Campbell Family Mental Health Research Institute, CAMH, Toronto, ON, Canada.
Department of Psychiatry, University of Toronto, Toronto, ON, Canada.
Curr Top Behav Neurosci. 2021;49:31-53. doi: 10.1007/7854_2020_210.
Initial reports supporting the possibility of inflammation in the brain in obsessive-compulsive disorder (OCD) evolved from the models of Sydenham's Chorea, and Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcus (PANDAS), which implicated excessive autoimmune responses following exposure to group A B-hemolytic streptococcal infections. Subsequently, this model was expanded to Pediatric Autoimmune Neuropsychiatric Syndrome (PANS) which applied the same concept but included other infections. A critical shortcoming of this model was that it was attributable to a small minority of OCD cases. The relationship between inflammation and OCD was more broadly demonstrated through translocator protein (TSPO) positron emission tomography imaging, a method that detects gliosis, an important component of brain inflammation, in neuropsychiatric diseases, including morphological activation and proliferation of microglia and to some extent astroglia. This method identified greater TSPO binding in the cortico-striatal-thalamo-cortical circuit in OCD, providing a direct brain measure of an important component of inflammation. To identify OCD cases with prominent elevations in TSPO binding in clinical research settings with lower cost peripheral markers, a promising approach is to apply blood serum biomarkers of inflammatory molecules produced by activated microglia and astroglia (gliosis). Such measures may aid stratification in future clinical trials. Several inflammatory-modifying interventions, including celecoxib, minocycline, and n-acetylcysteine, have been tested as treatments in randomized double-blind placebo controlled clinical trials and there is a tendency toward positive results, although these medications are not optimized for brain penetration and sample sizes for most trials were small. Future clinical trials of medications that target gliosis in OCD should apply larger sample sizes, ideally incorporating stratification approaches to enrich samples for the presence of gliosis.
最初有研究报告表明,强迫症(OCD)患者的大脑可能存在炎症,这些报告源于以下两种模型:其一为Sydenham 舞蹈病,其二为与链球菌相关的小儿自身免疫性神经精神障碍(PANDAS)。这两种模型都暗示了在接触 A 组乙型溶血性链球菌感染后,会出现过度的自身免疫反应。随后,该模型被扩展为小儿自身免疫性神经精神综合征(PANS),该模型应用了相同的概念,但纳入了其他感染。该模型的一个关键缺陷是,它仅适用于 OCD 患者中的一小部分。
通过正电子发射断层扫描(PET)成像技术检测神经精神疾病中的神经胶质增生(大脑炎症的一个重要组成部分),如小胶质细胞形态激活和增殖,在一定程度上也包括星形胶质细胞的增殖,来更广泛地证明炎症与 OCD 之间的关系。这种方法确定了 OCD 患者皮质-纹状体-丘脑-皮质回路中 TSPO 结合的增加,为炎症的一个重要组成部分提供了直接的大脑测量方法。为了在具有较低成本外周标志物的临床研究环境中识别 OCD 患者中 TSPO 结合的明显升高,一种很有前途的方法是应用由激活的小胶质细胞和星形胶质细胞(神经胶质增生)产生的炎症分子的血清生物标志物。这些措施可能有助于未来临床试验的分层。
几项炎症调节干预措施,包括塞来昔布、米诺环素和 N-乙酰半胱氨酸,已在随机双盲安慰剂对照临床试验中作为治疗方法进行了测试,结果有积极的趋势,尽管这些药物的脑穿透性并不优化,并且大多数试验的样本量较小。未来针对 OCD 中神经胶质增生的药物临床试验应采用更大的样本量,理想情况下,采用分层方法来丰富存在神经胶质增生的样本。