Painful menstruation (dysmenorrhea) affects an estimated 90% of women at some point during their reproductive years, with 10% to 15% of all women unable to function because of pain. Dysmenorrhea is generally divided into two broad classiﬁcations: Primary dysmenorrhea is painful menstruation without a clinically identiﬁable cause, whereas secondary dysmenorrhea is recurrent menstrual pain resulting from a clinically identiﬁable cause or abnormality. Because the common causes of secondary dysmenorrhea (such as ﬁbroids, pelvic adhesions, adenomyosis) are more frequent in older patients, the incidence of primary dysmenorrhea is greater in adolescents whereas secondary dysmenorrhea presents later in reproductive life. (Dysmenorrhea that begins after the age of 25 is most often secondary.) Although dysmenorrhea is uncommon during the ﬁrst 6 months of menstruation because of anovulation, 38% of women experience it in their ﬁrst year. The abrupt onset of painful vaginal bleeding should suggest the possibility of a complication of pregnancy (abortion or ectopic pregnancy) rather than dysmenorrhea.
The underlying cause of primary dysmenorrhea is the overproduction of
prostaglandin F2α by the endometrium, which
is a facilitator, if not originator, of nociceptive pain signals. In addition,
prostaglandin F2α is a strong stimulator of uterine contractions, resulting in resting
intrauterine pressures of 60 to 80 torr (mm Hg) and peak contractile pressures
that sometimes exceed 400 torr. The absence of an abnormality on pelvic
examination, combined with historical characteristics, is diagnostic of primary
The possible etiologies of secondary dysmenorrhea may be broadly
classiﬁed as being intrauterine and extrauterine. Diffuse lower abdominal
cramping, back or thigh pain, nausea, diarrhea, and headache may occur with
either intrauterine or extrauterine sources of secondary dysmenorrhea and
therefore these are not diagnostic. Extrauterine sources are the most likely to
provide hints of their presence through additional nonmenstrual symptoms.
Intrauterine processes are more likely to be associated with other disturbances
of menstruation, such as intermenstrual spotting or menorrhagia.
In secondary dysmenorrhea, the deﬁnitive treatment of the underlying
cause may have to be modiﬁed by considerations such as the preservation of
fertility. Although analgesics, antispasmodics, and birth control pills may
have some temporary beneﬁt, only speciﬁc therapy aimed at correcting the cause
will ultimately be successful. When these are not practical, modiﬁcation of the
period itself (oral contraceptives, long-acting progestins, or
gonadotropin-releasing hormone [GnRH] agonists) and analgesics (including
continuous low-level topical heat, oral pain medications, and transcutaneous
electrical nerve stimulation) should be considered and may be successful.
In primary dysmenorrhea, therapies directed toward the reduction of
prostaglandins or their effects have proven the most effective. Oral
contraceptives act to reduce the substrate available for formation of
prostaglandins, whereas nonsteroidal antiinﬂammatory drugs (NSAIDs) act to
block the synthesis pathway at two later enzymatic steps (including
cyclooxygenase, COX-1, and COX-2). These
drugs are generally well tolerated and need only be taken at the time of menstruation.
NSAID therapy is generally so successful at improving, if not removing,
symptoms that if no signiﬁcant beneﬁt is seen, the original diagnosis of
primary dysmenorrhea should be reevaluated. Suppression of menstruation (depot
medroxyprogesterone acetate, GnRH agonists) may be indicated for patients with
Recent experience with continuous low-level (topical) heat therapy suggests that this modality may provide pain relief that is comparable to NSAID therapy without the associated systemic side effects. The recent development of small, wearable, air-activated devices capable of supplying a low level of topical heat at a constant temperature over a prolonged period of time ma es this a viable treatment option for many patients.