神经系统疾病伴发抑郁焦虑障碍的诊断治疗专家共识__培训课件.ppt

* Key Point Antidepressants may affect neuronal survival and growth Background Neuronal atrophy and cell death are thought to occur as a result of hyperactivity of the stress–response system in depressed patients, which increases adrenal glucocorticoid release and decreases BDNF levels, a factor critical for the survival and function of neurons in the adult brain1 The damaging effects of prolonged stress/depressive symptoms could contribute to the selective loss of volume of the hippocampus (a structure essential to learning and memory, contextual fear conditioning, and neuroendocrine regulation) observed in patients with depression. These morphologic changes have been shown to persist long after the depressive symptoms have resolved2 In theory, antidepressants that affect serotonin and/or norepinephrine activity may affect neuronal survival and growth by decreasing glucocorticoid levels and increasing BDNF levels1 References 1. Duman RS, et al. Biol Psychiatry. 2000;48:732-739. 2. Sapolsky RM. Arch Gen Psychiatry. 2000;57:925-935. * Stress is a well-known factor in inducing neural sensitization. This phenomenon been suggested as one mechanism for the common overlap of some psychiatric disorders with each other and the observed overlap with certain medical conditions with 焦虑 disorders. Sensitivity to somatic sx in anxious individuals has been hypothesized to be driven via a process referred to in the neurological literature as “kindling” (Weiss and Post,1998; Antelman, 1988), as is cross-sensitization to uncomfortable “psychic” sensations such as fear and 焦虑 and other stress-related conditions. Emerging evidence suggests that uncontrolled 焦虑 is not only exacerbated by stress, but also represents the equivalent of chronic stress ( McEwen, 2003) and in this way may contribute to the cumulative adverse effects of stress. Dysregulation of the hypothalamic-pituitary-adrenal ( HPA) axis is observed in chronic pathological stress conditions and , and severe forms of