Anæmia of the cord-substance proper, like hyperæmia, is practically inseparable from the corresponding condition of the membranes. The influence of a reduced blood-amount on the functional activity of the spinal cord is more susceptible of exact demonstration than the corresponding nutritive disturbance of the brain. As the functions of this segment of the nervous axis are far simpler than those of the higher organ, there is more unanimity among observers as to the interpretation of their disordered states. In Stenon's experiment, and the more elaborate modifications made by those who have followed his method, it is found that interference with the supply of arterial blood to the spinal cord is followed by abolition of the function of the gray matter; if the supply be still further diminished, the functions of the white tracts become eliminated; next the peripheral nerves, and ultimately the muscles themselves, lose their normal excitability. On the re-establishment of the circulation these various parts regain their functional capacity in the inverse order of its suspension—the muscles first, next the nerves, then the white substance, and last the gray substance of the cord. The initial symptoms of some cases of myelitis from refrigeration correspond more nearly to such a result of artificial anæmia of the cord than they do to anything that is customarily regarded as hyperæmia.73
73I have seen distinct pallor of the spinal meninges on dipping the posterior extremities of a dog, whose cord had been exposed, into water. It is to be remarked, however, that other observers, notably Hammond, have either obtained different results or interpreted the consequences of refrigeration differently.
No one has gone farther than Hammond in erecting a theoretical anatomical framework which elaborately provides for the accommodation of various symptoms of spinal anæmia. He describes anæmia of the posterior columns, and sharply discriminates between it and anæmia of the antero-lateral columns. It is a question whether the conducting tracts of these columns are seriously affected in their functions by anæmia as long as the centres of innervation are well nourished. Undoubtedly, it is the gray substance of the cord which is most vulnerable to the influence ofdisturbed circulation and nutrition, as Stenon's experiment has shown; and a glance at the distribution of the blood-vessels will show that a partial anæmia or hyperæmia, limited to special cornua in any considerable length of the cord, is an exceedingly improbable occurrence. With regard to isolated anæmia of the white columns, it is to be admitted that the posterior are most vulnerable to malnutrition. But it is doubtful whether this vulnerability is so great as to allow of an exclusively posterior anæmia, or whether a protracted anæmia of this kind could exist for years as a purely symptomatic—or, as some designate it, functional—disorder.
Hammond candidly states that in specifically locating the lesions in these affections he is aware that post-mortem examinations are wanting to support them, and admits that what he calls anæmia of special parts of the cord is the spinal irritation of most authors, and in part the reflex paraplegia of others.
The most clearly-established form of cerebral anæmia is the one which is indicated by the ischæmic paraplegia of Jaccoud and the paraplegia following profuse hemorrhages. The former is produced by all causes which, by obstructing the flow of arterial blood in the abdominal or thoracic aorta, cut off the proper blood-supply to the cord, which the latter receives through the intercostal and upper lumbar arteries. Aneurism, compression by tumors, and embolism of the aorta produce this result. The consequence is paraplegia corresponding in all features of its development to the phenomena observed in Stenon's experiment. These features, already detailed, suffice to show that it is not the anæmia of the peripheral nerves and muscles that is chiefly responsible for the paraplegia, but the insufficient irrigation of the gray and white substance of the cord itself. The same is true of the paraplegia following hemorrhage which has been noted after uterine, renal, and enteric hemorrhages. Both affections are exceedingly rare.
The influence of general anæmia on the functions of the spinal cord is not susceptible of accurate study. The cerebral enlargement of the nervous axis is so much more unfavorably situated than the cord that it suffers first and most when general anæmia is present. The consequence is that the signs of cerebral anæmia mask those of spinal anæmia. It is supposed, however, by many authorities that the effect of anæmia on the cord may be regarded as an auxiliary factor in the production of hysterical and neurasthenic symptoms.
How far the spinal cord is liable to suffer from arterial spasm is as yet a matter of conjecture. It is supposable that just as a powerful psychical impression provokes a sudden spasm of the cerebral arteries, so a peripheral irritation may provoke a spasm of the spinal arteries. In this way the reflex paralyses, motor and vaso-motor, are explained by many writers.
The subject of reflex palsy has been so much confused by improper cataloguing—if it can be so called—that some of the best authorities have become sceptical as to its occurrence. Among the chief sources of error has been the attributing to irritation of the genital organs various convulsive, psychical, and paralytic disorders. Adherence of the prepuce and its excessive length were charged with being responsible for idiocy, imbecility, epilepsy, and every form of paraplegia and panplegia. It was further claimed that instances of complete cure of each of theseaffections had followed the removal of the exuberant or adherent prepuce. I cannot find a single instance recorded where such a cure was effected in any of our large medical centres, so as to prove convincing to critical colleagues. On the contrary, L. C. Gray74has shown that various surgical procedures have been needlessly resorted to on this erroneous theory in cases of organic diseases of the spinal cord. I have seen two unfortunate children suffering from the worst forms of anterior poliomyelitis, one afflicted with pseudo-hypertrophic paralysis, and several hydrocephalous and microcephalous idiots, whose prepuces had been sacrificed to the theory alluded to—it is needless to add without any result, good or bad.
74Reflex Irritation from Genital Irritation. In this paper written communications from all or nearly all neurologists in the United States—certainly including all those of national fame and large experience—are cited, in which they testify to never having seen a case of this character cured by operations on the penis (Annals of Anatomy and Surgery, Jan. and Feb., 1882.)
The possibility of a reflex paralysis occurring from genital irritation in the male cannot be denied; among the lower animals a ligature around the spermatic cords sometimes produces paraparesis, and paraplegia is a common complication of renal and vesical troubles in others. But analogous observations in man are rare, and becoming rarer with our increasing acumen in diagnosis. In females peculiar reflex disturbances are found associated with uterine and ovarian derangements. In one case of retroflexion, with possible dislocation of the ovary, referred to me by H. J. Boldt, there is a remarkable vaso-motor paralysis of the right arm during each menstrual period: this member becomes greatly enlarged, of a purplish-blue color, and cold. Equally remarkable are the reflex disturbances resulting from the presence of worms in the intestinal canal. Every form of spinal and cerebral paralysis, even aphasia, has been observed in connection with helminthiasis. Such disorders yield as rapidly as they are developed to the exhibition of vermifuges.
Special interest has been aroused by the discovery laid down in the joint treatise of J. W. Mitchell, Morehouse, and Keen of reflex paralysis following injuries, observed in the War of the Rebellion. The cases cited by them appear singular on first sight. The paralysis is often observed in parts of the body which are not only remote from the seat of injury, but have no direct connection, physiologically or otherwise, with it. The hand may be injured and the opposite leg paralyzed.
