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抗 N-甲基-D-天冬氨酸受体脑炎缓解后出现精神分裂症。

Schizophrenia after remission of anti-NMDA receptor encephalitis.

机构信息

Department of Neuropsychiatry, Wakayama Medical University, 811-1 Kimiidera, Wakayama, Wakayama 641-8510, Japan.

Department of Neuropsychiatry, Wakayama Medical University, 811-1 Kimiidera, Wakayama, Wakayama 641-8510, Japan; Department of Psychiatry, Hidaka Hospital, 116-2 Sono, Gobo, Wakayama 644-0002, Japan.

出版信息

Asian J Psychiatr. 2022 Apr;70:103027. doi: 10.1016/j.ajp.2022.103027. Epub 2022 Feb 12.

DOI:10.1016/j.ajp.2022.103027
PMID:35180463
Abstract

N-methyl-D-aspartate receptor (NMDAR) dysfunction is an attractive hypothesis regarding the etiology of schizophrenia. We present the unprecedented case of a woman diagnosed with schizophrenia without anti-NMDAR antibodies after history of NMDAR encephalitis. A first episode of psychosis was antibody-positive and was improved with steroid and immunoglobulin treatment. Second and third episodes were antibody-negative, each about three months postpartum (different pregnancies) and were improved with antipsychotics. Without NMDAR encephalitis-related findings, we diagnosed schizophrenia. After anti-NMDAR encephalitis, NMDAR dysfunction may decrease the threshold for the onset of psychosis. This case provides insight into NMDAR dysfunction on etiology of schizophrenia.

摘要

N-甲基-D-天冬氨酸受体(NMDAR)功能障碍是精神分裂症发病机制的一个有吸引力的假说。我们报告了首例在抗 NMDAR 抗体阴性的情况下被诊断为精神分裂症的女性病例,该患者有 NMDAR 脑炎病史。首次出现精神病症状时,抗体呈阳性,经类固醇和免疫球蛋白治疗后得到改善。第二次和第三次发作时,抗体呈阴性,均在产后约三个月(不同妊娠),抗精神病药物治疗后有所改善。由于没有发现与 NMDAR 脑炎相关的表现,我们诊断为精神分裂症。在抗 NMDAR 脑炎之后,NMDAR 功能障碍可能会降低精神病发作的阈值。该病例为 NMDAR 功能障碍在精神分裂症发病机制中的作用提供了新的见解。

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Schizophrenia after remission of anti-NMDA receptor encephalitis.抗 N-甲基-D-天冬氨酸受体脑炎缓解后出现精神分裂症。
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引用本文的文献

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BMC Psychiatry. 2024 Apr 2;24(1):248. doi: 10.1186/s12888-024-05689-0.
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NMDAR autoantibodies in psychiatric disease - An immunopsychiatric continuum and potential predisposition for disease pathogenesis.精神疾病中的N-甲基-D-天冬氨酸受体自身抗体——一种免疫精神病学连续体及疾病发病机制的潜在易感性
J Transl Autoimmun. 2022 Sep 21;5:100165. doi: 10.1016/j.jtauto.2022.100165. eCollection 2022.