Hyponatraemia caused by LGI1-associated limbic encephalitis

Limbic encephalitis (LE), once thought to be a rare paraneo-plastic phenomenon, is increasingly diagnosed in patients without malignancy. Autoimmune LE has emerged as a distinct clinical entity. Autoantibodies to neuronal cell sur-face proteins have been described and may now be tested for. This has led to an exponential increase in the number of cases being reported. The most recently implicated autoanti-body is to the leucine-rich anti-glioma 1 protein (LGI1). This protein is involved in synaptic transmission and inherited loss-of-function mutations cause autosomal dominant lat-eral temporal epilepsy. LGI1 is also expressed in specific tubules in the kidney. Anti-leucine-rich anti-glioma 1 protein (anti-LGI1) LE presents with sub acute onset of progressive neurological, cognitive and psychiatric disturbance. The con-dition is complicated in up to 60 % of cases with severe and life threatening hyponatraemia. As well as causing significant morbidity, the co-existence of hyponatraemia may confuse the initial diagnosis. We present a case of anti-LGI1 which was complicated by hyponatraemia with a comprehensive review of the literature