Guillain-Barre syndrome (GBS) is the commonest cause of acute polyradiculoneuropathy that requires hospitalization. Many of these patients experience systemic and disease-related complications during its course. Notable among them is hyponatremia. Though recognized for decades, the precise incidence, prevalence, and mechanism of hyponatremia in GBS are not well known. Hyponatremia in GBS patients is associated with more severe in-hospital disease course, prolonged hospitalization, higher mortality, increased costs, and a greater number of other complications in the hospital and worse functional status at 6 months and at 1 year. Though there are several reports of low sodium associated with GBS, many have not included the exact temporal relationship of sodium or its serial values during GBS thereby underestimating the exact incidence, prevalence, and magnitude of the problem. Early detection, close monitoring, and better understanding of the pathophysiology of hyponatremia have therapeutic implications. We review the complexities of the relationship between hyponatremia and GBS with regard to its pathophysiology and treatment.

Hyponatraemia is frequent in older people and induces marked motor and cognitive dysfunction, even in patients deemed ‘asymptomatic’. Nutritional status is worse than in euvolaemic-matched controls, and the risk of fracture is increased following incidental falls. Yet hyponatraemia is undertreated, in spite of the fact that its correction is accompanied by a clear improvement in symptoms. Both evaluation of neurological symptoms and classification by volaemia are essential for a correct diagnosis and treatment of the hyponatraemic elderly patient. The syndrome of inappropriate anti-diuretic hormone secretion (SIADH) is the most common cause of hyponatraemia in older people. Nutritional status and chronicity of SIADH should be taken into account when deciding therapy. We propose an 8-step approach to the management of the elderly patient with hyponatraemia.

A case of inappropriate ADH secretion, water intoxication, convulsion and unconsciousness occurring during abrupt withdrawal of benzodiazepines due to the patient under reporting her consumption is described.