AUTOPSIES OF RELATIVELY RECENT CASES.—In cases relatively recent all macroscopic changes in the cord may be entirely wanting. There may be some degree of asymmetry in the surface of section, patches of white coloration in the anterior gray substance, or of gray or yellow color in the white columns; the anterior roots may be congested or even already atrophied.⁹⁴ On the other hand, there have several times been found foci of visible red softening, much more frequently at a point corresponding to the origin of the paralyzed nerves, but not absolutely confined to them, and sometimes existing at points where they have given rise to no symptoms whatever.⁹⁵

⁹⁴ Roger's first case, No. 28 of Table V.

⁹⁵ Case 1st of Roger, Tab. V.

Microscopic Lesions.—In striking contrast with this paucity of macroscopic lesions are the interesting structural changes revealed under the microscope. These lesions are usually comprised within circumscribed foci whose size may vary from a long diameter of 2 mm.⁹⁶ to one of from 10 to 30 mm.⁹⁷ Sometimes bilateral foci are found with monoplegic paralysis; thus one side or the other preponderates in the morbid process.

⁹⁶ Case Roth, Tab. V.

⁹⁷ Case Schulze, Tab. V.

In recent cases (Damaschino's, at twenty-six days; Roger's, at two months; Turner's, at six weeks) patches of red softening existed at the portions of the cord containing the nuclei of origin of the paralyzed nerves. In Turner's case the focus contained hemorrhagic extravasation, and the traces of this were clearly perceptible in Roger's first case. The blood-vessels are dilated; their lymphatic sheaths infiltrated with leucocytes and with granular corpuscles; their walls are thickened, pigmented, or fatty.

Leucocytes are often disseminated through the diseased area, and in one case (Demme) were accumulated into a focus of pus. Besides the leucocytes, the foci are often infiltrated with large round granular cells that seem to be transformed neuroglia-cells (Leyden). In one case neuroglia nuclei were accumulated in a ring around the focus, seeming to indicate the beginning of encapsulation.

The most striking lesion, however, and the one which is common to the most recent as well as to old cases, is the deformation, atrophy, and final disappearance of the large ganglionic cells of the anterior cornua. The first change consists in granular pigmentation;⁹⁸ then the prolongations disappear, leaving the body of the cell shrunken and deformed; at last the whole cell disappears. Sometimes all the cells of an anterior horn have disappeared throughout the entire depth of the focus; quite as often, in certain sections at least, the atrophy is limited to certain groups, as the external,⁹⁹ or the external in one focus, the antero-lateral in another, situated on the opposite side of the cord.¹⁰⁰

⁹⁸ Case of Echeverria, Tab. V.

⁹⁹ Case by Schultze (this is a case of ancient lesion), Tab. V. (Virch. Arch., Bd. lviii.).

¹⁰⁰ Case by Taylor, Tab. IV. (Path. Trans., London, 1879.)

In a case rendered celebrated by Charcot it is stated that in many sections of the cord atrophy of ganglionic cells constituted the unique alteration, the tissue immediately surrounding the place whence they had disappeared being perfectly healthy. It is on this appearance that has been built up the theory of a primary idiopathic atrophy of the ganglionic cells as the characteristic lesion of infantile paralysis. But in other portions of the same cord Charcot himself describes destruction of the gray reticulum imbedding the cells; and this destruction is insisted upon in many other observations. In other words, there is a general disintegration of the gray nervous tissue of the anterior cornua which contain the focal lesion. The normal tissue is then replaced by a reticulum of conjunctive fibres, more or less dense according to the age of the case.

These focal lesions of the cord explain admirably, as will be seen, the permanent symptoms of the disease. But of great importance for understanding its initial period is the fact that structural changes—similar to, but less severe than, those just described—have beer found diffused throughout the cord. In several cases hyperæmia, partial atrophy of ganglionic cells and nerve-fibres, infiltration with exudation corpuscles, in the anterior cornua and even central gray canal from the lumbar to the cervical region.¹⁰¹ In Damaschino's case, besides the focal lesions which corresponded to the paralyses of the right arm and left leg, were others corresponding to the left arm and right leg where no paralysis existed.

