Johnson Evan Thomas, Eraly Sara George, Aandi Subramaniyam Bhaskaran, Muliyala Krishna Prasad, Moirangthem Sydney, Reddi Venkata Senthil Kumar, Jain Sanjeev
Department of Psychiatry, National Institute of Mental Health and Neuro Sciences, Bangalore, India.
Brain Behav Immun Health. 2022 Mar 10;22:100440. doi: 10.1016/j.bbih.2022.100440. eCollection 2022 Jul.
In recent years the neurobiological underpinnings of catatonia have been an emerging area of interest. Catatonia is frequently encountered in mood disorders, neurological disorders and systemic illnesses. Furthermore, the manifestation of catatonia in autoimmune disorders such as NMDA receptor antibody encephalitis and thyroiditis reinforces its neuropsychiatric nature. Irrespective of cause benzodiazepines and electroconvulsive therapy remain the standard treatments for catatonia, although a proportion fail to respond to the same. This report describes three women with pre-existing bipolar disorder presenting in catatonia. Interestingly in all three, while benzodiazepines and electroconvulsive therapy failed, a dramatic resolution of catatonia with corticosteroids was noted following the detection of Hashimoto's thyroiditis. Hashimoto's encephalopathy presenting as catatonia has been reported, but our patients' profile differed in having had an a priory diagnosis of bipolar disorder. Given that both catatonia and thyroid dysfunction are frequently encountered in bipolar disorder, Hashimoto's encephalopathy as a potential cause for this concurrent manifestation in bipolar disorder may be overlooked. Therefore, it is essential to suspect Hashimoto's encephalopathy when catatonia manifests in bipolar disorder. A timely evaluation would be prudent as they may fail to respond to standard treatments for catatonia but respond remarkably to corticosteroids, saving much time and angst. Recent evidence implicates immune system dysfunction, with neuroinflammation and peripheral immune dysregulation contributing to the pathophysiology of bipolar disorder as well as catatonia. Findings from this study reaffirm the role of immune system dysfunction common to the etiopathogenesis of all these disorders, highlighting the complex interplay between catatonia, thyroiditis and bipolar disorder.
近年来，紧张症的神经生物学基础一直是一个新兴的研究热点。紧张症在情绪障碍、神经系统疾病和全身性疾病中经常出现。此外，紧张症在自身免疫性疾病如NMDA受体抗体脑炎和甲状腺炎中的表现强化了其神经精神性质。无论病因如何，苯二氮䓬类药物和电休克治疗仍然是紧张症的标准治疗方法，尽管有一部分患者对此无反应。本报告描述了三名患有双相情感障碍且出现紧张症的女性。有趣的是，在这三名患者中，苯二氮䓬类药物和电休克治疗均无效，但在检测到桥本甲状腺炎后，使用皮质类固醇后紧张症戏剧性地得到缓解。已有报道称桥本脑病可表现为紧张症，但我们患者的情况有所不同，他们先前已被诊断为双相情感障碍。鉴于紧张症和甲状腺功能障碍在双相情感障碍中都很常见，桥本脑病作为双相情感障碍中这种并发表现的潜在原因可能会被忽视。因此，当双相情感障碍出现紧张症时，怀疑桥本脑病至关重要。及时评估是明智的，因为他们可能对紧张症的标准治疗无反应，但对皮质类固醇有显著反应，从而节省大量时间和减轻焦虑。最近的证据表明免疫系统功能障碍，神经炎症和外周免疫失调参与了双相情感障碍以及紧张症的病理生理过程。本研究结果再次证实了免疫系统功能障碍在所有这些疾病病因学中的作用，突出了紧张症、甲状腺炎和双相情感障碍之间复杂的相互作用。
