Dysmenorrhea - Pathophysiology

Pathophysiology

During a woman's menstrual cycle, the endometrium thickens in preparation for potential pregnancy. After ovulation, if the ovum is not fertilized and there is no pregnancy, the built-up uterine tissue is not needed and thus shed.

Molecular compounds called prostaglandins are released during menstruation, due to the destruction of the endometrial cells, and the resultant release of their contents. Release of prostaglandins and other inflammatory mediators in the uterus cause the uterus to contract. These substances are thought to be a major factor in primary dysmenorrhea. When the uterine muscles contract, they constrict the blood supply to the tissue of the endometrium, which, in turn, breaks down and dies. These uterine contractions continue as they squeeze the old, dead endometrial tissue through the cervix and out of the body through the vagina. These contractions, and the resulting temporary oxygen deprivation to nearby tissues, are responsible for the pain or "cramps" experienced during menstruation.

Compared with other women, women with primary dysmenorrhea have increased activity of the uterine muscle with increased contractility and increased frequency of contractions.

In one research study using MRI, visible features of the uterus were compared in dysmenorrheic and eumenorrheic (normal) participants. The study concluded that in dysmenorrheic patients, visible features on cycle days 1-3 correlated with the degree of pain, and differed significantly from the control group.