Dysmenorrhoea and premenstrual disorders

• Dysmenorrhoea is pain with menstruation. Primary dysmenorrhoea occurs without visible pelvic disease and is driven by excess prostaglandins; secondary means an underlying cause such as endometriosis or adenomyosis is present.
• Premenstrual syndrome is a recurring pattern of physical and mood symptoms in the premenstrual phase; PMDD is the severe, function-impairing end of the spectrum with at least five characteristic symptoms including a core mood symptom.
• NSAIDs are the first medicine for primary dysmenorrhoea, started 1-2 days before expected pain and taken on a schedule. Oral contraceptives and other ovulation-suppressing methods follow once NSAIDs fail or contraception is also needed.
• PMS and PMDD are diagnosed from prospective daily symptom ratings across at least two cycles rather than a single clinic visit. ^[2]
• SSRIs are first-line for moderate or severe PMS and PMDD, usable continuously or only luteally, supported by ACOG and by RCOG guidance.

By the end of this page you should be able to:

1. Distinguish primary from secondary dysmenorrhoea.
2. Explain the prostaglandin-driven mechanism of primary dysmenorrhoea.
3. Apply the diagnostic rules for PMS and PMDD.
4. Choose staged treatments for dysmenorrhoea and for PMS/PMDD including dose ideas from credible sources.
5. Investigate red flags and suspected secondary dysmenorrhoea.
6. Adapt care for adolescents, pregnancy, older adults and low-resource settings.

Dysmenorrhoea means painful menstruation. Primary dysmenorrhoea is recurrent pain with otherwise normal menstruation when no pelvic disease or anatomic anomaly is demonstrable. It is a diagnosis of exclusion, yet it accounts for about 90% of cases. ^[1] Secondary dysmenorrhoea is menstrual pain caused by an identifiable pelvic or systemic disorder. Endometriosis is the most common cause; others include adenomyosis, fibroids, infection, outflow obstruction and intrauterine devices.

Premenstrual syndrome is a recurring cyclical pattern of physical and psychological symptoms confined to the luteal phase, causing distress. PMDD is the more narrowly defined and more severe disorder in which at least five of eleven characteristic symptoms, with at least one being a core mood symptom, occur in the late luteal phase, improve within days of bleeding and resolve afterwards, cause significant functional impairment, and are confirmed prospectively over at least two symptomatic cycles. ^[2]

The clinical classification matters because ovulation drives both dysmenorrhoea and premenstrual disorders; therefore treatments that abolish ovulation often abolish the symptoms when simpler measures fail.

Dysmenorrhoea is one of the commonest gynaecological complaints of the reproductive years. Between 50 and 90% of adolescent girls and young women report menstrual pain during their lifetime ^[3], and a systematic review and meta-analysis of 21,573 women from 38 countries reported a pooled prevalence of 71.1% (95% CI 66.6-75.2) ^[7]. About 10% of adolescents have symptoms severe enough to disrupt school and daily life. ^[3] In some Middle-Eastern studies prevalence has reached 96% (for example, 96.3% among Palestinian adolescent refugees in Jordan and the West Bank); global estimates are lower (about 45-95%). ^[3]

Primary dysmenorrhoea usually begins between 6 and 24 months after menarche, most often within the first year; estimates differ by source (RCH Melbourne: 6-12 months; Merck: within a year; StatPearls: within about 2 years). ^[1] The pain usually starts within a few hours of bleeding and resolves within 72 hours. ^[1] Secondary dysmenorrhoea accounts for about 10% of cases. ^[3] Associated factors include family history, stress and negative mood around menses, insomnia, being underweight, irregular cycles, heavy bleeding, earlier or later menarche, and lower social support. ^[3]

Premenstrual complaints are even more common. Symptom experience of PMS is reported by 4 in 10 women on RCOG criteria (Green-top Guideline No. 48) and by 20-30% on the stricter ACOG criterion for clinically significant PMS (Clinical Practice Guideline No. 7, 2023); up to 90% report at least one premenstrual symptom. ^{[4] [5]} Severe PMS affects 5-8%. ^[4] Moderate to severe PMS and PMDD together affect 5-8% of women. ^[2] Prospectively confirmed PMDD affects about 2-5% or fewer of women. ^[6]

Primary dysmenorrhoea occurs without structural disease and is biochemical in nature. Excess prostaglandin F2 alpha and E2 from late-luteal menstrual endometrium causes hypercontractile, poorly coordinated uterine contractions and vasoconstriction. Risk increases with ovulatory cycles, because progesterone withdrawal after the corpus luteum fails triggers shedding and prostaglandin release.