¹⁰¹ See cases by Leyden, Roth, Schultze, Clarke, Damaschino.

This case (1883) is also interesting in bringing out another lesion not usually noticed. This is the breaking up into balls of the myeline in the medullated tubes, both of the anterior intraspinal nerve-roots and of such fibres as traversed the anterior nerves. In balsam preparations these myeline drops are dissolved; but in osmic acid and glycerin preparations they appear as black balls all over the field. The lesion is identical with that already described by Dejerine (1875) in both nerves, roots, and white columns. The columns of Clarke have always been found intact.

In the recent cases no lesions of the white columns have been observed—a fact upon which reposes the doctrine that such lesions, when existing, are secondary to those of the cornua.

SECOND GROUP OF CASES.—The next group of cases contains 16, where the autopsy was made more than two years after the début of the paralysis.

The date of these lesions varies from seven to seventy-six years. In two or three cases, where the autopsy was made on very old people, the early history of the disease was unknown, but the probable date of the paralysis was calculated.

In this group of cases patches of atrophy, semi-transparent and grayish in color, focal or diffused, are clearly perceptible to the naked eye. As a rule, the atrophy is unilateral, and sensibly affects the entire half of the cord. In some cases of paraplegia, however, there is a bilateral, symmetrical shrinkage of the entire lumbar cord, which has been reduced to the size of a quill.

The atrophy involves, first and most markedly, one or both anterior cornua; second, the anterior nerve-roots arising from them; third, the antero-lateral columns.

In both the latter localities the microscope will often find individual nerve-tubes wasted and deprived of their myeline. The atrophied patches are generally sclerosed as the seat of a proliferated neuroglia, coloring deeply with carmine. In Laborde's cases, published at the very beginning of what may be called the anatomical period, the atrophy and sclerosis were said to be limited to the antero-lateral columns and the nerve-roots, while the cornua remained intact. In all more recent observations, however, the lesion of the white columns and roots has been found strictly proportioned to that of the gray horns. The sclerosis extended into the latter, constituted by a reticulum of connective-tissue fibres, sometimes fine, sometimes so matted together as to form a dense felt-like substance, sometimes offering the ordinary aspect of sclerosis.

Amyloid corpuscles have been found infiltrated in great numbers through both the gray and white substance in these old cases (case by Cornil),¹⁰² seeming to replace the infiltration with exudation corpuscles observed in the more recent ones.¹⁰³ When the lesion is distinctly circumscribed the focus is often surrounded by a zone of embryonic cells, seeming to indicate a reactive proliferation on the periphery.¹⁰⁴

¹⁰² Loc. cit., Soc. Biol.,1863.

¹⁰³ Seguin (loc. cit.) observes that the opinion is gaining ground which ascribes these to a transformation of the neuroglia corpuscles.

¹⁰⁴ Case by Schultze, loc. cit.

As in the relatively fresh cases, the circumstance which has attracted the most attention is the atrophy of the ganglionic cells from the sclerosed patches of the anterior cornua. The completeness with which these have disappeared in any focus seems to be proportioned to the completeness of the paralysis in the corresponding limb. Partial atrophy or disappearance of spinal groups of cells from the cornua may sometimes be correlated with paralysis of special muscles.¹⁰⁵

¹⁰⁵ Thus in Schultze's case, already quoted, the external group of cells had disappeared from the focus in one gray horn, and the extensors of the foot were alone paralyzed. This seems to confirm the opinion advanced by Spitzka, that this external group of motor-cells corresponds to the extensor, the internal groups to the flexor muscles.

Study of the pathology of infantile paralysis is not completed when the above series of spinal lesions has been enumerated. Most various interpretations have been made of these lesions as they have been successively discovered. Thus, after the theory of congestion came the theory of primary sclerosis, built upon Laborde's two autopsies;¹⁰⁶ then the theory of primary atrophy of ganglionic cells;¹⁰⁷ then the theory of myelitis;¹⁰⁸ finally, a theory of complex and variable lesion.¹⁰⁹

¹⁰⁶ Laborde, loc. cit.; Cornil, loc. cit.