Since Mitchell, Morehouse, and Keen first announced the existence of this peculiar form of reflex paralysis a careful search has been made by military surgeons engaged in other campaigns for like results. Notably was this done in the Franco-Prussian War. A number of confirmatory instances have been collected, some of which rival in singularity those related by the discoverers of the affection. In one case a unilateral paralysis agitans followed a punctured wound of the opposite shoulder, and in another reflex aphasia followed a gunshot wound of the lumbar region.75A discrimination is to be made between such cases where the paralysis, anæsthesia, or neuralgia is an immediate result of the injury, and those where they follow after weeks or months. In the latter instance we have not true reflex disorders to deal with, an ascendingneuritis having been found in the few cases which could be carefully followed up.76
75Sanitäts Bericht über die deutschen Heere im Krieg gegen Frankreich, 1870-71, vol. vii.—abstracted inNeurologisches Centralblatt, 1886, p. 207.
76In a case of Mollenhauer's, vesical paralysis and paresis of the right leg occurred six years ago (1880) in a veteran of our civil war who had a gunshot wound of the right hand, with signs, which are still present, of occasional exacerbation of brachial neuritis. Prodromal signs of paresis were noticed at intervals since his return from the campaign. The bladder trouble and paresis are now apparently stationary. Such a case can be accounted for only on the assumption of an organic cord-change secondary to a neuritis.
The theory that the reflex paralysis from utero-ovarian, intestinal, and surgical affections, when acutely produced, is due to central anæmia, is as acceptable as any other would be in the absence of decisive observations.
Spinal anæmia will but rarely present itself as a subject for special and separate treatment. When not associated with an intrinsically grave condition, such as aortic obstruction, dysentery, fatal hemorrhage, or typhoid fever, it is an exceedingly benign affection, rapidly yielding to tonic and restorative measures combined with rest.
Although the spinal cord is a segment of the same central organ as the brain, nourished in a similar way, and subject to the same physiological and pathological laws, lesions of the vascular apparatus, which play so important a part in brain pathology, play a comparatively insignificant one in that of the spinal cord. Embolic, thrombic, and primary hemorrhagic lesions of the cord are so rare that their possible existence has even been denied. A primary thrombosis of the cord has not yet been satisfactorily demonstrated to occur independently of syphilitic lesions; and when it occurs the ensuing tissue-changes, as described by Heubner, Julliard, and Greiff, are usually in the background as compared to the gummatous, sclerotic, or meningitic changes which coexist. The clinical as well as the anatomical picture is accordingly either one of a myelitis or meningitis, as the cases of Charcot-Gombault, Heubner, McDowell, Wilks, Wagner, Zambaco, Homolle, Winge, Moxon, Schultze, Westphal, Julliard, and Greiff show. (See Myelitis and Spinal Meningitis.)
With regard to the occurrence of hemorrhage into the substance of the spinal cord (hæmato-myelia), it is so rare an occurrence that I can recall but a single case in which I entertained the diagnosis of this lesion; and in that very case I am unable to declare that it was not a hemorrhagic myelitis. Aneurismal changes of the spinal arteries are comparatively of rare occurrence, and as other predisposing causes to primary vascular rupture are rare in the cord, the probability of its occurrence is very much diminished. Hebold,77in a young girl who had developed severe cerebro-spinal symptoms during a period of nine months following an erysipelatous disorder, found the upper dorsal cord, on section, dotted with numerous reddish and round points. These points corresponded toaneurismal dilatations of the vessels. As there were other inflammatory and vascular lesions in the same subject, the author referred their causation to a general constitutional vice, the result either of the phlegmonous or of a tuberculous disorder.
77Archiv für Psychiatrie, xvi. 3. Rupture of miliary and other aneurisms in the meninges has been reported by Astley Cooper, Traube, and others. It is remarkable that such cases are more and more rarely recorded from year to year in inverse ratio to the accuracy of our spinal autopsies. I have never found a miliary aneurism below the uppermost cervical level of the cord. On the other hand, I have found extensive spinal hemorrhage in cases where the vessels of the cord proper were fairly healthy.
It is claimed that suppression of the menses, over-exertion, lifting heavy weights, and concussion are causes of spinal hemorrhage. The same causes are also mentioned for acute hemorrhagic myelitis; and it is a question whether the supposed hemorrhage is an initial lesion or secondary to congestive or anæmic softening.78
78I have never found vascular ruptures, although carefully searching for them, in the spinal cord of persons dying instantly after falls from a great height, or, as in one case which I was fortunately able to secure the cord of, where the subject had been violently thrown down. Where hemorrhages have been found under these circumstances they were, as far as I am able to learn from the cases recorded, meningeal.
The symptoms attributed to spinal hemorrhage are the same, taking the same locality of the cord, as those of a very rapidly-developed transverse myelitis. It is unnecessary to enumerate these here in anticipation of the next section. They are described as being much more sudden. This suddenness is the only diagnostic aid on which we can rely.79The fate of the patient is said by Erb to be decided within a few days. If he survive the immediate consequences of the hemorrhage, he is apt to recover, as to life, altogether, with such permanent atrophies, paralyses, and anæsthesias as are entailed by the destruction of the tracts and gray substance involved in the hemorrhage. The treatment recommended for this condition consists of rest, either in the lateral or prone position, local depletion and derivation to the intestinal canal, as well as the internal use of ergotin. The local application of ice, which is also advised, is probably based on illusory views.80After the immediate danger is past the case is to be treated as one of myelitis—a very safe recommendation in view of the probability that it was a case of myelitis from the beginning.
79And even this sign is unavailable as a distinguishing feature in supposed hemorrhage from concussion, as sudden paraplegias of motion and sensation are found in some cases of railway spine, and, although a number of cases terminating fatally have been examined, there was not always hemorrhage even in the meninges.
80Until authorities shall have agreed as to what effect the exposure of the bodily periphery to certain temperatures has on the circulation of the cord, it would be premature to make any special recommendations as to the temperature at which they should be kept. I am inclined to believe that while, as is universally accepted, a general cooling of the bodily surface tends to increase vascular fulness in the cord, as in all other internal organs, a partial cooling, as of the feet, produces local anæmia at the level of origin of the nerves supplying the cooled part. Certainly, the bilateral neural effects of unilateral cooling are in favor of this view.
The descriptions given of the hemorrhagic foci as observed after death strengthen the view that they were in the majority of cases of myelitic origin. Usually, they are stated to extend up and down the cord in the direction of least resistance—that is, in the gray substance—resembling an ordinary apoplectic clot. But in their neighborhood there was usually considerable softening, and, to judge by the descriptions given, this softening differed in no wise from that which is the characteristic feature of acute myelitis;81and often the transition from a peripheral zone of whitesoftening, through an intermediate zone of red softening, to a central compact clot, is so gradual as to leave it unquestionable that the softening pre-existed, and that a vessel had broken down in the midst of the myelitic detritus. Many ancient foci of myelitis betray the hemorrhagic complication of their initial period by the presence of pigmented residue of the absorbed clot.
