Catatonia and Autoimmune Encephalitis Triggered by <i>Mycoplasma pneumoniae</i> Infection with GAD-65 Antibodies: A Case Report

Background Autoimmune encephalitis (AE) is a rare but significant neurological condition characterized by immune-mediated inflammation of the central nervous system. This report highlights a case of AE associated with GAD-65 antibodies following a Mycoplasma pneumoniae infection, emphasizing the immunological underpinnings and diagnostic challenges. Case Presentation An 18-year-old male with a history of ADHD and tics presented with altered mental status, disorientation, and catatonia. Initial symptoms included sore throat and fever treated with dextromethorphan-containing over-the-counter medications. In the emergency department, a positive rapid strep test raised concern for PANDAS, while suspicion of dextromethorphan toxicity prompted supportive care. Persistent symptoms, including autonomic instability, catatonia, and cognitive decline, led to further investigations for infectious and autoimmune etiologies. Diagnostic workup revealed positive Mycoplasma pneumoniae respiratory panel and elevated inflammatory markers. Empirical treatments including ceftriaxone, vancomycin, and azithromycin were initiated. Neuroimaging was normal, and CSF analysis was unremarkable for infectious agents. Persistent encephalopathy and episodes of catatonia necessitated intravenous immunoglobulin (IVIG) for suspected autoimmune encephalitis, leading to significant clinical improvement. GAD-65 antibodies were later identified on the CSF encephalitis panel. Discussion The presence of GAD-65 antibodies, typically associated with neurological syndromes such as stiff-person syndrome and limbic encephalitis, underscores the autoimmune mechanism of this case. Mycoplasma pneumoniae is recognized as a trigger for postinfectious immune responses, further complicating the clinical presentation. This case highlights the interplay between infection and autoimmunity in precipitating encephalitis, necessitating a multidisciplinary approach involving neurology, psychiatry, infectious disease, and immunology. IVIG therapy demonstrated efficacy in reducing inflammatory markers and resolving catatonia. Conclusion This case emphasizes the importance of considering autoimmune mechanisms in encephalitis, particularly in the context of recent infections. The identification of GAD-65 antibodies and the role of Mycoplasma pneumoniae as a potential trigger provide critical insights into the immunopathogenesis of AE and its management.