AMNESIA FOLLOWING BASAL FOREBRAIN LESIONS
AMNESIA FOLLOWING BASAL FOREBRAIN LESIONS
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DOI：
10.1001/archneur.1985.04060030081013
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发表时间：
1985-01-01
影响因子：
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通讯作者：
KASSELL, N
中科院分区：
文献类型：
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作者：
DAMASIO, AR;GRAFFRADFORD, NR;KASSELL, N
5例基底前脑损伤患者中，4例继发于大脑前动脉瘤或前交通动脉瘤破裂，1例继发于动静脉畸形切除。计算机断层扫描和术中报告证实了基底前脑区域的损伤，包括隔核、伏隔核、无名质和相关通路。行为障碍表现为明显的健忘症和人格改变。这种健忘症与报告的HM和DRB患者的健忘症不同，与Korsakoff综合征患者的健忘症有共同的特征。记忆障碍可以用海马体系统的故障来解释，它继发于与之紧密相连的基底前脑结构的损伤。这种功能障碍部分可能是由于特异性神经递质神经支配的减少引起的，因为病变可能损害基底前脑内的胆碱能神经元和附近的儿茶酚胺通路。
Of 5 patients with damage to the basal forebrain, 4 had lesions secondary to rupture of anterior cerebral or anterior communicating artery aneurysms and 1 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. 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.