[3][4] In the current literature across several fields, including neurology, neurosurgery, nephrology, and critical care medicine, there is controversy over whether CSWS is a distinct condition, or a special form of syndrome of inappropriate antidiuretic hormone secretion (SIADH).
[5] CSWS is a diagnosis of exclusion and may be difficult to distinguish from the syndrome of inappropriate antidiuretic hormone (SIADH), which develops under similar circumstances and also presents with hyponatremia.
[1][14] In 1858, Claude Bernard first raised the possibility of a direct relationship between the central nervous system and renal excretion of osmotically active solutes.
Patients with extra-renal salt losses complicated by hyponatremia were found to be common-place, and consistent with McCance's description, they excreted urine virtually free of sodium.
Berry, Barnes and Richardson shared the production of this new device to measure sodium and potassium in solution of biological materials by means of the flame photometer in 1945.
[21] Almost a century after the pioneering work of Bernard in animals, Peters et al., in 1950, reported three patients seen at Yale New Haven Hospital with hyponatremia associated with varying cerebral pathologies and severe dehydration.
They postulated that this provided evidence of an extra-pituitary cerebral structure mediating normal sodium metabolism but were unsure of its location or mechanism of action.
[23] In 1953, Leaf et al., demonstrated that exogenous administration of the antidiuretic hormone vasopressin resulted in hyponatremia and a natriuresis dependent on water retention and weight gain.
Vasopressin-ADH administration to normal humans was shown to result in water retention and urinary loss of electrolytes (primarily sodium) in other studies at the time.
Given Bernard's ability to create a chloride diuresis without glycosuria though renal denervation, Cort postulated the existence of a neuronal connection between the hypothalamus and proximal tubule of the kidney influencing electrolyte reabsorption.
If correction of such a state is desirable, the most useful therapeutic measure would appear to be limitation of the intake of fluid to slightly more than the amount needed to cover water expenditure from insensible losses, obligatory urine volume and growth requirements.
Similarly, it has been suggested that inappropriate release of vasopressin is the cause of hyponatremia and renal salt wasting in certain diseases, including bronchogenic carcinoma, cerebral injuries, and malformations.
[28] In 1981, Nelson et al. studied hyponatremia in neurosurgical patients, primarily subarachnoid hemorrhage, and found that isotopically measured blood volumes were contracted; he attributed this finding to cerebral salt wasting (CSW).
[29] Other authors associated hyponatremia in subarachnoid hemorrhage with increased levels of natriuretic peptides, negative sodium balance, and low central venous pressure.
The first reports of hyponatremia and renal sodium loss corrected by fluid restriction in patients with bronchogenic carcinoma were published by Bartter.