Dysmenorrhea is defined as cramping pain in the lower abdomen occurring at the onset of menses. Dysmenorrhea is commonly divided into two main categories:

Primary dysmenorrhea, when there is no discernible pelvic pathology

Secondary dysmenorrhea, which is due to pelvic pathology such as endometriosis.

Primary dysmenorrhea is a diagnosis of exclusion. A thorough history and physical will help determine if there is any pelvic pathology.

Table 103.5 will help to differentiate primary from secondary dysmenorrhea.

Primary Dysmenorrhea

Primary dysmenorrhea is the most common menstrual disorder in women. Women with dysmenorrhea often experience sharp, intermittent spasms of pain, usually centered in the suprapubic area. Pain may radiate to the back of the legs or the low back. Systemic symptoms of nausea, vomiting, diarrhea, fatigue, fever, headache, or light-headedness are fairly common. Pain usually starts within hours of onset of menses and peaks within the first 1 to 2 days.

There are some theories that smoking, obesity, and alcohol consumption are related to more dysmenorrhea, but these remain controversial. The etiology of primary dysmenorrhea is not precisely understood, but most symptoms can be explained by the action of uterine prostaglandins, particularly PGF2. This prostaglandin is released as the endometrium sloughs, causing uterine contractions.

Treatment of Primary Dysmenorrhea

NSAIDs are the first choice for treatment. NSAIDs work through prostaglandin synthetase inhibition. Prostaglandins are felt to be responsible for the uterine contractions and the systemic symptoms mentioned such as nausea and diarrhea. If one particular NSAID is not effective, try one from another class.

Oral contraceptives are second-line therapy unless a woman is also seeking contraception, then they would become first-line therapy. Oral contraceptives are 90% effective in improving primary dysmenorrhea and work by reducing menstrual blood volume and suppressing ovulation. It may take up to 3 months for the oral contraceptives to become effective. Norplant and Depo-provera are also effective since these methods often induce amenorrhea.

For the 10% of patients who do not respond to NSAIDs and/or oral contraceptives, a wide range of alternative therapies have been proven effective, including transcutaneous electrical nerve stimulation (TENS), acupuncture, omega-3 fatty acids, transdermal nitroglycerin, thiamine, and magnesium supplements.

Secondary Dysmenorrhea

The onset of secondary dysmenorrhea generally occurs after age 25. The pelvic pathology can be divided into uterine causes and extrauterine causes. The uterine causes are adenomyosis, pelvic inflammatory disease, cervical stenosis, polyps, fibroids, and IUDs. The extrauterine causes are endometriosis; inflammation and scarring (adhesions); functional ovarian cysts; benign or malignant tumors of the ovary, bowel, or bladder; and inflammatory bowel disease. Some of these disorders can be determined by a careful pelvic exam. The two most important diagnostic steps are a pelvic ultrasound, including an intravaginal probe component, and laparoscopy.

Treatment of Secondary Dysmenorrhea

Treatment should focus on the underlying condition. For patients with a mass lesion or enlarged uterus on exam or ultrasound referral to a gynecologic specialist is indicated. For adenomyosis, gynecologic consultation is warranted. If a woman has an IUD, dysmenorrhea may be an indication for removal.

Although endometriosis (ectopic functioning endometrial tissue located in such places as the ovaries, uterosacral ligaments, cul de sac, and peritoneum) can be suspected on exam, it must be confirmed by laparoscopy. Endometriosis is a common cause of secondary dysmenorrhea. In fact, approximately 24% of women who complain of pelvic pain are subsequently found to have endometriosis. This condition is often associated with infertility. If pain relief is the goal, medical options include oral contraceptives, danazol, progestational agents, and GnRH agonists. If pain is severe or infertility is an issue, laparoscopic surgical excision and ablation of lesions is indicated. If pain is intractable and childbearing is not a factor, hysterectomy and oopherectomy are indicated.

