Electroconvulsive therapy can improve psychotic symptoms in anti‐NMDA‐receptor encephalitis

Abstract

ANTI-N-METHYL-d-ASPARTATE (NMDA) RECEPTOR encephalitis has recently been described as paraneoplastic encephalitis often associated with ovarian teratoma.1 This form of encephalitis is important to psychiatrists because of the possibility of misdiagnosis as schizophrenia. Tumor removal and immunotherapy are usually recommended for anti-NMDA-receptor encephalitis. Reports on the effectiveness of electroconvulsive therapy (ECT), however, are limited.2, 3 We present here a case of anti-NMDA-receptor encephalitis accompanied by schizophrenia-like psychosis with catatonia. To our knowledge, this is the first report on the successful treatment of this encephalitis with ECT, unaccompanied by immunotherapy or tumor removal. After recuperating from influenza, an 18-year-old Japanese man felt fatigue and vertigo. Five days later, he developed acute-onset behavioral abnormalities and personality change. Another 6 days later, he developed delusions and committed violence, and was admitted to hospital. At the first visit, he was found to be in a confusional state with catalepsy, stereotypy, convulsions, and involuntary movements of the tongue. Initial electroencephalography, brain magnetic resonance imaging, and cerebrospinal fluid (CSF) were normal. Full body computed tomography (CT) showed no malignant neoplasm. A CSF sample for anti-NMDA antibody testing was obtained at the time of admission. The first attempt to treat him for catatonic schizophrenia with antipsychotics, lorazepam, and sodium valproate only reduced his confusional states. Therefore, ECT was carried out. ECT improved catatonia and psychosis, and confusional states gradually. After 13 ECT sessions and use of antipsychotics, the patient made a full recovery. He did not show any central hypoventilation in the course of the disease. After discharge we were informed that the anti-NMDA antibody in his CSF was positive. At 1-year follow-up the patient had fully recovered, and required no medication. Without information on anti-NMDA-receptor antibody, we would have misdiagnosed the patient as having schizophrenia and passed over the encephalitis. Because treatment for anti-NMDA-receptor encephalitis differs from that of schizophrenia, the differential diagnosis is crucial. Pharmaceutical therapy for schizophrenia was not effective in the present case, but ECT ameliorated the psychotic symptoms. The present finding suggests that ECT is an effective treatment option for catatonia and psychosis in anti-NMDA-receptor encephalitis. The current literature shows only a limited effect of ECT for anti-NMDA-receptor encephalitis: one patient made a full recovery after ECT but only in conjunction with methylprednisolone pulse therapy,2 while another patient's symptoms were partially improved with ECT, but full recovery was attained only after tumor removal.3 We do not fully understand the mechanism of ECT in anti-NMDA-receptor encephalitis. In the present case, it is possible that ECT temporarily attenuated the symptoms while encephalitis was improved in the natural course.4 Recent studies, however, have shown that ECT modulates the glutamatergic synapses in animal models.5 Thus, studying anti-NMDA-receptor encephalitis may lead to a better understanding of the function of NMDA receptors and ECT. Further studies are needed to confirm the present observation.