Damasio A R, Graff-Radford N R, Eslinger P J, Damasio H, Kassell N
Arch Neurol. 1985 Mar;42(3):263-71. doi: 10.1001/archneur.1985.04060030081013.
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.
在五名基底前脑受损的患者中,四名患者的损伤继发于大脑前动脉或前交通动脉瘤破裂,一名患者的损伤继发于动静脉畸形切除术。计算机断层扫描和术中报告证实了基底前脑区域的损伤,这些区域包括隔核、伏隔核、无名质和相关通路。行为障碍的特征是明显的遗忘综合征和人格改变。这种遗忘症与HM和DRB患者所报告的不同,与科尔萨科夫综合征患者的遗忘症有共同特征。我们认为,记忆障碍可以用海马系统功能失调来解释,这是基底前脑结构受损的继发结果,而海马系统与基底前脑结构紧密相连。这种功能障碍可能部分是由特定神经递质支配减少引起的,因为这些损伤可能会损害基底前脑内的胆碱能神经元和附近的儿茶酚胺通路。