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The pathophysiology of premenstrual syndrome (PMS) is centred around the ovarian hormone cycle. This theory is based on the fact that patients do not exhibit symptoms before puberty, during pregnancy, after menopause, and during treatment with gonadotrophin-releasing hormone (GnRH) analogues (1).

Currently two theories predominate and appear interlinked.

  • first theory suggests that some women are ‘sensitive’ to progesterone and progestogens, since the serum concentrations of oestrogen or progesterone are the same in those with or without PMS
  • second theory implicates the neurotransmitters serotonin and γ-aminobutyric acid (GABA)
    • serotonin receptors are responsive to oestrogen and progesterone, and selective serotonin reuptake inhibitors (SSRIs) are proven to reduce PMS symptoms.
    • GABAA receptors are associated with alterations in mood, cognition, and affect. GABA levels are modulated by the metabolite of progesterone, allopregnanolone, and in women with PMS the allopregnanolone levels appear to be reduced (1,2)


  1. Walsh S, Ismaili E, Naheed B, O’Brien S. Diagnosis, pathophysiology and management of premenstrual syndrome. The Obstetrician &Gynaecologist 2015;17:99–104
  2. Management of Premenstrual Syndrome: Green-top Guideline No. 48. BJOG. 2017;124(3):e73-e105.

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