¹⁰⁷ Charcot, Leçons sur les Maladies du Syst. nerveux; Prévost, Soc. Biol., 1864; Joffroy, Arch. de Physiol., 1870; Petitfils, “De l'Atrophie aigue des Cellules matrices,” Thèse de Paris, 1873.

¹⁰⁸ Schultze, Virch. Arch., Bd. lxviii.; Roth, Ibid., Bd. lviii.; Henoch, loc. cit., p. 208; Ross, loc. cit., p. 125; Seguin, loc. cit., 1877; Erb, Ziemssen's Handbuch; Seeligmüller, Gerhardt's Handbuch; Roger and Damaschino, Gaz. méd., 1871; Turner, Path. Trans. Lond., 1879; Hammond, loc. cit.

¹⁰⁹ Leyden, Archiv für Psych., Bd. vi., 1876.

It was Prévost who first ascribed a predominant importance to the atrophy of the ganglionic cells of the anterior cornua; but it was in the hands of Vulpian, Joffroy, and more especially Charcot and his pupils, that the theory was fully developed. Infantile paralysis was ranked in a newly-formed group of diseases, all characterized by atrophy of these same cells, and differing from each other principally in the acuteness of the process and in its complications.¹¹⁰ Seguin, in his original lecture in 1874, supported the same views, but in 1877 fully adopted that of myelitis. The objections to this theory are: 1st, that by it two diseases so different in their course, localization, electrical reactions, and form of paralysis as atrophic paralysis and progressive muscular atrophy are essentially identified on account of the identity of one lesion, the atrophy of the anterior ganglionic cells;¹¹¹ 2d, the presence of other lesions or of traces of them peremptorily proves the pre-existence of a complex morbid process which involves the ganglionic cells, but is neither limited to them, nor, necessarily, originates in them.

¹¹⁰ Thus, acute anterior poliomyelitis, subacute anterior poliomyelitis, progressive muscular atrophy, amyotrophic lateral sclerosis, bulbar paralysis.

¹¹¹ When this objection is accepted, Barlow's remark falls to the ground, that “the similarity of lesion found in two such different diseases as infantile paralysis and progressive muscular atrophy proves the failure of anatomical characters, taken alone, to serve as a basis of nosology” (Brain, April, 1879, p. 74).

This inference was drawn by Roger from the hemorrhagic softening, dilatation, and degeneration of blood-vessels, infiltrations with exudation-corpuscles, and hyperplasia of conjunctive nuclei present in his case. Similarily, Schultze, in a case examined nineteen years after the occurrence of the paralysis, found traces of an extensive myelitis in the diffusion of the lesions,¹¹² in the exquisite cellular infiltration, the proliferation of the neuroglia, and the atrophy of axis-cylinders of nerve-fibres together with the cells; and inferred an anterior myelitis, diffused in the long axis of the cord, but limited to the antero-posterior region. Schultze defines Charcot's theory to be an hypothesis of such an acute atrophy of ganglionic cells as leads to a rapid melting down of these bodies, whereby reactionary inflammation is excited in the surrounding tissue. This implies that the dying cells are able to act like a virulent substance on the imbedding tissue, and of this, declares Schultze, “Charcot has offered no proof.”¹¹³

¹¹² In this case of paraplegia without lesion of the upper extremity, to which we have several times alluded, there was bilateral atrophy of the lumbar cord, atrophy of the right anterior nerve in the dorsal and lower cervical region, also in the cervical enlargement.

¹¹³ It might be said that the fall of the fever as soon as the paralysis is declared and the motor cells presumably melted down should contradict the idea that their dying substance acts as an irritant upon surrounding tissues.

A third objection has been brought forward by Leyden, and is really an enlargement on the second. It is, that various lesions or morbid processes may underlie the same clinical history. In four autopsies of cases presenting all the clinical history of acute anterior poliomyelitis this author has found three different lesions. In one an extensive lepto-meningitis, together with irregular focal sclerosis of the white columns, evidently depended upon the latter, and in turn caused sclerosis of the anterior cornua with consequent destruction of their cells.¹¹⁴ In two other cases an anterior poliomyelitis was accompanied by diffused lesions of the central canal. Finally, in a fourth case the lesions were limited to the anterior cornua, as is most usual.