Secondary dysmenorrhoea is a symptom of disease rather than a diagnosis. Major causes are endometriosis, adenomyosis, fibroids (especially submucosal), pelvic inflammatory disease and adhesions, obstructive mullerian anomalies, intrauterine contraceptive devices and rarely malignancy.

For the premenstrual disorders, the cause is best understood as altered sensitivity to normal ovarian steroid fluctuations. Symptoms occur in ovulatory cycles, peak in late luteal phase, resolve when steroid levels fall, disappear in anovulatory cycles, and can be re-triggered by exogenous progestogen. Serotonin dysregulation supports the mood symptoms, which is why serotonergic drugs are effective. ^[6]

The mechanism of primary dysmenorrhoea explains both its timing and its treatment. After ovulation, progesterone rises then falls. Falling progesterone destabilises lysosomes, releasing phospholipase A2, which produces arachidonic acid and then prostaglandins. ^[3] Prostaglandin F2 alpha and E2 create hypercontractility, increased resting tone and vasoconstriction; the resulting myometrial ischaemia sensitises pain fibres. Vasopressin rises and further increases contractility. ^[3]

This peak of pain in the first 48-72 hours of bleeding explains why NSAIDs started early and given on a schedule are effective, because they block cyclooxygenase and prostaglandin synthesis, and why hormonal contraception can help by suppressing ovulation and thinning the endometrium. ^[3] Premenstrual disorders share the same steroid trigger, with rapid response to serotonergic agents, particularly for mood symptoms. ^[6]

In primary dysmenorrhoea pain is typically midline and suprapubic, sometimes radiating to the back, groins or upper thighs. It is crampy, episodic and similar with each cycle, starts within hours of bleeding and resolves within 72 hours. ^[1] Associated symptoms include nausea, vomiting, diarrhoea, headache, dizziness, fatigue and sleep disturbance. ^[3]

Secondary dysmenorrhoea begins days before bleeding, continues after it, worsens over time, and may be lateralised. Dyspareunia, heavy or irregular bleeding, infertility, fever, bowel or bladder symptoms and postcoital bleeding all suggest a pelvic cause. ^[3]

Cycle details (menarche, regularity, flow, clotted tissue), pain onset and pattern, impact on function, sexual and reproductive history, contraception, fertility wishes and infection risk. Red flags include pain unrelieved by adequate NSAIDs, late new severe pain, pain outside menstruation, one-sided severe pain, intermenstrual or postcoital bleeding, weight loss and fever.

General examination should assess pallor, vital signs and abdominal tenderness. Pelvic examination is needed when secondary causes are suspected or the woman is sexually active: look for cervical motion tenderness, adnexal tenderness, uterine enlargement and nodularity. Uterosacral nodularity supports endometriosis; an enlarged tender "boggy" uterus supports adenomyosis. Adolescents with classic primary symptoms and no red flags often do not need pelvic examination.

PMS combines physical symptoms such as bloating, mastalgia, headache, breast swelling and fatigue with psychological ones such as irritability, low mood, anxiety, lability and loss of confidence. PMDD is defined by core symptoms such as depressed mood or hopelessness, marked anxiety or tension, marked affective lability or marked irritability or anger, plus additional symptoms such as decreased interest, poor concentration, lethargy, appetite change, sleep change, feeling overwhelmed, or physical symptoms such as breast tenderness, headache, joint pain, bloating and weight gain. ^[2] The defining problem in PMDD is not the symptom list alone but the severe functional impairment.

There are two questions: is this primary or secondary dysmenorrhoea, and if the complaint is premenstrual, is it PMS, PMDD or another illness that worsens premenstrually?

For premenstrual disorders, the main mimics are medical conditions that worsen premenstrually and premenstrual exacerbation of depression, anxiety, panic or personality disorder, which rarely show the clean symptom-free interval in the follicular phase seen with PMS and PMDD.

There is no test that proves primary dysmenorrhoea. Diagnosis is clinical after excluding causes that would alter management. In new pain, perform a pregnancy test in women who might be pregnant. Use a full blood count when bleeding is heavy, and screen for infection when tenderness, discharge or postcoital bleeding suggest pelvic inflammatory disease.

