- Author: Karim Anton Calis, PharmD, MPH; Chief Editor: Michel E Rivlin, MD more...
Dysmenorrhea refers to the symptom of painful menstruation. It can be divided into 2 broad categories: primary (occurring in the absence of pelvic pathology) and secondary (resulting from identifiable organic diseases).
Signs and symptoms
A complete history should include the following:
Age at menarche
Menstrual frequency, length of period, estimated menstrual flow, and presence or absence of intermenstrual bleeding
Onset, duration, type, and severity of pain, as well as its relation to the menstrual cycle
External factors affecting the pain
Impact of dysmenorrhea on physical and social activity
Progression of symptom severity
Sexual and obstetric history
Clinical features of primary dysmenorrhea include the following:
Onset shortly after menarche (≤6 months)
Usual duration of 48-72 hours (often starting several hours before or just after the menstrual flow)
Cramping or laborlike pain
Background of constant lower abdominal pain, radiating to the back or thigh
Often unremarkable pelvic examination findings (including rectal)
The following may indicate secondary dysmenorrhea[1, 2] :
Dysmenorrhea beginning in the 20s or 30s, after previous relatively painless cycles
Heavy menstrual flow or irregular bleeding
Dysmenorrhea occurring during the first or second cycles after menarche
Pelvic abnormality with physical examination
Poor response to nonsteroidal anti-inflammatory drugs (NSAIDs) or oral contraceptives (OCs)
A complete physical examination should be performed. A pelvic examination is crucial for excluding uterine irregularities, cul-de-sac tenderness, or suggestive nodularities and includes the following:
Inspection of the external genitalia
Inspection of the vaginal vault
Inspection of the cervix
See Presentation for more detail.
No tests are specific to the diagnosis of primary dysmenorrhea. The following laboratory studies may be performed to identify or exclude organic causes of secondary dysmenorrhea:
Complete blood count with differential
Gonococcal and chlamydial cultures, enzyme immunoassay, and DNA probe testing
Quantitative human chorionic gonadotropin level
Erythrocyte sedimentation rate
Cancer antigen 125 assay
If pelvic pathology is suspected, the following imaging studies may be considered:
Abdominal or transvaginal ultrasonography
Magnetic resonance imaging
Other more invasive studies that may be considered are as follows:
Dilatation and curettage
See Workup for more detail.
Pharmacotherapy is the most reliable and effective treatment for relieving dysmenorrhea. Treatment of secondary dysmenorrhea involves correction of the underlying organic cause.
NSAIDs specifically approved by the FDA for treatment of dysmenorrhea are as follows:
Other NSAIDs and analgesics that have been used include the following:
Although not approved by the FDA for treating dysmenorrhea, the following OCs are also used:
Combination OCs (eg, ethinyl estradiol with progestin or drospirenone)
Levonorgestrel intrauterine device
Depot medroxyprogesterone acetate
Preventive measures for outpatient management of dysmenorrhea include the following:
See Treatment and Medication for more detail.
Dysmenorrhea is defined as difficult menstrual flow or painful menstruation. It is one of the most common gynecologic complaints in young women who present to clinicians. Optimal management of this symptom depends on an understanding of the underlying cause. Dysmenorrhea can be divided into 2 broad categories: primary (spasmodic) and secondary (congestive).
Primary dysmenorrhea is defined as menstrual pain that is not associated with macroscopic pelvic pathology (ie, occurs in the absence of pelvic disease). It typically occurs in the first few years after menarche and affects as many as 50% of postpubertal females. Secondary dysmenorrhea is defined as menstrual pain resulting from anatomic or macroscopic pelvic pathology,[5, 7] as is seen in women with endometriosis or chronic pelvic inflammatory disease. It is most often observed in women aged 30-45 years.
The following risk factors are associated with more severe episodes of dysmenorrhea :
Earlier age at menarche
Long menstrual periods
Heavy menstrual flow
Positive family history
Some (not all) studies have found obesity and alcohol consumption to be associated with dysmenorrhea.[9, 10, 11] Physical activity and the duration of the menstrual cycle do not appear to be associated with increased menstrual pain.
Although dysmenorrhea is not life-threatening, it can be debilitating and psychologically taxing for many women. Some choose to self-medicate at home and never seek medical attention for their pain. Dysmenorrhea is responsible for significant absenteeism from work, and it is the most common reason for school absence among adolescents.
The history is critical in establishing the diagnosis of dysmenorrhea and should include an assessment of the onset, duration, type, and severity of pain. A thorough menstrual history is also essential. A complete physical examination should be performed. For younger adolescents who have never been sexually active, a careful abdominal examination is appropriate. In older adolescents or those known to be sexually active, a pelvic examination is crucial. (See Presentation.)