¹¹⁴ This case of Leyden's throws light on the two autopsies by Laborde with sclerosis of the white columns and intact cornua. It seems probable that a process originating in the cornua had then been arrested or had receded, while continuing its evolution in the white columns.

The theory of acute atrophy of ganglionic cells is not sensibly different from that of a parenchymatous myelitis.¹¹⁵ But all the objections which can be urged against the former theory apply to the latter also, with the exception that the hypothesis of inflammation suggests a cause for the otherwise inexplicable atrophy. Observation of the pathological appearances alone could not decide whether the irritation started in the parenchymatous or interstitial tissues. Reference to the etiology of the disease shows that of the two most frequent apparent causes, blood-poisoning and traumatisms, the first would indicate that the inflammation started in the connective tissue supporting the blood-vessels; the second suggests that the irritation began in the spinal elements constituting the origin of the nerves.

¹¹⁵ Hammond assumes such a form of myelitis in his classification of inflammations limited to the anterior part of the gray matter of the spinal cord:

1. Inflammation of motor and trophic nerve-cells: (a) Infantile spinal paralysis; (b) Spinal paralysis of adults; (c) Pseudo-hypertrophic spinal paralysis.

2. Inflammation of motor cells: (a) Glosso-labia-laryngeal paralysis.

3. Inflammation of trophic cells: (a) Progressive muscular atrophy; (b) Progressive facial atrophy (Dis. Nerv. Syst., 6th ed., p. 464).

We think this classification open to several fundamental criticisms.

Whatever be the starting-point, however, it is very evident that the morbid process soon involves all the tissues contained in the gray matter of the anterior horns, and constitutes, therefore, a real anterior poliomyelitis.

A question of much interest is the relation to this of the lesions of the anterior roots and of the white columns. Is the atrophy of nerve-tubes a passive consequence of their separation from the ganglionic cells, the sclerosis a secondary consequence of this? or is the sclerosis the cause of the atrophy, itself the result of an irritation propagated downward from the myelitic focus, according to the usual law for secondary degenerations in motor tracts? or, finally, is it a residuum of a leucomyelitis (or of the white substance), complicating by simple extension the inflammation of the gray substance?

Review of the autopsies recorded would indicate that the lesions in question are brought about sometimes in one, sometimes in another, of these ways—sometimes even, as in Leyden's case, by extension from a meningitis. That sclerosis of the white columns is most frequently a secondary degeneration is indicated by the frequency with which it appears below the lesion of the cornua, by the rarity with which it is found above, and also by the general proportion between its intensity and that of the disease of the gray matter.

We have devoted so much space to consideration of spinal-cord lesions, because they are by far the most constant and the most important; after these rank the structural alterations of the muscles, which received for a while such a preponderance of attention.

Hammond has studied the progress of these changes on the living subject by fragments of fibre successively removed with Duchenne's harpoon. In an incipient stage of degeneration the fibrillæ are found to be irregular and torn,¹¹⁶ the transverse striæ dim; oil-globules are seen arranged according to the long axis of the fibre. In a more advanced stage the transverse striæ nearly disappear, the oil-globules are in large numbers, and fat-corpuscles are also abundant. Finally, the whole specimen is seen as a mass of air-globules. Six weeks later, however, these had in turn disappeared, and there remained a mass of connective tissue.

¹¹⁶ Though, from the method of removal, this appearance cannot be considered as certainly pathological.

This series of changes, however, does not always take place, as Hammond himself recognizes. Laborde¹¹⁷ first described a granular form of muscle atrophy, where the muscular substance gradually wastes away without ever becoming fatty, and leaving a transparent and hyaline sheath. The two forms of fatty and of simple atrophy can be distinguished by the naked eye. In the latter the muscle begins by being thinner or lighter and softer than usual, ultimately turning light brown. The fatty muscle becomes a homogeneous yellowish-white, diversified by occasional remnants of reddish fibres.

¹¹⁷ Loc. cit., p. 131.

