676 DR JAMES W. DAWSON ON 



lying processes, but more probably on the varying intensity of one causal agent and 

 the varying factors which modify its action in individual cases and at individual 

 times. It is concluded therefore that : 



(ii) Disseminated sclerosis is probably not due to a developmental process, and 

 there are no sufficient grounds for distinguishing between primary and secondary 

 disseminated sclerosis in the sense used by Ziegler, Strumpell, and Muller. 



It is important to observe that this conclusion has been qualified by the addition 

 of the words " in the sense used by Ziegler, Strumpell, and Muller." I differ 

 fundamentally from those writers in their grouping of the forms of disseminated 

 sclerosis into true, primary disseminated sclerosis — a developmental disease, with 

 characteristic clinical and anatomical features — and secondary disseminated sclerosis, 

 one of a group of allied diseases, without such. Yet it is considered that the clinical 

 and anatomical picture of disseminated sclerosis stands out clearly and well defined, 

 that it is probably due to a specific but unknown morbid agent, and that it is 

 probably quite distinct from other diseases of the central nervous system, which, in 

 virtue of the disseminated distribution of their lesions, call forth clinical symptoms 

 resembling disseminated sclerosis. Two of the chief of such disseminated affections 

 are those due to multiple arterio-sclerotic and multiple syphilitic endarteritic pro- 

 cesses, in both of which, however, a careful clinical and anatomical examination 

 makes the differential diagnosis possible. Rarer forms are those due, e.g. to thrombi 

 in the cerebral vessels, formed by malarial parasites, and to multiple tumour- 

 formations, e.g. multiple neuromata of the central nervous system. The most 

 important form, however, is that due to toxi-infective conditions, which may give 

 rise to disseminated areas of myelo-encephalitis. From what has already been said 

 about the varying intensity of the "noxa" and from the assumption that when this was 

 stronger in its intensity areas might arise of an acute myelitic type, it may legiti- 

 mately be assumed that such disseminated areas may arise in immediate relation, 

 e.g. to the acute infective diseases, and produce symptoms impossible to distinguish 

 clinically from disseminated sclerosis except in the acuteness of their onset and their 

 severity. It is further probable that the clinical course of such cases, if they become 

 chronic, would not be characterised by definite remissions and relapses, and, 

 anatomically, the end-result of such areas would be characterised by a reparatory 

 sclerosis or, the opposite extreme, an absence of evidence of glia reaction and the 

 so-called " areolierte " areas of Muller. It seems unlikely that the specific toxi- 

 infective agents of the different acute infective diseases can each produce a clinical 

 and pathological condition so characteristic as that of disseminated sclerosis, while 

 it is conceivable, and we know from experimental and other evidence that it is 

 possible, that the various toxi-infective agents can call forth an acute disseminated 

 myelitis which runs its course and remains stationary. The clinical symptoms would 

 resemble disseminated sclerosis, but the characteristic remissions and relapses would 