No tests are specific to the diagnosis of primary dysmenorrhea. Studies that may be indicated to elucidate the cause of secondary dysmenorrhea include laboratory tests, abdominal or transvaginal ultrasonography, hysterosalpingography, hysteroscopy, or laparoscopy. (See Workup.)
Treatment of dysmenorrhea is aimed at providing symptomatic relief as well as inhibiting the underlying processes that cause symptoms. Grading dysmenorrhea according to the severity of pain and the degree of limitation of daily activity may help guide the treatment strategy. Medications used may include NSAIDs and opioid analgesics, as well as oral contraceptives (OCs). In addition to pain relief, mainstays of treatment include reassurance and education. Other therapies have been proposed, but most are not well studied. (See Treatment.)
Historical attitudes toward menstrual pain were often dismissive. Pain was often attributed to women’s emotional or psychological states or to misconceptions about sex and sexual behaviors. Although the etiology and pathophysiology of dysmenorrhea have not been fully elucidated, research has led to data supporting concrete physiologic explanations for dysmenorrhea, which discredit these prior dismissive theories.[12, 13, 14]
Current evidence suggests that the pathogenesis of primary dysmenorrhea is due to prostaglandin F2α (PGF2α), a potent myometrial stimulant and vasoconstrictor, in the secretory endometrium. 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. A 3-fold increase in endometrial prostaglandins occurs from the follicular phase to the luteal phase, with a further increase occurring during menstruation. The increase in prostaglandins in the endometrium after the fall in progesterone in the late luteal phase results in increased myometrial tone and excessive uterine contraction.
Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. Substantial amounts of leukotrienes have been demonstrated in the endometria of women with primary dysmenorrhea that does not respond to treatment with prostaglandin antagonists.[10, 18, 19, 20, 21]
The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea.[22, 23, 12, 24] Vasopressin’s role in the endometrium may be related to prostaglandin synthesis and release.
In addition, a neuronal hypothesis has been advocated for the pathogenesis of primary dysmenorrhea. Type C pain neurons are stimulated by the anaerobic metabolites generated by an ischemic endometrium. Women with dysmenorrhea appear to have enhanced pain sensitivity compared to women without dysmenorrhea, even during phases of the menstrual cycle when they are not experiencing menstrual pain. This enhanced pain sensitivity may increase the risk of affected women to other chronic conditions (eg, fibromyalgia) as well as negatively impact their quality of life.
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.
In primary dysmenorrhea, there is a highly complex interplay between hormones and mediators, basal body temperature, sleep patterns, and the central nervous system (CNS), the extent of which is not completely understood.
Elevated prostaglandins may also play a role in secondary dysmenorrhea, but by definition, concomitant pelvic pathology must be present. A number of factors may be involved in the pathogenesis of secondary dysmenorrhea, including the following:
Pelvic inflammatory disease (PID)
Ovarian cysts and tumors
Cervical stenosis or occlusion
Congenital malformations (eg, bicornuate uterus or subseptate uterus)
Intrauterine contraceptive device (IUCD), or intrauterine device (IUD)
Transverse vaginal septum
Pelvic congestion syndrome
Almost any process that can affect the pelvic viscera can produce cyclic pelvic pain.
Risk factors for primary dysmenorrhea include the following:
Early age at menarche (< 12 years)
Heavy or prolonged menstrual flow
Positive family history
Risk factors for secondary dysmenorrhea include the following :
In the following sections, the more common causes of secondary dysmenorrhea are briefly summarized.
Uterine leiomyomata are benign tumors of the uterine musculature that are a common cause of dysmenorrhea because they enlarge when stimulated by estrogen. They are up to 9 times more common in black women than in white women.
In addition to pain with menses, patients may present with menorrhagia, abdominal distention, or pressure. Pelvic examination may reveal a uterine mass or irregularity. Ultrasonography is often used for determining size and location of fibroids, though computed tomography (CT) is used if ultrasonographic information is limited.[26, 27] Unless patients are symptomatic from profound anemia, these patients can be safely discharged with appropriate gynecologic follow-up. Potential complications are anemia and infertility.
Pelvic inflammatory disease
PID is an infection of the uterus and fallopian tubes, with or without ovarian or parametrial involvement. It is an ascending infection that develops during or immediately after menses; if chronic, it can lead to dysmenorrhea. The most common causative pathogens are Chlamydia trachomatis and Neisseria gonorrhoeae, though PID also can be caused by other organisms, such as Gardnerella vaginalis, anaerobes, and gram-negative rods.
Previously, the diagnosis of PID, though primarily clinical, was based on the presence of 3 major criteria (abdominal pain, adnexal pain, and cervical motion tenderness), and 1 minor criterion (fever, vaginal discharge, leukocytosis, positive cervical cultures, gram-negative stain, intracellular diplococci, or white blood cells [WBCs] on vaginal smear).
