Adolescents presenting with CPP may be experiencing dysmenorrhea (see this section for a more complete discussion of dysmenorrhea). Adolescents are often unable to keep accurate records of their menstrual cycles making it difficult for many of them to recognize a cyclic pattern to their pain.

Dysmenorrhea is very common in the adolescent population with surveys reporting up to 92% of teenagers experience dysmenorrhea and up to 50% of them missing school or work because of debilitating symptoms. However, the vast majority of them do not report the symptoms to their parents, and only 14 - 31% seek help from healthcare providers.

Dysmenorrhea is classified as primary dysmenorrhea if it occurs with the absence of pelvic pathology and secondary dysmenorrhea if it occurs in the presence of pelvic pathology. Possible causes of secondary dysmenorrhea include endometriosis, obstructive müllerian malformations, cervical stenosis, uterine polyps or myomas, PID, and ovarian cysts.

Primary dysmenorrhea is much more common than secondary dysmenorrhea and usually presents once ovulatory cycles are established, usually about 6 - 12 months after menarche. Symptoms usually start with or just prior to the menses. Patients may present with a broad range of symptoms including crampy, spasmodic, labor-like pain over the lower abdomen and back, dull aching or stabbing pain, nausea, vomiting, diarrhea, headache, fatigue, low back pain, thigh pain, dizziness, and syncope. Primary dysmenorrhea occurs due to the metabolism of arachidonic acid through the cyclooxygenase pathway leading to the synthesis of prostaglandins, thromboxanes, and prostacyclin. The human endometrium catalyzes prostaglandins PGF2 and PGE2 in increased amounts during the first 36 - 48 h of menses.

The symptoms of primary dysmenorrhea typically begin after ovulatory cycles are established, progress during the teen years, and improve when the patient enters her early twenties. Treatment should include education, reassurance and the maximization of healthy lifestyles with the use of medical interventions as indicated. NSAIDS interfere with the metabolism of arachidonic acid and therefore represent a mainstay of dysmenorrhea treatment. Therapy should be initiated at the first sign of discomfort or menstrual flow and should be taken in the prescribed doses to gain the most relief. Patients can look forward to a high response rate with NASAs alone within 6 months of therapy. If the patient fails NASAs or is sexually active, oral contraceptive pills decrease dysmenorrhea by diminishing the production of prostaglandins from the endometrium. Other therapeutic methods include: TENS (electrical stimulation) units, calcium channel blockers, acupuncture, and depot medroxyprogesterone acetate.

Patients who continue to experience dysmenorrhea despite treatment with NSAIDS and oral contraceptives should be further evaluated for secondary causes of dysmenorrhea such as endometriosis and obstructive müllerian abnormalities. Additional evaluation may include pelvic ultrasound and/or diagnostic laparoscopy.