Depression and Anxiety in the Epilepsies: from Bench to Bedside.
Depression and Anxiety in the Epilepsies: from Bench to Bedside.
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DOI：
10.1007/s11910-020-01065-z
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发表时间：
2020-07-14
影响因子：
5.6
通讯作者：
Krishnan, Vaishnav
中科院分区：
文献类型：
--
作者：
Krishnan, Vaishnav
关键词：
抑郁和焦虑在很大程度上有助于癫痫患者（PWE）的发作间期残疾。本文综述了目前的研究，揭示了并发症的机制。越来越多的流行病学数据暗示焦虑/抑郁和癫痫发作倾向的共同风险因素，但这些因素在很大程度上仍然难以捉摸，可能因癫痫类型而异。在PWE中，这些症状似乎与独特的遗传、神经病理和连接特征相关。颞叶癫痫已经得到了极大的重视，特别是在临床前研究的comorbidirectionality，候选人的神经生物学机制的双向性已经过测试，没有精神药理学的混淆。癫痫患者的抑郁和焦虑反映了广泛分布的边缘网络功能障碍，可能是癫痫发生的原因或后果。在难治性癫痫中，癫痫发作和/或某些抗惊厥药物可能会扭曲中枢情绪稳态机制，从而永久提高癫痫发作的风险。开发未来安全有效的抗惊厥-抗抑郁联合治疗将需要详细了解多效性增加癫痫发作风险和负面改变情绪的解剖和分子节点。
Depression and anxiety substantially contribute to interictal disability in patients with epilepsy (PWE). This review summarizes current studies that shed light on mechanisms of comorbidity. Mounting epidemiological data implicate shared risk factors for anxiety/depression and seizure propensity, but these remain largely elusive and probably vary by epilepsy type. Within PWE, these symptoms appear to be associated with unique genetic, neuropathological, and connectivity profiles. Temporal lobe epilepsy has received enormous emphasis particularly in preclinical studies of comorbidity, where candidate neurobiological mechanisms underlying bidirectionality have been tested without psychopharmacological confounds. Depression and anxiety in epilepsy reflect dysfunction within broadly distributed limbic networks that may be the cause or consequence of epileptogenesis. In refractory epilepsy, seizures and/or certain anticonvulsants may distort central emotional homeostatic mechanisms that perpetually raise seizure risk. Developing future safe and effective combined anticonvulsant-antidepressant treatments will require a detailed understanding of anatomical and molecular nodes that pleiotropically enhance seizure risk and negatively alter emotionality.
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