Data from the PEACH (Pelvic inflammatory disease Evaluation And Clinical Health) trial shows that the presence of adnexal tenderness has a sensitivity of 95.5% for histologic endometritis. The findings of this trial support empiric treatment of all women at risk for PID with adnexal tenderness and no other obvious cause.
On the basis of data from the PEACH trial, the Centers for Disease and Control and Prevention (CDC) recommends that all women who are at risk for PID and who exhibit adnexal, uterine, or pelvic tenderness on bimanual examination in the absence of any other explanation for these findings be treated empirically for PID.
In addition to appropriate analgesia, patients require appropriate antibiotic coverage. The most commonly used regimen consists of ceftriaxone 250 mg IM and doxycycline 100 mg daily for 14 days. Patients should be hospitalized if outpatient therapy fails, if they have intractable nausea or vomiting, if they have a complicating tubo-ovarian abscess, or if they are immunocompromised. Complications include tubo-ovarian abscess and Fitz-Hugh Curtis syndrome (perihepatitis) if pus from the fallopian tubes leaks into the peritoneum.
Tubo-ovarian abscess is a loculated infection within the fallopian tubes or ovaries, usually occurring as a sequela of PID. It is often polymicrobial.
Most commonly, patients present with fever and gradually worsening pelvic pain and tenderness; nausea, vomiting, and vaginal bleeding or discharge may be present as well. Examination may elicit tenderness on cervical motion and in the adnexal area. A pelvic mass may be present, though it is often difficult to palpate. Tubo-ovarian abscesses can be detected on pelvic ultrasonography or abdominal CT as a complex cystic structure in the pelvis, with or without loculations.
Patients are often admitted for intravenous (IV) antibiotic therapy covering Neisseria gonorrhoeae, Chlamydia, anaerobes, and gram-negative organisms. If medical therapy fails or if peritoneal signs are found on examination, surgical drainage is indicated. Infertility is almost always a complication of tubo-ovarian abscess. The most feared complication, however, is rupture, which can lead to septic shock and death; this is a true surgical emergency.
Ovarian torsion involves twisting of the adnexal structures, which leads to ischemia and ultimately necrosis if the process is not reversed in time. In a nonpregnant woman, it is almost always caused by an abnormality in the ovary, such as a cyst or a tumor. Torsion can occur in pregnancy without a requisite adnexal abnormality, and in one large series, 20% of the patients found to have torsion were pregnant.
Patients often present with severe, intermittent, colicky, unilateral pelvic or lower abdominal pain, frequently associated with nausea and vomiting. The diagnosis is often delayed because the presentation of ovarian torsion can resemble those of other disease entities, such as appendicitis or renal colic.[26, 28]
Because of these resemblances and the consequent potential for diagnostic uncertainty, CT is often performed before any other imaging modality. It is important to be familiar with the typical CT findings for torsion: ovarian enlargement exceeding 5 cm with a corkscrew appearance of the ipsilateral fallopian tube. A sonogram will usually show a large ovarian mass or cyst, but ultrasonographic evidence of torsion is difficult to obtain, because the appearance changes depending on the length of time elapsed.
If there is a high level of suspicion for ovarian torsion, a gynecologic consultation should be obtained early. Laparoscopy is not only diagnostic but also therapeutic and potentially fertility-saving. These patients are all admitted.
Ovarian cyst rupture or hemorrhage
A hemorrhagic ovarian cyst comes from an ovarian follicle in the absence of ovulation; consequently, these cysts are exclusively found in menstruating females.
Patients often present with the acute onset of pelvic or abdominal pain, along with nausea and vomiting. Examination may reveal an adnexal mass, but almost all patients with ruptured ovarian cysts have some level of adnexal tenderness. Signs of peritoneal irritation may be apparent as well. Although CT and ultrasonography can be used to visualize hemoperitoneum and the cyst, laparoscopy is required for the definitive diagnosis.
Endometriosis is the presence of endometriumlike tissue found outside of the uterus, most commonly in the ovaries. Women often present with dyspareunia and pelvic and back pain. Although endometriosis is a diagnosis of exclusion, patients may give a history of dysmenorrhea that was cyclic with menses. It is important to note, however, that endometriosis can exist concomitantly with other disease processes causing dysmenorrhea; this makes the diagnosis even more difficult.
The history may also include chronic pelvic pain unresponsive to antibiotics or analgesics. In addition, a good obstetric history may elicit frequent miscarriages or difficulty conceiving.[26, 31] The classic examination finding is a fixed uterus with “ash” spots (purple-blue discolorations) on the cervix, though this finding is not always present.
In the future, CT may hold some promise as a diagnostic tool, but at present, endometriosis can be definitively diagnosed only via laparoscopy or laparotomy. Some argue that definitive diagnosis may not even be necessary. Often, endometriosis, if found, is assumed to be the cause of discomfort when it may not be. Even if endometriosis is the cause of dysmenorrhea, surgery may not be necessary if pain is controlled with hormonal therapy or analgesia. The main complication of endometriosis is rupture of an endometrioma.
