Dysmenorrhea

Dysmenorrhea (from Greek dys – disorder, men – month, rhoia – course) is a common gynecological disorder manifested by intense pain syndrome in the lower abdomen occurring cyclically on the eve or during menstruation.

It is often combined with metabolic-endocrine and psychovegetative disorders.

Etiology and pathophysiology

Primary (functional) dysmenorrhea is not associated with anatomical changes in the pelvic organs. Its mechanism is due to impaired synthesis and metabolism of eicosanoids in the endometrium: hyperproduction of prostaglandins F2α and E2, as well as leukotrienes causes powerful, spastic and discoordinated contractions of the myometrium.

Intrauterine pressure may exceed 400 mmHg, which is higher than the perfusion pressure in uterine arteries. This leads to transient ischemia of myometrium, accumulation of metabolites of anaerobic glycolysis and irritation of painful nerve endings (“uterine angina”).

Secondary (organic) dysmenorrhea is caused by pathologic processes that obstruct the outflow of blood or irritate the peritoneum.

Clinical significance

Secondary dysmenorrhea, which occurs not from the moment of menarche, but at a later age, tends to progression and resistance to NSAIDs. It is a cardinal clinical symptom of external genital endometriosis and adenomyosis, as well as hyperplastic processes of the endometrium. The nature of pain may indicate the localization of the process: irradiation to the rectum or coccyx often indicates the lesion of the retrocervical space and sacrococervical ligaments.