THE HISTOLOGY OF DISSEMINATED SCLEROSIS. 657 



one, and therefore feels justified in falling back on his view of a developmental cause 

 to which any of the other factors may be an exciting agent. Franqois, also, believes 

 that only this congenital degenerescence of the central nervous system can explain 

 the characteristics of disseminated sclerosis, and that infectious disease, chill, trauma, 

 etc., allows this to come into play. It has already been pointed out that the assump- 

 tion of the developmental genesis of the disease is insufficiently founded, and such a 

 conception must appear, in the light of modern pathological knowledge, untenable, 

 and justifiable only when every other factor has been eliminated. 



The essential problem, then, lies still before us : What is the nature of the special 

 stimulus which originates this process ? In the attempt to answer this question it 

 is important to remember that the causal factor must be in operation over long 

 stretches of years, allowing remissions of the disease and relapses. It would, 

 therefore, appear necessary to exclude those agents which actually attack the 

 organism and then disappear rapidly. It is admitted by all, except the supporters 

 of the developmental nature of the process, that the topographical distribution of the 

 areas points to the blood-vessels or their lymphatic sheaths as the route of convey- 

 ance of this agent, and the assumption of an infection or intoxication harmonises with 

 this relation to the blood-vessels. 



In spite of the absence of any positive evidence for the presence of bacteria the 

 organismal cause of disseminated sclerosis cannot be excluded, especially in view of 

 the conditions existing in syphilitic and para-syphilitic affections on the one hand 

 and poliomyelitis on the other. It has just been stated that the clinical and 

 anatomical picture requires that the agent must be one whose influence extends over 

 many years. We know that in syphilis we have an actual living organism remaining 

 present in the body for years, therefore the chronic and variable course of the disease 

 in disseminated sclerosis is not against the assumption of an infectious genesis. But 

 with none of the acute infectious diseases which have been considered by Pierre 

 Marie as etiological factors can we assume that the organism is preserved in activity 

 in the central nervous system, and the supposition that in consequence of these 

 infective diseases mixed infections, with persistent micro-organisms, establish them- 

 selves rests on no sufficient proof. 



In acute poliomyelitis the earliest changes described in the nervous system are 

 hypersemia, and a collection of small round cells in the peri-vascular spaces of the 

 blood-vessels of the soft membranes : this peri-vascular cell infiltration flows along 

 the vessels as they enter the cord and reaches its height in the grey matter around 

 the branches of the central vessels. Together with this cell infiltration there is 

 marked oedema and the presence of minute or extensive haemorrhages. These three 

 features are all dependent on inflammatory vascular changes, and may be regarded 

 as the primary reaction of the nervous system to the virus of poliomyelitis. Again, 

 as a result of the acute infective diseases, we may get an acute infective myelitis, and 

 probably one portion of the cases ascribed to disseminated sclerosis, following such 



