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Mesolimbocortical DementiaA Clinicopathologic Case Study of a Putative Disorder
Richard M. Torack, MD;
John C. Morris, MD
Arch Neurol. 1986;43(10):1074-1078.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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The term "limbic dementia" has been proposed to describe the cognitive and behavioral changes resulting from damage to those brain regions that comprise the limbic system: Cingulate and parahippocampal gyri, hippocampal formation, amygdala, hypothalamus, and dorsomedial and other thalamic nuclei.1 The disorder is clinically characterized by amnesia in combination with elements of the Klüver-Bucy syndrome,2 particularly hyperphagia, distractability, and hypersexuality, and its pathologic substrate rests in the selective and complete destruction of limbic structures and their connections. Certain elements of the disorder, such as the amnestic syndrome, have been produced with partial limbic involvement by a wide variety of disease processes, including acute necrotizing herpes simplex encephalitis,3,4 cerebrovascular insults,5,6 neoplastic invasion,7 paraneoplastic effects,8,9 surgical lesions,10 and inflammatory reactions of uncertain origin.11 Careful study of these cases has permitted valuable insight into the importance of the limbic system for both emotional behavior
. . . [Full Text PDF of this Article]
Author Affiliations
From the Departments of Pathology (Dr Torack) and Neurology and Neurological Surgery (Neurology) (Dr Morris), Washington University School of Medicine, St Louis.
Footnotes
Accepted for publication July 3, 1986.
Reprint requests to Department of Pathology, Washington University School of Medicine, 660 S Euclid Ave, St Louis, MO 63110 (Dr Torack).
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