TY - JOUR
T1 - Amnesia Following Basal Forebrain Lesions
AU - Damasio, Antonio R.
AU - Graff-Radford, Neill R.
AU - Eslinger, Paul J.
AU - Damasio, Hanna
AU - Kassell, Neal
PY - 1985/3
Y1 - 1985/3
N2 - 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.
AB - 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.
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U2 - 10.1001/archneur.1985.04060030081013
DO - 10.1001/archneur.1985.04060030081013
M3 - Article
C2 - 3977657
AN - SCOPUS:0021909686
SN - 0003-9942
VL - 42
SP - 263
EP - 271
JO - Archives of Neurology
JF - Archives of Neurology
IS - 3
ER -