650 DR JAMES W. DAWSON ON 



sclerotic areas, in which the changes may be the effect of the sclerotic process 

 and not its cause. 



Ribbert thought that the exciting cause of the inflammation circulates in the 

 blood : that owing to its presence a clot is formed at some part of a small blood- 

 vessel ; and that at this point an irritation of the vessel wall is set up with a peri- 

 vascular inflammation, which extends to involve the surrounding tissue — causing 

 degeneration of the nerve fibres and an active proliferation of the glia. The 

 liability to thrombosis after the acute specific infections is well recognised, and 

 French writers especially have suggested that multiple thrombi form owing to an 

 altered condition of the blood or of the vessel wall. In the area of supply of such 

 vessels there would appear ischaemic degeneration, followed by phagocytic cells, and 

 a substitution glia proliferation. It is pointed out that such areas, unless examined 

 shortly after the thrombus formation, would reveal no trace in the vessel of the 

 cause of the focal degeneration. Amongst recent writers Siemerling and Raecke 

 have attached considerable importance to the presence of capillary haemorrhages. 

 In all the areas examined by them, and especially marked in the cortical areas, were 

 minute haemorrhages which were looked upon as the first evidence of the inflam- 

 matory process, and the cause of the initial fibre degeneration. 



During the course of this investigation, a large number of small isolated areas, 

 both in the brain and spinal cord, have been cut in serial section with the object of 

 tracing the possible presence of thrombosis or of capillary haemorrhages. In a few 

 instances, especially in the lateral vessels of the cord and medulla, there have been 

 found aggregations of white cells and the presence of fibrin, which have been taken 

 as indications of intra-vital thrombosis, but nowhere has evidence been present of 

 organisation of such thrombi nor of alterations in the vessel walls in relation to 

 them, nor have these been always in relation to sclerotic areas. Again, in close 

 relation to the engorgement of the blood-vessels, both within and without the areas,' 

 small haemorrhages have been found. These, however, show no changes, and were 

 looked upon as probably the result of the respiratory difficulties before death. The 

 vessel walls also showed no changes which would explain the haemorrhages, nor 

 were there any signs of inflammation around them. Keeping in mind the 

 difficulties in recognising small thromboses after actual sclerosis has set in, and 

 also the admitted long time that extravasated blood may remain unchanged in 

 the nervous tissues, it is difficult to account for the origin of sclerotic areas in such 

 primary changes. The absence of any histological evidence of changes in the vessel 

 walls associated with thrombosis or haemorrhages . is quite incompatible with a 

 primary vascular lesion in this sense. 



To true inflammatory changes in the walls of the blood-vessels a primary 

 significance has. been ascribed by a very large number of writers. :< In the early 

 stages inflammatory alterations, with small-celled infiltrations, can be recognised 

 in the vessel walls/' 'The primary vascular inflammation determines a peri- 



