640 DR JAMES W. DAWSON. ON 



disease. This study will reveal- the fact — at first sight paradoxical — that the funda- 

 mental features of the clinical condition are in the great majority of cases absolutely 

 the same. There is usually no real exciting cause : it may commence suddenly, but 

 more commonly has a subacute or chronic onset ; and it shows sudden exacerbations 

 with marked remissions, but is, on the whole, a progressive and chronic disease. 



MtiLLER holds that the relationship between infectious diseases and disseminated 

 sclerosis has apparent justification only in cases where the one disease immediately 

 precedes the other, or where there is a direct transition of the one into the other. 

 True disseminated sclerosis shows a marked preference for youth, and the fully- 

 developed syndrome is very rare in childhood during the years when infectious 

 diseases are most common. Cases showing a close time-relationship are very 

 numerous, and clinical experience shows that external factors are quite insignificant 

 in the etiology of disseminated sclerosis. Further, the idea of a direct causal rela- 

 tionship appears incompatible with a satisfactory explanation of many of the char- 

 acteristic features of the course of the disease. Disseminated sclerosis runs a chronic 

 course, and Muller asks if the typical exacerbations in its course are to be explained 

 by inferring that the various exciting agents of scarlet fever, diphtheria, etc., circu- 

 late for months or years and become deposited in the foci to give rise later to fresh 

 infection. On the same grounds, Muller thinks it unlikely that disseminated 

 sclerosis is caused by the action of metabolic products derived from bacteria (toxins), 

 as in post-diphtheritic nephritis or polyneuritis. For this we would have to suppose 

 that the products of metabolism from absolutely different bacteria and of entirely 

 different chemical composition could give rise to absolutely similar foci, and also that 

 a paroxysmal increase and decrease in the action of the toxin accounts for the exacer- 

 bations and remissions. He further thinks that such meta-infectious diseases are 

 more likely to produce diffuse and system diseases than focal processes. True dis- 

 seminated sclerosis, just as Friedreich's ataxia and psychoses due to congenital 

 disposition, may develop at the conclusion of an acute infective disease, but all 

 recognisable exogenous factors, which in a small minority of cases have a definite 

 time-relationship with the commencement of the clinical symptoms, are capable only 

 of acting as agents provocateurs — given an existing predisposition to the disease — 

 making manifest or aggravating the condition. Infectious diseases may, however, 

 give rise to a disseminated disease of the central nervous system, which may develop 

 into a secondary disseminated sclerosis, but its pathogenesis, course, and histological 

 details differ from true disseminated sclerosis. So-called acute disseminated sclerosis 

 is to Muller simply a disseminated affection of the central nervous system, which 

 really belongs to disseminated myelo-encephalitis. In the rare cases in which it is 

 difficult to make a pathological diagnosis between true disseminated sclerosis and the 

 secondary forms, a consideration of the whole clinical condition and especially of the 

 course of the disease will decide. 



Muller points to the fact that, so far as we are aware, there are no exogenous 



