THE HISTOLOGY OF DISSEMINATED SCLEROSIS. 645 



When, therefore, the inflammatory nature of the process is referred to, it is as a 

 reaction process and one not necessarily associated with exudation of fluid and cell 

 infiltration of the vessel walls. All changes which reveal any kind of progressive 

 phenomena in any of the tissue elements are therefore included in this view of 

 inflammation. Later the relations of disseminated sclerosis to acute and chronic 

 myelitis must be referred to, but the widely varying views regarding the true nature 

 of " acute myelitis " may here be touched upon. Many clinicians have given this 

 name to all diseases of the spinal cord, the symptoms of which cannot be traced to 

 an isolated affection of individual portions of the cord or systems of the cord. Others, 

 before applying the term, make the additional condition that an inflammatory process 

 should really be present. The conditions under which it is justifiable to entitle a 

 disease " myelitis " are not yet defined either clinically or anatomically, and it is the 

 anatomical substratum of the disease, when known, that usually defines the idea of 

 the disease. Bastian, arguing largely from the similarity of the morbid changes to 

 those occurring in the brain, which are due to thrombosis, has long maintained that 

 the great majority of cases are really "thrombotic softening of the cord" rather 

 than an infiltrative myelitis. An ischsemic softened area in the brain, in which great 

 numbers of phagocytic cells, associated later with proliferation of the supporting 

 tissue, are present, is not usually looked upon as an encephalitis. It is the custom to 

 identify this finding by the name of " softening," and yet it is much rather a reactive 

 condition that has set in secondarily, and is a secondary inflammatory reaction — 

 secondary to the presence of the degenerated products. A similar condition may 

 occur in the spinal cord as a result of thrombosis of the spinal vessels, and the reactive 

 phenomena are here again not due to the primary cause which produced the tissue 

 necrosis. On the other hand, as a result of toxi-infective agents, it is possible to get 

 (l) typical cell infiltrations of the vessels and surrounding tissue ; (2) simple degenera- 

 tions of the tissue, in which the so-called inflammatory vascular changes may be 

 absent ; or, further (3), actual inflammatory softenings of the tissue. In the latter two 

 forms we again get later reactive changes in the tissue elements, and these may be 

 secondary to the tissue degeneration, or simultaneously called forth by the primary 

 causal stimulus. Are such conditions to be termed inflammatory only when the 

 primary blood-vessel wall changes are inflammatory ? or is it not possible to recognise 

 the complicated inter-reaction as an inflammatory process ? Clinically, we cannot 

 yet distinguish parenchymatous and infiltrative myelitis, nor these from acute 

 inflammatory softening and acute thrombotic softening. Pathologically, it is sufficient 

 to distinguish two main types in which myelitis may show itself: (l) Infiltration — 

 a form to which some would limit the term "acute" myelitis; (2) softening— to 

 which the term "myelomalacia" has been recently applied — a form which may be 

 very varied in degree from the degeneration of a limited number of nerve fibres, in 

 which the process is more probably subacute, to the necrosis of a large area, in 

 which the process is more likely to be acute in onset. 



TRANS. ROY. SOC. EDIN., VOL. L, PART III (NO. 18). 90 



