Around 50% of patients with LGI1 antibodies and FBDS are hyponatraemic.4 6 15 The mechanism may involve the established capacity of LGI1 antibodies to bind anti-diuretic hormone (ADH)-secreting hypothalamic neurons.13 Although hyponatraemia may be seen with CASPR2 antibody positivity, this is typically at significantly lower rates, and the CASPR2 antibodies do not bind the ADH-secreting neurons, suggesting an alternative mechanism is required to explain the observation. This evidence concerns the gene LGI1 and Hyponatremia.