Department Neurology and Institute of Health Science, Gyeongsang National University School of Medicine, Jinju, Korea.
Department of Neurology, School of Medicine, Kyungpook National University, Daegu, Korea.
J Clin Neurol. 2014 Jul;10(3):175-88. doi: 10.3988/jcn.2014.10.3.175. Epub 2014 Jul 3.
Many recent epidemiological studies have found the prevalence of depression and anxiety to be higher in people with epilepsy (PWE) than in people without epilepsy. Furthermore, people with depression or anxiety have been more likely to suffer from epilepsy than those without depression or anxiety. Almost one-third of PWE suffer from depression and anxiety, which is similar to the prevalence of drug-refractory epilepsy. Various brain areas, including the frontal, temporal, and limbic regions, are associated with the biological pathogenesis of depression in PWE. It has been suggested that structural abnormalities, monoamine pathways, cerebral glucose metabolism, the hypothalamic-pituitary-adrenal axis, and interleukin-1b are associated with the pathogenesis of depression in PWE. The amygdala and the hippocampus are important anatomical structures related to anxiety, and γ-aminobutyric acid and serotonin are associated with its pathogenesis. Depression and anxiety may lead to suicidal ideation or attempts and feelings of stigmatization. These experiences are also likely to increase the adverse effects associated with antiepileptic drugs and have been related to poor responses to pharmacological and surgical treatments. Ultimately, the quality of life is likely to be worse in PWE with depression and anxiety than in PWE without these disorders, which makes the early detection and appropriate management of depression and anxiety in PWE indispensable. Simple screening instruments may be helpful for in this regard, particularly in busy epilepsy clinics. Although both medical and psychobehavioral therapies may ameliorate these conditions, randomized controlled trials are needed to confirm that.
许多最近的流行病学研究发现,癫痫患者(PWE)中抑郁和焦虑的患病率高于非癫痫患者。此外,患有抑郁或焦虑症的人比没有抑郁或焦虑症的人更容易患癫痫。几乎三分之一的 PWE 患有抑郁和焦虑,这与耐药性癫痫的患病率相似。包括额叶、颞叶和边缘区域在内的各种大脑区域与 PWE 中抑郁的生物学发病机制有关。有人提出,结构异常、单胺途径、脑葡萄糖代谢、下丘脑-垂体-肾上腺轴和白细胞介素-1b 与 PWE 中抑郁的发病机制有关。杏仁核和海马是与焦虑相关的重要解剖结构,γ-氨基丁酸和 5-羟色胺与焦虑的发病机制有关。抑郁和焦虑可能导致自杀意念或尝试以及被污名化的感觉。这些经历也可能增加与抗癫痫药物相关的不良反应,并与对药物和手术治疗的反应不佳有关。最终,患有抑郁和焦虑症的 PWE 的生活质量可能比没有这些疾病的 PWE 更差,这使得早期发现和适当管理 PWE 中的抑郁和焦虑症必不可少。简单的筛查工具可能对此有所帮助,特别是在繁忙的癫痫诊所。尽管医学和心理行为疗法都可能改善这些情况,但仍需要随机对照试验来证实这一点。