Adenomyosis is defined as an invasion of myometrium by uterine adrenal glands. It is a rare disease and can resemble uterine leiomyomas and endometrial carcinoma in its presentation; accordingly, diagnosis is difficult.
Definitive diagnosis is typically accomplished by means of transvaginal ultrasonography or magnetic resonance imaging (MRI). When the latter is used, the key finding is a thickened junctional zone (JZ line)—that is, the border between myometrium and endometrium. One paper showed that adenomyosis should be in the differential diagnosis when a patient is treated for presumptive endometriosis and has chronic persistent pain.
Intrauterine contraceptive device
IUCDs (IUDs) may cause bladder or uterine perforation. The sooner a patient has a uterine perforation after IUCD placement, the more likely it is that she will present with peritoneal signs. Patients with bladder perforation may have recurrent cystitis that is unresponsive to antibiotics. The IUCD must be removed immediately to prevent further damage to the uterine or bladder walls. Abdominal radiographs may reveal the location of an IUCD if the string is not seen in the vaginal vault. A gynecologist should be consulted early.
Premenstrual dysphoric disorder
Besides dysmenorrhea, patients with premenstrual dysphoric disorder (formerly premenstrual syndrome) may have bloating, body aches, migraine headaches, breast tenderness, and emotional complaints. The effects of these symptoms are occasionally debilitating. Aside from possible vaginal brownish discharge or bleeding, pelvic examination findings are normal. It is the emergency physician’s responsibility to ensure adequate analgesia and appropriate follow-up with a gynecologist.
United States statistics
Dysmenorrhea may affect more than 50% of menstruating women, and its reported prevalence has been highly variable (eg, 45-95% ). A survey of 113 patients in a family practice setting showed a prevalence of 29-44%, but figures as high as 90% in women aged 18-45 years have been reported. The use of oral contraceptives (OCs) and nonsteroidal anti-inflammatory drugs (NSAIDs), both of which are effective in ameliorating symptoms of primary dysmenorrhea, may hinder accurate assessment of prevalence.
Primary dysmenorrhea peaks in late adolescence and the early 20s. The incidence falls with increasing age and with increasing parity. In many studies,[9, 35, 36] though not all, the reported prevalence and severity of dysmenorrhea in parous women are substantially lower. An epidemiologic study found no significant differences in prevalence and severity of dysmenorrhea between nulligravid women and those in whom pregnancy had been terminated by either spontaneous or induced abortion.
In an epidemiologic study of an adolescent population (age range, 12-17 years), Klein and Litt reported that dysmenorrhea had a prevalence of 59.7%. 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 were (12.3%), even after socioeconomic status was adjusted for.
The prevalence of dysmenorrhea worldwide is similar to that in the United States. Reported prevalences have ranged from 15.8% to 89.5%, with higher rates reported in adolescent populations.[38, 39, 40, 9, 41, 35, 42, 43]
A study of 408 young Italian women found that the prevalence of dysmenorrhea was 84.1% when only menstrual pain was considered, 55.2% when menstrual pain was associated with a need for medication, 31.9% when menstrual pain was associated with absenteeism, and 25.3% when menstrual pain was associated with both a need for medication and absenteeism.
In a longitudinal population study of 9,067 Australian women, researchers found that those who began smoking by age 13 had the greatest risk of developing chronic dysmenorrhea. Overall, approximately 60% of the women reported experiencing dysmenorrhea symptoms at some time during the study period.[45, 46]
The prevalence of period pain was higher among current smokers (29%) than nonsmokers (23%). Compared with never-smokers, ex-smokers had a 33% increased risk of chronic symptoms (odds ratio, 1.33; 95% confidence interval, 1.05 - 1.68), while current smokers had a 41% increased risk (odds ratio, 1.41; 95% CI, 1.17 - 1.70). After adjustment for socioeconomic status, lifestyle, and reproductive factors, women who began smoking before or by age 13 had a 59% increased risk (odds ratio, 1.59; 95% CI, 1.18 – 2.15), those who began at ages 14-15 had a 50% increased risk (1.50; 95% CI 1.18 to 1.90), and those who began at age 16 or older had a 26% increased risk (1.26; 95% CI 1.03 to 1.55).[45, 46]
In a cross-sectional study of 311 female Iranian undergraduate students (aged 18-27 y), the prevalence of primary dysmenorrhea was 89.1%. Factors that were significantly associated with higher dysmenorrhea pain intensity included younger age as well as familial factors (eg, low maternal formal education, family history of dysmenorrhea), social factors (living at home), and menstruation factors (eg, higher menstrual bleeding severity and shorter menstrual intervals).
