Abstract

10.2217/17455057.2.2.183 © 2 ‘It is assumed that ovulationrelated mechanisms trigger premenstrual symptoms in women with a vulnerability to CNS dysregulation. Several studies have identified abnormal serotonergic parameters during the entire menstrual cycle and the luteal phase in women with premenstrual dysphoric disorder.‘ s p t t h t D h a r T t s c Premenstrual dysphoric disorder (PMDD) is a combination of emotional, behavioral and physical symptoms that occur in the luteal phase of the menstrual cycle, abate shortly after the onset of menses, and cause impairment in social and role functioning [1]. The hallmark emotional symptoms of PMDD include irritability, anxiety or tension, mood swings and depressed mood. PMDD occurs in approximately 5% of menstruating women and is considered the severe end of the spectrum of clinically significant premenstrual symptoms. Reduced quality of life (QoL), increased healthcare costs and reduced productivity at work have been documented in women with PMDD [2,3]. Recent reviews and expert guidelines summarize the diagnostic criteria, recommended forms for the prospective daily charting of symptoms and the importance of identifying a premenstrual exacerbation of an underlying mood or medical illness prior to the initiation of treatment [4–7]. The etiology of PMDD is likely to be multifactorial, and many possible etiological factors have been reviewed [8]. It is assumed that ovulation-related mechanisms trigger premenstrual symptoms in women with a vulnerability to CNS dysregulation [9]. Several studies have identified abnormal serotonergic parameters during the entire menstrual cycle and the luteal phase in women with PMDD [8]. Studies also suggest an abnormal response to allopregnanolone and other γ-aminobutyric acid (GABA)-ergic agonists during the luteal phase of the cycle [10]. The

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