Anti-GAD65 encephalitis-like other autoimmune encephalitis conditions-poses a significant diagnostic challenge; its heterogeneous neuropsychiatric phenotypes mimic primary psychiatric disorders. The broad pathophysiological spectrum, ranging from limbic dysfunction to catatonia, underscores the need for systematic approaches that integrate immunotherapy with neuromodulation when standard interventions fail. We present a 78-year-old woman with no prior psychiatric history who developed acute-onset catatonia with visual hallucinations. Neurological evaluation revealed markedly elevated anti-GAD65 antibodies despite unremarkable neuroimaging and electroencephalography. Initial treatment with lorazepam and intravenous immunoglobulin achieved partial response. Recurrent catatonia and treatment-refractory psychosis prompted a trial of electroconvulsive therapy (ECT), which led to sustained remission through maintenance ECT. This case illustrates three critical clinical practice points: (1) late-onset catatonia necessitates comprehensive evaluation of autoimmune etiologies, including paired serum-cerebrospinal fluid antibody testing; (2) partial response to immunotherapy does not preclude more aggressive symptomatic management; and (3) ECT can effectively treat catatonia secondary to autoimmune illnesses. We conclude that successful management of anti-GAD65 encephalitis necessitates a multidisciplinary team for thorough neuro-immunological assessment, nuanced psychopharmacology, and timely neuromodulation.
Song et al. (Sun,) studied this question.