Menopause

Menopause is the permanent cessation of menstruation resulting from loss of ovarian follicular activity. It is confirmed retrospectively after twelve consecutive months of amenorrhoea in the absence of any other identifiable cause. It typically occurs at a median age of approximately fifty-one years.

It is a natural, physiological life transition accompanied by a characteristic constellation of symptoms reflecting oestrogen deficiency.

The perimenopausal transition is the period of fluctuating, declining ovarian function preceding the final menstrual period. It frequently extends over several years and carries a substantial symptomatic burden.

Individualised management addresses both symptomatic relief and longer-term health, including bone and cardiovascular health.

Pathophysiology and classification

• Natural menopause reflects progressive, age-related depletion of the ovarian follicular reserve. Declining follicular numbers produce increasingly erratic ovarian hormone production during the perimenopausal transition.
• The perimenopausal transition is characterised by fluctuating, sometimes markedly elevated, oestrogen levels alongside progressively rising follicle-stimulating hormone. This reflects reduced negative feedback from the declining, though still intermittently functional, follicular pool.
• Complete cessation of ovarian follicular activity follows, with the sustained fall in oestrogen production that characterises established postmenopausal status.
• Premature menopause (before age forty, more precisely termed primary ovarian insufficiency) and early menopause (between age forty and forty-five) are distinct categories. The subsequent duration of oestrogen deficiency is substantially longer, so hormone replacement therapy for bone and cardiovascular protection is more relevant.
• Surgical menopause, resulting from bilateral oophorectomy, produces abrupt, immediate cessation of ovarian hormone production, in contrast to the gradual, fluctuating transition of natural menopause. Symptom onset is frequently more abrupt and severe because there is no gradual physiological adaptation.

• Vasomotor symptoms (hot flushes and night sweats) are the most characteristic and commonly reported symptom. They affect a substantial majority of women to some degree during the perimenopausal transition and early postmenopausal period.
• Severity and duration vary considerably. A meaningful proportion of women have significant, persistent vasomotor symptoms for many years beyond the final menstrual period.
• Genitourinary syndrome of menopause reflects the direct effect of oestrogen deficiency on the vulvovaginal and lower urinary tract epithelium. It produces vaginal dryness, dyspareunia, and urinary symptoms including urgency and recurrent urinary tract infection.
• This is a chronic, progressive symptom complex that, unlike vasomotor symptoms, characteristically does not improve spontaneously without specific treatment.
• Additional commonly reported symptoms: sleep disturbance (related to night sweats and, independently, to hormonal effects on sleep architecture), mood disturbance and increased anxiety, cognitive symptoms (subjective difficulty with concentration and memory, sometimes termed "brain fog"), joint aches, and reduced libido. The combination and severity of symptoms vary substantially between women.
• Menstrual irregularity, reflecting the fluctuating ovarian function of the perimenopausal transition, typically precedes the final menstrual period. Cycle length and flow become increasingly irregular and unpredictable before complete cessation.
• Longer-term health implications of sustained postmenopausal oestrogen deficiency include accelerated bone loss, increased osteoporosis risk and changes in cardiovascular risk profile. These matter for longer-term menopausal health management beyond symptomatic relief.

• Diagnosis is generally clinical, based on the characteristic symptom pattern and menstrual history in a woman of the relevant age range. Hormonal confirmation is not routinely needed in the great majority of straightforward presentations at a typical age.
• Follicle-stimulating hormone measurement may be considered in specific circumstances, including assessment of suspected premature or early menopause, or where the clinical picture is atypical or diagnostic clarity is otherwise required.
• It is not generally required or particularly useful in a woman with typical symptoms at a typical age. Substantial hormonal fluctuation in the perimenopausal transition limits the reliability of a single measurement.
• Assess carefully for alternative causes of the symptom pattern where relevant, including thyroid dysfunction, which can produce overlapping symptoms.
• Assess the individual risk factor profile relevant to subsequent treatment decisions, including cardiovascular risk factors and personal or family history of venous thromboembolism or hormone-sensitive malignancy. This supports individualised management planning.

• Hormone replacement therapy is the most effective treatment for vasomotor and genitourinary symptoms. It comprises oestrogen, given alone in women who have had a hysterectomy, or combined with progestogen in women with an intact uterus to protect against unopposed oestrogen-related endometrial hyperplasia and malignancy.
• Discuss relative risks and benefits individually, as essential to informed, shared decision-making. The risks relate to breast cancer, venous thromboembolism and cardiovascular disease. They are generally modest and context-dependent, varying with formulation, route of administration, and timing of initiation relative to the menopausal transition.
• Route and formulation (oral, transdermal, or other) can be individualised to the woman's risk profile and preference. Transdermal oestrogen is generally associated with a more favourable venous thromboembolism risk profile than oral preparations, which matters in women with risk factors for this complication.
• Topical vaginal oestrogen, applied locally with minimal systemic absorption, is highly effective and generally very well tolerated for genitourinary syndrome of menopause. Use it alongside systemic hormone replacement therapy where additional local relief is required, or alone for women with genitourinary symptoms only, or where systemic hormone therapy is not desired or is contraindicated.
• Non-hormonal options for vasomotor symptoms are evidence-based alternatives for women unable or unwilling to use hormone replacement therapy.
• Certain antidepressants (particularly selective serotonin and serotonin-noradrenaline reuptake inhibitors) are used at doses and for an indication distinct from their typical use in depression.
• More recently, neurokinin-3 receptor antagonists, a targeted non-hormonal class developed for vasomotor symptoms, are available.
• Attend to longer-term health, including bone health and cardiovascular risk factor optimisation, together with general lifestyle measures (regular exercise and, for some women, dietary modification).
• Individualised counselling and shared decision-making address the woman's symptom burden, risk profile and preferences. Discuss the appropriate duration of treatment and arrange structured, ongoing follow-up and reassessment.