Etiological mechanisms of post-stroke depression: a review

Abstract

Post-stroke depression (PSD) has become a prominent negative factor of stroke recovery. Different etiological mechanisms may be involved, and there forms two major hypotheses: biological hypothesis and psychological hypothesis. Biological hypothesis included four mechanisms: lesion location mechanism, neurotransmitters mechanism, inflammatory cytokines mechanism and gene polymorphism mechanism. As for lesion location, the specific location of a lesion (e.g., basal ganglia or left frontal lobe lesions) played an important role in the etiology of PSD. For neurotransmitters, decreased serotonin and norepinephrine in the brain were associated with PSD. In inflammatory cytokines, increased cytokines [including interleukin (IL) 1β, IL-18, tumor necrosis factor α] after stroke lead to depression. For gene polymorphism, there was significant association between serotonin transporter gene-linked promoter region short variant genotype and post-stroke major depression. Psychological hypothesis suggested that social and psychological stressors associated with stroke may be the primary cause of depression. Up to now, there is no definitive evidence to support or refute either a solely biological or solely psychosocial mechanism. It appears to be a kind of biopsychosocial multifactorial mental illness.     

以压迫阻滞针效定位的方法测试人体体表心包经的循行路线

以心功能和心电图为指标,以机械压迫阻滞针效为手段,比较压迫心包经穴位、经线上非穴位点和该穴点两侧对照点对针刺内关穴针效的影响,检测心包经在体表的循行轨迹。结果,压迫经上穴点针后各项指标变化微小,针效显著降低;压迫两侧对照点则对针效无明显影响。两者比较,差异非常显著。证明上肢屈侧确有一条与心包经一致的机能路线,并与心脏机能活动调节密切相关。