40 patients with premenstrual symptoms were randomly allocated to receive placebo patches or active treatment with transdermal oestradiol patches (2 x 100 micrograms) to suppress ovulation. Norethisterone 5 mg was given in each group from day 19-26 of the cycle to ensure a regular withdrawal bleed. Treatment was for 6 months with crossover at 3 months. Patients completed the Moos menstrual distress questionnaire (MDQ) and the premenstrual distress questionnaire (PDQ) daily throughout the study. 5 patients withdrew, 4 because of skin reactions and 1 because of considerable improvement with initial (active) treatment. After 3 months, both groups showed improvement in MDQ and PDQ scores. In general, between 3 and 6 months, patients who switched from active treatment to placebo had deteriorating scores while patients who switched from placebo to active treatment maintained or improved upon their initial gains. Significant improvements occurred after changing to active treatment in five of six negative MDQ symptom clusters and in six of ten PDQ symptoms.
"At the higher doses of 600–800 mg per day required to suppress ovulation, danazol is associated with side effects such as weight gain, mood changes, fluid retention and acne. High-dose transdermal estradiol 200 mcg provided via patch can prevent ovulation and reduce symptoms of PMS (Watson et al., 1989). However, this high-dose estrogen therapy with cyclic low-dose progestin supplementation for the last 7 days of the cycle has not been clearly demonstrated to eliminate the risk of endometrial hyperplasia associated with estrogen administration. "
[Show abstract][Hide abstract] ABSTRACT: Severe premenstrual syndrome (PMS) and, more recently, premenstrual dysphoric disorder (PMDD) have been studied extensively over the last 20 years. The defining criteria for diagnosis of the disorders according to the American College of Obstetricians and Gynecologists (ACOG) include at least one moderate to severe mood symptom and one physical symptom for the diagnosis of PMS and by DSM IV criteria a total of 5 symptoms with 1 severe mood symptom for the diagnosis of PMDD. There must be functional impairment attributed to the symptoms. The symptoms must be present for one to two weeks premenstrually with relief by day 4 of menses and should be documented prospectively for at least two cycles using a daily rating form. Nonpharmacologic management with some evidence for efficacy include cognitive behavioral relaxation therapy, aerobic exercise, as well as calcium, magnesium, vitamin B(6) L-tryptophan supplementation or a complex carbohydrate drink. Pharmacologic management with at least ten randomized controlled trials to support efficacy include selective serotonin reuptake inhibitors administered daily or premenstrually and serotonergic tricyclic antidepressants. Anxiolytics and potassium sparing diuretics have demonstrated mixed results in the literature. Hormonal therapy is geared towards producing anovulation. There is good clinical evidence for GnRH analogs with addback hormonal therapy, danocrine, and estradiol implants or patches with progestin to protect the endometrium. Oral contraceptive pills prevent ovulation and should be effective for the treatment of PMS/PMDD. However, limited evidence does not support efficacy for oral contraceptive agents containing progestins derived from 19-nortestosterone. The combination of the estrogen and progestin may produce symptoms similar to PMS, such as water retention and irritability. There is preliminary evidence that a new oral contraceptive pill containing low-dose estrogen and the progestin drospirenone, a spironolactone analog, instead of a 19-nortestosterone derivative can reduce symptoms of water retention and other side effects related to estrogen excess. The studies are in progress, however, preliminary evidence suggests that the drospirenone-containing pill called Yasmin may be effective the treatment of PMDD.
"For example, in a study which reported the positive benefits of fluoxetine, Menkes et al. (1993) reported findings that " support the proposed role of serotonergic hypoactivity in the etiology of PMS " (p.101). Similarly, in a study of estradiol patches, Watson et al. (1989) argue that their positive result " supports the earlier observation of a link between premenstrual syndrome and ovarian function " (p. 731). "
[Show abstract][Hide abstract] ABSTRACT: This paper will examine the way in which premenstrual symptomatology has been represented and regulated by psychology and psychiatry. It questions the “truths” about women's premenstrual experiences that circulate in scientific discourse, namely the fictions framed as facts that serve to regulate femininity, reproduction, and what it is to be “woman.” Hegemonic truths that define Premenstrual Dysphoric Disorder (PMDD) and its nosological predecessor Premenstrual Syndrome (PMS) are examined to illustrate how regimes of objectified knowledge and practices of “assemblage” come to regulate individual women through a process of subjectification. Five interconnected “truths” are presented as objects of scrutiny: PMDD is a thing that can be objectively defined and measured; PMDD is a pathology to be eradicated; PMDD is caused and can be treated by one factor; PMDD is a bodily phenomenon; PMDD causes women's problems or symptoms. I examine the way in which these hegemonic truths function in framing the reproductive body as a cause of disorder or distress that leads women to interpret premenstrual experiences within a pathological framework deserving medical or psychological treatment. Finally, I offer an alternative framework drawing on Eastern models of selfhood that provides a more empowering model of women's premenstrual experiences.
Journal of Medical Humanities 06/2003; 24(1):131-146. DOI:10.1023/A:1021366001305
"However, as discussed above, in some but not in all women, progesterone 'add-back' will produce a return of symptoms (Henshaw et al., 1996; Schmidt et al., 1998). Likewise when ovulation is prevented by means of estradiol implants or patches, the cyclical addition of a progesterone analogue required to induce endometrial shedding may lead to PMSlike complaints (Magos et al., 1986; Watson et al., 1989). The combination of estradiol patches and a progesterone-releasing intrauterine device would be an attractive strategy and appears to be effective (PMS O'Brien, unpublished), but, to date, has not been evaluated in controlled trials. "
[Show abstract][Hide abstract] ABSTRACT: Premenstrual dysphoric disorder was discussed by a panel of European researchers. The criteria for diagnosis of the condition,
its categorisation as a mental disorder, and its differentiation from depression and premenstrual syndrome are all considered.
Data on the treatment of premenstrual dysphoric disorder, using serotonin reuptake inhibitors and other therapies, are reviewed.
An algorithm for the treatment of premenstrual dysphoric disorder is proposed.
Archives of Women s Mental Health 04/2002; 4(4):111-119. DOI:10.1007/s007370200009 · 2.16 Impact Factor
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