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卒中后抑郁是脑血管病后的常见并发症,严重影响了患者的生活,延长了康复治愈的时间,增加了致残率和致死率,加重了患者和家属的疾病负担。其发病机制尚未完全明了,治疗上主要以抗抑郁的精神药物为主。但是目前常用的抗抑郁药绝大多数以增加5-羟色胺和去甲肾上腺素的突触利用率为目标。这些抗抑郁药的效果不超过60%～65%,并需要2～4周才能发挥其疗效,近年的研究发现“谷氨酸及其受体”也参与抑郁症的发病机制。本文就卒中后抑郁与谷氨酸及其受体的关系方面的研究进行综述。
Post-stroke depression is a common complication after cerebrovascular disease, seriously affecting the patient’s life, prolonging the healing time, increasing the morbidity and mortality, and increasing the disease burden on patients and their families. The pathogenesis is not yet fully understood, the main treatment of antidepressants mainly psychotropic substances. However, most commonly used antidepressants nowadays aim at increasing synaptic utilization of serotonin and norepinephrine. The efficacy of these antidepressants does not exceed 60% ~ 65%, and take 2 ~ 4 weeks to play its efficacy, recent studies have found that “glutamate and its receptor ” is also involved in the pathogenesis of depression. This article reviews the research on the relationship between post-stroke depression and glutamate and its receptors.