Disturbances of water and sodium ion (Na+) metabolism in acute brain diseases are presented. Hyponatraemia accompanies two etiopathogenetically quite different syndromes, the cerebral salt wasting syndrome (CSWS) and the syndrome of inappropriate secretion of natriuretic hormone (SIADH). The first one is caused by increased urinary Na+ loss and accompanied by increased loss of water and elevated plasmatic atrial and brain natriuretic peptides (ANP, BNP). The second one is caused by water retention with subsequent dilutional hyponatremia, caused by an increased antidiuretic hormone (ADH) level. The CSWS was discovered and described more than 50 years ago, SIADH a few years later. During the approximately 30 years there after the hyponatraemic states developing in acute brain diseases were considered to be SIADH and treated by water restriction and diuretics. Only 10 years ago renal functional parameters were introduced as part of the differential diagnosis between both syndromes. Since that time, CSWS is much more frequently diagnosed as the cause of hyponatraemia. In therapy intensive supplementation of Na+ salts and fluids is required. The third disturbance of Na+ metabolism is the diabetes insipidus centralis with typical development of hyponatraemia. The paper also describes parameters typical for its diagnosis. Attention is also paid to the possible share of renal diabetes insipidus in polyuria in critically ill patients. Data about the frequency and time-dependency of development of hyper- or hyponatraemia are presented. Hyponatraemia is more frequent and usually accompanied by hypernatriuria and by depletion of the circulating volume. Hypernatraemia is prognostically more serious. Hyponatraemia treated by fluid restriction and diuretics was complicated by a higher frequency of cerebral vasospasms and infarctions. Increased water nad salt supplementation rectified the situation. Plasmatic ADH elevation is usually described during days 0–2 after onset of acute brain disease or closely to neurosurgical operation. During the following days, when natriuresis and hyponatraemia develops, the ADH values return into the reference ranges. In the CSWS pathogenesis no significant role of digoxin-like-substances was found. Unambigous are the increased plasmatic ANP and BNP levels. This elevation lasts up to two weeks (when monitoring is unfortunately usually stopped). So far the origin of natriuretic peptides in acute brain disease is not known, but most authors place it into the cardiac tissue. However possible mechanisms of their liberation are only discussed. Significant correlations are found between natriuretic peptide changes and hyponatremia, natriuresis and intracranial pressure.

        Key words: hypernatraemia, hyponatraemia, natriuretic peptides, syndrome of inappropriate antidiuretic hormone secretion (SIADH), cerebral salt wasting syndrome (CSWS).