Proliferation of the interstitial connective tissue may be combined with either simple or fatty atrophy. A combination of abundant sclerosis and abundant fatty infiltration may lead to a pseudo-hypertrophy of the muscles.

“There cannot be the slightest doubt,” observes Erb, “that the lesions described constitute a degenerative atrophy similar to what may be caused by section or sense traumatism of a peripheric nerve.”

The peripheric nerves have been much less thoroughly studied than the spinal cord. Leyden first directed special attention to the nerves. He found the sciatic altered in two cases,¹¹⁸ in the first by an interstitial neuritis; in the second by partial atrophy. In 1880 the same writer, in an extensive article on poliomyelitis and neuritis,¹¹⁹ greatly extends his views as earlier expressed. Not only does he claim the coexistence of neuritis with spinal-cord disease in atrophic paralysis, but thinks that many cases of this, and also of other forms of paralysis, “lately supposed to originate in the spinal cord, may really begin in any part of the motor apparatus,” thence sometimes generalize throughout the whole apparatus, sometimes remain limited to the original portion affected. Thus, progressive muscular atrophy may sometimes begin in the nerves, sometimes in the muscles, and sometimes in the ganglionic cells of the cord; and this variety of origin explains the discrepancies of opinion which have been held upon the nature of this disease. Similarly, all forms of acute or chronic atrophic paralysis in either children or adults may begin in either the nerves or cord, thence become generalized to both, or remain limited to one part of the spinal motor system. Cases of atrophic paralysis which recover are probably not cases of poliomyelitis at all, but of multiple neuritis, rheumatic, traumatic, or infectious in nature. The regeneration of peripheric nerves is a well-demonstrated possibility, but not that of the cells of the cord. Lead-paralysis is usually confined to the nerves, but sometimes extends to the cord. In diphtheritic paralysis Buhl has found injection, thickening, and granular infiltration of nerves at the union of their anterior and posterior roots;¹²⁰ and as long ago as 1876, Dejerine, in a case of atrophic paralysis in a syphilitic woman, found varicose swelling of the medullary sheath in the nerves of the paralyzed lower extremities, together with heaping up of the myeline into large drops, colored black in glycerin and osmic-acid preparations. Coincidently, in the cord, at the origin of the same nerves, the number of motor-cells was diminished, and of those that remained the prolongations, and even the body, of the cell were atrophied.¹²¹

¹¹⁸ Cases 34 and 35 of Table V., quoted from Arch. de Psychiatrie, Bd. vi., 1876.

¹¹⁹ Zeitschrift für Klin. Med., 1880.

¹²⁰ Zeitschrift für Biol., 1867.

¹²¹ Arch. de Phys., 1876.

These views of Leyden's are extremely interesting, and should stimulate future research into the condition of nerves in all cases of atrophic paralysis. It is quite incorrect to say, as Archambault and Damaschino have recently done,¹²² that Leyden denies the existence of anterior poliomyelitis in such cases, especially in such as prove permanent. He only insists on the frequent coincidence of neuritis, on a varying point of departure for the morbid process, and on the probability that in cases of recovery this process has always remained peripheric.

¹²² Le Union méd., 1883, 7, 35, case quoted in Table V. It is much to be regretted that Damaschino, who strongly controverts Leyden's views, did not examine the nerves in his own most interesting case.

The strongest objection to Leyden's theory is the absence in most recorded cases, either infantile or adult, of the usual signs of nerve inflammation, local pain, or tenderness. Autopsies of old cases are not able to differentiate an inflammation from an atrophic process in the nerves, followed by a secondary thickening of the endoneurium. This thickening was found in three cases examined by Edmonds in 1882, whose subjects had suffered from infantile paralysis in early life, and had had the paralyzed limb amputated at the age of fifteen or sixteen. Transverse sections were made from the internal popliteal nerves. The specimens showed some healthy nerve-fibres, presumed to be sensory; others much smaller, with the axis-cylinders wasted or degenerated; while strands of connective tissue traversed the nerve-bundles, resulting from hypertrophy of the endoneurium. The vessels showed inflammation of their coats, with proliferation of the endothelium.¹²³

¹²³ Trans. Path. Soc. London, 1883.

