Menstrual pain: its origin and pathogenesis

Abstract

A variety of misconceptions about the etiology of dysmenorrhea have existed in the past. Experimental and clinical research of the last 15 years, however, has identified uterine prostaglandins as substantially contributing to the pathogenesis of primary dysmenorrhea. This paper reviews the various current theories of pathogenicity. It is now known that at the end of the menstrual cycle, prostaglandins increase myometrial contractions and cause constriction of small endometrial blood vessels, with consequent tissue ischemia, endometrial disintegration, bleeding and pain. Dysmenorrhea may be due to tissue ischemia resulting from increased intrauterine pressure, vessel constriction and decreased uterine blood flow. The most compelling evidence for the "prostaglandin theory" is the success of prostaglandin synthesis inhibitors in the treatment of dysmenorrhea. The pain relief achieved with these drugs is accompanied by a suppression of prostaglandin synthesis and a decrease in intrauterine pressure.