Hyponatremia is the most common electrolyte disorder encountered in neurosurgical patients. The aggressive treatment of hyponatremia in this group is critical, as hyponatremia can lead to mental status changes, seizures, vasospasm, cerebral edema, and even death. When it occurs, it represents a failure of one of several homeostatic mechanisms that tightly regulate serum sodium. In these patients, hyponatremia is most commonly due to the syndrome of inappropriate antidiuretic hormone (SIADH) or cerebral salt wasting (CSW). It can be problematic to differentiate between these 2 as they share key features, including low serum sodium, low serum osmolality, a higher urine osmolality than serum osmolality, and an elevated urinary sodium concentration. Furthermore, distinctions between CSW and SIADH, namely extracellular fluid (ECF) volume and total sodium balance, are often difficult to establish. Syndrome of inappropriate antidiuretic hormone is characterized by a volume-expanded state, whereas CSW is characterized by a volume-contracted state. Determining the exact cause remains a clinical imperative as the treatment for each is different. The rate at which serum sodium is corrected must be attended to, as rapid shifts in serum sodium pose potential risk of cerebral pontine myelinolysis.