Age- and race-related demographics
The most common causes of dysmenorrhea differ by age. The prevalence of this condition is estimated to be 25% among adult women and as high as 90% among adolescents.
No data suggest that race affects the incidence of dysmenorrhea.
With the use of NSAIDs, the prognosis for primary dysmenorrhea is excellent. The prognosis for secondary dysmenorrhea varies, depending on the underlying disease process. If a diagnosis of secondary dysmenorrhea is missed, the underlying pathology may lead to increased morbidity, including difficulty conceiving.
Although dysmenorrhea itself is not life-threatening, it can have a profound negative impact on a woman’s day-to-day life. Besides missing work or school, she may be unable to participate in sports or other activities and thus experience additional emotional distress. Some 10% of dysmenorrheal women have severe pain that can be incapacitating. Dysmenorrhea is a public health problem associated with substantial economic loss related to work absences (an estimated 600 million work hours and 2 billion dollars in the United States).
Smith RP. Cyclic pelvic pain and dysmenorrhea. Obstet Gynecol Clin North Am. 1993 Dec. 20(4):753-64. [Medline].
Smith RP. Gynecology in Primary Care. Baltimore: Williams & Wilkins; 1997. 389-404.
Jamieson DJ, Steege JF. The prevalence of dysmenorrhea, dyspareunia, pelvic pain, and irritable bowel syndrome in primary care practices. Obstet Gynecol. 1996 Jan. 87(1):55-8. [Medline].
Dawood MY. Dysmenorrhea. J Reprod Med. 1985 Mar. 30(3):154-67. [Medline].
Koltz MM. Dysmenorrhea, endometriosis and pelvic pain. Lemeke DP, Pattison J, Marshall LA, Cowley DS, eds. Primary Care of Women. Norwalk Conn: Appleton & Lange; 1992. 420-32.
Dawood MY. Nonsteroidal anti-inflammatory drugs and changing attitudes toward dysmenorrhea. Am J Med. 1988 May 20. 84(5A):23-9. [Medline].
Dawood MY. Dysmenorrhea. Clin Obstet Gynecol. 1990 Mar. 33(1):168-78. [Medline].
Harlow SD, Park M. A longitudinal study of risk factors for the occurrence, duration and severity of menstrual cramps in a cohort of college women. Br J Obstet Gynaecol. 1996 Nov. 103(11):1134-42. [Medline].
Andersch B, Milsom I. An epidemiologic study of young women with dysmenorrhea. Am J Obstet Gynecol. 1982 Nov 15. 144(6):655-60. [Medline].
Sundell G, Milsom I, Andersch B. Factors influencing the prevalence and severity of dysmenorrhoea in young women. Br J Obstet Gynaecol. 1990 Jul. 97(7):588-94. [Medline].
Parazzini F, Tozzi L, Mezzopane R, Luchini L, Marchini M, Fedele L. Cigarette smoking, alcohol consumption, and risk of primary dysmenorrhea. Epidemiology. 1994 Jul. 5(4):469-72. [Medline].
Durain D. Primary dysmenorrhea: assessment and management update. J Midwifery Womens Health. 2004 Nov-Dec. 49(6):520-8. [Medline].
Proctor ML, Murphy PA, Pattison HM, Suckling J, Farquhar CM. Behavioural interventions for primary and secondary dysmenorrhoea. Cochrane Database Syst Rev. 2007 Jul 18. CD002248. [Medline].
Iacovides S, Avidon I, Baker FC. What we know about primary dysmenorrhea today: a critical review. Hum Reprod Update. 2015 Nov. 21 (6):762-78. [Medline].
Willman EA, Collins WP, Clayton SG. Studies in the involvement of prostaglandins in uterine symptomatology and pathology. Br J Obstet Gynaecol. 1976 May. 83(5):337-41. [Medline].
Eden JA. Dysmenorrhea and premenstrual syndrome. NF Hacker, JG Moore, eds. Essentials of Obstetrics and Gynecology. 3rd ed. Philadelphia: WB Saunders; 1998. 386-92.
Speroff L. Postmenopausal hormone therapy into the 21st century. Int J Gynaecol Obstet. 1997 Oct. 59 Suppl 1:S3-10. [Medline].
Demers LM, Hahn DW, McGuire JL. Newer concepts in dysmenorrhea research: leukotrienes and calcium channel blockers. Dawood MY, McGuire JL, Demers LM, eds. Premenstrual Syndrome and Dysmenorrhea. London: Pitman; 1984. 205-13.
Chegini N, Rao CV. The presence of leukotriene C4- and prostacyclin-binding sites in nonpregnant human uterine tissue. J Clin Endocrinol Metab. 1988 Jan. 66(1):76-87. [Medline].
