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N-Methyl-D-aspartate receptor antibody could be a cause of catatonic symptoms in psychiatric patients: case reports and methods for detection

Authors Tsutsui K, Kanbayashi T, Takaki M, Omori Y, Imai Y, Nishino S, Tanaka K, Shimizu T

Received 26 October 2016

Accepted for publication 9 December 2016

Published 8 February 2017 Volume 2017:13 Pages 339—345


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Taro Kishi

Ko Tsutsui,1 Takashi Kanbayashi,1,2 Manabu Takaki,3 Yuki Omori,1 Yumiko Imai,4 Seiji Nishino,5 Keiko Tanaka,6 Tetsuo Shimizu1,2

1Department of Neuropsychiatry, Akita University Graduate School of Medicine, Akita, 2International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Tsukuba, 3Department of Neuropsychiatry, Okayama University, Okayama, 4Biological Informatics and Experimental Therapeutics, Akita University Graduate School of Medicine, Akita, Japan; 5Sleep and Circadian Neurobiology Laboratory, Stanford University School of Medicine, Palo Alto, California, USA; 6Brain Research Institute, Niigata University, Niigata, Japan

Abstract: The symptoms of catatonia have been reported to be similar to the initial symptoms of anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis. Subsequently, this autoimmune limbic encephalitis has been noticed by many psychiatrists. For a differential diagnosis of catatonic state, it is important to detect anti-NMDAR encephalitis. This encephalitis is expected to be in remission by early detection and treatment. We should be more cautious about catatonic symptoms of schizophrenia. When a patient is being doubted with encephalitis, we should screen for anti-NMDAR antibodies in cerebrospinal fluid samples using a cell-based assay. We describe the methods of NMDAR antibody detection and the etiology of this encephalitis with case reports. Two representative cases with catatonia and non-catatonia (brief psychotic disorder) were reported. Schizophrenia is a general, heterogeneous, and complicated disorder, and its pathophysiology is unknown. There is an established evidence of NMDAR hypofunction, which is the functional disconnection of the central component; this is one of the most recognized models for schizophrenia. Furthermore, it is said that autoimmune mechanisms have been involved, at least in subgroups of schizophrenia patients. Further study of anti-NMDAR antibody and its related encephalitis would give essential clues for the research of schizophrenia, catatonia, and atypical psychosis.

Keywords: NMDA receptor, encephalitis, antibody, psychosis, catatonia

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