Dysmenorrhea 

  • Author: Karim Anton Calis, PharmD, MPH, FASHP, FCCP; Chief Editor: Michel E Rivlin, MD   more...
 
Updated: Mar 8, 2011
 

Background

Dysmenorrhea is defined as difficult menstrual flow or painful menstruation. The term dysmenorrhea is derived from the Greek words dys, meaning difficult/painful/abnormal, meno, meaning month, and rrhea, meaning flow.

Dysmenorrhea is one of the most common gynecologic complaints in young women who present to clinicians.[1] The optimal management of this symptom depends on an understanding of the underlying cause. Dysmenorrhea is classified as primary (spasmodic) or secondary (congestive).[2]

Primary dysmenorrhea is defined as menstrual pain not associated with macroscopic pelvic pathology (ie, absence of pelvic disease). It typically occurs in the first few years after menarche[3] and affects up to 50% of postpubescent females.[4]

Secondary dysmenorrhea is defined as menstrual pain resulting from anatomic and/or macroscopic pelvic pathology,[3, 5] such as that seen in women with endometriosis or chronic pelvic inflammatory disease. This condition is most often observed in women aged 30-45 years.

The following risk factors have been associated with more severe episodes of dysmenorrhea:[6]

  1. Earlier age at menarche
  2. Long menstrual periods
  3. Heavy menstrual flow
  4. Smoking
  5. Positive family history

Obesity and alcohol consumption were found to be associated with dysmenorrhea in some (not all) studies.[7, 8, 9] Physical activity and the duration of the menstrual cycle do not appear to be associated with increased menstrual pain.[7]

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Pathophysiology

The etiology and pathophysiology of dysmenorrhea have not been fully elucidated. Nonetheless, the following may be involved.

Primary dysmenorrhea

Current evidence suggests that the pathogenesis of primary dysmenorrhea is due to prostaglandin F2alpha (PGF2alpha), a potent myometrial stimulant and vasoconstrictor, in the secretory endometrium.[10] The response to prostaglandin inhibitors in patients with dysmenorrhea supports the assertion that dysmenorrhea is prostaglandin mediated. Substantial evidence attributes dysmenorrhea to prolonged uterine contractions and decreased blood flow to the myometrium.

Elevated prostaglandin levels were found in the endometrial fluid of women with dysmenorrhea and correlated well with the degree of pain.[11] A 3-fold increase in endometrial prostaglandins occurs from the follicular phase to the luteal phase, with a further increase occurring during menstruation.[12] The increase in prostaglandins in the endometrium following the fall in progesterone in the late luteal phase results in increased myometrial tone and excessive uterine contraction.[5]

Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. Significant amounts of leukotrienes have been demonstrated in the endometrium of women with primary dysmenorrhea that does not respond to treatment with prostaglandin antagonists.[8, 13, 14, 15, 16]

The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea.[17, 18] Vasopressin's role in the endometrium may be related to prostaglandin synthesis and release.

A neuronal hypothesis has also been advocated for the pathogenesis of primary dysmenorrhea. Type C pain neurons are stimulated by the anaerobic metabolites generated by an ischemic endometrium.

Primary dysmenorrhea has also been attributed to behavioral and psychological factors. Although these factors have not been convincingly demonstrated to be causative, they should be considered if medical treatment fails.

Secondary dysmenorrhea

A number of factors may be involved in the pathogenesis of secondary dysmenorrhea. The following pelvic pathologies can lead to the condition:

  • Endometriosis
  • Pelvic inflammatory disease
  • Ovarian cysts and tumors
  • Cervical stenosis or occlusion
  • Adenomyosis
  • Fibroids
  • Uterine polyps
  • Intrauterine adhesions
  • Congenital malformations (eg, bicornate uterus, subseptate uterus)
  • Intrauterine contraceptive device
  • Transverse vaginal septum
  • Pelvic congestion syndrome
  • Allen-Masters syndrome

Almost any process that can affect the pelvic viscera can produce cyclic pelvic pain.[19]

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Epidemiology

Frequency

United States

Dysmenorrhea may affect more than half of menstruating women, and its reported prevalence has been highly variable. A survey of 113 patients in a family practice setting showed a prevalence of dysmenorrhea of 29-44%,[20] but prevalence rates as high as 90% in women aged 18-45 years have been reported.[1] The use of oral contraceptives (OCs) and nonsteroidal anti-inflammatory drugs (NSAIDs), both of which are effective in ameliorating symptoms of primary dysmenorrhea, may confound the prevalence.

