The pathophysiologic background for current treatments of premenstrual syndromes
Multiple hypotheses on the etiology of premenstrual syndromes (PMS) that have been proposed during the past 70 years have led to a multitude of treatment modalities. During the past two decades, the following two classes of pharmacologic interventions have emerged: hormonal interventions—mostly suppression of ovulation; and neurotransmitter’s activity stimulation—mostly by specific serotonin reuptake inhibitors. These treatment modalities are based on the hypothesis that the etiology and pathophysiology of PMS are related to ovulation-related luteal activity of gonadal hormones, and their interaction with serotonin and other neurotransmitters. Two other components of the pathophysiology of PMS—the genetic propensity and the dynamically evolving-vulnerability—have not yet been addressed for treatment. Environmental inputs to pathophysiology, which are not discussed here, have been addressed by attempts at changes of lifestyle, coping style, and environment.