Nigam S, Benedetto C, Zonca M, Leo-Rossberg I, Lubbert H, Hammerstein J. Increased concentrations of eicosanoids and platelet-activating factor in menstrual blood from women with primary dysmenorrhea. Eicosanoids. 1991. 4(3):137-41. [Medline].
Rees MC, DiMarzo V, Tippins JR, Morris HR, Turnbull AC. Leukotriene release by endometrium and myometrium throughout the menstrual cycle in dysmenorrhoea and menorrhagia. J Endocrinol. 1987 May. 113(2):291-5. [Medline].
Akerlund M, Stromberg P, Forsling ML. Primary dysmenorrhoea and vasopressin. Br J Obstet Gynaecol. 1979 Jun. 86(6):484-7. [Medline].
Akerlund M. Pathophysiology of dysmenorrhea. Acta Obstet Gynecol Scand Suppl. 1979. 87:27-32. [Medline].
French L. Dysmenorrhea. Am Fam Physician. 2005 Jan 15. 71(2):285-91. [Medline].
Proctor M, Farquhar C. Diagnosis and management of dysmenorrhoea. BMJ. 2006 May 13. 332(7550):1134-8. [Medline]. [Full Text].
Baines PA, Allen GM. Pelvic pain and menstrual related illnesses. Emerg Med Clin North Am. 2001 Aug. 19(3):763-80. [Medline].
Kalish GM, Patel MD, Gunn ML, Dubinsky TJ. Computed tomographic and magnetic resonance features of gynecologic abnormalities in women presenting with acute or chronic abdominal pain. Ultrasound Q. 2007 Sep. 23(3):167-75. [Medline].
Kamaya A, Shin L, Chen B, Desser TS. Emergency gynecologic imaging. Semin Ultrasound CT MR. 2008 Oct. 29(5):353-68. [Medline].
Walker CK, Wiesenfeld HC. Antibiotic therapy for acute pelvic inflammatory disease: the 2006 Centers for Disease Control and Prevention sexually transmitted diseases treatment guidelines. Clin Infect Dis. 2007 Apr 1. 44 Suppl 3:S111-22. [Medline].
Houry D, Abbott JT. Ovarian torsion: a fifteen-year review. Ann Emerg Med. 2001 Aug. 38(2):156-9. [Medline].
Levy BS, Apgar BS, Surrey ES, Wysocki S. Endometriosis and chronic pain: a multispecialty roundtable discussion. J Fam Pract. 2007 Mar. 56(3 Suppl Diagnosis):S3-13. [Medline].
Parker JD, Leondires M, Sinaii N, Premkumar A, Nieman LK, Stratton P. Persistence of dysmenorrhea and nonmenstrual pain after optimal endometriosis surgery may indicate adenomyosis. Fertil Steril. 2006 Sep. 86(3):711-5. [Medline].
Sobczyk R, Braunstein ML, Solberg L, Schuman SH. A case control survey and dysmenorrhea in a family practice population: a proposed disability index. J Fam Pract. 1978 Aug. 7(2):285-90. [Medline].
Fraser IS. Prostaglandins, prostaglandin inhibitors and their roles in gynaecological disorders. Baillieres Clin Obstet Gynaecol. 1992 Dec. 6(4):829-57. [Medline].
Osuga Y, Hayashi K, Kobayashi Y, et al. Dysmenorrhea in Japanese women. Int J Gynaecol Obstet. 2005 Jan. 88(1):82-3. [Medline].
Latthe P, Mignini L, Gray R, Hills R, Khan K. Factors predisposing women to chronic pelvic pain: systematic review. BMJ. 2006 Apr 1. 332(7544):749-55. [Medline]. [Full Text].
Klein JR, Litt IF. Epidemiology of adolescent dysmenorrhea. Pediatrics. 1981 Nov. 68(5):661-4. [Medline].
Ohde S, Tokuda Y, Takahashi O, Yanai H, Hinohara S, Fukui T. Dysmenorrhea among Japanese women. Int J Gynaecol Obstet. 2008 Jan. 100(1):13-7. [Medline].
Sharma P, Malhotra C, Taneja DK, Saha R. Problems related to menstruation amongst adolescent girls. Indian J Pediatr. 2008 Feb. 75(2):125-9. [Medline].
Lee LK, Chen PC, Lee KK, Kaur J. Menstruation among adolescent girls in Malaysia: a cross-sectional school survey. Singapore Med J. 2006 Oct. 47(10):869-74. [Medline].
El-Gilany AH, Badawi K, El-Fedawy S. Epidemiology of dysmenorrhoea among adolescent students in Mansoura, Egypt. East Mediterr Health J. 2005 Jan-Mar. 11(1-2):155-63. [Medline].
Cakir M, Mungan I, Karakas T, Girisken I, Okten A. Menstrual pattern and common menstrual disorders among university students in Turkey. Pediatr Int. 2007 Dec. 49(6):938-42. [Medline].