Primary dysmenorrhea peaks in late adolescence and the early 20s.[21] The incidence falls with increasing age and with increasing parity. The prevalence and severity of dysmenorrhea in parous women are reportedly significantly lower in many[7, 22, 23] but not all[1] studies. No significant difference with respect to prevalence and severity of dysmenorrhea was found between nulligravid women and those in whom pregnancy had been terminated by either spontaneous or induced abortion.[7]

In an epidemiologic study of an adolescent population (aged 12-17 y), Klein and Litt reported a prevalence of dysmenorrhea of 59.7%.[24] Of patients reporting pain, 12% described it as severe; 37%, as moderate; and 49%, as mild. Dysmenorrhea caused 14% of patients to miss school frequently. Although black adolescents reported no increased incidence of dysmenorrhea, they were absent from school more frequently (23.6%) than whites (12.3%), even after adjusting for socioeconomic status.

International

The prevalence of dysmenorrhea worldwide is similar to that in the US, with rates ranging from 15.8-89.5%, with higher prevalence rates reported in adolescent populations.[25, 26, 27, 7, 28, 22, 29, 30]

Mortality/Morbidity

Dysmenorrhea can disrupt personal life and is a significant public health problem associated with substantial economic loss related to work absences. Ten percent of women with the condition have severe pain that can be incapacitating. In the United States, the annual economic loss has been estimated at 600 million work hours and 2 billion dollars.[31]

Race

No data suggest that race affects the incidence of dysmenorrhea.

Sex

See Frequency.

Age

See Frequency.

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Contributor Information and Disclosures
Author

Karim Anton Calis, PharmD, MPH, FASHP, FCCP  Adjunct Clinical Investigator, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health; Clinical Professor, Medical College of Virginia, Virginia Commonwealth University School of Medicine; Clinical Professor, University of Maryland School of Medicine

Karim Anton Calis, PharmD, MPH, FASHP, FCCP is a member of the following medical societies: American College of Clinical Pharmacy, American Society of Health-System Pharmacists, and Endocrine Society

Disclosure: Nothing to disclose.

Coauthor(s)

Vaishali Popat, MD, MPH  Clinical Investigator, Intramural Research Program on Reproductive and Adult Endocrinology, National Institutes of Child Health and Human Development, National Institutes of Health

Vaishali Popat, MD, MPH is a member of the following medical societies: American College of Physicians and Endocrine Society

Disclosure: Nothing to disclose.

Devra K Dang, PharmD, BCPS, CDE  Associate Clinical Professor, University of Connecticut School of Pharmacy, Clinical Faculty, Burgdorf Health Center

Disclosure: Nothing to disclose.

Sophia N Kalantaridou, MD  Assistant Professor, Department of Obstetrics and Gynecology, University of Ioannina Medical School, Greece

Disclosure: Nothing to disclose.

Specialty Editor Board

Anthony Charles Sciscione, DO  Professor, Department of Obstetrics and Gynecology, Drexel University College of Medicine; Director, Maternal and Fetal Medicine, Christiana Care Health System; Director, Delaware Center for Maternal and Fetal Medicine

Anthony Charles Sciscione, DO is a member of the following medical societies: American College of Obstetricians and Gynecologists and American Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

A David Barnes, MD, PhD, MPH, FACOG  Consulting Staff, Department of Obstetrics and Gynecology, Mammoth Hospital (Mammoth Lakes, California), Pioneer Valley Hospital (Salt Lake City, Utah), Warren General Hospital (Warren, Pennsylvania), and Mountain West Hospital (Tooele, Utah)

A David Barnes, MD, PhD, MPH, FACOG is a member of the following medical societies: American College of Forensic Examiners, American College of Obstetricians and Gynecologists, American Medical Association, Association of Military Surgeons of the US, and Utah Medical Association

Disclosure: Nothing to disclose.

Frederick B Gaupp, MD  Consulting Staff, Department of Family Practice, Hancock Medical Center

Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians

Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD  Professor, Coordinator of Quality Assurance/Quality Improvement, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine

Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

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