Dysmenorrhea is defined as recurrent pelvic pain associated with menstruation. It is generally classified into two broad categories:

  • Primary dysmenorrhea refers to menstrual pain in the absence of any underlying pelvic pathology.
  • Secondary dysmenorrhea refers to menstrual pain associated with a specified organic etiology.



Dysmenorrhea is the most common gynecologic complaint in adolescents, occurring in 60-93% of women in this demographic group. It is more prevalent during late adolescence, with the beginning of ovulatory cycles two to three years after the commencement of menstruation. Peak incidence occurs during the late teenage years and early 20s. Dysmenorrhea is the leading cause of school and work absenteeism among young women, with one report estimating the resultant annual economic cost to be $2 billion and 600 million lost work hours.


Risk factors associated with primary dysmenorrhea include early age of menarche, heavy menstrual flow, and a positive family history. No correlation has been found with BMI or history of abortion.


Secondary dysmenorrhea is much more rare in the adolescent age group: an organic cause is implicated in approximately 10% of cases. Secondary dysmenorrhea is more likely to be associated with mid-cycle pain, dyspareunia, and metrorrhagia. The most common cause of secondary dysmenorrhea in adolescents is endometriosis. Other potential causes include complications of pregnancy, infection (e.g., PID, abscess), uterine fibroids, Mullerian anomalies, pelvic adhesions, ovarian cysts, and, rarely, ovarian tumors.


Pathogenesis of Primary Dysmenorrhea

A depiction of the described inflammatory pathway, along with a schematic of the normal menstrual cycle, is presented below for clarity.


Following ovulation, there is a buildup of phospholipids in the cell membrane of the endometrial lining in response to progesterone. With the degeneration of the corpus luteum and the onset of progesterone withdrawal, arachidonic acid is released from the endometrial cell membrane, initiating an inflammatory cascade. It is this inflammatory response, mediated by the synthesis of prostaglandins and leukotrienes, which is responsible for producing cramps, nausea, and vomiting in primary dysmenorrhea. Prostaglandin F2-alpha (PGF2-alpha) in particular has been implicated. It contributes to uterine arteriolar vasoconstriction and myometrial contractions, the combination of which leads to uterine ischemia and pain. The intensity of menstrual cramping and associated symptoms in primary dysmenorrhea have been demonstrated to be directly proportional to the amount of PGF2-alpha released. The pathophysiology of the concurrent leukotriene pathway has not been studied to the same degree and represents one potential avenue for future research.



 Primary Dysmenorrhea

  1. Typically occurs before the age of 20
  2. No underlying pathology is discovered in the pelvis
  3. Most common etiology of pain with menstruation
  4. Pathophysiology- increased production of prostaglandins and leukotrienes leading to vasoconstriction, myometrial stimulation and inflammation.  There may also be a psychological component based on attitudes towards menstruation.
  5. Clinical Symptoms
    1. Cramping pain in the midline in the suprapubic area
    2. Usually begins right before or with the start of menstruation and lasts 1-2 days
    3. May not develop symptoms until months or years after menarche because will not have symptoms with anovulatory cycles
    4. May have associated backache, leg pains, nausea, vomiting, light-headedness and headache
    5. Physical examination is usually benign except for mild suprapubic tenderness.  A thorough abdominal exam and inspection of the external genitalia is important to rule out other etiologies of the pain
    6. Pelvic examination ultrasonography, and laboratory evaluation only necessary if there is suspicion of other pathology and/or poor response to medical treatment.
    7. Clinical suspicion of another etiology if there is a history of pelvic inflammatory disease (PID), menorrhagia, and inter-menstrual bleeding.
  6. Diagnosis
    1. Diagnosis based on history and lack of organic causes
    2. Complete history should include: age at menarche, duration menstrual cycles, onset and duration of cramps, presence of other symptoms and their severity, medication use, sexual history
    3. Most often confused with endometriosis, but endometriosis pain typically begins 1-2 weeks prior to menstruation, worsens just before onset of menstruation, and is relieved by menstrual flow (as opposed to primary dysmenorrhea, which occurs within 1st or 2nd day of menstruation)
  7. Treatment
    1. NSAIDS (1st line tx- commonly aspirin, ibuprofen, naproxen)- they decrease the production of prostaglandins within the endometrium.  Must be used in the proper dosage and intervals.  Often patients do not take adequate amounts and may need prescription strength doses to obtain satisfactory symptom relief.
      1. NSAIDS should be taken 24 hours prior to expected onset of symptoms and continued throughout menses
    2. Oral Contraceptives (2nd line treatment)- inhibits the production of prostaglandins secondary to inhibiting ovulation and/or decrease in endometrial proliferation.  90% success rate.
    3. Nonmedical therapy- heating pads, exercise, massage, transcutaneous electrical nerve stimulation, etc
    4. Failure of therapy warrants a diagnostic work-up


Secondary Dysmenorrhea

Symptoms of dysmenorrhea caused by an identifiable cause

  1. Endometriosis- consider if no response to therapy.  May require laparoscopy
  2. Adenomyosis- consider US or MRI if clinical suspicion
  3. Uterine fibroids
  4. Vaginal or uterine congenital anomalies causing obstruction to flow (e.g. Cervical stenosis, pelvic adhesions)
  5. Foreign bodies



  1. Davis, A.R., and Westhoff, C.L. (2001). Primary dysmenorrhea in adolescent girls and treatment with oral contraceptionJ Pediatr Adolesc Gynecol, 14(1), 3-8. 
  2. Davis, A.R., et. al. (2005). Oral contraceptives for dysmenorrhea in adolescent girls: a randomized trialObstet Gynecol, 106(1), 97-104.
  3. Harel, Z. (2006). Dysmenorrhea in adolescents and young adults: etiology and managementJ Pediatr Adolesc Gynecol, 19, 363-371.
  4. Hillard, P. (2006). Dysmenorrhea. Pediatrics in Review, 27(2), 64-71.