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January 1937

PATHOGENESIS OF THE CORTICAL ATROPHY OBSERVED IN DEMENTIA PARALYTICA

Author Affiliations

BOSTON; EDINBURGH, SCOTLAND

From the Neurological Unit, the Boston City Hospital, and the Department of Neurology, Harvard University Medical School.

Arch NeurPsych. 1937;37(1):75-90. doi:10.1001/archneurpsyc.1937.02260130085006
Abstract

It is universally recognized that the cortical atrophy observed in dementia paralytica may be entirely independent of the inflammatory phenomena. Jahnel,1 in a recent authoritative review of the subject, stated: "The parenchymal degeneration corresponds neither in its intensity nor in its extent with the infiltrative processes." The mechanism of production of the inflammatory changes is obvious, but the sequence of events leading to the degeneration of ganglion cells has been the subject of much discussion. It has been supposed, for example, that the nerve cells are actually invaded and destroyed by the spirochetes. This appears unlikely, since, according to Jahnel,1 spirochetes have never been satisfactorily demonstrated within ganglion cells. Also, spirochetes are usually rare or absent from areas showing the greatest degree of cortical atrophy,2 and they have never been observed free in the white matter, even in cases in which there were extensive lesions of the

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