Burnett MA, Antao V, Black A, et al. Prevalence of primary dysmenorrhea in Canada. J Obstet Gynaecol Can. 2005 Aug. 27(8):765-70. [Medline].
Grandi G, Ferrari S, Xholli A, et al. Prevalence of menstrual pain in young women: what is dysmenorrhea?. J Pain Res. 2012. 5:169-74. [Medline]. [Full Text].
Swift D. Smoking may increase risk for dysmenorrhea. Medscape Medical News from WebMD. 2014 Nov 18. Available at http://www.medscape.com/viewarticle/835082. Accessed: November 29, 2014.
Ju H, Jones M, Mishra GD. Smoking and trajectories of dysmenorrhoea among young Australian women. Tob Control. 2014 Nov 17. [Medline].
Habibi N, Huang MS, Gan WY, Zulida R, Safavi SM. Prevalence of primary dysmenorrhea and factors associated with its intensity among undergraduate students: a cross-sectional study. Pain Manag Nurs. 2015 Aug 29. [Medline].
Dawood MY. Ibuprofen and dysmenorrhea. Am J Med. 1984 Jul 13. 77(1A):87-94. [Medline].
Simpson JL, Elias S, Malinak LR, Buttram VC Jr. Heritable aspects of endometriosis. I. Genetic studies. Am J Obstet Gynecol. 1980 Jun 1. 137(3):327-31. [Medline].
Jamieson DJ, Steege JF. The association of sexual abuse with pelvic pain complaints in a primary care population. Am J Obstet Gynecol. 1997 Dec. 177(6):1408-12. [Medline].
Propst AM, Storti K, Barbieri RL. Lateral cervical displacement is associated with endometriosis. Fertil Steril. 1998 Sep. 70(3):568-70. [Medline].
Barbieri RL, Propst AM. Physical examination findings in women with endometriosis: uterosacral ligament abnormalities, lateral cervical displacement and cervical stenosis. J Gynecol Tech. 1999. 135:102.
Milsom I, Andersch B, Sundell G. The effect of flurbiprofen and naproxen sodium on intra-uterine pressure and menstrual pain in patients with primary dysmenorrhea. Acta Obstet Gynecol Scand. 1988. 67(8):711-6. [Medline].
Chan WY, Fuchs F, Powell AM. Effects of naproxen sodium on menstrual prostaglandins and primary dysmenorrhea. Obstet Gynecol. 1983 Mar. 61(3):285-91. [Medline].
Dawood MY, Khan-Dawood FS. Clinical efficacy and differential inhibition of menstrual fluid prostaglandin F2alpha in a randomized, double-blind, crossover treatment with placebo, acetaminophen, and ibuprofen in primary dysmenorrhea. Am J Obstet Gynecol. 2007 Jan. 196(1):35.e1-5. [Medline].
Zhang WY, Li Wan Po A. Efficacy of minor analgesics in primary dysmenorrhoea: a systematic review. Br J Obstet Gynaecol. 1998 Jul. 105(7):780-9. [Medline].
Rosenwaks Z, Jones GS, Henzl MR, Dubin NH, Ghodgaonkar RB, Hoffman S. Naproxen sodium, aspirin, and placebo in primary dysmenorrhea. Reduction of pain and blood levels of prostaglandin F2-alpha metabolite. Am J Obstet Gynecol. 1981 Jul 1. 140(5):592-8. [Medline].
Daniels SE, Torri S, Desjardins PJ. Valdecoxib for treatment of primary dysmenorrhea. A randomized, double-blind comparison with placebo and naproxen. J Gen Intern Med. 2005 Jan. 20(1):62-7. [Medline].
Morrison BW, Daniels SE, Kotey P, Cantu N, Seidenberg B. Rofecoxib, a specific cyclooxygenase-2 inhibitor, in primary dysmenorrhea: a randomized controlled trial. Obstet Gynecol. 1999 Oct. 94(4):504-8. [Medline].
Fujiwara H, Konno R, Netsu S, et al. Efficacy of montelukast, a leukotriene receptor antagonist, for the treatment of dysmenorrhea: a prospective, double-blind, randomized, placebo-controlled study. Eur J Obstet Gynecol Reprod Biol. 2010 Feb. 148(2):195-8. [Medline].
Wong CL, Farquhar C, Roberts H, Proctor M. Oral contraceptive pill as treatment for primary dysmenorrhoea. Cochrane Database Syst Rev. 2009 Apr 15. CD002120. [Medline].
Sillem M, Schneidereit R, Heithecker R, Mueck AO. Use of an oral contraceptive containing drospirenone in an extended regimen. Eur J Contracept Reprod Health Care. 2003 Sep. 8(3):162-9. [Medline].
