Etiology
Dysmenorrhea can be divided into 2 subcategories, although it is not always easy to distinguish between these based on history and exam alone:
Primary dysmenorrhea occurs in the absence of pelvic pathology
Secondary dysmenorrhea occurs in the presence of pelvic pathology.
Primary dysmenorrhea
During ovulatory cycles, the sequential exposure to estrogen and progesterone causes sloughing of the endometrium and prostaglandin release with the onset of menstruation. The biosynthesis of prostaglandins from the precursor, arachidonic acid, occurs via the cyclooxygenase (COX) pathway. The underlying mechanism of primary dysmenorrhea is thought to be prostaglandin-stimulated uterine myometrial contractions, leading to decreased blood flow with ensuing uterine hypoxia. The hypoxia then triggers the spasmodic pain described by affected women.[20][21][22]
Increased concentrations of prostaglandin F-2 alpha (PGF-2 alpha) in menstrual fluid are found in women with primary dysmenorrhea. These increased concentrations of PGF-2 alpha lead to frequent and dysrhythmic contractions and a higher basal uterine tone. Increased contractility correlates with the severity of symptoms as with the concentrations of PGF-2 alpha.[23][24][25] Leukotrienes and vasopressin may also play a role in the etiology of primary dysmenorrhea.[26][27][28]
Further effects of prostaglandins on smooth muscle may manifest as GI symptoms (e.g., nausea, vomiting, diarrhea), which frequently coexist in women with primary dysmenorrhea.
As PGF-2 alpha production is increased in ovulatory cycles, any treatment that inhibits ovulation, such as hormonal contraception, may be considered as a treatment option.[29][30]
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Treatments that decrease the production of prostaglandins, such as nonsteroidal anti-inflammatories (NSAIDs), are also usually successful in treating primary dysmenorrhea.[31]
Differences have been observed in neuroimaging studies between women who experience dysmenorrhea and those who do not, suggesting an additional role of central pain pathways.[32]
Secondary dysmenorrhea
The mechanisms underlying secondary dysmenorrhea due to a pelvic pathology overlap with those of primary dysmenorrhea.
Common causes of secondary dysmenorrhea
Endometriosis: the most common cause of secondary dysmenorrhea.[6] Presents as pelvic pain and discomfort that is exacerbated during the premenstrual and menstrual period. It is, as yet, unclear how ectopic endometrial tissue can result in pelvic pain, although prostaglandins may play a role. Increased concentrations of prostaglandins have been documented in the peritoneal fluid and in the circulation in women with endometriosis.[33]
Pelvic inflammatory disease (PID): an infectious process often preceded by uterine instrumentation or a history of sexually transmitted infection. The pain may be related to the release of inflammatory mediators or prostaglandins, which subsequently lead to vasoconstriction and uterine contractions. Delay in treatment of acute PID can increase the risk of infertility and chronic pelvic pain. Approximately 1 in 5 women may develop chronic pelvic pain after an initial episode.
Adenomyosis: extrauterine pain and uterine enlargement, often accompanied by heavy vaginal bleeding. It is thought to be a result of invasion of the endometrium into the myometrium, resulting in ectopic endometrial glands and stroma.
Uterine leiomyoma (fibroids): common benign tumors arising from the myometrium, identified on pelvic examination (or ultrasound) as a firm (smooth or multinodular) enlarged uterus. Often presenting symptoms include heavy and prolonged bleeding.
Less common causes of secondary dysmenorrhea
Ovarian cyst with hemorrhage: characterized by unilateral pain and tenderness and an adnexal mass. The mechanism by which ovarian masses result in dysmenorrhea is not well elucidated and may be due to an acute-onset pain due to torsion, rupture, or hemorrhage.
Ovarian torsion: sometimes accompanied by ovarian pathology with symptoms similar to those of hemorrhagic ovarian cyst. However, this commonly has an acute onset and is unlikely to cause long-standing dysmenorrhea.
Obstructive Mullerian duct anomalies: manifesting as cyclical pain soon after menarche and, in the presence of hematometra (trapped blood within endometrial cavity), an emerging pelvic mass.
Cervical stenosis: typically in postsurgical patients with pain further exacerbated by the collection of fluid in the uterine cavity, which may be visible on pelvic ultrasound.
Further uncommon causes of secondary dysmenorrhea include Asherman syndrome, pelvic congestion syndrome, and other congenital uterine abnormalities. Intrauterine contraceptive devices may be associated with dysmenorrhea, which is a commonly reported reason for discontinuation.[34] However, levonorgestrel-containing devices are associated with a reduction in primary dysmenorrhea and may be used in the treatment of conditions such as endometriosis.[35] Intrauterine polyps and submucosal fibroids can also cause pain, but are more frequently associated with abnormal bleeding.
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