648 DR JAMES W. DAWSON ON 



therefore, on the one hand, secondary to the parenchymatous degeneration, or, on 

 the other, also productive — passing beyond the bounds of a substitution process. 

 The view that the toxic agent has an affinity for myelin has been supported by 

 numerous recent writers : e.g. Marburg speaks of the process as essentially a 

 " lecitholysis," and Mott thinks it might be explained by the slow, limited, and 

 localised action of some " lipolytic " ferment which attacks the myelin covering 

 of the nerve fibres. 



In our histological study it has been pointed out that numerous small areas 

 occur in which there is no appreciable change but a demyelination of the affected 

 tissue. This is well brought out in Weigert myelin sheath sections, but in 

 normally-evolving areas it is more apparent than real, for sections stained by 

 Heidenhain's iron-hsematoxylin almost invariably show that in such small areas 

 the slightest demyelination is accompanied by a commencing glia cell proliferation, 

 which continued parallel to, or even exceeded in proportion, the destruction of the 

 myelin sheath. On the other hand, numerous areas are present in which there is 

 a complete absence not only of the myelin sheath but of all signs, in the presence 

 of fat granule cells and proliferating glia cells, either within the area or at its 

 periphery, of an extending process, and in such areas the abundance of the glia 

 does not justify the name of sclerosis. Here, again, it is probable that varying 

 factors have been at work to alter what may be looked upon as the normal evolu- 

 tion of a sclerotic area. Arguing, however, from the presence of such areas, I am 

 in entire agreement with the view that the most constant and uniform change is 

 the absence of the myelin sheath : this usually commences as an early swelling, 

 varicosity, and faint staining, which passes into a finely granular degeneration. 



The glia proliferation, in the great majority of the areas, is, therefore, called 

 forth by two factors : it is immediately occasioned by the stimulant action of the 

 " noxa " which caused the degeneration of the nerve fibre, and it is secondarily 

 brought about by the degenerated products of the parenchyma. The latter effect 

 is explained in part by the irritant action of these products and in part by the 

 well-known conception of Weigert (" Wegall von Wachstumhindernisse " ) that the 

 constituent tissues of an organ are usually in a state of equilibrium, so correlated 

 to one another that no cell can disappear without its place being taken by hyper- 

 plasia of the surrounding tissue. Thoma has suggestively applied this conception 

 to explain the comparative absence of glia in the cortical areas. He points out 

 the importance of considering two factors in the sclerosis : (l) the proved resisting 

 power that the ganglion cells and axis cylinders show, and (2) the non-resistance 

 of the myelin sheath, and he thinks that these two opposing factors account for 

 the proportionate development of a sclerosis. In the medullary rays and at the 

 base of the radiations in the cortex, where the myelinated fibres lie close together, 

 their extensive degeneration brings about a marked sclerosis, but in the actual 

 cortical layers two unfavourable factors — few myelin sheaths and a trifling glia 



