THE HISTOLOGY OF DISSEMINATED SCLEROSIS. 639 



tions and inflammations, and, on the other hand, into a morbid condition which 

 has one uniform circumscribed pathogenesis, being due not to any known external 

 cause but to a congenital abnormal disposition of the glia. Among the former, he 

 states, are those " comparatively rare " processes which have resulted in injury to 

 the nervous tissue due to some apparently primary blood-vessel condition, e.g. 

 syphilitic or arterio-sclerotic disease of the vessels, or to a toxi-infective inflamma- 

 tion in the form of a disseminated myelitis or encephalitis. In all these cases the 

 histogenetic terminal product is a secondary disseminated sclerosis in the sense of 

 Schmaus and Ziegler. In contrast to these is the "comparatively common" 

 disease caused by congenital disturbances of development, and termed by Schmaus 

 and Ziegler primary disseminated sclerosis. This form, which presents distinct 

 clinical and anatomical signs and may be looked upon as a multiple gliosis 

 (Strumpell), is the only true disseminated sclerosis. 



The essential anatomical signs of this condition are the following : (l) the foci 

 are situated only in those parts of the nervous system which normally contain much 

 glia ; they tend to develop symmetrically and are often of considerable size, e.g. in 

 the cord they may occupy the whole transverse section ; their relation to the blood- 

 vessel can be explained by the layer of glia — the glia limitans perivascularis — normally 

 around the vessels. (2) Microscopically the foci consist of an excessive proliferation 

 of glia, leading to a dense tissue which is never areolar : there is comparative 

 integrity of the ganglion cells and axis cylinders in the area and a marked degenera- 

 tion of the myelin sheath, with no secondary degeneration ; and there is never 

 evidence of a primary disease of the blood-vessels within the area. The foci, stained 

 by means of Weigert's myelin sheath stain, appear clearly defined and as if punched 

 out, but, stained by Weigert's glia method, the areas have not the same abrupt 

 transition to the normal tissue — the proliferated glia becoming gradually lost in the 

 periphery. In this circumstance Muller found an argument for the primary glia 

 origin of the process. He bases much of his description of the areas on sections, 

 stained by Weigert's glia method, lent to him by Weigert himself. Sections so 

 stained bring out very forcibly the enormous proliferation of the glia, and give the 

 impression of a primary glia growth so out of proportion to the relative integrity of 

 the ganglion cells and axis cylinders as to contradict any mere substitution pro- 

 liferation. Muller thinks it very striking that this colossal glia proliferation — the 

 maximum found in pathological conditions (Weigert) — should be met with in a 

 disease in which there is relative integrity of the true nervous tissue. 



The clinical signs are also typical, and Muller thinks that secondary dis- 

 seminated sclerosis can never successfully simulate Charcot's classical picture in the 

 marked distinctness of each symptom and the peculiarly characteristic course. In 

 spite of the great variableness in the symptoms, which may simulate widely-differing 

 diseases of the brain or cord, the diagnosis can always be established by a study of 

 certain individual symptoms and groups of symptoms, and of the course of the 



