646 DR JAMES W. DAWSON ON 



(2) Its Origin. 



It is necessary now to discuss the question of the structural element of the 

 nervous tissue in which this inflammatory process has its origin. In the fully 

 developed sclerotic area changes are evident in relation to the myelin sheath of the 

 nerve fibre, the glia, and the blood-vessels. It is important to recognise on which 

 tissue element the causal agent, circulating presumably in the blood-vessels or lymph 

 sheath of the blood-vessels, first produces its effect. 



1 . Changes in the Neuroglia Tissue. 



Charcot defined the histological picture of disseminated sclerosis as a chronic 

 interstitial inflammation leading to a gradually increasing glia hyperplasia. This 

 view is so frequently confused with that formulated by Strumpell, Ziegler, and 

 Muller, in which there is also a gradually increasing glia hyperplasia, that at the 

 risk of a too frequent repetition the distinction between the two must be emphasised. 

 Strumpell's view is that abnormally placed glia cells take on a latent vegetative 

 activity, and produce a multiple gliosis, while Charcot holds that an exogenous causal 

 factor stimulates the glia anywhere within its range to a marked glia fibril formation. 

 The sequence of the process appeared to him to be the following : the multiplication of 

 the glia nuclei and concomitant hyperplasia of the reticulated fibrils of the glia consti- 

 tute the initial fundamental fact and necessary antecedent ; the degenerative atrophy 

 of the nerve elements is consecutive and secondary, and the hyperplasia of the vessel 

 walls plays merely an accessory part. Disseminated sclerosis is, therefore, looked upon 

 as a primary and multilocular chronic interstitial myelitis and encephalitis. The con- 

 tention of a primary glia change is based on the presence of glia hyperplasia, while 

 as yet there is little or no evidence of either an alteration of nerve fibres or changes 

 in the blood-vessels, and also on the fact that at the periphery of the areas, where 

 presumably the morbid process is still active, there is a marked increase of glia cells ; 

 here, also, are the evidences of the strangling of the nerve fibres by the glia fibril 

 formation. The substance of the argument of those who support this view seems to 

 lie in the acknowledged fact that in many areas the glia proliferation is far in excess 

 of that required as a mere reparatory or substitution process, and that it must there- 

 fore be looked upon as a productive primary stimulation. Weigert, whose views 

 on such a subject necessarily carry great weight, believes that the maximum of 

 pathological glia fibril formation is seen in this disease. 



The presence of areas, especially in the lateral columns of the cord, of a gradually 

 increasing glia hyperplasia, has already been indicated, and their comparative rarity 

 in this study emphasised. I am, therefore, not in general agreement with this 

 view, seeing it applies to so few of the areas, but in isomorphous sclerosis it is 

 probable that the reaction phenomena may be all the more marked when the tissue 

 is not greatly altered, and this would account for the colossal glia proliferation. 



