Definition and Epidemiology

The term dysmenorrhea, from the Greek word meaning “difficult monthly flow,” refers to painful menstruation. Dysmenorrhea is classified as either a primary or a secondary gynecologic disorder. Primary dysmenorrhea is defined as painful menses despite normal pelvic anatomy and ovulation occurring within 6 to 12 months after menarche, when ovulatory cycles are established.^1,2 However, primary dysmenorrhea can begin as late as 1 to 3 years after menarche and is characterized by cramping pelvic pain just before or with the onset of menstrual flow and typically lasting 1 to 3 days,³ with a peak in the second and third decades of life and subsequently decreasing with advancing age. Secondary dysmenorrhea usually appears later in life, after some years of painless menstruation, and is associated with underlying pathologic processes such as endometriosis, uterine fibroids, adenomyosis, pelvic inflammatory disease, infertility problems, ovarian cysts, polyps, intrauterine adhesions, cervical stenosis, other pelvic pathologic conditions, or an intrauterine contraceptive device (IUD).^2,4

Dysmenorrhea prevalence rates around the world vary widely and range between 20% and 90%.⁴ In the United States, dysmenorrhea is one of the most commonly encountered gynecologic disorders, estimated to affect 50% to 60% of reproductive age women overall and up to 90% of adolescents.⁵ The peak incidence of dysmenorrhea is highest during adolescence, and approximately 15% of women who experience dysmenorrhea have discomfort that interferes with normal daily activity for 1 to 3 days each month, with 51% of women having missed work or school because of their symptoms.^1,5,7 It is difficult to estimate the economic burden of missed work from dysmenorrhea, but clearly it accounts for significant lost wages and diminished quality of life. Nevertheless, many women “suffer silently” and do not discuss dysmenorrhea with any health care provider. Adolescents, in particular, are unlikely to consult a health care provider about dysmenorrhea and have a tendency to self-medicate with over-the-counter medications.¹ Providers should be aware that the quality of a woman’s life can be improved by reducing or relieving the discomfort of dysmenorrhea. In addition, the willingness to discuss this common but possibly sensitive issue may pave the way to a more satisfying patient-provider relationship.

Pathophysiology

Primary dysmenorrhea has been attributed to ovulatory cycles, with the maturation of the hypothalamic-pituitary-gonadal axis.² Dysmenorrhea is caused by an excess or imbalance of prostaglandins, vasopressin, and chemical substances originating from phospholipids. These chemicals cause uterine contractions, cramping, nausea, vomiting, and diarrhea. Risk factors for dysmenorrhea include adolescence, anxiety, depression, stress, body mass index below 20 or above 30 kg/m², menorrhagia, metrorrhagia, nulliparity, and smoking. Contractions in the menstruating uterus and pain have been attributed to the production of prostaglandins, specifically PGF_2α and PGE₂.^2,3 The prostaglandins also cause the nausea and diarrhea associated with dysmenorrhea. Current evidence shows that the menstrual fluid of women with primary dysmenorrhea has higher-than-normal levels of these prostaglandins.^1,8,9 Anovulatory cycles are associated with lower levels of prostaglandins and as a result usually no dysmenorrhea.³

Despite the supporting evidence for a link between higher prostaglandin levels and dysmenorrhea, it is likely that the explanation for menstrual pain is not as simple as the cyclic production of one hormone. Women with dysmenorrhea may have complex alterations in hormonal patterns that exist throughout the cycle and affect a number of factors, including higher basal body temperature and disrupted sleep patterns.² Vasopressin may also play a role by increasing uterine contractility and causing ischemic pain as a result of vasoconstriction. Elevated vasopressin levels have been reported in women with primary dysmenorrhea.¹ In addition, women have differing perceptions of pain, and this may affect how they experience dysmenorrhea.² Research suggests that many factors are related to dysmenorrhea, including younger age, low body mass index, smoking, early menarche, pelvic infections, genetic influence, and history of pelvic assault.⁴

There is no convincing evidence that mechanical cervical obstruction or severe uterine flexion causing obstructed uterine flow is present in patients with primary dysmenorrhea, although heavy menstrual flow is associated with dysmenorrhea. Some studies have suggested that young age and nulliparity are associated with dysmenorrhea, but the correlation with age was not substantiated in other studies once parity and other factors were controlled for.¹ There is also no evidence to support an association between tubal sterilization and the prevalence of dysmenorrhea.^1,10

Although dysmenorrhea is no longer considered a psychological disorder, risk factors for dysmenorrhea have been investigated, including the varied socioeconomic and behavioral variables in many studies. Factors such as smoking; higher body mass index, which can also include obesity; earlier age at menarche; nulliparity; longer and heavier menstrual flow; and family history of dysmenorrhea have been examined.² In addition, depression, stress, level of education attained, marital status, employment, alcohol consumption, and physical activity levels have also been investigated.

