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March 1937


Author Affiliations


From the Department of Nervous and Mental Diseases and the Institute of Neurology, the Northwestern University Medical School.

Arch NeurPsych. 1937;37(3):479-504. doi:10.1001/archneurpsyc.1937.02260150009001

Evidence has accumulated to indicate that poliomyelitis is propagated within the central nervous system along axonal channels and that the clinical manifestations of the disease are explainable on the basis of advance of the infection solely through and within the nervous system. The excellent studies of Hurst1 and Pette, Demme and Környey2 disclosed that the early spread of virus within the neuraxis after experimental intraneural inoculation follows rather narrowly a unilateral, decussating pathway. After unilateral intracerebral inoculation the early cerebral lesions are more marked ipsilaterally (Fairbrother and Hurst3), and the lesions in the spinal cord are more severe contralaterally (Pette and his associates2).

In the present study an endeavor was made to establish the nature and pattern of distribution of the histopathologic process in fully developed experimental poliomyelitis following intracerebral inoculation with a particular strain of virus and to study the evolution of the histopathologic changes

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