THE HISTOLOGY OF DISSEMINATED SCLEROSIS. 651 



vascular embryonic infiltration." " In recent areas the reactionary vascular 

 phenomena are entirely out of proportion to the myelin degeneration." Such 

 statements, asserting the primary inflammatory character of the lesion in the 

 vessels, can be found extensively throughout the literature of this subject, together 

 with statements which show that the " granular cell myelitis " is also taken as a 

 proof of the presence of an acute inflammation in the vessel walls. The sequence 

 of the process is either that the primary affection of the vessel wall is transmitted 

 direct, by a progressive diffusion, to the surrounding tissues, causing a solution of 

 the myelin and a reactive interstitial inflammation, or the agent causing the 

 inflammation is restricted to the vessels and causes in these first of all alterations, 

 through which are produced changes in the nutrition of the surrounding tissue, 

 which are no longer inflammatory but purely degenerative. 



It would a 'priori be thought natural that an irritative substance circulating in 

 the blood would, in its filtration and diffusion into the tissues, stimulate the 

 capillary endothelium and cells of the adventitia to proliferate, and that its first 

 effect would thus be on the vessel wall through which it passed. In this investiga- 

 tion special importance was attached to this point, and a reference to the histological 

 study will show that it was impossible to trace, except in rare instances, a primary 

 proliferation 'of the capillary endothelium, or a primary increase in the nuclear 

 content of the adventitia. The first cell infiltration of the vessel wall was one of 

 fat granule cells in the adventitial lymph spaces, secondary to the resorptive 

 processes : this called forth a secondary proliferation in the endothelial and other 

 cellular elements of the adventitia, and at a later stage there was a cell infiltration 

 of lymphocyte-like cells analogous to those found in all chronic processes. In the 

 event, therefore, of a disease-producing agent, either bacterial or toxic, being- 

 carried with the blood or circulating in the lymph sheaths, it must be assumed 

 that this poison leaves the blood channels in so slight an amount or in such weak 

 concentration that a recognisable injury of the vessel wall does not result. The 

 only part played by the blood-vessels would thus be the bringing of the " noxa " to 

 the tissues. Bielschowsky, who looks upon the vessel changes as entirely 

 secondary, has come to the conclusion that only a "noxa" that has penetrated 

 by the vessel into the tissue but has left the vessel wall intact has occasioned the 

 process. Taylor, who was unable to find any trace of vessel changes in the 

 examination of eight cases of disseminated sclerosis, thinks that it is perfectly 

 conceivable that the manifestation of the toxic agent may occur without evidence 

 of local inflammation in the vessel wall. Marburg and other writers, who have 

 described cases of " acute multiple sclerosis," have given this designation instead of 

 " acute myelitis," " in virtue of the absence of any marked signs of actual inflamma- 

 tion in the vessel w r alls." The explanation of the numerous findings of such 

 inflammation by other writers must be found either in- the presence of areas of an 

 acuter type than were observed by me, or in the possibility that areas were described 



