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Antonio R. Damasio, MD; Neill R. Graff-Radford, MBBCh, MRCP; Paul J. Eslinger, PhD; Hanna Damasio, MD; Neal Kassell, MD

Arch Neurol. 1985;42(3):263-271.

Abstract
• Of five patients with damage to the basal forebrain, four had lesions secondary to rupture of anterior cerebral or anterior communicating artery aneurysms, and one to the resection of an arteriovenous malformation. Computed tomographic scans and intraoperative reports confirmed damage to basal forebrain regions, which include septal nuclei, nucleus accumbens, substantia innominata, and related pathways. Behavioral disturbances featured a prominent amnesic syndrome and personality changes. The amnesia was distinguishable from that reported in patients HM and DRB and shared features with that seen in patients with Korsakoff's syndrome. We propose that the memory disorder can be explained by malfunctioning in the hippocampal system, secondary to damage in the basal forebrain structures with which it is strongly interconnected. The dysfunction might, in part, be caused by reduction of specific neurotransmitter innervation because the lesions are likely to damage cholinergic neurons and nearby catecholamine pathways within the basal forebrain.

Author Affiliations
From the Departments of Neurology (Drs A. Damasio, Graff-Radford, Eslinger, and H. Damasio) and Surgery (Dr Kassell), University of Iowa College of Medicine, Iowa City.

Footnotes
Accepted for publication June 23, 1984.

Reprint requests to Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242 (Dr A. Damasio).

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