Studies have elucidated the regulatory interplay between ovarian hormonal changes, prostaglandin levels and the evolution of intrauterine pressure that leads to dysmenorrhea. These studies substantiated the premise that primary dysmenorrhea is caused by endogenous prostaglandin excess and prompted clinical trials with naproxen sodium (Anaprox) in patients with primary dysmenorrhea. The primary action of prostaglandin is constriction of uterine blood vessels, with consequent anoxia and sustained myometrial contraction. Cyclic uterine contractions evolve later but gradually, with the progress of time. However, the cyclic contractions are not perceived as painful. It is important to realize that the source of uterine pain in dysmenorrhea is the high resting intrauterine pressure (tonus). Penetration of excess prostaglandins into general circulation fully accounts for the systemic symptoms of dysmenorrhea (nausea, vomiting, diarrhea, headache, etc). Rational treatment of dysmenorrhea should be directed at elimination of the excess prostaglandin action. Naproxen sodium and other prostaglandin synthesis inhibitors decrease intrauterine resting pressure as well as amplitude and frequency of uterine contractions and reduce the uterine concentrations of prostaglandins. These changes are associated with substantial pain relief. Thus, naproxen sodium and other prostaglandin synthesis inhibitors present a logical treatment modality to be used in dysmenorrhea.