater, thus allowing the puru- lent products to come in direct contact with the cord, giv- ing rise to a lepto-meningitis. Finally, then, our researches have led us to conclude that the original lesion is, as a rule, non-inflammatory, and we have endeavored to demonstrate this from a pathological standpoint, support it by experimental physiology, and cor- roborate it by clinical manifestations. We must await further researches in neuro-pathology to clear away certain obstacles which we recognize exist. When the pathology of the so-called combined sclerosis is thor- THE PRESSURE PARALYSIS OF POTT'S DISEASE. 27 oughly understood, together with all the facts pertaining to the physiological and pathological role played by the pos- terior root ganglia and the vascular mechanism of the cord, it will doubtless be possible to complete the patho- logical picture of this peculiar form of paralysis, and establish as certainties what at present exist but as proba- ble hypotheses. 48 East Twenty-sixth Street. jgr ft REASONS WHY Physicians Should Subscribe >or The New York Medical Journal, Edited by FRANK P. FOSTER, M. D., Published by D. APPLETON & CO., 1, 3, & 5 Bond St. 1. BECAUSE : It is the LEADING JOURNAL of America, and contains more reading-matter than any other journal of its class. 2. BECAUSE: It is the exponent of the most advanced scientific medical thought. 3. BECAUSE: Its contributors are among the most learned medical men of this country. 4. BECAUSE : Its "Original Articles" are the results of scientific observation and research, and are of infinite practical value to the general practitioner. 5. BECAUSE : The "Reports on the Progress of Medicine," which are published from time to time, contain the most recent discov- eries in the various departments of medicine, and are written by practitioners especially qualified for the purpose. 6. BECAUSE: The column devoted in each number to "Therapeu- tical Notes " contains a resume of the practical application of the most recent therapeutic novelties. 7. BECAUSE : The Society Proceedings, of which each number con- tains one or more, are reports of the practical experience of prominent physicians who thus give to the profession the results of certain modes of treatment in given cases. 8. BECAUSE : The Editorial Columns are controlled only by the desire to promote the welfare, honor, and advancement of the sci- ence of medicine, as viewed from a standpoint looking to the best interests of the profession. 9. BECAUSE : Nothing is admitted to its columns that has not some bearing on medicine, or is not possessed of some practical value. IO. BECAUSE : It is published solely in the interests of medicine, and for the upholding of the elevated position occupied by the profession of America. Subscription Price, 85.00 per Annum. Volumes begin in January and July.