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.