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This page is an AI-assisted Turkish summary of the study presented at the 26th World Congress of Psychiatry. The study belongs to the presenting authors; please refer to the original source when citing it.

EV0675

Recognizing autoimmune psychosis: clinical warning signs and a diagnostic framework for early psychiatric practice

RECOGNIZING AUTOIMMUNE PSYCHOSIS: CLINICAL RED FLAGS AND A DIAGNOSIS FRAMEWORK FOR EARLY PSYCHIATRIC PRACTICE

Because autoimmune psychosis can be mistaken for primary psychiatric disorders, a stepwise diagnostic framework based on clinical warning signs is essential for early immunotherapy.

The poster aims to present a practical framework for the early recognition of autoimmune psychosis (AP), a clinical entity in which immune dysregulation and neuronal autoantibodies directly cause psychiatric symptoms. AP mimics schizophrenia and bipolar disorder, frequently leading to misdiagnosis and treatment delays; unlike primary psychiatric disorders, it is resistant to antipsychotics but responds well to timely immunotherapy. Autoimmune diseases are reported to affect up to 9.4% of the global population, and up to 39% of confirmed cases are reported to have previously been misdiagnosed as primary psychiatric disorders. The first step of the proposed framework involves recognizing warning signs: psychiatric signs include new-onset psychosis, mania, catatonia, and poor response to antipsychotics; neurological signs include rapid cognitive decline, new-onset seizures, movement disorders, and autonomic instability; historical features include a personal or family history of autoimmune disease and onset following a viral prodrome; investigation findings include epileptiform discharges on EEG, mesiotemporal hyperintensities on MRI, and cerebrospinal fluid (CSF) pleocytosis. The second step, the diagnostic workup, includes excluding infectious encephalitis, preferring CSF over serum for autoantibody testing (e.g., anti-NMDAR), identifying hippocampal hyperintensity on T2-FLAIR MRI and an extreme delta brush pattern on EEG, using FDG-PET where available, as it is more sensitive than MRI and EEG, and screening for malignancy in paraneoplastic cases; faciobrachial dystonic seizures are considered pathognomonic for anti-LGI1, and a normal MRI does not rule out the diagnosis. In terms of antibody subtypes, anti-NMDAR is associated with psychosis, mania, and catatonia; anti-LGI1 with mood disorders and memory impairment; and anti-CASPR2 with confusion and possible psychosis. Recommended first-line treatment consists of steroids, intravenous immunoglobulin, or plasma exchange, with second-line rituximab or cyclophosphamide if there is no improvement within two to four weeks; antipsychotics and benzodiazepines are reserved for cautious symptomatic use only.

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