In spite of brief periods of enthusiasm about the potential diagnostic utility or etiological insights to be gained from neuroendocrine tests associated with depression, there has been an overall lack of success of neuroendocrine testing in primary depression. Similarly, among patients with poststroke depression, neuroendocrine tests have not been successful in establishing either an alternative method of diagnosing poststroke depression or illuminating neuroendocrine abnormalities which may contribute to the mechanism of poststroke depression.

Since the early 1960s, it has been known that patients with depression secrete an excess amount of cortisol (Gibbons and McHugh 1962; Sachar et al. 1973). The dexamethasone suppression test (DST) has been used extensively to study states of hypercortisolism (Carroll et al. 1981). Patients given 1 mg of dexamethasone orally will suppress serum cortisol secretion over the following 24 h. In a significant number of patients with primary major depression, especially the melancholic form of depression, there is a failure to suppress serum cortisol following dexamethasone administration. This lack of suppression is referred to as a positive DST response. Sensitivity of a positive DST in identifying patients with melancholic depression is determined by dividing the number of DST-positive depressed patients as a percentage of the total number of depressed patients.