686 DR JAMES W. DAWSON ON 



fibril-forming cells, and, later, glia fibril formation at the expense of this protoplasm : 

 glia cells which have produced fibrils undergo slow, regressive changes, the glia 

 nuclei subsequently atrophy and disappear, and to such a disappearance is due the 

 fact that the old sclerotic areas have fewer nuclei than the normal tissue : the course 

 and direction of the glia fibrils is, as a rule, in the direction of the normal longi- 

 tudinal course of the nerve fibres, especially in the posterior columns of the cord, 

 but frequent whorls are found or a dense tangle with very fine meshes. 



In the progressive alteration in the glia all its component parts share — nucleus, 

 protoplasm, and specific fibres: the "glia limitans peri-vascularis " is the first to 

 show signs of reaction : the abundance of the glia in an area justifies the name 

 " sclerosis," but the process may stop short of complete sclerosis and so areas are 

 present showing all degrees of density of the glia meshes : the sclerotic tissue is 

 more loosely constructed in the grey matter of the cord and the analogous nuclei. 



The glia changes in the cortex lend support to the view that the adult glia 

 consists of (l) cells — with nuclei, cell bodies, and protoplasmic processes ; (2) differ- 

 entiated fibrils — whether anatomically independent or not ; (3) intercellular 

 fibreless glia. 



It seems unnecessary to postulate areas of glia abnormality and that the blood- 

 vessels carry the morbid agent to such points : but this can neither be proved 

 nor disproved. 



(xv) Blood-vessels. The topographical relation of the areas points to the blood- 

 vessels, or their lymphatic sheaths, as the route by which the " noxa " is conveyed 

 to the tissues : in its diffusion through the vessel walls the morbid agent causes no 

 recognisable primary alteration, but probably there is an abnormal permeability 

 and diminished resistance to the oscillations of the blood-pressure by which an 

 increased transudation of (toxic) lymph is made possible — the only anatomical 

 expression of this is dilatation and engorgement. 



On the ground of numerous serial sections of areas it has been concluded that it 

 is the branches of one vessel stem which are affected, and that the primary minute 

 areas, related to each branch, subsequently coalesce. 



There is no evidence of a primary nuclear increase in the endothelium or in the 

 adventitia : the first cellular increase is secondary to the resorptive processes 

 — an infiltration of fat granule cells : this is followed by a proliferation in all 

 the cell elements of the adventitia and, at a later stage, by a modified infiltration 

 of lymphocyte-like cells and a few plasma cells. The derivation of the nuclear 

 content of the adventitia at a later stage is, therefore, a very varied one. The 

 later changes in the vessel walls are related to a condensation of its adventitia, 

 such as is found in all chronic conditions : the separate layers of the adventitia 

 gradually blend, its nuclear contents break up, and are carried away in the lymph 

 spaces or fuse with the adventitia ; and finally, both adventitia and media show a 