Secondary-cause investigations proceed in order: transvaginal ultrasound identifies fibroids, adenomyosis, ovarian endometriomas and other masses but not superficial peritoneal endometriosis, MRI is reserved for deep disease or anomalies, and laparoscopy is the reference test when imaging is negative but symptoms are severe or fertility is required. ^[3]

The diagnosis is syndromic, with no blood test. The current criteria paraphrase as follows:

The Daily Record of Severity of Problems is the usual prospective instrument, completed for at least two consecutive cycles, with a third if the first two disagree. ^[6]

Management starts with reassurance and education, because many young women have been told that pain is a normal part of growing up. A woman with classic primary dysmenorrhoea, normal examination and no red flags can be treated without immediate investigation. ^[1]

The menstrual pain algorithm should separate primary from secondary causes, use NSAIDs and heat first, and escalate to hormonal suppression when those fail.

NSAIDs are first-line for primary dysmenorrhoea because they inhibit cyclooxygenase and reduce prostaglandin production and uterine hypercontractility. Taken on a schedule starting 1-2 days before expected pain and continuing 2-3 days, they are more effective than use only as needed. ^[3] A pooled analysis of 80 randomised trials in 5,820 women found NSAIDs 4.5 times more effective than placebo, with an OR of 4.37 (95% CI 3.76-5.09), and about twice as effective as paracetamol, with an OR of 1.89 (95% CI 1.05-3.43). ^[3] About 20% of patients do not respond. ^[3]

Fenamates such as mefenamic acid may be slightly more effective than phenylpropionic acid derivatives such as ibuprofen and naproxen because they inhibit both prostaglandin synthesis and action. ^[3] Mefenamic acid can be started at 500 mg at onset of menses or pain, followed by 250 mg every six hours for up to three days; some paediatric guidelines use 500 mg three times daily with food (RCH Melbourne). ^[3] Overall no NSAID is clearly superior, although pooled analyses single out agents such as flurbiprofen and tiaprofenic acid. ^[3] Selective COX-2 inhibitors such as celecoxib are not shown to be more effective than non-selective NSAIDs for dysmenorrhoea (Merck Manual; NICE CKS) and carry cardiovascular and gastrointestinal risk and a reversible delay of ovulation, so they are not first-line and are avoided in practice. ^[3]

NSAID adverse effects include nausea, heartburn, nephrotoxicity, bronchospasm, fluid retention and bleeding. ^[3] Paracetamol is a good alternative when NSAIDs are contraindicated and is more effective than placebo, with greatest relief two, three and four hours after dosing. ^[3]

Non-drug measures have strong evidence. Heat matches NSAIDs and outperforms paracetamol in some studies. ^[3] Regular exercise improves uterine perfusion. ^[3] Diet and herbal approaches help some women but evidence varies. ^[3] TENS and acupuncture are reasonable additions once first-line therapy has been used. ^[3]

When NSAIDs fail or contraception is also wanted, combined hormonal contraception is the usual next step, with continuous regimens more effective than cyclic ones. ^[3] Progestin-only methods, implants, injections and intrauterine systems may be especially useful for secondary dysmenorrhoea due to endometriosis, with their role in primary disease still under study. ^[3] The levonorgestrel-releasing intrauterine system suits women needing long-term contraception or with heavy bleeding. ^[3]

GnRH agonists and oral GnRH antagonists with add-back oestrogen and progestogen treat endometriosis-related pain but are expensive, short term and not appropriate for uncomplicated primary dysmenorrhoea. ^[3] Aromatase inhibitors and calcium channel blockers have limited evidence and are not routine. ^[3]

Education is the most useful starting point: explaining the link to ovulation and giving reliable information relieves much anxiety. ^[4]

Guidelines endorse regular aerobic exercise, reducing caffeine and refined sugar, avoiding excess salt, eating small frequent meals with complex carbohydrates, and cognitive behavioural therapy. ^{[4] [6]} Calcium 600 mg twice daily was superior to placebo for emotional and physical symptoms in a large randomised trial. ^[6] Pyridoxine 100 mg daily has weak superiority over placebo in meta-analyses, but doses above 200 mg daily risk neuropathy. ^[6]

Women whose symptoms are mostly physical may benefit from a prostaglandin inhibitor or diuretic; spironolactone may help fluid retention. Luteal-phase danazol can help breast pain but not the full syndrome and requires counselling and contraception because of virilisation and fetal risk. ^[6]

SSRIs are first-line therapy for PMS and PMDD, supported by a meta-analysis of 29 trials. ^[6] This is the position reflected in ACOG Clinical Practice Guideline No. 7 (2023) and in RCOG Green-top Guideline No. 48 (2016, reviewed 2023). ^{[5] [4]} Effective agents include fluoxetine, sertraline, paroxetine and escitalopram, and the SNRI venlafaxine may also help. ^[6]

