Definition

Dysmenorrhoea is defined as cyclic lower abdominal pain that occurs with, or precedes, menstruation.¹ Depending on the aetiology of the condition, dysmenorrhoea may be classified as either primary or secondary. Primary dysmenorrhoea is a functional disorder that has no identifiable pathological aetiology and is typically associated with ovulation. Pain caused by a demonstrable pathology to the pelvic or reproductive structures, however, is referred to as secondary dysmenorrhoea.¹

Epidemiology

The prevalence of dysmenorrhoea varies across the globe, affecting between 16.8 and 81 per cent of women.² Of the two categories of menstrual pain, primary dysmenorrhoea is the most common, contributing to around ninety per cent of dysmenorrhoeic cases.³ Primary dysmenorrhoea usually begins during adolescence or the early twenties, generally after regular ovulation is established, and usually after the first three to six menstrual cycles.⁴ Unlike the prevalence of secondary dysmenorrhoea, which increases with advancing age, the prevalence of primary dysmenorrhoea diminishes with age and, in some cases, following pregnancy.⁴

Aetiology and pathophysiology

Primary dysmenorrhoea is caused by abnormal eicosanoid production, specifically, an abnormal increase in endometrium-derived prostaglandin (PG) F_2α and PGE₂. These proinflammatory compounds are formed under the influence of progesterone, but can also rise following endometrial shedding, endometrial cell necrosis,⁴ excess omega 6 fatty acid intake, low omega 3 fatty acid consumption and/or abnormal fatty acid metabolism.^3,5,6 The PGs implicated in the pathogenesis of dysmenorrhoea exhibit a wide range of effects. PGF_2α, for instance, affects the gastrointestinal (GI) tract, causing nausea, vomiting and diarrhoea.⁴ PGF_2α is also a potent smooth muscle stimulant and vasoconstrictor, which, in sufficient quantities, can cause uterine ischaemia, myometrial contractions and uterine pain.³ In contrast, PGE₂ is a potent vasodilator and a possible contributor to excessive menstrual bleeding.⁴ While the cytokine hypothesis of dysmenorrhoea is theoretically plausible, evidence from clinical studies is mixed.^7,8

As opposed to the proinflammatory state of primary dysmenorrhoea, the cause of secondary dysmenorrhoea is primarily pathological. Conditions usually associated with secondary dysmenorrhoea include endometriosis, uterine adenomycosis, leiomyomata or fibroids, pelvic adhesions, cervical stenosis, pelvic inflammatory disease, in situ intrauterine device and endometrial polyps.^1,4

Other factors that may increase the severity or duration of dysmenorrhoea are anxiety, low levels of exercise, low fish consumption and cigarette smoking.^1,3 Several studies also report a higher risk of dysmenorrhoea among women with high stress (i.e. occupational or perceived stress) compared to those with low stress.^9,10

Clinical manifestations

Dysmenorrhoea typically presents as recurrent, spasmodic lower abdominal or suprapubic pain that is sharp or dull in quality.⁴ In many cases, the pain radiates to the lower back or thighs. Some women also report symptomatic improvement following the application of heat to the abdomen or by assuming the fetal position.⁴ In primary dysmenorrhoea symptoms usually begin 1–3 days before menses, peak 24 hours after the onset of menstruation and subside 2–3 days later. In secondary dysmenorrhoea, menstrual pain may commence long before menses begins and continue well after menstruation has ceased.¹ It is not uncommon for women with either type of dysmenorrhoea to also experience concomitant nausea, vomiting, diarrhoea, constipation, headache, fatigue, irritability, nervousness, urinary frequency, dizziness, sleeplessness and depression.^1,3