THE HISTOLOGY OF DISSEMINATED SCLEROSIS. 679 



exciting factors in lowering the resistance of the organism, and thus allowing the 

 final determining factor to operate. 



The most important question yet remains : What is the nature of this postulated 

 specific morbid agent which is the final and determining factor in the process ? It 

 has already been frequently stated that this is quite uncertain, and that there is 

 not sufficient evidence to show whether it is microbial or of the nature of a toxin. 

 There is much in favour of the view that the disease is toxic in origin ; the histo- 

 logical evidence, which is far from conclusive, is related to the absence of cell 

 infiltration of the vessel walls, for it is admitted by most writers that areas of 

 degeneration without cell infiltration are more usually due to toxic influences, while 

 infective agents more uniformly call forth an infiltrative form of myelitis. More 

 decisive, however, is the clinical evidence : many of the early symptoms, symptoms 

 which sometimes last for years, are slight motor palsies and transient psychical 

 symptoms, which pass off readily under treatment with faradism or suggestion — 

 such transient symptoms are very suggestive of the persistence in the body of some 

 toxin which exercises its action on the nervous system. The variability of the 

 early symptoms, which has so frequently led to the diagnosis of hysteria, suggests 

 that at this stage areas may be affected by a "nutritional" rather than a structural 

 change. The possibility of dynamic modification of function is now well recognised, 

 in diseases of the nervous system, while as yet structural change is slight, and this 

 being so, it is therefore more likely that the agent producing this varying disturb- 

 ance of function is some form of toxin. The importance of determining the relation 

 of the so-called Westphal-Striimpell pseudo-sclerosis to disseminated sclerosis is very 

 great, for in this affection the symptoms of disseminated sclerosis are present with 

 negative pathological findings. 



If we assume the presence of a toxin as the essential stimulus, we must further 

 decide the route of its conveyance to the nervous tissues. The histological evidence 

 in favour of hsematogenous and lymphogenous spread has been given in a previous 

 section : it was there stated that although certain circumstances, such as the 

 frequent marked peri -ventricular sclerosis, and recent experimental evidence in 

 favour of the toxicity of the cerebro-spinal fluid, point to a lymphogenous spread, 

 there is no histological evidence to support this view. 



(iv) The causal agent is, therefore, probably of the nature of a soluble toxin, and 

 it is conveyed to the nervous tissues probably by the blood channel. 



We have still to explain the restriction of the action of this circulating toxin 

 to certain areas. The difficulty of explaining how the degeneration connects itself 

 with special vascular tracts, and avoids others, has led many writers to fall back 

 upon the assumption of developmental defects or minimal tissue injuries, which 

 form " loci minoris resistentise " where the circulating toxin might settle. In the 