81In the latest treatise on nervous diseases published in our language (Ross,loc. cit., vol. ii. p. 325) the insufficient foundation on which a whole chapter has been built up is illustrated by the admission that the usual evidence of acute central myelitis may be observed far beyond the limits of the hemorrhagic infiltration. If a large area of softening in the brain were found to contain a central or peripheral clot of blood, and histologically resembling a typical embolic or thrombic softening, no one would be in doubt as to which of the two was the primary lesion.
Embolisms and embolic softenings of that part of the spinal cord which is supplied by the small spinal vessels are so rarely observed in the dead-house that our knowledge of their possible occurrence and character is almost entirely the result of experimental observations or based on analogy. The situation of these vessels, the angle at which their supply-tubes are given off from the aorta, all act as protectors of the cord against what is one of the chief dangers to which the brain is exposed. No definite symptoms have been attributed to the few doubtful cases of simple embolic occlusion of the spinal arteries found accidentally in human subjects. Even those emboli which, when once let loose in the circulation, are found distributed in nearly every organ of the body, those derived from ulcerative endocarditis and those due to the invasion of micrococci, are comparatively rare in the cord. Leyden found multiple capillary emboli in the spinal cord from the former cause. Small grayish white foci in a similar distribution were found to be due to an invasion of cocco-bacteria from a decubitus by Rovigli.82In this latter case an increase of pain and muscular spasm in the history of the case of sclerosis which was thus complicated was attributed to the parasitic affection.
82Rivista sperimentale di Freniatria, 1884, x. p. 227.
Just as simple and infectious embolic lesions are frequent in the brain and rare in the cord, so purulent inflammation or abscess is an exceptional occurrence in spinal as compared with cerebral pathology, and probably for the same reasons.
SYNONYMS.—Spontane (primäre) acute Rückenmarkserweichung, Softening of the spinal cord, Ramollissement blanc de la moelle, Myélite aiguë.
As Leyden, whose treatise83may be regarded as the foundation of our knowledge on this subject, correctly avers, it is to Abercrombie and Ollivier that we owe the determination of the existence of that acute structural disease of the spinal cord, now termed myelitis, as an affection independent of meningeal changes. The anatomical descriptions given by these older writers may be accepted at the present day as models of accurate observation by the naked eye. Their statement that in acute myelitis the substance of the spinal cord is softened and changed into a puriform, yellowish, diffluent mass; that while the disorganization is sometimes more marked in the posterior, at others in the anterior, and occasionally in the lateral half, it is most pronounced in the axis of the cord, because the central gray substance is the favorite starting-pointof the morbid process,—requires no modification to-day. Considerable doubt existed in the minds of the contemporaries of Ollivier and Abercrombie as to whether this change was the result of a true inflammation; and one of the clearest thinkers of the day, Recamier,84regarded myelitic softening as a lesion peculiar to the nervous apparatus, and different from ordinary inflammation. I believe that the most profound investigators of the present day have not been able to rid themselves of a similar doubt. The discovery of Gluge's so-called inflammatory corpuscles, which was regarded as settling the question, only served to confuse the student by the confidence with which it was urged that they were infallible criteria of the inflammatory process. Under the non-committal designation of granule-cells these bodies still flourish in the annals of cerebro-spinal pathology. As we shall see, a number of products of real disease, of artifice, and of cadaverous change have passed and do pass muster under this name. The first substantial progress in our knowledge of the minute processes underlying inflammation of the spinal cord was made by Frommann and Mannkopf, but it applied altogether to the chronic inflammatory or cirrhotic affections of the cord. The difference between acute and chronic myelitis is greater than is the difference between acute and chronic inflammation in any other organ; and it must be admitted that if Recamier is to be regarded as having erred in asserting that acute myelitis is not a true inflammation, he is justified in so far as he asserted many features of the process to be altogether peculiar to the organ affected. Leyden himself attempted to throw light on the subject by provoking myelitis experimentally in dogs. He injected Fowler's solution into the spinal cords of three dogs, and in each instance produced changes which he interpreted as comparable to the myelitis of human pathology. But the inflammation thus provoked was not of the cord-substance alone; it also involved the membranes, and the inflammatory foci were in several instances purulent. Now, pus never85forms in ordinary myelitis. An abscess of the cord never occurs where a septic agency can be excluded. In six dogs whose spinal cords I wounded in the dorsal and lumbar regions by aseptic methods, and who survived from two to seven days, I never found purulent or indeed any active inflammatory process, as that term is ordinarily understood, but exactly such passive and necrotic or reactive changes as occur in the acute myelitis of human pathology.
83Klinik der Rückenmarkskrankheiten, ii. p. 115.
84Cited by Leyden.
85In the textbooks and encylopædias, without an exception, the statement that pus may be a product of myelitis is made. This is true of traumatic cases and of such depending on septic and zymotic causes alone. I am unable to find a single carefully observed case of the occurrence of pus in simple myelitis in the literature.
Owing to the advance of clinical and anatomical knowledge made within the past fifteen years many forms of spinal disease classed with the inflammations have been recognized as distinct pathological entities, no longer to be confounded with simple acute myelitis, ordinarily so called. Special forms of acute spinal paralysis, notably acute poliomyelitis anterior of children and the corresponding chronic affection among adults, have become separated in this way, and are accordingly treated of in separate parts of this volume.86
86For other and practical reasons the traumatic and compression forms of myelitis are also assigned a separate place.
Some dispute exists as to the propriety of making a distinction between acute and chronic myelitis, since an acute myelitis, if the initial attack be recovered from with life, presents a similar condition clinically as chronic myelitis; and this quiescent or slowly-progressing condition may extend over many years. The term acute with reference to inflammation of the spinal cord refers only to the active period of the disease. Just as an embolic softening of the brain is an acute affection, but may be followed by a chronic paralysis or aphasia, so the acute myelitic process may be followed by a chronic paraplegia. It is improper to call the latter a chronic myelitis. It is merely a protracted symptomatic sequel of the acute process. The latter is distinguished from chronic myelitis both clinically (by the rapidity of its onset) and anatomically (by the early dissolution of nerve-elements in the focus of disease). Limited in this sense, acute myelitis, excluding the special clinical forms already adverted to, is rather a rare disease.
MORBIDANATOMY.—The most recognizable change noted in an acute myelitic focus is one of consistency: the spinal substance is softened. In some cases the softening is so slight that the observer may doubt whether he has a pathological or cadaveric softening to deal with, the dorsal cord, which is most apt to be the site of an acute transverse myelitis, being precisely the part which is most apt to show the latter change even in fairly well-preserved bodies. In extreme cases the softening may be so intense that the cord-substance, completely fluidified, runs out of the meningeal sac, leaving the latter a collapsed membranous cylinder to mark the place where the cord once was. Where the cord-substance is sufficiently firm to permit of sections being made through it, the normal outline of the gray and white substance is found obliterated, either presenting the appearance as if the gray and white matter had been stirred up together or of a more uniform color-change. The color may be either white, reddish, yellowish, or chocolate-like. It depends upon the participation of the blood-vessels in the change. If there be much hyperæmia, there will be developed what is known as red softening; if there be much extravasation and commingling of blood with the diffluent cord-tissue, a chocolate color will mark the diseased area; and similarly one and the same focus may present different tints in different parts according to the age and intensity of the process and the more or less advanced retrogressive metamorphosis of the extravasated fluid. As already stated, the purulent form of softening or abscess does not occur in ordinary myelitis.
