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脑损伤后去抑制的机制。

Mechanism of disinhibition after brain lesions.

作者信息

Starkstein S E, Robinson R G

机构信息

Department of Neuropsychiatry, Rául Carrea Institute of Neurological Research, Buenos Aires, Argentina.

出版信息

J Nerv Ment Dis. 1997 Feb;185(2):108-14. doi: 10.1097/00005053-199702000-00007.

Abstract

Disinhibition syndromes, ranging from mildly inappropriate social behavior to full blown mania, may result from lesions to specific brain areas. Several studies in patients with closed head injuries, brain tumors, stroke lesions, and focal epilepsy have demonstrated a significant association between disinhibition syndromes and dysfunction of orbitofrontal and basotemporal cortices of the right hemisphere. Based on the phylogenetic origin of these cortical areas and their main connections with dorsal regions related to visuospatial functions, somatosensation, and spatial memory, the orbitofrontal and basotemporal cortices may selectively inhibit or release motor, instinctive, affective, and intellectual behaviors elaborated in the dorsal cortex. Thus, dysfunction of these heteromodal ventral brain areas may result in disinhibited behaviors.

摘要

去抑制综合征,从轻度不适当的社会行为到全面发作的躁狂症,可能由特定脑区的损伤引起。对闭合性颅脑损伤、脑肿瘤、中风损伤和局灶性癫痫患者的多项研究表明,去抑制综合征与右半球眶额皮质和基底颞叶皮质功能障碍之间存在显著关联。基于这些皮质区域的系统发生起源及其与与视觉空间功能、躯体感觉和空间记忆相关的背侧区域的主要连接,眶额皮质和基底颞叶皮质可能选择性地抑制或释放背侧皮质中产生的运动、本能、情感和智力行为。因此,这些异模态腹侧脑区的功能障碍可能导致去抑制行为。

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