Institute of Clinical Neurobiology, Alberichgasse 5/13, Vienna, A-1150, Austria.
J Neural Transm (Vienna). 2024 Aug;131(8):847-869. doi: 10.1007/s00702-024-02792-0. Epub 2024 Jun 13.
Depression and anxiety are the most frequent neuropsychiatric symptoms of multiple sclerosis (MS), an autoimmune-mediated demyelinating neurodegenerative disease. Their prevalence is 25-65% and 20-54%, respectively, often associated with chronic fatigue and cognitive impairment, but usually not correlated with motor and other deficits, suggesting different pathophysiological mechanisms. Both disorders often arise before MS diagnosis, lead to faster disability and impair the quality of life. Risk factors are (young) age, genetic and family history burden. While no specific neuropathological data for depression (and anxiety) in MS are available, modern neuroimaging studies showed bilateral fronto-temporal, subcortical and limbic atrophies, microstructural white matter lesions and disruption of frontoparietal, limbic and neuroendocrine networks. The pathogenesis of both depression and anxiety in MS is related to shared mechanisms including oxidative stress, mitochondrial dysfunction, neuroinflammation and neuroendocrine mechanisms inducing complex functional and structural brain lesions, but they are also influenced by social and other factors. Unfortunately, MS patients with anxiety, major depression or suicidal thoughts are often underassessed and undertreated. Current treatment, in addition to antidepressant therapy include transcranial magnetic stimulation, cognitive, relaxation, dietary and other healthcare measures that must be individualized. The present state-of- the-art review is based on systematic analysis of PubMed, Google Scholar and Cochrane Library until May 2024, with focus on the prevalence, clinical manifestation, neuroimaging data, immune mechanisms and treatment options. Depression and anxiety in MS, like in many other neuroimmune disorders, are related, among others, to multi-regional patterns of cerebral disturbances and complex pathogenic mechanisms that deserve further elucidation as a basis for early diagnosis and adequate management to improve the quality of life in this disabling disease.
抑郁和焦虑是多发性硬化症（MS）最常见的神经精神症状，这是一种自身免疫介导的脱髓鞘神经退行性疾病。其患病率分别为 25-65%和 20-54%，常与慢性疲劳和认知障碍相关，但通常与运动和其他缺陷无关，提示存在不同的病理生理机制。这两种疾病通常在 MS 诊断之前出现，导致更快的残疾并损害生活质量。危险因素包括（年轻）年龄、遗传和家族病史负担。虽然目前尚无 MS 中抑郁（和焦虑）的特定神经病理学数据，但现代神经影像学研究显示双侧额颞叶、皮质下和边缘萎缩、白质微观结构病变以及额顶叶、边缘和神经内分泌网络中断。MS 中抑郁和焦虑的发病机制与共享机制有关，包括氧化应激、线粒体功能障碍、神经炎症和神经内分泌机制导致复杂的功能性和结构性脑损伤，但也受到社会和其他因素的影响。不幸的是，患有焦虑、重度抑郁症或自杀念头的 MS 患者通常评估不足和治疗不足。除了抗抑郁治疗外，目前的治疗方法还包括经颅磁刺激、认知、放松、饮食和其他医疗保健措施，这些措施必须个体化。本综述基于 2024 年 5 月之前对 PubMed、Google Scholar 和 Cochrane Library 的系统分析，重点关注患病率、临床表现、神经影像学数据、免疫机制和治疗选择。MS 中的抑郁和焦虑，与许多其他神经免疫疾病一样，与大脑多个区域的紊乱模式和复杂的发病机制有关，这些机制需要进一步阐明，作为早期诊断和适当管理的基础，以改善这种致残疾病的生活质量。