There is considerable variation in the extent of the affected areas of acute myelitis. In the typical and severe transverse form the whole thickness of the cord may be disorganized, and the disorganization may extend in the length of the cord, so as to involve the level of exit of from two to five pairs of nerves. In less furibund cases the area of absolute softening is confined to the gray substance and its immediate neighborhood, the submeningeal white substance being but slightly affected or escaping. Sometimes several foci of intense softening are scattered through a short length of the cord and connected by less severely involved areas of softening or œdema. Leyden distinguishes three types of distribution—the transverse, the longitudinal, and the disseminated insular or multiple form. He includes under thelongitudinal type the so-called central softening of Albert, but undoubtedly many cases of syringo-myelia have passed under this designation. The submeningeal form of softening which, with Ollivier, he states to occur in association with spinal meningitis, must be a very rare affection, as it is difficult to find a well-established case recorded. The longitudinal form shows the same predilection for the gray substance which the acute myelitic process generally does, but I have seen a finely demarcated fascicular myelitis limited to the lateral column in a paretic negro. In this case the pyramid tract and the contiguous area in front of it were so intensely softened that for a length of twelve centimeters a hollow canal ran through the cord in the place previously occupied by the diseased substance. In recent cases of myelitis the diseased area is usually found surrounded by a transition zone in which, the morbid change gradually becoming less intense, the consistency is firmer, and which merges into that of the normal cord. In cases where death occurs after a few weeks a more abrupt demarcation is usually found; this is due to the reactive changes occurring in the neighborhood. The connective tissue becomes firmer, and thus the softening centre becomes surrounded by a sclerosing capsule. Ultimately, the centre undergoes complete disintegration and absorption, and a cavity is left behind filled with a clear fluid; in short, a cyst surrounded by a firm capsule represents the residua of disease. In cases where the softening at the centre of the focus does not proceed so rapidly nor reach so high a degree as to result in liquefaction, the less vulnerable elements, the blood-vessels and supporting tissues, survive the death of the ganglionic and conducting substance; the connective elements hypertrophy, and thus a firm sclerotic patch is formed, indicating the location of the previously softened field.
It seems to be generally admitted, with Hayem, that the blood found exuded in the hemorrhagic form of myelitis does not necessarily indicate an active determination, but is rather, like some forms of so-called red softening of the brain, the result of capillary rupture or necrosis in the midst of the disintegrated tissue, now rendered incapable of supporting the vessels. The existence of a purely white form of myelitic softening shows that a textural change is the primary occurrence, and that the participation of hyperæmia or congestion is not an essential feature of myelitis. The assumption of an initial inflammatory congestion is made rather on theoretical grounds than on the basis of observation. It is simply incredible that, as Ross87claims, white softening should be a third stage, preceded by red and yellow softening as a first and a second stage! How the extravasated blood, which pathologists generally allow to leave long-lasting traces, manages to disappear, and how blood-vessels in the midst of necrotic or œdematous surroundings suddenly acquire such contractile energy as to produce a total emptying of their contents while the perishable nerve-elements remain behind, are problems which should be solved before attempting to assign to a condition which is often found to be a primary phase of myelitis the position of a late and regressive stage. Erb admits that red softening, to which he also assigns the position of a first stage, is very rarely seen, only traumatic and rapidly fatal cases of central myelitis offering opportunities of examining it. None of thevarious forms of exudation claimed to occur at this period under the names of vitreous, colloid, or hyaline deposit have been confirmed in any recently well-studied case.88The great mass of authorities, however, still agree in regarding the minute changes of the initial stage of myelitis to correspond to those of ordinary inflammation. The vessels are described as injected, the adventitial spaces as crowded with the formed elements of the blood, and the vascular walls and the neuroglia infiltrated with granule-cells and fatty granular matter. By some, inflammatory changes of the neuroglia are described, but I am unable to find a single case in which these were determined in early fatal cases. As far as our observation goes, the hypertrophy of the neuroglia is a later occurrence.
87A Treatise on Diseases of the Nervous System, 1882, vol. ii. p. 280. The author states no authority, nor does he advance his own observations in support of this statement.
88Baumgarten's case of hyaline exudation,Archiv der Heilkunde, vol. xvii. 276, was an infectious myelitis and associated with anthrax.
As to the nervous elements themselves, they are always found affected. The nerve-cells appear inflated, their processes fragile, sometimes suddenly swollen in their course, at others very thin and brittle. Multiplication of the nuclei of the large multipolar cells has been described. It must be an unusual occurrence, as it has been confirmed by but a few of the numerous observers who have examined into this question. The protoplasm of the nervous elements loses its normal striation and fine molecular granulation; it becomes either coarsely granular or hyaline. The axis-cylinders, both in their intracinereal and their intramyelinic course, show changes similar to those of the cell-processes in the gray matter. Particularly frequent are swellings in their course, the diameter of the cylinder being so much increased as to almost equal that of the myelin tube. This increase in diameter is regarded as an inflammatory swelling by some, as secondary to disturbed nutrition by others; it precedes disintegration: the substance becomes granular, fragile, and in the end dissolves. In the mean time the myelin loses its continuity, irregular segments of it fusing into round and oval masses.89
89Many of the bodies represented as granule and colloidal cells are in reality round spheres of myelin, whose resemblance to a nucleated cell is sometimes heightened by their occasional inclusion of a fragment of an axis-cylinder which has not yet lost its power of imbibing carmine and other dyes. Where softening has proceeded farthest, there the spherical and other forms of myelin are found crowding the field, and mingled with them are blood-corpuscles, fragments of blood-pigment, granular detritus, and bodies known as fatty granular cells. A number of bodies of very different origin have received this name, some of them, like the fragments of myelin alluded to, not even meriting the name of cells. Others, however, are veritable formed histological elements, either leucocytes or cellular ingredients of the neuroglia, which, having fed on the products of myelin disintegration, have become enlarged and coarsely granular. The longer the duration of the process the more numerous are these bodies, showing that they are not the coarse and essential factor of the inflammation, but an accompaniment, subserving some conservative process, inasmuch as they either remove effete material or contribute to the permanent organization of the cicatricial or atrophic tissue.
The period now reached by the morbid process may be regarded as a sort of interregnum. The necrotic tissues have not yet disappeared on the one hand, the products of inflammation have not yet organized themselves on the other. It is in this period that the ganglionic elements are described as undergoing certain changes in outline and in appearance. Above all, one change has interested observers, which, consisting in the development of what appear to be spherical vacuoles in the interior of the cell, is termed vacuolization. I can compare it to nothing so nearly as tothe appearance which is produced by the formation of gas-bubbles in a putrefying albumen or other semifluid substance.
