压力会使诸如抑郁等精神疾病恶化，还可能增加痴呆风险，这提示压力导致的精神疾病发展和痴呆损害存在着共同的机制。因此，加拿大学者们对焦虑是否损害大脑进行了评估，并对压力和神经精神疾病之间相关联的潜在机制进行了识别。

近期的研究显示，焦虑症与恐惧神经的改变有关，以致杏仁核“自下而上”由前额皮质(PFC)和海马调控过程对威胁的反应被夸大，同时这些过程的调控受损。 同样，长期压力暴露通过增强杏仁核功能而改变恐惧神经，进而导致PFC和海马结构的退化，从而抑制PFC/海马对压力反应的控制。

药物(如抗抑郁药物)和非药物干预(认知行为治疗、运动)可能部分逆转压力导致的大脑损害。情绪稳定剂、抗抑郁药治疗和体育锻炼均可增加海马神经形成。杏仁体-PFC功能连接通路可在使用抗抑郁药治疗抑郁后正常化。治疗老年人广泛性焦虑症的选择性5-羟色胺再摄取抑制剂西酞普兰可增加d1PFC和 v1PFC之间的功能连接，同时增加涉及注意力的顶叶区域。

此外，焦虑症的认知行为治疗可减少杏仁核反应性，增加PFC区域活性。对广泛性焦虑症患者进行正念训练也可改变杏仁核-PFC连接，甚至对儿童进行简单的认知指导不仅可以减少焦虑的发生，还可以减少杏仁核反应性。

总之，长期压力可增加罹患严重精神疾病(如抑郁)和痴呆风险。其潜在机制为，长期压力增强杏仁核活性，但压力也会引起海马神经神经受损和PFC结构退化， 进而导致情绪调节和认知受损。焦虑/压力可损伤大脑，但这种损伤可能在进行药物和非药物干预下被逆转。抗焦虑干预是否可减少罹患神经精神疾病风险，尚需纵 向研究来验证。

参考文献：Linda Mah,et al. Geriatric psychiatry .Volume 29 Number 1 January 2016

Can anxiety damage the brain?
Linda Maha,b, Claudia Szabuniewiczb, and Alexandra J. Fioccoc
Purpose of review Stress exacerbates mental illnesses such as depression but also appears to increase risk of dementia,suggesting a common mechanism for development of stress-induced affective and cognitive impairment. The purpose of this review is to address the question of whether anxiety ‘damages’ the brain, and to identify potential mechanisms for the link between stress and neuropsychiatric illness.
Recent findings Anxiety disorders are associated with alterations in fear neurocircuitry such that ‘bottom-up’ processes in the amygdala which respond to threat are exaggerated, and regulation of these processes by the
prefrontal cortex (PFC) and hippocampus is impaired. Chronic stress exposure similarly alters fear
neurocircuitry by enhancing amygdalar functioning while causing structural degeneration in the PFC and hippocampus thereby inhibiting PFC/hippocampus control over the stress response. Pharmacological (e.g.,antidepressant medications) and nonpharmacological interventions (cognitive-behavioral therapy, exercise)may reverse stress-induced damage in the brain.
Summary
Pathological anxiety and chronic stress lead to structural degeneration and impaired functioning of the hippocampus and the PFC, which may account for the increased risk of developing neuropsychiatric disorders, including depression and dementia. Longitudinal studies are needed to determine whether reversal of stress-induced brain changes by interventions such as cognitive-behavioral therapy can reduce risk of neuropsychiatric illness.