668 DR JAMES W. DAWSON ON 



and the former inflammatory, but both are occasioned by the same causal agent 

 acting with different intensity and over a longer time. Such a slowly increasing 

 interstitial change is, therefore, an illustration in the central nervous system of 

 the fact that the first evidence of reaction, when the action of an irritant is slow 

 enough for us to follow clearly its results, is a proliferative change. 



If we assume still further that the toxin is in greater concentration and acting 

 more quickly, the first effect would be solely on the myelin sheath, which would 

 degenerate rapidly. If this were not followed by a compensatory glia proliferation, 

 there would result the type of area described by numerous writers as " areolierte " 

 areas, in which the myelin sheath is dissolved away, leaving the original network 

 of the glia and the axis cylinders persisting. If there were an attempt at a 

 substitution glia proliferation, the glia nuclei would form the nodal points of a 

 brush-like formation of fibrils, but this fibril formation would yet be insufficient 

 to fill up all the meshes of the tissue, and the resultant area would be midway in its 

 sclerosis between an "areolierte" area and a dense sclerotic area. Both of these 

 latter types of areas are very numerous, and give the justification for looking upon 

 the change in the myelin sheath as the most constant and uniform one. 



It is possible to go a stage further and assume that the toxin is so concentrated, 

 or acts so rapidly, that it attacks not only the myelin sheath, but destroys the axis 

 cylinders and goes on to destroy the meshes of the glia, which thus break into one 

 another, giving the appearance of the so-called " Luckenfelder." We would thus 

 get true myelitic areas, and this is the present writer's view of the relation of 

 disseminated sclerosis to acute myelitis. The areas in disseminated sclerosis are 

 areas of lesser degeneration, and the difference in the pathological process is one 

 only of degree. I assume, therefore, that the changes are not so intense in degree 

 as in acute myelitis, and I regard disseminated sclerosis as a localised disseminated 

 subacute inflammation, which gradually tends to sclerosis. In such subacute 

 processes the general architecture of the tissue is retained. Chronic myelitis is a 

 term which is becoming obsolete. It can represent the remaining stage of a 

 previous acute myelitis, of a process which has begun chronically, or is healing 

 slowly. Taylor and Buzzard state that disseminated sclerosis has some claim to 

 be regarded as a chronic inflammatory disease of the spinal cord, and is sometimes 

 held to be the only true instance of chronic myelitis. 



It is difficult to answer the question whether an acute encephalo-myelitis can 

 pass over into a disseminated sclerosis. The pathological conceptions of the disease, 

 as have been indicated, pass over into one another, and with this conception is 

 admitted the inflammatory nature of the process. Whether it can be regarded as 

 inflammation, as degenerative inflammation, or as purely degenerative, depends 

 fundamentally upon different definitions of the same process. It seems defensible 

 to regard certain forms of disseminated sclerosis, especially those occurring in close 

 relation to the acute infectious diseases, as having their origin in an acute dis- 