This vacuolization of ganglion-cells is now regarded as a cadaveric change. It is not agreed, as yet, whether its occurrence in myelitis is so frequent as to suggest its ante-mortem occurrence as a veritable feature of the disease. I have been struck by this change in the neighborhood of wounds artificially produced in dogs, even in the fresh specimen. It must be remembered, however, that under these circumstances, the nutrition of the cell being destroyed and exposure to the macerating effect of the cerebro-spinal and pathologically exuded fluids occurring, a cadaveric change may take place intra vitam.
The influence of phosphorus and alkaloid as well as metallic poisons on the cord has been experimentally studied by a number of observers. Unfortunately, Popow, Tschisch, and Danillo—who described as characteristic a resulting change in the staining reaction of the cells, the development of vacuoli in them, and an atrophy of their processes—had not made a sufficient number of examinations of normal cords under like methods of preparation to recognize which of these deviations is without the physiological confines. Kreyssig90demonstrated the existence of all these conditions in the cords of perfectly healthy animals preserved in chromic acid;91and Schultze confirms him, and expresses a surprise, which must be shared by all reflecting investigators, that poisons of so widely different a character should have an identical effect on the cord-substance, as is claimed by the writers named.
90Virchow's Archiv, cii.
91He attributes the remarkable difference in staining of nerve-cells of the same ganglionic group and in the same section to the sudden transferral of the hardened specimens to strong alcohol, which seems to be the custom in some German laboratories. He claims that uniformity in staining is effected if the specimen be transferred from the chromic preparation to weak alcohol, then to stronger, and thus by gradual increase of the strength to strong spirit. Possibly, instead of approximating the real structural indications by this method, Kreyssig may obliterate them. In specimens which alcohol is not permitted to touch before staining is completed, very deeply and very lightly stained cells will be found almost side by side. The shorter the hardening process, the more perfect the staining method, the more likely are these differences to be found. It is reasonable to assume that the difference in dye-absorbing power indicates slight differences in the cell-protoplasm, marking the nutritive state of the latter and occurring within physiological limits.
If life be prolonged and the conservative processes assert themselves, the disintegrated material disappears, and as the white color of the greater area of the cord was due to the myelin, and the latter has now become destroyed within the diseased area, the latter presents a grayish color. This phase is often termed gray softening. The consistency is, however, much firmer than in the previous stage. Trabeculæ of connective tissue form, enclosing in their meshes a large number of neuroglia-nuclei and sometimes spaces filled with fluid. According as condensation and retraction or rarefication preponderate the process will terminate either in the formation of a sclerotic focus or of a cyst. Occasionally an irregular spongy tissue containing several small cysts results.
Charcot claims that a restitution of anatomical continuity, and therefore of physiological potentiality, may occur in a myelitic cicatrix. But the experiments of Kahler92and Homén93prove that when a nerve-tractis once destroyed within the spinal cord all hope of restoring that tract in structure, and thus to restore its functions, is at an end. Unlike the fibres of the peripheral nerves, those of the spinal cord and brain do not seem capable of regeneration.94If a restoration of function is to occur at all, it must occur through other channels than those destroyed—in other words, by vicarious action.
92Prager medizinische Wochenschrift, 1884, No. 31.
93Contribution expérimentale à la Pathologie et à l'Anatomie pathologique de la moelle épinière, Helsingfors, 1885, abstracted inCentralblatt für die medizinisches Wochenschriften, 1886, No. 16.
94According to the first observer, this is probably due to structural differences. The extramedullary fibres have a sheath and annular constrictions which are absent in the intramedullary.
In a large number of cases myelitis is a limited affection; that is, its ravages remain confined to the area originally involved. But occasionally the morbid process involves the next segments above or below, extending with specially great rapidity through the anterior gray horns. Exceptionally, the entire cord may thus become the site of a generalized myelitis. There is one segment of the cord which may be regarded as possessing an acquired vulnerability when a myelitic focus is in its neighborhood, and that is the lower end. It seems that while the results of a transverse myelitis in the middle dorsal cord may remain stationary for ten or more years, those of a transverse myelitis at the upper lumbar level do not; on the contrary, the entire cord below the lesion appears to be doomed to undergo the same degeneration by contiguity. This is the only occurrence which seems to deserve the name of a descending myelitis: an ascending extension is more frequently noted in other parts of the cord, but the frequency of both the so-called ascending and descending types has been unduly magnified by the inclusion of the secondary degenerations, which are constant sequelæ of all complete destructive transverse lesions of the cord, but which are rather passive phenomena, and probably influence the clinical progress of the case but little, except under such conditions as are potent in that chronic form of myelitis which underlies tabes dorsalis.
CLINICALHISTORY.—The symptoms of acute myelitis usually correspond to those of any more or less completely transverse lesion of the cord, and accordingly vary with the altitude of the upper level of the lesion. In a general way, they may be stated as consisting of—
First, paralysis of movement in the parts supplied from the nerves given off below the level of the lesion. The reason for this can be easily recognized in those cases where the pyramid tract, which conveys voluntary impulses centrifugally, is interrupted by the softening.
Second, paralysis of sensation in the parts supplied by the same nerves. This is equally explained by the pathological interruption of the centripetal impressions normally conveyed brainward.
Third, alterations in the nutrition of the parts supplied by the nerves arising in the affected level.
Fourth, abolition of those reflexes which are translated in the level of the lesion.
Speaking crudely, then, the symptoms of a transverse myelitis fall into two natural groups. The one which includes the first and second categories enumerated are symptoms due to interruption of cerebral functions; the other, which comprises the last two categories, being due to abolition or perversion of spinal functions. There is a third group comprising certain constitutional symptoms.
Aside from those variations due to the distribution, extent, and intensity of the lesion there are others which depend on the rapidity of its invasion. There are three types in this respect—the apoplectiform, the ordinary acute, and the subacute. The term apoplectiform has been used in two different senses, one being clinical, and referring to the rapidity of onset of the symptoms; the other anatomical, and referring to the nature of the lesion. It is, however, doubtful if a distinction in the latter sense is practically valuable. The presence of a blood-clot in a myelitic focus is itself secondary to the softening, and the intensity and rapidity of the process must have shown itself in the development of the latter.95The term ought, therefore, to be used in a clinical sense only.
95I am able to recall but a single case in which, even clinically speaking, a primary hemorrhage into the cord-substance was plausible. In this instance a sudden arrest of menstruation had occurred nearly simultaneously with a combined strain and exposure in a young girl.
