Bechter K
Abteilung Psychiatrie, Bezirkskrankenhaus Günzburg.
Fortschr Neurol Psychiatr. 2013 May;81(5):250-9. doi: 10.1055/s-0033-1335253. Epub 2013 Apr 29.
The mild encephalitis (ME) hypothesis describes a subgroup of severe psychiatric disorders, with a focus on a subgroup of schizophrenias, in which low-level neuroinflammation (LLNI) represents the core in pathogenesis. LLNI is increasingly recognised in experimental neuroimmunology and is in principle able to explain various types of psychopathology. Epidemiology and course of schizophrenia are well compatible with the ME hypothesis, indirectly indicating that the ME subgroup may be rather large. With the ME model connected is a set of three contributing factors: genes, environment (especially infectious agents) and the immune system. The type of psychopathology observed in the individual case may heavily depend upon other conditions, e. g. pre-existing vulnerabilities. The first large-scale epidemiological study in psychiatry identified two factors during lifetime, severe infectious diseases and autoimmune diseases, as risk factors. This and clinical findings more and more support the ME hypothesis, e. g., activated monocytes or proteome changes in blood and slight CSF pathologies in more than 60 % of therapy-resistant schizophrenia, or activated microglia and dysconnectivity in neuroimaging.
轻度脑炎（ME）假说描述了一组严重精神障碍，重点是精神分裂症的一个亚组，其中低水平神经炎症（LLNI）是发病机制的核心。LLNI在实验神经免疫学中越来越受到认可，原则上能够解释各种类型的精神病理学。精神分裂症的流行病学和病程与ME假说高度契合，间接表明ME亚组可能相当大。与ME模型相关的有三个促成因素：基因、环境（尤其是感染因子）和免疫系统。个体病例中观察到的精神病理学类型可能在很大程度上取决于其他条件，例如预先存在的易感性。精神病学领域的第一项大规模流行病学研究确定了一生中的两个因素，即严重传染病和自身免疫性疾病，为风险因素。这一点以及临床发现越来越支持ME假说，例如，超过60%的难治性精神分裂症患者血液中活化的单核细胞或蛋白质组变化以及轻微的脑脊液病变，或者神经影像学中活化的小胶质细胞和神经连接障碍。