The brain is usually normal, unless indeed the paralysis has affected children previously rendered idiotic by congenital atrophia cerebri. Sandie, however, examined one brain with an interesting positive result.¹²⁴ The brain was taken from a boy of fifteen paralyzed since the age of three in almost all his muscles, with even paresis of the muscles of the trunk and neck. The paralysis was more marked upon the right than on the left side. At the autopsy, in addition to atrophy of the muscles and of the motor nerves, with exquisite atrophy of the anterior columns and anterior cornua, was found a decided atrophy of the left central convolution, and, less marked, of the paracentral lobule. This was shown by comparative measurements with the opposite side of the same brain, and also with the corresponding convolution and lobule in two other brains. The child's intelligence had not been affected.

¹²⁴ Centralblatt f. d. Med. Wissensch., No. 15, 1875.

The arrest of development of the bones has been already mentioned, as well as that of their epiphyses and apophyses. The compact osseous tissue is atrophied: the medullary, on the contrary, abundantly developed and rich in fat.

PATHOGENY OF INFANTILE PARALYSIS.—In the pathological anatomy of infantile paralysis there are two principal facts to be correlated with its clinical phenomena—namely, the limitation of the myelitis to the anterior gray horns of the spinal cord; the destruction of the ganglionic nerve-cells in these gray horns. That the other lesions observed are subordinate to these is shown by their variableness as compared with the constancy of the anterior poliomyelitis. These lesions are, in the cord, the atrophy and sclerosis of the anterior nerve-roots and white columns; in the muscle, the fatty degeneration or simple atrophy of the fibre; in the nerve, breaking down, and finally atrophy of the myeline sheath, sometimes of the axis-cylinder; proliferation of the endoneurium.

Consequence of Limitation of Myelitis.—Limitation of the morbid process to a portion of the motor tract, the anterior cornua, and exclusion of the posterior horns and roots, readily explain the predominant positive symptom of motor paralysis, together with the absence of sensory disturbance. The absence of muscular rigidity, spasm, active contraction, and of exaggerated reflexes is similarly explained by the immunity from the morbid process of the posterior white columns and the portion of the lateral columns immediately adjacent to them. The motor paralysis resulting from destruction of the anterior ganglionic cells of the cord is much more complete than that which depends on simple interruption of the motor tracts passing from the brain. The manner in which the motor tracts are connected by a succession of arching fibres with these cells already indicates that the latter are dépôts for the reinforcement of the motor impulses. We must believe, indeed, that the centrifugal impulses reaching the anterior cornua are not yet motor in character, but to become so must sustain a new elaboration in the ganglionic cells of this region. Evidently, the network of gray fibres connecting the arcuate strands of the antero-lateral columns with the cells become, in virtue of that fact alone, essential to the process. But it is also probable that the multiplied transmission of impressions, which lies perhaps at the basis of the process of their higher elaboration in ganglionic centres, is carried on in the larger network of gray fibres as well as in the smaller network contained in the ganglionic cells. Destruction of a portion of this network would therefore interfere with the elaboration of the motor impulse, in the same manner, though to a relatively less extent, as destruction of the ganglionic cells themselves.

Trophic Lesions.—The rapid wasting of the paralyzed muscles, with their degenerative electrical reactions, seems, however, to be an effect altogether peculiar to lesions of the ganglionic bodies.¹²⁵ According to Charcot, who has so especially formulated the laws of amyotrophic paralysis, all the ganglionic cells essential to the elaboration of motor impulses exercise a trophic influence upon muscles. The spinal cell, nerve-fibre, and muscle-fibre combine into a complex indissoluble unity or element. One part of this lesion of complex elements is necessarily followed by proportionate lesion of all its other parts.

¹²⁵ The amyotrophic lateral sclerosis of Charcot exhibits in an exquisite manner the difference between paralysis without atrophy, caused by sclerosis of the antero-lateral columns, and paralysis with atrophy when the morbid process has extended to the anterior cornua.