The constitutional symptoms of acute myelitis—which, however, are often absent—are its most distinctive features in one sense. Disorders of motion and sensation and perversions of nutrition are signs common to all destructive affections of the cord, whether of a traumatic, neoplastic, or a chronic inflammatory character. But fever, headache, and delirium,96associated with gastric and visceral disturbances of acute development, are not found to be initial and intrinsic symptoms with them as with acute myelitis. In their absence the mode of onset is characteristic. A high degree of paralysis, motor or sensory, is developed with a rapidity unequalled in any chronic affection of the cord. Sometimes there is a prodromal period in which formication, numbness, and disorders of movement are observed in the same part of the body which are destined to become paralyzed at a later stage of the malady. Within a few hours, days, or at most weeks, complete paraplegia may become developed. The prodromal symptoms may include any form of disturbed sensation. Lancinating pains, tingling, a feeling of the limbs falling asleep, peculiar and indescribable sensations attending the acts of micturition and defecation or of placing the feet violently on the ground, are common. Occasionally they are found in one limb only, although motor and sensory paralysis may ultimately occupy the symmetrical member as completely as the one first involved. In some cases it has been noted that the patient is unable to lie down, or, if lying, to occupy the dorsal recumbent position. This feature has been utilized to support the theory of an initial congestion, which is supposed to be relieved or aggravated according as the cord is kept elevated or depressed.
96These symptoms are to be regarded as actual parts of the myelitic symptoms only when they accompany the prodromal or initial periods. The later complications, uræmia and septicæmia, the latter arising from pyelitis, cystitis, or decubitus, often lead to constitutional disturbance which is not due to the myelitis as such.
In most cases of transverse myelitis, when the anterior cornua are destructively involved, we possess in the electrical tests valuable and unerring means of determining the altitude and extent of the lesion. Whenever we find the atrophy of a paralyzed muscle accompanied by qualitative electrical changes in myelitis, we must conclude that the cell-group from which that muscle receives its nerve-supply is destructively involved.97These changes are particularly well demonstrable when thecervical or lumbar enlargements are affected. They are not as readily ascertainable in the case of a transverse myelitis in the upper dorsal region, on account of the situation of the muscles supplied by the upper dorsal nerves, and the consequent difficulty of application of the necessary tests.
97The proposition, originally, I believe, made by myself, that there are distinct cell-groups in the spinal cord which are constant with certain animal species, and correspond in relative development to ventral, dorsal, and appendicular muscular groups (“Architecture and Mechanism of the Brain,”Journal of Nervous and Mental Diseases, April, 1880), appears to be confirmed in a general way by the researches and cases of Edinger, Kahler-Pick, Dejerine-Major, Genzmer, Von Monakow, Sahli, Prévost-David, F. Schultze, Remak, and Parrot-Joffroy; for the knowledge of the first and last of which I am indebted to the review of the subject by Starr (“Localization of the Functions of the Spinal Cord,”American Journal of Neurology and Psychiatry, August, 1883).
The disturbance of the deep reflexes with very few exceptions affects the same peripheries as are represented in the destroyed and impaired gray nuclei. Thus, if the lower part of the lumbar enlargement be affected, the reflexes of the Achilles tendon and the gluteal muscles will disappear; if the upper lumbar enlargement, the knee-jerk disappears.98Disease of the lower part of the cervical enlargement is in like manner associated with absence of the wrist-tendon reflexes, while the disappearance of the elbow-tendon reflex suggests a higher involvement at the levels of the fifth and sixth cervical nerve-roots.
98The disappearance of the knee-jerk and similar reflexes was originally supposed to be a phenomenon exclusively pertaining to spinal disease and to a destructive lesion anywhere in the track of the centripetal and centrifugal nerves connected with that segment of the cord in which the reflex is supposed to be translated. But aside from a number of physiological observations99which prove that cerebral conditions may influence the intensity of the jerk, there are pathological ones which show that it may be permanently abolished in disease of the pons and cerebellum, and temporarily abolished or diminished immediately after capsular and ventricular hemorrhage. The associated symptoms in the former case, and the history of the onset and total hemiplegia in the latter, serve to distinguish them from destructive spinal lesions should the occasion for discriminating between them ever arise; which is not likely.
99S. Weir Mitchell and M. J. Lewis found that voluntary effort increases the jerk at first, but if continued diminishes its excursiveness (The Medical News, 1886, Feb. 13th and 20th).
In complete transverse acute myelitis of the cervical region high fever is a constant symptom. In unilateral myelitis of this region flushing of the face and unilateral sweating are produced, together with iridoplegia, sometimes preceded by dilatation, owing to initial irritation and succeeding paralysis of the sympathetic branches originating at this level of the cord.
Just as the disturbed reflexes and the belt sensations enable us to distinguish at what levels of the cord the myelitis is situated, so the distribution of the motor and sensory paralysis affords corroborative evidence of such location and additional proof of its extent and intensity.
Transverse myelitis at and above the level of origin of the phrenic nerve is almost immediately fatal, through its interference with the innervations required in respiration. In the upper part of the cervical enlargement it produces complete paraplegia of motion and sensation in the trunk and all four extremities. In the lowest part of the cervical enlargement it produces paralysis of the same parts, but the serratus magnus and scapular muscles escape. The nuclei of origin of the muscles moving the upper extremity are situated so that those which are farthest removed from the axis of the body when the arms are extended are situated lowest in the cord. The sensory paralysis is distributed in harmony with the motor paralysis; that is, when there is paralysis of motion in the handand forearm the anæsthesia or subjective numbness is also in the hand and forearm. The same correspondence is not found in affections of the lumbar enlargement, for anæsthesia of the gluteal region accompanies paralysis of the crural muscles when the lesion is low down at the level of the lower lumbar and upper sacral nerves. The distribution of the anæsthesia, in other words, is not by segments of the limb, but by surfaces. The gluteal, posterior femoral, gastrocnemial, and outer pedal surfaces are affected together with the muscles moving the foot, while the thigh and inner side of the leg and foot become anæsthetic, with lesion of the upper part of the lumbar enlargement accompanying paralysis of the quadriceps and deep muscles. It is not difficult to understand this discrepancy when we bear in mind the different plan of distribution followed by the brachial plexus as compared with the lumbar and sacral plexuses. It is not, in my experience, found that the anæsthesia affects that surface which covers the part moved by the paralyzed muscle; which is characteristic of associated paralysis and anæsthesia from cortical disease.
One of the most dreaded occurrences in acute myelitis is the malignant bed-sore. The ordinary decubitus which results from the protracted sojourn of the patient in bed, coupled with the prominence of his trochanters and sacrum resulting from general or atrophic emaciation, is also common, but is comparatively benign and easy to prevent or to manage when established. The malignant bed-sore, on the other hand, is a spontaneous occurrence, due to the same obscure but undeniable trophic influences exerted for good by the normal and for evil by the diseased nerve-centres, which play so large a part in the symptomatology of tabes dorsalis. It cannot be avoided; it is not due to pressure alone, or, as some have claimed, to the macerating influence of the dribbling and decomposing urine. The development of this lesion is exceedingly rapid, and it may be regarded as a sort of local gangrene. The skin shows a livid color; vesicles appear, then burst; the part becomes denuded; and within a few days a deep ulcer with a dark border and base appears, discharging a sanious fluid. The subsequent history is that of a rapid extension and destruction of the neighboring tissues, even down to the bone, and if situated over the sacrum opening into the spinal canal through the necrotic arches of the sacral vertebra, thus leading either to general septicæmia or to putrid infection of the spinal meningeal sac. Occasionally, gangrenous spots coexist on other parts of the body, notably the lower extremities, where neither pressure nor maceration can be accused of playing a part, proving that the process is primarily due to the spinal affection.
