Acute psychosis due to non-paraneoplastic anti-NMDA-receptor encephalitis in a teenage girl: Case report

Anti‐N‐methyl‐d‐aspartate receptor (NMDAR) encephalitis is a disease occurring when antibodies produced by the body's own immune system attack NMDA‐type glutamate receptors in the brain. Most anti‐NMDAR encephalitis cases are associated with paraneoplastic syndrome. We analyze the case of a 15‐...

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Veröffentlicht in:PsyCh journal 2015-12, Vol.4 (4), p.226-230
Hauptverfasser: Kramina, Sandra, Kevere, Laura, Bezborodovs, Nikita, Purvina, Santa, Rozentals, Guntis, Strautmanis, Jurgis, Viksna, Zane
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Sprache:eng
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Zusammenfassung:Anti‐N‐methyl‐d‐aspartate receptor (NMDAR) encephalitis is a disease occurring when antibodies produced by the body's own immune system attack NMDA‐type glutamate receptors in the brain. Most anti‐NMDAR encephalitis cases are associated with paraneoplastic syndrome. We analyze the case of a 15‐year‐old girl who was hospitalized in a child psychiatry clinic in Riga, Latvia, with de novo acute polymorphic psychotic disorder gradually progressing to a catatonic state. The patient received antipsychotic and electroconvulsive therapy with no beneficial effect. The council of doctors discussed differential diagnoses of schizophrenia‐induced catatonia and the autoimmune limbic encephalitis‐induced catatonic condition. When the diagnosis of anti‐NMDAR autoimmune encephalitis was finally confirmed by repeated immunological assays (specific immunoglobulin [Ig] G and IgM in her blood serum and cerebrospinal fluid), and a paraneoplastic process was ruled out, she was started on immunomodulating therapy (methylprednisolone, Ig, plasmapheresis, rituximab), which changed the course of her disease. On immunomodulating treatment, her physical and mental health have gradually improved to almost complete reconvalescence. Psychiatrists should consider anti‐NMDAR encephalitis as a differential diagnosis in first‐episode psychosis patients presenting with disorientation, disturbed consciousness, pronounced cognitive deficits, movement disorder, dysautonomia, or rapid deterioration, and test for specific IgG NR1 autoantibodies, even if there are no specific findings on routine neuroimaging, electroencephalography (EEG), or cerebrospinal fluid tests.
ISSN:2046-0252
2046-0260
DOI:10.1002/pchj.121