THE HISTOLOGY OF DISSEMINATED SCLEROSIS. 683 



—sometimes over long stretches of tissue — may be caused by several factors, among 

 which may be mentioned: (l) a diffuse spread of the toxic lymph in the lymph 

 spaces, (2) circulatory derangements in consequence of numerous foci, (3) considerable 

 participation of the axis cylinders causing a certain degree of secondary degeneration. 

 Finally, especially in the cord, there are frequent evidences of an early degenera- 

 tion of the myelin sheath (Marchi staining), over the whole myelinated tissue and 

 the nerve roots. This must be referred to the general somatic disturbances. 



(ix) Sites of predilection are probably related (l) to the vessels : to the terminal 

 ramifications of end-arteries, e.g. on the ventricular surfaces, and to the points where 

 vessels break up, e.g. in the transition zone between grey and white matter — both in 

 the central and cortical grey matter ; and (2) to areas where much glia is normally 

 present : again, therefore, to the peri-ventricular and to the peri-central tissue, to 

 the optic chiasma, to the postero-median and para-median septa, to the marginal glia 

 zone, and to the peri-vascular glia layer. The peri-ventricular affection was very 

 marked in six of the cases, slight in other two, and scarcely noticeable in one. The 

 optic chiasma and one or both optic nerves were affected in seven out of the eight 

 cases in which they were examined, and in six cases there was an extensive involve- 

 ment of the optic radiations on both sides — an involvement which seemed to 

 extend laterally and posteriorly from the sclerosis around the posterior horn of 

 the lateral ventricle. 



The frequent marked symmetry of the areas may be related to both of these 

 circumstances. 



(x) Cortical areas. The essential change is a demyelination, and the cyto- 

 architecture of the cortex is frequently retained. On the other hand, the ganglion 

 cells may show a marked increase of their satellite cells or all stages of degeneration, 

 but these changes are not strictly limited to the area of demyelination. The glia 

 cells in the deepest layers are markedly proliferated and show all stages of glia fibril 

 formation : in the layer of the deep pyramids there is an hypertrophy of the normal 

 glia cell content with formation of fibrils — insufficient to lead to sclerosis : in the 

 upper layers the glia cell changes diminish in intensity, but fine glia cell forms with 

 long processes of uniform calibre are present, especially around the ganglion cells and 

 capillaries ; and in the sub-pial marginal layer there is again an increase of both cells 

 and fibrils. Cortical and subcortical areas were numerous in six of the cases, few in 

 two, and in the ninth case not evident — but this brain was the only one not examined 

 microscopically in large sections. 



The changes in the cortex have been held to account for the psychical symptoms, 

 often so marked a feature in the clinical picture. Such symptoms, however, have been 

 present in cases which anatomically showed little cortical change, and, again, marked 

 involvement of the cortex has been noted in cases which clinically presented no 



