卒中后抑郁神经生物学发病机制研究进展

Research progress on post-stroke depression neurobiological mechanisms

卒中后抑郁发病机制复杂,涉及生物学、心理学及社会学等多个方面,具有发病率、漏诊率高,治愈率低等特点.由脑卒中引起的神经内分泌功能紊乱,重要脑区功能缺失及神经递质缺乏均可引发抑郁情绪,而卒中后炎症反应导致的脑损害亦可加重病情,导致卒中后抑郁的产生.近年来,科学提供的便利使卒中后抑郁的遗传易感性得到深入研究,敏感基因的发现为卒中后抑郁预测提供了可能性,成为目前研究热点.本文对其神经递质、神经内分泌、神经解剖等神经生物学方面发病机制的相关研究进行了回顾,旨在为提高对卒中后抑郁的认识、诊断及治疗提供帮助.

The pathogenesis of poststroke depression is complex, is involved multiple aspects such as biology, psychology, sociology and so on, and is characterized by high disease incidence and rate of missed diagnosis and low cure rate. Neuroendocrine dysfunction due to stroke, afunction of important encephalic region and neurotransmitters＇ deficiency all can cause depressive emotion, brain damage caused by poststroke inflammatory reaction can aggratate patient＇s condition and lead to the generation of poststroke depression. In recent years the genetic susceptibility to poststroke depression has been deeply studied on the basis of the convenience provided by science, the discovery of sensitive gene provide the possibility for poststroke depression prediction and become research hotspot. In this paper pathogeneses involving neurobiological aspects such as neurotransmitter, neuroendocrine and neuroanatomy were reviewed in order to improve the understanding of poststroke depression and provide help for diagnosis and treatment.