Abstract / Summary
We report the case of a 55-year-old man who presented with recurrent, brief episodes of isolated speech arrest lasting 10-30 seconds, during which awareness and comprehension were preserved.Initial neurological examination and neuroimaging were unremarkable, and the episodes were initially attributed to suspected transient ischaemic attacks (TIAs).Subsequently, the patient developed a generalised tonic-clonic seizure, prompting initiation of antiepileptic therapy.Over the following months, he experienced an increasing frequency of transient aphasic episodes alongside focal seizures with left-sided motor involvement, which proved refractory to multiple antiepileptic medications.Further investigation during hospital admission revealed significant hyponatraemia and characteristic magnetic resonance imaging (MRI) findings, including bilateral medial temporal lobe enlargement with fluid-attenuated inversion recovery (FLAIR) hyperintensity involving the amygdala and hippocampi.The detection of LGI1 antibodies, in conjunction with the clinical presentation and radiological features, confirmed the diagnosis of LGI1 antibody-associated autoimmune limbic encephalitis.The patient was treated with intravenous methylprednisolone followed by oral corticosteroid therapy, resulting in a marked reduction in seizure frequency and severity.This case underscores the importance of recognising aphasic seizures as a potential manifestation of autoimmune encephalitis (AIE), particularly LGI1-associated disease, to avoid diagnostic delay and facilitate early initiation of immunotherapy.