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Premenstrual Syndrome (P.M.S.)


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Premenstrual Syndrome (P.M.S.)
Premenstrual Stress (PMS)

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Premenstrual Syndrome (P.M.S.)

  1. 1. Dr. Sami Shawer P.M.S. Premenstrual Syndrome
  2. 2. Definition “A condition which manifests with distressing physical, behavioural and psychological symptoms, in the absence of organic or underlying psychiatric disease, which regularly recurs during the luteal phase of each menstrual cycle and which disappears or significantly regress by the end of menstruation” RCOG green-top guideline No. 48
  3. 3. History Katharina Dalton wrote about it for the first time in 1953. In 1980, took it to the British court to defend Anna Reynolds which was accepted by the court in this and other later trials. Nowadays; promoting PMDD as a psychiatric disorder.
  4. 4. Epidemiology Varies with different definitions of PMS. (RCOG – American Psychiatric Association – WHO). 80% of women experienced at least one symptom attributed to PMS. 5% suffer from severe PMS (withdrawal from social and professional activities).
  5. 5. Service Delivery GPs should deal with most cases of PMS. Ideally, severe PMS should be managed by a multidisciplinary team (gynaecologist, psychiatrist, dietician and counsellor). Practically, gynaecologist and psychiatrist should be involved in severe cases.
  6. 6. Types of P.M.S. Mild: Does not interfere with personal/social and professional life. Moderate: Interferes with personal/social and professional life but still able to function and interact. Severe: Unable to interact personally/socially or professionally – withdraws from social and professional activities. PMDD (Premenstrual Dysphoric Disorder): Severe PMS (USA institutes).
  7. 7. Aetiology  Remains unknown.  Effect of cyclic ovarian hormones on neurotransmitters (Serotonin – GABA) appears to be a key factor.  Recent studies: high glutamate levels prior to menstruation in rats.  40% of symptomatic women have significant decline in beta-endorphins.  In one study, elevated serum psedocholinesterase were found.  May have genetic factor: (93% of identical twins will both C/O PMS compared to 44% in dizygotic twins).  Cultural factors (reported to be of less intensity in war times).  Evolutionary rationales.
  8. 8. Risk Factors High caffeine intake. Alcohol abuse. Stress. Anxiety. History of Depression. Increasing age (worse in late 30s). Overweight. Family history. Dietary Factors (low levels of certain vitamins and minerals).
  9. 9. Symptoms Psychological:Psychological: Irritability. Mood swings. Depression. Feeling out of control Behavioural:Behavioural: Aggression. Reduced cognitive abilities and forgetfulness. Increase in accidents (reduced concentration).
  10. 10. Symptoms Physical:Physical: Fatigue. Headaches. Breast tenderness. Bloating. Pelvic pain. Joints pain. Acne. Appetite changes. Swelling.
  11. 11. How to diagnose?! Symptoms should be recorded prospectively for at least two cycles using symptoms diary. Daily record of severity of problems (DRSP):
  12. 12. Treatment Traditional and Complementary medicines should be considered. Although many complementary therapies are not evidence-based but it is generally agreed that it is beneficial and may be used. Most efficacious treatments used in PMS are unlicensed for PMS.
  13. 13. Complementary therapies Data limited . Interactions with conventional medicines should be considered. Regular monitoring of the response using charts should be done. Best data appear to exist for: Vitamin D/Calcium Magnesium Agnus Castus
  14. 14. Cognitive Behavioural Therapy (CBT) In a RCT lasting 6 months; CBT proved to have same efficacy as Fluoxetine but with better maintenance.
  15. 15. SSRIs and SNRIs Should be considered as 1st line of treatment in severe PMS. Prescribing restriction to health professionals with expertise in this area. (few suicides in young women using SSRIs for depression reported) Luteal phase use is superior to continuous use in relation to symptoms resolution and withdrawal. Citalopram may be effective where other SSRIs failed. No evidence for better results if combined therapy with ovulation suppression.
  16. 16. Ovulation Suppression 1. Combined oral contraceptive pills: (Yasmin, Yaz) - should be considered as a 1st line of treatment. - continuous use is superior to cyclic (risk ?!) 2. Percutaneous Estradiol: (patch, implant) - 100 micrograms twice weekly as effective as 2oo. - alternative contraception should be used as barrier or intrauterine method. - low-dose progestogen to be added minimize adverse effects (cyclogest pessary – crinone 8% gel) - not licensed for treatment of PMS. 3. Danazol: (200 mg BD) - beneficial. - potential irreversible virilising effects. - advise to use contraception. - not licensed for treatment of PMS.
  17. 17. 4. GnRHa: -Retained for those with the most severe symptoms. -Should be considered as a 2nd or 3rd line of treatment. -Add-back hormone therapy should be used. -Low-dose therapy in not recommended (no benefit). -Treatment for 6 months if used alone. -If combined with HRT; annual bone density measurement. -Not licensed for treatment of PMS. 5. Progesterone: of no benefit in most of the clinical trials. Ovulation Suppression
  18. 18. Surgical Approach (TAH + BSO) Rarely done for treatment of PMS. For severe cases where medical treatment failed. GnRHa should be use pre- operative as test of cure. HRT should be considered.
  19. 19. Summary PMS is usually underestimated. Symptoms diary should be used at least for 2 cycles before making a diagnosis and to evaluate treatment plans. Multi-disciplinary team should be involved. Lifestyle change, diet, exercise and complementary therapies should be considered. C.O.C. and SSRIs in severe cases. GnRHa and Surgical approach as last lines of treatment.