The atypical form of dementia paralytica described by Lissauer and Storch1 is characterized by transient apoplectic or epileptic attacks followed by residual focal symptoms to which correspond localized anatomic lesions. Discussions in the literature of the nature of the disorder have centered about the pathogenesis of the specific histologic picture of the lesions, namely, status spongiosus and its tendency to laminar distribution. It is the purpose of this contribution to analyze the pathogenic factors suggested by various other investigators and by a study of four additional cases.
REVIEW OF THE LITERATURE
Since a comprehensive summary of the literature has been outlined by Merritt and Springlova,2 only contributions to the pathogenesis will be reviewed.Status spongiosus may occur in both the gray and the white matter in different diseases of the central nervous system. It is characterized histologically by transformation of the tissue into a honeycombed spongy structure with
MALAMUD N. LISSAUER'S DEMENTIA PARALYTICA: A STUDY OF ITS PATHOGENESIS. Arch NeurPsych. 1937;38(1):27–42. doi:10.1001/archneurpsyc.1937.02260190037003
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