The initial report of the syndrome of Inappropriate Antidiuresis (SIAD) was published as recently as 1960 in the American Journal of Medicine. Schwartz and colleagues described an elegant series of physiological studies, in which two patients with hyponatraemia and lung carcinoma were shown to have an inability to excrete a water load, and who responded to water restriction with a rise in plasma sodium concentration. They termed this syndrome SIADH; in the 60 years since then, the basic diagnostic requirements for SIAD hyponatraemia, concentrated urine, elevated urine sodium concentration, euvolaemia, and exclusion of cortisol and thyroid hormone deficiency remain the gold standard for definition of the syndrome. Neoplasia, particularly lung carcinoma, remains a major cause of the syndrome. In addition, all recent published guidelines recommend that the treatment employed in these index cases fluid restriction should remain as first line therapeutic choice. However, much has changed. The development of RIA methods for measurement of plasma vasopressin (AVP) has led to more complex definition of SIAD, and molecular biology techniques have shown that AVP is produced ectopically in tumour tissue. Recent data has shown that cortisol deficiency is commoner than previously recognised as a cause of SIAD, and that the need to exclude hypothyroidism is of questionable value. Data has also questioned the clinical value of fluid restriction in the reversal of hyponatraemia; the AVP-receptor antagonists, the vaptans are clearly more effective clinically, though cost effectiveness remains an issue. The need to treat SIAD actively is emphasised by the prospective data which shows that SIAD is associated with increased mortality which cannot be attributed solely to co-morbidity. Finally, guidelines for management of acute hyponatraemia recommend bolus treatment with hypertonic saline rather than continuous infusion; clinical data shows this to be safe, and effective in restoring cognitive function.