Signs and symptoms

  • Mild - pelvic discomfort or cramping or heaviness on first day of bleeding with no associated symptoms
  • Moderate - discomfort occurring on first 2-3 days of menses and accompanied by mild malaise, diarrhea and headache
  • Severe - intense, cramp-like pain lasting 2-7 days; often with nausea, diarrhea, back pain, thigh pain, and headache

Incidence/Prevalence in USA:

  • > 50% of adult females have menstrual pain
  • 10% are incapacitated for 1-3 days each cycle

Predominant age:

  • Primary - teens to early 20’s
  • Secondary - 20’s to 30’s


  • Primary:
    • History is characteristic
  • Secondary:

    1. Pelvic or genital infection  
    2. Complication of pregnancy  
    3. Missed or incomplete abortion  
    4. Ectopic pregnancy  
    5. Uterine or ovarian neoplasm  
    6. Endometriosis  
    7. Urinary tract infection  
    8. Complication of uterine device

Cyclic pain associated with ovulatory cycles without demonstrable lesions affecting reproductive structures.

The pain is thought to result from uterine contractions and ischemia, probably mediated by prostaglandins produced in secretory endometrium; therefore, primary dysmenorrhea is almost always associated with ovulatory cycles. Contributing factors may include the passage of tissue through the cervix, a narrow cervical os, malposition of the uterus, lack of exercise, and anxiety about menses. This common disorder usually starts during adolescence and tends to decrease with age and after pregnancy.

Symptoms and Signs
Low abdominal pain is usually crampy or colicky but may be a dull constant ache and radiate to the lower back or legs. The pain may start before or with menses, tends to peak after 24 h, and usually subsides after 2 days. Sometimes endometrial casts (membranous dysmenorrhea) or clots are expelled. Headache, nausea, constipation or diarrhea, and urinary frequency are common; vomiting occurs occasionally. PMS symptoms (see above) may persist during part or all of the menses.

A woman should be assured that her reproductive organs are normal. Many women do not need drugs, but for women with substantially bothersome symptoms, the most effective drugs are prostaglandin synthetase inhibitors (eg, ibuprofen, naproxen, mefenamic acid). A drug may be more effective if started 24 to 48 h before and continued 1 or 2 days after menses begins. If pain continues to interfere with normal activity, suppression of ovulation with low-dose estrogen-progesterone oral contraceptives is advisable. Antiemetics may be used. Adequate rest and sleep and regular exercise may help.

Secondary Dysmenorrhea (ACQUIRED DYSMENORRHEA)
Pain with menses caused by demonstrable pathology.
Endometriosis is a common cause of dysmenorrhea; adenomyosis may also cause it. A few women have an extremely tight cervical os (secondary to conization, cryocautery, or thermocautery); pain occurs when the uterus attempts to expel tissue through the os. A pedunculated submucosal fibroid or an endometrial polyp extruding from the uterus occasionally causes cramping pain. Pelvic inflammatory disease may cause diffuse continuous low abdominal pain that tends to increase with menses. Sometimes, a cause cannot be found.

The first line of treatment is medical (eg, prostaglandin synthetase inhibitors, oral contraceptives, danazol, progestins).  If possible, the underlying disorder or anatomic abnormality is corrected, thus relieving symptoms. Dilation of a narrow cervical os may give 3 to 6 mo of relief (and allows diagnostic curettage if needed). Myomectomy, polypectomy, or dilation and curettage may be needed. Interruption of uterine nerves by presacral neurectomy and division of the sacrouterine ligaments may help selected patients. Hypnosis may be useful.


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3. McIver B, Romanski SA, Nippoldt TB. Concise review for primary-care physicians: evaluation and management of amenorrhea. Mayo Clin Proc 1997;72:1164.

4. Speroff L, Glass RH, Kase NG. Clinical gynecologic endo-crinology and infertility. 6th ed. Philadelphia: Lippincott Williams & Wilkins, 1999;421-8.

5. Hull MG. Epidemiology of infertility and polycystic ovarian disease: endocrinological and demographic studies. Gynecol Endocrinol 1987;1:235-45.


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Revision date: June 20, 2011
Last revised: by Amalia K. Gagarina, M.S., R.D.