PCN reports : psychiatry and clinical neurosciences · 2026
Pre-corticosteroid delusional psychosis and olanzapine-responsive behavioral dyscontrol in autoimmune glial fibrillary acidic protein astrocytopathy: A case report.
СтатьяНазвание и аннотация: Перевод в очереди
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Sugisaki Tomomi, Sato Yoshiteru, Fujita Hiroaki, Kawamata Yasushi, Sugawara Norio, Suzuki Keisuke, Yasui-Furukori Norio
Аннотация
BACKGROUND: Autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy is an immunotherapy-responsive inflammatory central nervous system disorder. Psychiatric manifestations include delirium, cognitive or behavioral change, apathy, depressive symptoms, and anxiety; however, frank delusional psychosis before corticosteroid exposure is rarely characterized. Timing is critical because corticosteroids can themselves cause psychosis.
CASE PRESENTATION: A 42-year-old man with no previous psychotic disorder developed a progressive subacute syndrome over several months, beginning with headache and followed by impaired fine motor function, dysarthria, dysphagia, tremor, and cognitive decline. Cerebrospinal fluid (CSF) showed inflammation, and CSF GFAP-immunoglobulin G (IgG) was confirmed by qualitative cell-based and tissue-based assays. Before corticosteroid pulse therapy or oral prednisolone, his family observed a new persecutory delusion that someone was outside the window. Immunotherapy was led by neurologists, and psychiatric symptoms were assessed by psychiatrists through consultation and later psychiatric hospitalization. After corticosteroid therapy, neurological symptoms partially improved, but persecutory ideas, grandiosity, insomnia, irritability, aggression, and escape behavior became prominent. Prednisolone was continued because of the autoimmune neurological disease. Olanzapine was titrated to 15 mg/day. Behavioral dyscontrol improved markedly despite continued prednisolone, and physical restraint was no longer required; however, residual grandiose delusional ideas persisted.
CONCLUSION: This case suggests that delusional psychosis can be an early manifestation of autoimmune GFAP astrocytopathy. Because the first delusion preceded corticosteroid exposure, steroid-induced psychosis was excluded as the mechanism of onset. Olanzapine may stabilize severe behavioral dyscontrol while necessary corticosteroid therapy is maintained, although residual delusions may persist.
CASE PRESENTATION: A 42-year-old man with no previous psychotic disorder developed a progressive subacute syndrome over several months, beginning with headache and followed by impaired fine motor function, dysarthria, dysphagia, tremor, and cognitive decline. Cerebrospinal fluid (CSF) showed inflammation, and CSF GFAP-immunoglobulin G (IgG) was confirmed by qualitative cell-based and tissue-based assays. Before corticosteroid pulse therapy or oral prednisolone, his family observed a new persecutory delusion that someone was outside the window. Immunotherapy was led by neurologists, and psychiatric symptoms were assessed by psychiatrists through consultation and later psychiatric hospitalization. After corticosteroid therapy, neurological symptoms partially improved, but persecutory ideas, grandiosity, insomnia, irritability, aggression, and escape behavior became prominent. Prednisolone was continued because of the autoimmune neurological disease. Olanzapine was titrated to 15 mg/day. Behavioral dyscontrol improved markedly despite continued prednisolone, and physical restraint was no longer required; however, residual grandiose delusional ideas persisted.
CONCLUSION: This case suggests that delusional psychosis can be an early manifestation of autoimmune GFAP astrocytopathy. Because the first delusion preceded corticosteroid exposure, steroid-induced psychosis was excluded as the mechanism of onset. Olanzapine may stabilize severe behavioral dyscontrol while necessary corticosteroid therapy is maintained, although residual delusions may persist.