A systematic review of several studies has suggested a significant inverse relationship between age and the risk of dysmenorrhea. A concurrent family history of dysmenorrhea, perceived stress levels, and heavy or irregular menstrual cycles have also been linked to dysmenorrhea in many studies. Stress has been demonstrated to indirectly affect prostaglandin synthesis and concentrations through the release of corticotropin-releasing hormone. Prostaglandins affect uterine muscle and vascular tone, and an imbalance of prostaglandins has been linked to the occurrence of dysmenorrhea.^1,9,11 Stress inhibits the release of follicle-stimulating hormone and luteinizing hormones, leading to impaired follicular development. This pathway can alter progesterone synthesis and release, which can alter the activity of prostaglandin. Stress-related hormones also appear to influence prostaglandin synthesis and/or binding in the myometrium of the uterus.

Fruit and vegetable intake has been found to have some benefit in the treatment of dysmenorrhea. The protective effect of oral contraceptives or other hormonal contraceptive forms such as IUDs has been evident and consistent across different study types²; IUDs containing hormones were found to have a positive effect on dysmenorrhea pain. Interestingly, there was no significant association between tubal ligation and dysmenorrhea.

Conflicting results were found in studies examining sociodemographic factors such as employment, socioeconomic status, body mass index, and the effect of exercise on dysmenorrhea. No associations between alcohol consumption and dysmenorrhea were found, and the association with cigarette smoking yielded mixed results.^1,2 The lack of data and the conflicting data are attributed to the limited number of studies as well as the small study samples in examining variables and the biases noted in systematic reviews.

Cultural and family influences may have a profound effect on how a woman experiences dysmenorrhea. The attitudes a woman has toward menstruation are often formed early in life and may be influenced by factors that include culture, religion, family, friends, and sexual partners. Additional emotional influences may be related to perceptions of fertility, the ability to bear children, or the relationship with the sexual partner. Many women begin menstruating with little or no accurate information, and menstrual sensations and discomfort may be distressing, frightening, or viewed as punishment. A woman’s beliefs about menstruation may directly affect the way she experiences it and her willingness to report any problems to her provider or to seek treatment. The variation rates examining the prevalence globally in studies are attributed to the lack of standard methods for assessing the severity of dysmenorrhea in various cultures.¹

Secondary dysmenorrhea is associated with underlying pelvic pathology and needs to be investigated to determine the cause. Secondary dysmenorrhea is caused by a pathologic process that affects the uterus, fallopian tubes, ovaries, or pelvic peritoneum. These processes can cause pain by altering pressures in or around pelvic structures, changing or restricting blood flow, or irritating the pelvic peritoneum. They can occur with the normal physiology of menstruation or act completely independently, with symptoms appearing during specific points in the menstrual cycle. Extrauterine causes must also be considered in the differential diagnosis; associated pelvic, bladder, and abdominal structural problems as well as causes related to previous surgical history may exist with chronic pelvic pain syndromes that suggest dysmenorrhea.⁵

Clinical Presentation

The diagnosis of primary dysmenorrhea is based on clinical features determined with a careful and detailed history of symptoms. The history should include age at menarche, menstrual history, last menstrual period, location and severity of discomfort, associated symptoms (headache, dizziness, nausea, vomiting, diarrhea, dyschezia), amount of school or work missed, medications, method of birth control, and whether the birth control is being used correctly. Abdominal and pelvic pain not related to the menstrual cycle should also be considered in the differential diagnosis.

Pain descriptions can vary significantly from individual to individual. Young women will generally report recurrent sharp, crampy pelvic pain, spasmodic lower abdominal pain, or pain over the suprapubic area.⁴ The pain will often radiate to the back, sacrum, or inner thighs. The pain usually begins a few hours before or just after the onset of menstruation and lasts the first 1 to 3 days of menstruation; it can be associated with nausea, vomiting, diarrhea, low back pain, or headache. Some young women also have associated systemic symptoms, including nausea, vomiting, loose bowel movements, and dizziness. Consideration should be given to symptoms exacerbated by dysmenorrhea such as irritable bowel syndrome, interstitial cystitis, or migraines.^2,3

Secondary dysmenorrhea is distinguished from primary dysmenorrhea by a history of pain that is inconsistent with the kind of low anterior pelvic pain described as beginning in adolescence and associated specifically with menstrual cycles. The signs and symptoms of secondary dysmenorrhea are related to an underlying pathologic process. The onset of secondary dysmenorrhea usually occurs in women 30 or 40 years of age rather than shortly after menarche. The pain is often not limited to the menses and is less related to the 48 to 72 hours of menstrual flow. There may be an array of associated symptoms in secondary dysmenorrhea including dyspareunia, infertility, and abnormal bleeding.