Acute central myelitis, as described by Dujardin-Beaumetz, Hayem, Hallopeau, and Erb, usually runs its course very rapidly. Indeed, all of these observers speak of it as the most violent and quickly fatal variety of spinal inflammation. I have, however, seen one case with T. A. McBride at the Presbyterian Hospital in which all the characteristic symptoms of acute central myelitis were markedly developed and present in their characteristic groupings, and yet the patient had been suffering from progressing symptoms of myelitis for one year and a half before that time.100Usually, complete anæsthesia and paralysis of the lower half of the body occur in this form. But the most characteristic feature is a rapidly progressive atrophy not only of the paralyzed muscles, but also of some which are still partially under the dominion of the will. With this there is extreme vesical and rectal trouble, the sphincters being paralyzed. As a rule, the deep and superficial reflexes are destroyed—they are always diminished—and trophic disturbances of a malignant type, such as acute decubitus, joint-changes, and œdema, are common. The paraplegia is characterized by the flaccid condition of the limbs; the contractures and spastic symptoms found with other forms of myelitis are entirely absent, and qualitative electrical changes, beginning with disappearance of farado-muscular contractility, are found in the atrophying muscles. There are marked constitutional symptoms with this form; the tendency to an ascent of the process and successive involvement of one segment after another of the gray matter is great, and a fatal issue, as far as known, is inevitable.
100At the time the patient had undergone such a profound change in appearance that I failed to remember him, and it was only by accident I learned that I had seen him in private consultation with his family attendent, F. A. McGuire, a year previous. On the latter occasion I had made the diagnosis of subacute myelitis chiefly limited to the posterior columns; there were ataxia, both static and locomotor, slight incontinence, belt sensation, and ocular symptoms, with abolition of the deep reflexes in the lower limbs.
DIAGNOSIS.—The principles governing the determination of the affected region of the cord in acute myelitis are exactly the same as those detailed in the later sections on Chronic Myelitis or Sclerosis, the acuteness of the onset, and the relapses which sometimes occur, and the predominance of irritative spasms—which, however, is an inconstant criterion—serving to distinguish between the acute and chronic form of spinal inflammation. In the present state of our knowledge it is impossible to always differentiate between acute central myelitis and syringo-myelus—a condition in which the formation of a periendymal neoplasm, and its subsequent breaking down in the axis of the cord, lead to the formation of a tubular cavity.101The neoplasm in this instance is classified among the gliomatous new formations. The symptoms depend, exactly as do those of myelitis, on the distribution of the destructive lesion. In some cases the posterior cornua and columns are chiefly involved, and extreme anæsthesia is found; in others the anterior columns are affected, and the symptoms of a poliomyelitis or an imperfect transverse myelitis may be imitated.102
101This cavity, unlike that of hydro-myelus, is not a dilatation of the central canal, but, lying to one side of it, is excavated in the cord-substance.
102Repeated fractures have been noted in cases marked by profound analgesia. It is believed that they are not always due to trophic changes, but may be the result of muscular action, exaggerated on account of the patient's inability to gauge his efforts. Still, in the majority of cases the presence of positive trophic disturbances of the skin seems to indicate the probability of some textural change facilitating the fracture.
As a rule, the sensory disturbance in syringo-myelus is out of proportion to the muscular atrophy developed; that is, it involves a far more extensive province. It is usually of a peculiar character: some forms of sensation are involved but slightly, or even escape, and others may be nearly destroyed. Commonly, it is the pain and temperature-sense which suffer most, while the cutaneous space and pressure, as well as the muscular sense, are not materially disturbed. These peculiarities are not commonly found in cases of myelitis, and when present, and particularly when the paralytic or sensory affections involve all four extremitiesalike, they suggest the existence of syringo-myelus. As yet we are unable to make more than a probable diagnosis between the two diseases.
DURATION ANDPROGNOSIS.—The duration of the disease varies. Cases of the apoplectiform variety are mentioned, in which the process reached its height in a few minutes, or where the patient, having retired in good health the night before, awoke finding himself paralyzed in the lower half of his body. Death may terminate such a case in a few days or weeks. In another class of cases, complicated by serious involvement of the bladder, the fatal termination is often precipitated by putrid cystitis, pyelitis, or uræmic poisoning, and even in cases which have passed the dangers of the early period in safety these ominous complications may develop with the usual result many years after the beginning of the illness. In a number of cases the first period, that in which the morbid process becomes developed, is followed by one of comparative quiescence, in which the paralyses of sensation and motion then established remain stationary for months and years. A number of authors, Erb, Leyden, Strümpell, and Ross, speak of such a case as one in which chronic myelitis has followed an acute myelitis. It seems improper to use the terms acute or chronic in this way. As it is generally understood that the term acute applies to myelitis in which disintegration of the nerve-elements predominates over interstitial proliferation, and in which the secondary sclerosis is rather like the cicatrix of an acute inflammation and necrosis, it should not be confounded at any period, no matter how similar the clinical signs may be, with a process which is essentially an interstitial one from the start. If chronic amaurosis results from an acute glaucoma, we do not change the latter designation to chronic glaucoma.
In cases where the symptoms at the acme indicate rather an involvement of the peripheral than the central paths of the cord, and in which an incomplete motor and sensory paralysis develops, the patients often regain a considerable amount of motor power and sensation, so that they may reach a good age, suffering at most from a paresis of some one muscle or muscular group, occasional bladder trouble, and pains. It has been laid down as a rule that where paraplegia and other signs remain stationary for years, there is no hope of even partial recovery. The following remarkable and well-attested case proves that this rule is not without exceptions:
Isidor K——, æt. forty-four years, worker in tobacco. After over-exertion in the fall of the year 1879 he had numbness, tingling, dorsal pain, and paresis rapidly developed, which induced him to consult the physicians at the clinic of the University of the City of New York. After some slight improvement a relapse occurred, and several others followed, usually provoked by over-exertion, till he became completely paraplegic. He was, according to his account, several times exhibited to a medical class by William A. Hammond, and remembers that this authority spoke of a possible ascent of the affection and ensuing involvement of the arms. His bladder was at no time seriously disturbed. For four years and three months he was totally paraplegic; his lower extremities were without life; and for the greater part of the time he could not move his toes. The limbs were cold and pale, but underwent little atrophy. The only exercise obtained during this time was in a roller carriage. His sexual power was abolished throughout the wholefour years and over. Nothing can be learned as to his reflexes in this period.103The paralysis of sensation was as complete as that of motion, and the lower limbs never perspired. The arms remained free. There was a dorsal belt sensation.
