Experimentally produced disseminated allergic encephalomyelitis closely resembles certain spontaneously occurring demyelinating diseases in humans for which no etiologic agent has been discovered.1 These include the postinfectious encephalitides and the encephalomyelitis which sometimes follows rabies and smallpox vaccinations. These conditions present the same clinical symptoms and identical histopathological manifestations.
The pathogenesis of multiple sclerosis may be primarily a biochemical derangement of the central myelin.2 The breakdown process is usually restricted to segments of myelin sheaths within the central nervous system. This has suggested that the hypothetical biochemical lesion occurs in myelin segments, in axons, or in the oligodendrocytes, but not primarily in the neuron bodies. It may be that the demyelination is related to an enzyme concerned with the physiology of conduction rather than with any of the lipases.3
The limitations of microscopic histochemistry are twofold: (a) It is not quantitative, although the methods proposed by Coujard,4
de SIBRIK I, O'DOHERTY DS. Phosphatases and Phospholipases in the Central Nervous SystemA Study in Normal States and in Experimentally Induced Disseminated Allergic Encephalomyelitis. AMA Arch Neurol. 1960;2(5):537–546. doi:10.1001/archneur.1960.03840110051006
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