Dysmenorrhea is a Greek term for “painful monthly bleeding”. More than half of women who menstruate have some pain for 1 to 2 days each month. Usually, the pain is mild. But for some women, the pain is so severe that it keeps them from engaging in their normal activities for several days each month. Primary dysmenorrhea begins within about 2 years of menarche or once ovulatory cycles have been established. It is more often a diagnosis made in adolescents and young adults. The cyclic pain starts within a few hours of the onset of menses and usually resolves within 72 hours. The pain is located midline in the pelvis and may radiate to the lumbar area of the back or upper legs. It may be crampy and episodic and is usually similar in each menstrual cycle. Concomitant symptoms may include nausea, vomiting, headaches, dizziness, fatigue, and sleep difficulties.
The cause of pain is believed due to the hypersecretion of Prostaglandins (PGs) from the endometrium, the lining of the uterus. Prostaglandins cause pain by increasing uterine contractions, thus increasing uterine pressure and impaired uterine perfusion, a condition where the blood supply to the uterus is insufficient, leading to a lack of oxygen and nutrients needed for the proper function of the uterus. This hypoxia or lack of sufficient oxygen caused by impaired uterine profusion, and the metabolites from anaerobic metabolism the, cellular process that breaks down glucose without using oxygen (glycolysis) also play a role in the origin pain experienced during dysmenorrhea.
The mechanism by which prostaglandins are produced involves the breakdown of endometrial tissue which frees phospholipids, that are then converted to arachidonic acid. The arachidonic acid is further converted to prostacyclins, prostaglandins and thromboxane via the enzyme cyclooxygenase. The products prostaglandin F2 alpha (PGF-2α) and Prostiglandin E2 (PGE2) are responsible for the increase in uterine tone and the resulting high-amplitude contractions of the uterus.
The hormone vasopressin works by causing vasoconstriction; a narrowing of the blood vessels and by reducing blood flow as well as stimulating painful uterine contractions which are directly linked to the pain seen in primary dysmenorrhea. Another variable is the presence of Leukotrienes that play an important role in the immune system especially in inflammation and are also associated with an increase in uterine contractions. Leukotrienes C4 and D4 are seen at levels higher in women with dysmenorrhea than those who are free of the disorder.
Progesterone has an anti-inflammatory effect, during the luteal phase, the latter half of the menstrual cycle. During the luteal phase progesterone inhibits uterine contractions which plays a role in keeping the uterus quiescent to favor implantation should fertilization take place. If no pregnancy occurs progesterone levels drop sharply just before menstruation. This sudden drop causes the endometrium to break down, releasing arachidonic acid and ultimately prostaglandins, which increase uterine contractions and cause vasoconstriction, leading to ischemia and pain. This sudden drop in progesterone just prior to menses explains the timing menstrual cramps: dysmenorrhea
NSAIDs such as aspirin, ibuprofen and naproxen have been shown to be effective in the treatment of dysmenorrhea. The main mechanism of action of NSAIDs is the inhibition of the enzyme cyclooxygenase (COX). Cyclooxygenase is required to convert arachidonic acid into thromboxanes, prostaglandins, and prostacyclins. Use of an NSAID on a scheduled basis starting 1 to 2 days prior to the onset of pain has been shown to work better than when an NSAID is used on an as-needed basis.