103Hammond has no notes of the case, having discontinued the clinic, and Ludwig Weiss, the physician in charge, saw him only occasionally in behalf of a benefit society.
On July 23, 1884, shortly before mid-day, while lying on the bed, in which he had lain a helpless cripple for over four years, except when lifted into the roller carriage, he felt a sudden rush of warmth. Surprised at this first sensation he had felt for years in limbs which had been quasi-foreign appendages, he raised up the bed-clothes and saw that they changed color. There was some tingling for about three minutes, and a perspiration broke out in the affected members. With this he found he could move his feet: half alarmed, half exulting, he sent for his physician, L. Weiss, who found that the patient could stand and walk with considerable freedom. I was then consulted, and found the patient presenting a picture of incomplete transverse myelitis. He could walk, turn about, stand with closed eyes with slight swaying, and his knee-phenomenon was of short excursiveness, but exceedingly spasmodic, and this symmetrically so. He was carefully watched, and against the advice of his physician engaged in peddling cigars, and subsequently took a position as attendant at the pauper asylum on Ward's Island. Here he was on his feet fully twelve hours a day, and his motion, which had continued improving until it was to all practical intents and purposes normal, aside from a slight stiffness, again became impaired, and a joint trouble in the metacarpo-phalangeal articulation of the right little toe, which had troubled him a week after his partial recovery, recurred.104On January 15th of the present year I again examined him. His knee-phenomenon was greatly exaggerated, cutaneous sensations scarcely impaired, gait paraparetic, but he could walk great distances, and claimed to suffer less from the exertion than from the tenderness accompanying the joint trouble referred to. There had, therefore, occurred, without any assignable cause—for the patient was not under treatment for a year or more before the event—an almost instantaneous restoration of sensation, locomotion, and sexual power; all of which faculties, notwithstanding the infraction of every medical direction given, remained established for two years, with prospects of so continuing a longer period.
104This was a trophic joint trouble.
TREATMENT.—Most of the therapeutic propositions relating to the treatment of the acute myelitic process are based on the theory that it is of a congestive character or associated with congestion. Accordingly, the internal administration of such drugs as ergotin, which diminish the calibre of the blood-vessels, and local measures, such as depletion, wet cupping, and counter-irritation, intended to act in the same way by derivation, are unanimously recommended by authorities. The suggestion of Hammond, that the patient occupy a ventral or lateral, and not the dorsal, position, is based on, and entirely consistent with, this same view. It is difficult to say what effect is attributable to these measures. Remarkable spontaneous changes—retrogressions as well as advances of the morbid process—occur equally under expectant as under active treatment. I have never seen any improvement in the active phase of simple myelitis whichI felt confident I could attribute to any special remedy employed with a view of acting directly on the morbid process. Indeed, improvement has been claimed by Jewell as a result of the use of strychnia—a drug which under the very dogmas governing the orthodox treatment of the disease might be expected to do positive damage.105
105Jewell gives very large doses of this alkaloid. L. C. Gray, in a discussion held before the American Neurological Association, cited numerous observations directly conflicting with those of Jewell. I cannot, in view of a recent observation in a typical case of acute anterior poliomyelitis, in which by accident the toxic effects of strychnia were obtained, consider this dispute as at all settled. In direct connection with the toxic symptoms the abolished patellar jerk returned in an exaggerated form; motion also returned, and rapid improvement ensued.
In relapses of acute myelitis which had been brought on by chilling of the feet I have obtained good results by derivation to the lower extremities, and on many grounds think that the morbid process in the cord, if it can be affected at all, can be affected by treating the periphery where the symptoms are noted more readily than by applying the cautery or bleeding over the proven site of the disease. Exposure of the dorsal region to cold has not yet been noted as a cause of acute myelitis, whereas such exposure of the lower extremities is a frequent one. This seems to show that the spinal cord is more vulnerable to influences affecting its nervous distribution than to those which are topographically nearer. If this is true as regards morbid influences, it may be urged that it is plausible as regards remedial influences if these are to drive out the disease tendency by the same door it entered.
Rest is imperative during the active progress of the disease. It may be stated as a canon that the earlier the patient takes to his bed, and the more thoroughly he obeys the injunction to attempt no motion of the affected members, the better, cæteris paribus, will the result obtained be. Countless cases are on record where a relapse was directly traceable to a walk undertaken prematurely or carried farther than was wise. As convalescence or partial restitution advances, gradually increasing exercise is to be attempted, not waiting for the danger-signal of a tired feeling to discontinue it; for that feeling, developed, means positive harm already done. It is therefore necessary to allow the returning function to be utilized only within small limits at first, and extending them slowly.
In all cases of severe myelitis where the formation of bed-sores is to be apprehended the water-bed should be employed. Owing to the low temperature which the rubber sac constituting it has, it is necessary to cover it with some well-warmed and non-conducting material and to have the room well warmed. If bed-sores are already formed, they are to be treated according to ordinary surgical principles. Antiseptic means should be in the foreground in the case of the malignant bed-sore. It is to be remembered that the latter is a gangrenous process, and, in so far as the formation of a line of demarcation between the necrotic and the conserved tissue is concerned, the ordinary expectant rules of surgery govern the case: the water-bath appears to yield the best results. Ordinary bed-sores yield readily to mechanical protection and stimulating ointments or the balsam of Peru. Iodoform is recommended, but it produces granulations of an indolent character as compared with those obtained through the use of resinous ointments.
The warm bath is probably the most useful measure in acute myelitis.In cases due to exposure I do not believe it can be applied too soon. Its temperature should, in the beginning at least, not be higher than about 88° F., and the duration about seven minutes. The continued administration will depend on the immediate effect on the patient, and the sittings can be ultimately prolonged to half an hour or even longer. It should be administered once daily, and, when the patient is not disturbed by the manipulation connected with its use, even oftener. Cold baths are recommended by the Germans, but it seems rather in the passive period of the disease than during its active phase.
The management of the bladder trouble is one of the most critical points in the treatment of most cases. The results of retention of urine are more frequently the cause of a fatal issue than any other single complication. Where there is complete retention continuous catheterization is to be employed, as recommended by Strümpell.106In other cases the bladder should be emptied thrice in the twenty-four hours. The catheter is to be thoroughly disinfected, and if the slightest sign of cystitis is noted the bladder should be washed out with astringent and disinfectant solutions. The continuous irrigation with a solution of corrosive sublimate, 1:2000, appears to give the best results.
106A. Nelaton's catheter is introduced into the bladder, and kept in place by strips of adhesive plaster fixed to the inner aspect of the thighs. A perforated condom fixed to the catheter, and then fastened to the inguinal region, is in my opinion a better measure, especially in patients who have some motor power left. The catheter is connected with a rubber tube, which should run on a decline in order to effect complete drainage.