Dysmenorrhea

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DESCRIPTION

Menses-associated pain in pelvis, lower abdomen, or lower back

  • Primary dysmenorrhea: functional menses-associated pain due to amplification of normal menstrual physiologic processes
  • Secondary dysmenorrhea: menses-associated pain due to other pelvic pathology, such as endometriosis or müllerian anomalies

EPIDEMIOLOGY

  • Primary dysmenorrhea
    • Typically begins 6 to 24 months postmenarche
    • More likely as more cycles become ovulatory
  • Secondary dysmenorrhea
    • More common later in adolescence and in young adults
    • Müllerian anomalies that partially obstruct the outflow tract from the uterus may present with pain with or shortly after menarche.

Prevalence

  • Most common gynecologic condition among those of reproductive age, affecting 45–95% of menstruating persons
  • Up to 62% of adolescents with dysmenorrhea have endometriosis.

RISK FACTORS

  • Early menarche
  • Increased duration or amount of menstrual flow
  • Nulliparity
  • Cigarette smoking
  • Alcohol consumption
  • Family history of dysmenorrhea
  • Higher body mass index

Genetics

  • Dysmenorrhea more common in persons with a positive family history
  • Hereditary predisposition to endometriosis; polygenic mode of inheritance, multifactorial, with expression varying with interaction with environmental factors
  • Even when not in pain, persons with primary dysmenorrhea have proinflammatory cytokine gene upregulations and anti-inflammatory response gene downregulations.

PATHOPHYSIOLOGY

  • Ovulation is followed by increased progesterone release by the corpus luteum in the second half of the menstrual cycle. With the progesterone drop late in the menstrual cycle, arachidonic acid and other omega-6 fatty acids are released, triggering an inflammatory response cascade involving prostaglandins (PGs) and leukotrienes (LTs).
  • Uterine PGs and LTs cause myometrial contractions and endometrial artery vasoconstriction, resulting in uterine ischemia and pain.
    • PGF2alpha is thought to stimulate the myometrium and cause vasoconstriction.
    • Dysmenorrhea severity is directly proportional to endometrial PGF2alpha concentrations.
  • Vasopressin is also elevated among women with dysmenorrhea and may play a secondary role by potentiating uterine contractions and ischemic pain.
  • PGs and LTs can affect other body systems/organs, leading to dysmenorrhea-associated symptoms such as nausea/vomiting, diarrhea, and headache.
  • Inappropriate local aromatase activity in endometriosis lesions leads to a local estrogen synthesis, which induces cyclooxygenase (COX)-2 transcription and PGE2 synthesis. Aberrant cytokine expression also mediates inflammation/pain.
  • Secondary dysmenorrhea may be caused by a müllerian abnormality.

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