According to Erb, however, who extends Samuel's doctrine of special trophic nerves, it is not the motor cells which influence the nutrition of the muscle-fibres with which they are connected, but special trophic cells lying among the others in the anterior cornua. This theory is principally based on the existence of muscular atrophies of central origin (progressive muscular atrophy, bulbar paralysis), unaccompanied for a long time by paralysis.¹²⁶ Hammond cites as a converse example the anterior poliomyelitis “where the peripheric disturbance is, in the first place, solely one of motility; this is paralysis without atrophy. After a time, which may be as much as six months or even more, the trophic changes begin.”¹²⁷

¹²⁶ Ziemssen's Handbuch.

¹²⁷ Loc. cit., p. 429.

But surely this is an exaggerated emphasis on the exception, rather than the true inference from the rule of rapid wasting in anterior poliomyelitis—a rule so general as to have originated the title atrophic paralysis. Erb gives an ingenious scheme (Fig. 55) of the mental relations of motor and trophic cells with cerebral and spinal nerve-fibres. It will be seen that isolated lesions of one or the other trophic apparatus might occur without paralysis of motor tracts, while simultaneous lesion of the trophic apparatus and of the ganglion-cells, or of the latter, involving the tracts coming from the trophic cells, would cause, as in anterior poliomyelitis, motor paralysis, muscular atrophy, loss of the reflexes, degenerative reaction in nerves and muscles.

Duchenne and Joffroy¹²⁸ also argue the existence of special trophic nerve-cells. The absence¹²⁹ of the nutritive lesions of the skin and cellular tissue which are so conspicuous when the gray matter around the central canal or posterior to it is involved,¹³⁰ the dependence of the nutrition of the motor apparatus, nerves, muscles, bones on the integrity of the anterior horns, are facts which, taken together, seem to indicate that the maintenance of nutrition depends on the unbroken continuity of the motor or sensory apparatus from the periphery to the ultimate central element, rather than on any special central cells endowed with trophic functions.¹³¹ Erb's hypothesis, as his own scheme moreover denotes, demands not only trophic cells distinct from motor cells, but separate trophic cells for the muscles, for the motor, and for the sensory nerves.

¹²⁸ “De l'Atrophie aigue et chronique des Cellules nerveuses,” Arch. de Phys., No. 4, 1870.

¹²⁹ Money, and also Gowers, have signalized a condition of the skin resembling myxœdema (Tr. Path. Soc. London, 1884, and Brit. Med. Journ., 1879).

¹³⁰ Mayer (Herman's Handbuch Physiol.) sums up the great mass of evidence now accumulated, which demonstrates the trophic influence of the central gray mass of the cord upon the tissue.

¹³¹ Nepveu (La France médicale, 1879) mentions some cases of infantile paralysis complicated with trophic lesions of the skin. The facts, if accepted, could only indicate an extension of the myelitis to the central and posterior regions of the gray columns. The relations between non-atrophic paralysis caused by interruptions of the motor tracts and muscular atrophy dependent on lesion of the anterior cornua are exquisitely shown in a case reported by Sander. An adult suffered from chronic motor paralysis, gradually increasing, in the right arm, with paresis of the lower extremities. In the hand, arm, and shoulder the paralysis was followed by gradual atrophy and diminution of the faradic contractility; in the lower extremities no atrophy occurred. At the autopsy was found a gliomatous tumor seated in the anterior cornua predominating on the right side, extending from the level of the sixth dorsal to that of the eighth cervical vertebra. The ganglion-cells were pigmented and compressed, not altogether destroyed. The lumbar cord was intact, and the non-atrophic paresis of the lower extremities evidently resulted from the interruption of the motor tract above.

The peculiar grouping of nerve-centres within the cord that seems to be indicated by some of the groupings of infantile paralysis shows, as has been said, a probable divergence within the cord of nerve-fibres which run together in the same nerve-stem. The associations to be expected from the data of functional association and of clinical history are by no means fully decided. It is even a matter of dispute whether the tibialis anticus is functionally more associated with the flexors or with the extensors of the thigh, and whether its experimental irritation or clinical paralysis really coincides with that of the first or of the second group. This entire field of observation is new and promises fertile results.¹³²

¹³² It is from this field that has come a new argument for the spinal nature of lead-paralysis, from its peculiar grouping, and from analogy with that of anterior poliomyelitis of the upper extremities (Remak, “Ueber die Local. Atropa. Spinal Lahm.,” Archiv für Psych., Bd. ix.; also, Ferrier, loc. cit.).

