536 DR JAMES W. DAWSON ON 



(2) Process underlying Multiple Sclerosis founded upon a Disturbance 



of Development. 



A. Deficient "Anlage " of the Nerve Elements, with Hypoplasia or 

 "Agenesia " of the Myelin Sheath. 



Schiff and other writers have thought it possible to trace disseminated sclerosis 

 to partial or total absence of the myelin sheath formation. We know that the 

 appearance of the myelin represents a definite stage in the development of the nerve 

 fibre. This myelination sets in at different periods in different tracts, and even in 

 different fibre areas of related tracts. The naked axis cylinders might, therefore, be 

 looked upon as incompletely developed nerve fibres. Friedreich's ataxia has been 

 traced to such a deficient development, and Schiff sees in the fact that in Friedreich's 

 ataxia the glia development approximates in intensity to that found in disseminated 

 sclerosis a possible analogy. He thinks that disseminated sclerosis may be due to a 

 deficient or arrested development of the myelin sheath in the affected areas. Kahler 

 and Pick have ascribed system diseases to such an arrest of development. Schmaus 

 thinks this view worthy of consideration ; but Borst, while acknowledging that 

 certain parts remain at an early stage of development, thinks that such an explana- 

 tion is possible only for system diseases, and that it is improbable that multiple 

 scattered arrests of development can occur. Most writers have agreed with this 

 attitude, and supporters of the developmental nature of the process relate it rather 

 to disseminated defects in the glia framework of the central nervous system. 



B. Multiple Defects in the Glia Framework of the Central Nervous System. 



Strumpell (1896) was one of the earliest advocates of this view. He speaks of 

 a " multiple gliosis," and draws comparisons with multiple fibromata, lipomata, 

 neuromata, etc. He looks upon the etiological factors of an exogenous nature only 

 as exciting causes, and he thinks it very unlikely that we should find a primary 

 affection of the smallest vessels in the central nervous system and not in the other 

 organs of the body. Strumpell further recognises it to be necessary, in other 

 cord affections, e.g. hydromyelia and syringomyelia, in which we have marked 

 glia proliferation, to have recourse to congenital anomalies of development. In 

 disseminated sclerosis he thinks that the proliferation of the glia gives the im- 

 pression of a primary process, and that it cannot be traced to a previous degenera- 

 tion of the nerve elements. 



Schmaus holds that both the view of a congenital hypoplasia or agenesia of the 

 myelin sheath and that of the possibility of inserted islets of glia with a special 

 capacity for proliferation are worthy of consideration, at least so long as no other 

 proof is brought forward, He thinks that the most important objection to the 