SSRIs can be taken continuously or only in the luteal phase because of their rapid onset in this disorder. Luteal dosing starts 14 days before expected bleeding and stops at onset. ^[6] A meta-analysis found no significant difference between intermittent and continuous regimens overall, but luteal dosing is less reliable for somatic symptoms. ^[6] Fluoxetine, sertraline and paroxetine are approved for both continuous and luteal-phase dosing. ^[6]

The dose should be at least the dose used for depression; an insufficient response in the first cycle justifies a rise the next cycle. ^[6] Nausea is the commonest side effect and usually settles within 4-5 days; sexual side effects may be reduced by intermittent dosing. ^[6] Overall response is 50-90%. ^[6]

When SSRIs and self-help fail, suppressing ovulation is the main alternative: drospirenone-containing combined pills in a 24/4 regimen (FDA-approved for PMDD), GnRH agonists with add-back therapy, high-dose transdermal estradiol with minimal progestogen, rarely danazol and, after a dramatic response to medical suppression, occasionally hysterectomy with bilateral oophorectomy. ^[6]

Complications of the disorders include missed school or work, reduced quality of life, disturbed sleep and relationships, anaemia from heavy bleeding and depression. PMDD can extend into perinatal mood risk, so follow mood in pregnancy and after delivery. ^[5] Treatment complications include NSAID gastro-intestinal, renal and bronchospasm problems, SSRI sexual and gastrointestinal effects, thromboembolism or mood change with hormonal suppression and irreversible operative risk.

Primary dysmenorrhoea may start in adolescence and often persists into adulthood, so treatment should adapt across life stages. ^[3] Severe premenstrual disorders are usually confined to reproductive life. With a correct diagnosis, the serotonergic response and ovulation-suppressing options give a good outlook for PMDD.

There is no proven prevention and no population screening test for dysmenorrhoea. Helpful public health themes are education before menarche, prompt treatment of severe adolescent dysmenorrhoea, good infection treatment and contraception where pregnancy is unwanted. For premenstrual disorders a quick screening question about whether symptoms peak before menses and improve once bleeding starts is a low-cost prompt to start prospective rating.

Primary dysmenorrhoea is dominant in young teenagers. ^[1] Centrally useful are education, reassurance, heat and early NSAIDs, followed by hormonal suppression when needed. Pelvic examination is normally reserved for red flags or treatment failure. PMS and PMDD can occur once ovulatory cycles are established and follow the same stepwise ladder. ^[3]

Dysmenorrhoea is uncommon in pregnancy because ovulation stops; cyclical early pain needs exclusion of ectopic pregnancy and miscarriage. NSAIDs are generally avoided or contraindicated, so paracetamol is the usual analgesic. ^[3] Many women improve from PMS and PMDD in pregnancy, although mood symptoms may persist and need multidisciplinary management.

New dysmenorrhoea after years of pain-free cycles is secondary until proved otherwise; consider fibroids, adenomyosis, polyps, stenosis, prolapse and malignancy. PMDD usually resolves after menopause, but cyclical mood symptoms on cyclical hormone treatment can imitate it.

Pelvic infections such as pelvic inflammatory disease or tuberculosis may be more severe and atypical; broader cultures and longer treatment may be needed, although basic diagnostic principles remain the same.

• Education, heat and exercise have good evidence and low cost.
• Over-the-counter NSAIDs are inexpensive and effective, but they should be stored cool and dry with expiry dates checked; heat and humidity can degrade medicines. ^[3]
• Hormonal methods used for contraception are the most affordable ovulation-suppressing components for the dysmenorrhoea and PMS algorithms.
• Transvaginal ultrasound is the key secondary-cause test where available; otherwise pelvic examination and history carry more weight.
• Refer early for incapacitating pain, suspected anomaly or endometriosis, or treatment failure.

• Dysmenorrhoea is menstrual pain; primary is common and prostaglandin driven, secondary implies disease.
• Suspect secondary disease when pain precedes bleeding, persists, worsens, is lateralised or comes with red flags.
• Use scheduled NSAIDs 1-2 days before pain, with heat and exercise; about 20% do not respond. ^[3]
• Escalate to continuous combined hormonal contraception or levonorgestrel systems; reserve GnRH agonists for confirmed disease.
• Diagnose PMDD only with characteristic symptoms and prospective rating, at least two cycles.
• SSRIs are first-line for moderate or severe PMS and PMDD, continuous or luteal.
• Calcium 600 mg twice daily and vitamin B6 100 mg daily have trial support; pyridoxine over 200 mg daily is neurotoxic. ^[6]
• Always consider psychiatric and medical mimics.

No written related topics were specified for this topic; cross-link with endometriosis, heavy menstrual bleeding and contraception once the relevant gynaecology topics are verified.