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Mechanism of Demyelinating Diseases of the Central Nervous System

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Abstract

Ten years after Arthus1 presented the histopathology of a local anaphylactic reaction in the skin of sensitized animals, Rachmanow2 described degenerative alterations in the neurone cells of animals that had died in anaphylactic shock. That the Arthus phenomenon could be produced in the brain was demonstrated when rabbits sensitized to horse serum were shocked by intracerebral injection of that antigen. The site of the injection became one of violent pathology, for hemorrhages, thrombi, necrosis, scavenger cells, and microglial and oligodendroglial infiltrations were demonstrated.3

Experimental cerebral anaphylaxis in monkeys produced neuropathologic changes comprising two types of lesions.4 The first was at the site of injection of the shocking dose of antigen and was similar to that described above. The second type of lesion was that of a disseminated encephalopathy in which the areas of demyelination were perivascular. The microscopic picture of these dispersed lesions revealed (1) perivascular infiltration by a variety of cellular elements; (2) axis cylinder destruction; (3) occlusion of small blood vessels by thrombi and endarteritic processes, and (4) intra and perivascular edema. Chronicity of the condition and protracted sensitization with the antigen were reflected in a change in the nature of the perivascular reaction. The change in reaction was from that of an acute hemorrhagic type associated with an exudate of polymorphonuclear leukocytes to the more chronic picture involving lymphocytes and finally granulomas and giant cells.

Basically the similarities and identities between the pathology of experimental cerebral allergy and the pathology of demyelinating diseases such as multiple sclerosis. . .


 

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