Summary: Serum prolactin (HPR) levels are influenced by waking and sleep states, as reflected by surges in serum concentrations during daytime naps and nocturnal sleep. Other physiological causes of hyperprolactinemia include sexual activity, pregnancy, and lactation. Drugs may stimulate or inhibit HPR secretion. Pathological causes for HPR secretion include destructive lesions of the hypothalamus, prolactin-secreting neoplasms of the pituitary gland, lesions of the spinal cord, and occasionally Parkinson's disease. The most predictable postictal changes are increased serum Cortisol levels and hyperprolactinemia. Serum HPR rises after virtually all generalized tonic-clonic seizures, most complex partial seizures, and some simple partial seizures. Absence and myoclonic seizures do not affect serum HPR levels. Repeated epileptic seizures and electroconvulsive therapy treatments produce successively less marked rises in serum HPR. The postictal elevation of serum Cortisol has a longer latency than for HPR and follows an earlier rise in serum ACTH. Other postictal hormonal changes are much more variable. Because of the normal diurnal variation in serum Cortisol levels and the relative delay in the postictal elevation of serum Cortisol, HPR is more useful as a diagnostic measure of epileptic seizures. This application of HPR requires an understanding of other factors that influence serum HPR and the use of baseline serum HPR levels for comparison. HPR data must be correlated with behavioral and electroencephalographic events.