Autoimmune limbic encephalitis (LE) with leucine-rich glioma-inactivated 1 (LGI1) antibodies is rare but treatable, often presenting as rapidly progressive cognitive decline, behavioural changes, and hyponatraemia. These features can resemble psychiatric or neurodegenerative disorders, delaying diagnosis. We report a case of a 63-year-old man with confusion, memory loss, dream enactment, hallucinations, severe hyponatraemia, and specific higher cortical features, including apraxia, anomia, and executive dysfunction. Faciobrachial dystonic seizures (FBDS), a recognised hallmark of LGI1 antibody-mediated LE, were not clearly appreciated at initial presentation in this case. MRI revealed bilateral medial temporal lobe abnormalities, while CSF and EEG results were unremarkable. LGI1 antibodies were identified only after initial neuronal antibody tests were negative. Treatment with corticosteroids and intravenous immunoglobulin (IVIg) stabilised his condition and led to partial improvement. This case underscores the diagnostic challenges of LGI1 antibody-associated LE and the importance of early recognition, antibody testing, and prompt immunotherapy to prevent irreversible neurological damage. The objective of this case report is to highlight the diagnostic pitfalls and management considerations in LGI1 antibody-mediated LE presenting predominantly with psychiatric and cognitive symptoms.
Zeb et al. (2026) studied this question.