Vercellini P, Frontino G, De Giorgi O, Pietropaolo G, Pasin R, Crosignani PG. Continuous use of an oral contraceptive for endometriosis-associated recurrent dysmenorrhea that does not respond to a cyclic pill regimen. Fertil Steril. 2003 Sep. 80(3):560-3. [Medline].
Cheewadhanaraks S, Choksuchat C, Dhanaworavibul K, Liabsuetrakul T. Postoperative depot medroxyprogesterone acetate versus continuous oral contraceptive pills in the treatment of endometriosis-associated pain: a randomized comparative trial. Gynecol Obstet Invest. 2012. 74(2):151-6. [Medline].
Petraglia F, Parke S, Serrani M, et al. Estradiol valerate plus dienogest versus ethinylestradiol plus levonorgestrel for the treatment of primary dysmenorrhea. Int J Gynaecol Obstet. 2014 Jun. 125(3):270-4. [Medline].
Barnard ND, Scialli AR, Hurlock D, Bertron P. Diet and sex-hormone binding globulin, dysmenorrhea, and premenstrual symptoms. Obstet Gynecol. 2000 Feb. 95(2):245-50. [Medline].
Harel Z, Biro FM, Kottenhahn RK, Rosenthal SL. Supplementation with omega-3 polyunsaturated fatty acids in the management of dysmenorrhea in adolescents. Am J Obstet Gynecol. 1996 Apr. 174(4):1335-8. [Medline].
Ziaei S, Zakeri M, Kazemnejad A. A randomised controlled trial of vitamin E in the treatment of primary dysmenorrhoea. BJOG. 2005 Apr. 112(4):466-9. [Medline].
Smith CA, Zhu X, He L, Song J. Acupuncture for primary dysmenorrhoea. Cochrane Database Syst Rev. 2011 Jan 19. CD007854. [Medline].
Witt CM, Reinhold T, Brinkhaus B, Roll S, Jena S, Willich SN. Acupuncture in patients with dysmenorrhea: a randomized study on clinical effectiveness and cost-effectiveness in usual care. Am J Obstet Gynecol. 2008 Feb. 198(2):166.e1-8. [Medline].
Ma YX, Ye XN, Liu CZ, et al. A clinical trial of acupuncture about time-varying treatment and points selection in primary dysmenorrhea. J Ethnopharmacol. 2013 Jul 9. 148(2):498-504. [Medline].
Abaraogu UO, Tabansi-Ochuogu CS. As acupressure decreases pain, acupuncture may improve some aspects of quality of life for women with primary dysmenorrhea: a systematic review with meta-analysis. J Acupunct Meridian Stud. 2015 Oct. 8 (5):220-8. [Medline].
Chen MN, Chien LW, Liu CF. Acupuncture or acupressure at the Sanyinjiao (SP6) acupoint for the treatment of primary dysmenorrhea: a meta-analysis. Evid Based Complement Alternat Med. 2013. 2013:493038. [Medline]. [Full Text].
Direkvand-Moghadam A, Khosravi A. The impact of a novel herbal Shirazi Thymus Vulgaris on primary dysmenorrhea in comparison to the classical chemical Ibuprofen. J Res Med Sci. 2012 Jul. 17(7):668-70. [Medline]. [Full Text].
Azima S, Bakhshayesh HR, Kaviani M, Abbasnia K, Sayadi M. Comparison of the effect of massage therapy and isometric exercises on primary dysmenorrhea: a randomized controlled clinical trial. J Pediatr Adolesc Gynecol. 2015 Dec. 28 (6):486-91. [Medline].
Akin M, Price W, Rodriguez G Jr, Erasala G, Hurley G, Smith RP. Continuous, low-level, topical heat wrap therapy as compared to acetaminophen for primary dysmenorrhea. J Reprod Med. 2004 Sep. 49(9):739-45. [Medline].
Akin MD, Weingand KW, Hengehold DA, Goodale MB, Hinkle RT, Smith RP. Continuous low-level topical heat in the treatment of dysmenorrhea. Obstet Gynecol. 2001 Mar. 97(3):343-9. [Medline].
Gurgan T, Urman B, Aksu T, Develioglu O, Zeyneloglu H, Kisnisci HA. Laparoscopic CO2 laser uterine nerve ablation for treatment of drug resistant primary dysmenorrhea. Fertil Steril. 1992 Aug. 58(2):422-4. [Medline].
Chen FP, Chang SD, Chu KK, Soong YK. Comparison of laparoscopic presacral neurectomy and laparoscopic uterine nerve ablation for primary dysmenorrhea. J Reprod Med. 1996 Jul. 41(7):463-6. [Medline].
Latthe PM, Proctor ML, Farquhar CM, Johnson N, Khan KS. Surgical interruption of pelvic nerve pathways in dysmenorrhea: a systematic review of effectiveness. Acta Obstet Gynecol Scand. 2007. 86(1):4-15. [Medline].