Causes of Period Pain: Primary and Secondary Dysmenorrhoea Explained

The prostaglandin mechanism, all causes of secondary dysmenorrhoea, and red flags that warrant assessment.

Part of the Access Doctor period pain guide.

Primary Dysmenorrhoea: The Prostaglandin Mechanism

Primary dysmenorrhoea is period pain with no identifiable underlying gynaecological cause. It typically begins in adolescence within 1–2 years of the first period and is the most common type of period pain.

The mechanism involves prostaglandins — specifically prostaglandin F2α (PGF2α) and prostaglandin E2 (PGE2). As progesterone falls at the end of the luteal phase:

• The endometrium (uterine lining) releases prostaglandins in large quantities as it begins to shed
• Prostaglandins trigger powerful uterine muscle contractions to help expel the shed lining
• Simultaneously, prostaglandins cause vasoconstriction — narrowing of blood vessels supplying the uterine muscle
• The combination of intense contraction and reduced blood supply creates ischaemia — the uterine muscle is temporarily deprived of oxygen, producing cramping pain similar in mechanism to angina

Women with primary dysmenorrhoea produce significantly higher levels of prostaglandins than women without period pain. Prostaglandin levels are highest in the first 24–48 hours of menstruation, which is why pain is typically worst on day one or two.

Secondary Dysmenorrhoea: Overview

Secondary dysmenorrhoea is period pain caused or significantly amplified by an underlying gynaecological condition. It typically:

• Begins later in life (20s–40s) or worsens progressively after previously manageable periods
• Is often more severe and starts earlier — sometimes days before menstruation
• May not respond fully to standard NSAID doses
• Is frequently accompanied by additional symptoms (heavy bleeding, dyspareunia, bowel/bladder symptoms)

Endometriosis

In endometriosis, tissue similar to the uterine lining grows outside the uterus — most commonly on the ovaries, fallopian tubes, uterosacral ligaments, bladder, or bowel. This tissue responds to monthly hormonal changes: it thickens, breaks down, and bleeds internally each cycle. Unlike uterine lining tissue, it has no route of escape, causing:

• Local inflammation and adhesions between organs
• Ovarian endometriomas (“chocolate cysts”)
• Progressively worsening dysmenorrhoea — often the defining symptom
• Deep dyspareunia (pain during sex, particularly deep penetration)
• Bowel symptoms (pain with defecation, rectal bleeding at menstruation)
• Bladder symptoms (pain when urinating around periods)

Endometriosis affects approximately 1 in 10 women. The average time to diagnosis in the UK is 8 years — a widely-documented failing of the healthcare system for this condition. Diagnosis requires specialist assessment; laparoscopy (keyhole surgery) remains the gold standard for confirmation. See the full guide: Endometriosis & Period Pain.

Adenomyosis

Adenomyosis occurs when endometrial tissue grows into the muscular wall of the uterus (myometrium) rather than outside it. The uterus becomes enlarged, boggy, and tender. Adenomyosis causes:

• Heavy, prolonged periods
• Severe dysmenorrhoea — often worse than in primary dysmenorrhoea
• Chronic pelvic pain
• Uterine tenderness on examination

Adenomyosis predominantly affects women aged 35–50 and is frequently underdiagnosed. Unlike endometriosis, it cannot be removed without hysterectomy, but hormonal treatments (Mirena IUS, combined pill, norethisterone) are highly effective at managing symptoms.

Uterine Fibroids

Fibroids (uterine myomas) are non-cancerous growths of uterine muscle. They are common — present in up to 70% of women by age 50 — but most cause no symptoms. Those in certain positions can worsen period pain:

• Submucosal fibroids (projecting into the uterine cavity) — most likely to cause heavy and painful periods
• Intramural fibroids (within the uterine wall) — can increase uterine size and worsen cramping
• Subserosal fibroids (on the outer surface) — less likely to affect menstruation

Polycystic Ovary Syndrome (PCOS)

PCOS disrupts the normal hormonal pattern of ovulation. When periods do occur in PCOS (often after a prolonged absence due to anovulation), a thicker-than-usual uterine lining has built up. Shedding this thicker lining generates higher prostaglandin levels and more intense cramping. The associated hormonal imbalance can also amplify the prostaglandin response.

Pelvic Inflammatory Disease (PID)

PID is an infection of the upper reproductive tract (uterus, fallopian tubes, ovaries) most commonly caused by sexually transmitted organisms (chlamydia, gonorrhoea, Mycoplasma genitalium) ascending from the lower genital tract. PID causes:

• Pelvic pain that may worsen around periods
• Abnormal vaginal discharge
• Pain during sex
• Fever and general malaise in acute cases

Prompt antibiotic treatment is essential — untreated PID can cause tubal scarring, ectopic pregnancy risk, and infertility.

Other Causes

• Ovarian cysts — functional cysts often resolve spontaneously; endometriomas cause more persistent symptoms; rupture causes sudden severe pain
• Cervical stenosis — narrowing of the cervical canal creates outflow obstruction, causing severe cramping as the uterus contracts forcefully to expel blood
• Intrauterine device (IUD/copper coil) — non-hormonal copper IUDs increase prostaglandin production and are a known cause of increased period pain, particularly in the first 3–6 months after insertion

Red Flags: When Period Pain Warrants Assessment

• Period pain that has worsened progressively over months or years
• Pain that begins before the period or persists after it ends
• Pain with deep dyspareunia (pain during sex)
• Period pain with bowel or bladder symptoms around menstruation
• Pain that does not respond to prescription-strength NSAIDs
• New significant period pain after age 30
• Period pain with difficulty conceiving
• Pain with fever and abnormal discharge (suggests PID)