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1.
Neuroimmunology Reports ; 2 (no pagination), 2022.
Article in English | EMBASE | ID: covidwho-2285849

ABSTRACT

Introduction: Post-COVID-19 autoimmune encephalitis is a rare manifestation following COVID-19. Most cases have not demonstrated solid evidence regarding their pathogenesis. Some believe it to be an immune process. Case presentation: In this case report, we present a case of a young female who presented to our emergency department with visual, auditory, and olfactory hallucinations after successfully treating COVID-19 two weeks prior to this visit. On examination, her vital signs were stable, but she was agitated, distressed, and hallucinating. Neurological examinations were normal. Laboratory investigations, including autoimmune profiles, were all negative. Magnetic resonance imaging of the brain showed non-specific changes in the bilateral frontal area. Electroencephalography (EEG) showed lateralized rhythmic delta activity (LRDA) arising more from the right occipital lobes. Autoimmune psychosis was suspected due to psychosis, abnormal imaging, and abnormal EEG findings. She was given corticosteroids and antipsychotic medication. Her symptoms improved within ten days. On follow-up, she remained well without any return of psychosis. Conclusion(s): Possible autoimmune pediatric encephalitis following COVID-19 is a rare entity that has scarcely been reported. The majority of the cases were reported to have been related to stress following the infection. To establish the correct diagnosis, an extensive workup, including an autoimmune profile, lumbar puncture, magnetic resonance imaging, and electroencephalography, is recommended.Copyright © 2022 The Author(s)

2.
Biol Psychiatry ; 92(4): 261-274, 2022 08 15.
Article in English | MEDLINE | ID: covidwho-2122338

ABSTRACT

BACKGROUND: Autoimmune psychosis may be caused by well-characterized anti-neuronal autoantibodies, such as those against the NMDA receptor. However, the presence of additional anti-central nervous system (CNS) autoantibodies in these patients has not been systematically assessed. METHODS: Serum and cerebrospinal fluid (CSF) from patients with schizophreniform and affective syndromes were analyzed for immunoglobulin G anti-CNS autoantibodies using tissue-based assays with indirect immunofluorescence on unfixed murine brain tissue as part of an extended routine clinical practice. After an initial assessment of patients with red flags for autoimmune psychosis (n = 30), tissue-based testing was extended to a routine procedure (n = 89). RESULTS: Based on the findings from all 119 patients, anti-CNS immunoglobulin G autoantibodies against brain tissue were detected in 18% (n = 22) of patients (serum 9%, CSF 18%) following five principal patterns: 1) against vascular structures, most likely endothelial cells (serum 3%, CSF 8%); 2) against granule cells in the cerebellum and/or hippocampus (serum 4%, CSF 6%); 3) against myelinated fibers (serum 2%, CSF 2%); 4) against cerebellar Purkinje cells (serum 0%, CSF 2%); and 5) against astrocytes (serum 1%, CSF 1%). The patients with novel anti-CNS autoantibodies showed increased albumin quotients (p = .026) and white matter changes (p = .020) more frequently than those who tested negative for autoantibodies. CONCLUSIONS: The study demonstrates five novel autoantibody-binding patterns on brain tissue of patients with schizophreniform and affective syndromes. CSF yielded positive findings more frequently than serum analysis. The frequency and spectrum of autoantibodies in these patient groups may be broader than previously thought.


Subject(s)
Autoantibodies , Endothelial Cells , Animals , Brain , Granulocyte-Macrophage Colony-Stimulating Factor , Humans , Immunoglobulin G , Mice , Mood Disorders
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