Ribbert and Zacher consider the sclerosis of tabes and the disseminated affection to be much more similar than Leyden and Charcot supposed. They locate the starting-point of the morbid process in the vascular and connective tissues; and Greiff, in harmony with this view, finds that the foci occur most frequently in those parts of the cord where the connective-tissue trabeculæ are most numerous, as in the posterior columns and at the junction of the anterior and lateral columns.
Although the morbid foci appear to the naked eye to be uniform, and to be sharply demarcated in the normal tissue, closer examination shows that the areas of maximum lesion are surrounded by a narrow transition zone by which the lesion seems to mark its eccentric progress, and occasionally a focus of intense disease lies in a diffused area of slight changes, resembling those of diffuse myelitis. Sometimes the cord appears to be almost continuously involved by a lesion of moderate intensity, and a few disseminated foci in the brain alone prove that the case belongs to this form of sclerosis.
A few years ago Greiff described what he considered a new lesion in multiple sclerosis, under the name of disseminated vitreous degeneration of the cerebral cortex.136 I have been familiar with this lesion since 1876: it can be produced at will in perfectly healthy brains, and consists in a precipitation of leucine crystals extracted from the brain-substance by the action of alcohol. His accompanying figure137 represents this artificial lesion very accurately; and Greiff, if he fails to recognize that his vitreous degeneration is a spurious lesion, at least identifies it with the miliary sclerosis of Bucknill and Tuke and the spheres of Schüle, which are now generally recognized to be the results of post-mortem manipulations and not actual lesions.138
136 Archiv für Psychiatrie, xiv. p. 286.
137 Ibid., xiv., Plate ii. Fig. 5.
138 Attention was first called to the artificial nature of these bodies by the writer in the Journal of Nervous and Mental Diseases, October, 1877, and a more accurate description was given in the Chicago Medical Review of 1880, and in a demonstration before the New York Neurological Society in 1883. In commenting on the latter a German critic stated that the facts related had been long known in Germany (Neurologisches Centralblatt, 1883, p. 283). On inquiring of the critic what publication contained any reference to this discovery, he frankly stated that he knew of none, but had had in mind what he considered a tradition of the laboratory. It was in the same year that Greiff worked at the Heidelberg laboratory under the eminent supervision of Fürstner, and it was a few years previous that Schüle, one of the collaborators of Ziemssen's Cyclopædia, had made the same mistake. So it seems that the tradition is in some danger of expiring, and that it would do no harm to accept the caution, even though it travel across the Atlantic in the reverse of the usual direction. It has been amply confirmed by Savage and Plaxton (Journal of Mental Science, October, 1882, and April, 1883).
In judging as to the nature and intensity of the inflammatory process which leads to the development of the sclerotic foci, it must be remembered that we are acquainted thus far only with the terminal period of the disease, when, as is to be presumed, the active inflammatory changes have gone by or are in the background. It is very probable that the newly-formed tissue is more nucleated in early periods than is found in the cases which constitute the material of pathological laboratories. In a case of protracted nervous exhaustion accompanied by spinal irritation in an alcoholic subject who was murdered, and whose brain and cord I had an opportunity of examining, I found, both in the cord and brain, districts in which the white substance showed a slight grayish discoloration and increased consistency. Minute examination failed to show any qualitative change in the conducting elements, but the interstitial tissue was hypertrophied, richly nucleated, and showed Frommann's cells in abundance.
ETIOLOGY.—Heredity has been observed in a number of cases by Duchenne, Erb, and Frerichs. The latter two had each an opportunity of recording this inheritance in several members—sisters or brothers—of the same family. In these cases the transmitted affection developed in adult life. Dreschfeld, however, cites a case where two brothers developed its symptoms in a marked degree in infancy. As an associated feature it is found with some cases of congenital defect. Thus Pollak139 discovered disseminated sclerosis in an infant which had a defective corpus callosum and exhibited the characteristic signs of the focal affection side by side with the imbecility due to imperfect cerebral development. As a rule, the disease is developed after the twentieth year. But cases have been related (De Fleury) where the patient developed the disease and died with an apoplectiform onset in earlier life. One of the youngest on record is described by Hödemacker.140 The subject developed the disease at the seventh year, and died with it at the fourteenth, having shown the characteristic symptoms, besides more muscular atrophy than is common. The sclerosis in this case belonged to the type which has been referred to as a connecting-link between diffuse and disseminated sclerosis. Pelizæus141 reports five cases developing in the same family in early life, corresponding somewhat in their relation to multiple sclerosis of advanced life, as the family forms of tabes and spastic paralysis correspond to the typical adult forms of those diseases. All the cases were of males, and the ancestral taint had been present in male members of the family, passing through the females to their progeny without breaking out in the mothers. Each branch of this family appeared to develop its own peculiar type of the disorder.
139 Deutsches Archiv für klinische Medizin, Bd. xxiv. p. 404.
140 Ibid., vol. xxiii. p. 442.