Relation between Limitation of Myelitis and Age.—From the relative frequency of anterior poliomyelitis in childhood, as compared with its much greater rarity in adult life, we must infer the existence of some special conditions in childhood which tend to limit the morbid process to such a portion of the cord. The theory of a primitive spontaneous atrophy of the motor cells would serve, indeed, to explain this limitation. The reasons already alleged for regarding the morbid process as a systematic myelitis decisively hinder the acceptance of such an explanation as it stands. On the assumption, however, that the myelitis is usually of functional origin, and starts, therefore, in the elements of the anterior cornua essentially involved in the motor functions, the morbid susceptibility of these elements may be ranked with the liability to disease of the entire locomotor system which is known to be so predominant in children. From pathological evidence, even without anatomical proof, we may reasonably infer an incompleteness of development in the anterior cornua of the cord correlative with that well demonstrated in the bones and functionally inexperienced muscles. If the antero-posterior fibres which connect the anterior cornua with the central and posterior gray masses be also incomplete, the radiation of irritations, and consequent vascular irritation, would also be arrested within the boundaries of the original lesion. Thus a peculiarly circumscribed, instead of the common diffused, myelitis of adults.

Money¹³³ points out that for the gray matter of the cord, as of the brain, the centre or maximum force of the circulation is on the periphery, and the nutritive supply of the centre is thus easily cut off. Moreover, while the blood-vessels of the cervical and dorsal regions of the cord pass to it transversely, the vessels of the lumbar region are compelled to describe a somewhat prolonged vertical course before reaching their point of distribution. From these circumstances, even transitory congestions in the circulation of the cord are easily followed by irreparable injury of its delicate elements.

¹³³ Loc. cit., Path. Trans., 1884.

Finally, in all discussions on pathogeny must not be forgotten the doctrine of Leyden¹³⁴ that infantile paralysis, also progressive muscular atrophy, is a disease which may begin at the periphery and extend to the centres, as well as the reverse. It must also be remembered that, as yet, only very scanty evidence exists to support this, in itself, plausible theory.

¹³⁴ See loc. cit., ut supra.

COURSE OF INFANTILE PARALYSIS.—The most ordinary course of infantile paralysis is that already described as typical—namely, extremely rapid development to a maximum degree of intensity, then apparent convalescence, retrocession of paralysis, atrophy, and ultimate deformities in limbs in which paralysis persists.

Several variations from this typical course are observed. Complete recovery may take place, as in the so-called temporary paralysis of Kennedy¹³⁵ and of Frey.¹³⁶ These cases are very rare. But their possibility seriously complicates the estimate we may make of the efficacy of therapeutic measures.¹³⁷

¹³⁵ Dublin Quarterly Journal, 1840.

¹³⁶ Berlin. Klin. Wochensch., 1874. I have described one such temporary case in the article already quoted. These cases seem about as frequent in adults. (See Frey, loc. cit.; also case of Miles, etc. etc.)

¹³⁷ As of the case of complete recovery, the only one the author had seen, related by Dally, Journal de Thérap., 1880, 1, vii.

On the other hand, there may be a complete absence of regression; and this is observed sometimes in cases where the paralysis is originally limited; sometimes where it is extremely extensive, involving nearly all the muscles of the trunk or limbs;¹³⁸ or muscles or limbs originally spared may become involved in a fresh attack. Laborde relates cases of this kind. In Roger's first case paraplegia occurred under the influence of scarlatina two months after paralysis of one arm.

¹³⁸ Thus in Eulenburg's case, quoted ut supra.

The form of anterior poliomyelitis most frequent in adults is the subacute, and after that the chronic. Both are extremely rare in children, the latter excessively so. Seeligmüller and Seguin¹³⁹ both admit the possibility of a chronic form in children, and the latter has kindly communicated to me one case from his private practice: