STUDIES of the experimental allergic neuropathy, which can be produced in animals by immunization with peripheral nervous tissue, have been largely concerned with the phenomena observed in the acute stage. As originally demonstrated by Waksman and Adams1in the rabbit, the pathological changes are confined to the peripheral nervous system, sparing structures of the central nervous system (CNS) except for the occasional accumulation of inflammatory cells in the meninges. The clinical features of a gradually ascending symmetrical polyneuropathy, accompanied by an increase in the cerebrospinal fluid protein, resemble certain human polyneuropathies such as the Guillain-Barré syndrome. Usually single severe attacks characterize the experimental rabbit disease with occasional repeat episodes being observed. Heitmann and Mannweiler2noted a shorter incubation period in the rabbit when the inoculation was repeated several months after primary immunization. In the monkey Heitmann et al3noted a predilection for the neuropathy to affect cranial
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Allan L. Sherwin (1966) studied this question.
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