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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Harv Rev Psychiatry. Author manuscript; available in PMC 2011 May 19.
Published in final edited form as:
Harv Rev Psychiatry. 2009; 17(2): 120–137.
doi:  10.1080/10673220902891836
PMCID: PMC3098121

Update on Research and Treatment of Premenstrual Dysphoric Disorder


Many women in their reproductive years experience some mood, behavioral. or physical symptoms in the week prior to menses. Variability exists in the level of symptom burden in that some women experience mild symptoms, whereas a small minority experience severe and debilitating symptoms. For an estimated 5%–8% of premenopausal women, work or social functioning are affected by severe premenstrual syndrome. Many women in this group meet diagnostic criteria for premenstrual dysphoric disorder (PMDD). Among women who suffer from PMDD, mood and behavioral symptoms such as irritability, depressed mood, tension, and labile mood dominate. Somatic complaints, including breast tenderness and bloating, also can prove disruptive to women's overall functioning and quality of life. Recent evidence suggests that individual sensitivity to cyclical variations in levels of gonadal hormones may predispose certain women to experience these mood, behavioral, and somatic symptoms. Treatments include: antidepressants of the serotonin reuptake inhibitor class, taken intermittently or throughout the menstrual cycle; medications that suppress ovarian cyclicity; and newer oral contraceptives with novel progestins. (Harv Rev Psychiatry 2009;17:120–137.)

Keywords: mood disorders, premenstrual dysphoric disorder, premenstrual syndrome

Emotional and physical symptoms are common premenstrual complaints from women, with most experiencing one or more symptoms during the final premenstrual and the initial days of the menstrual cycle.16 For the majority, such symptoms are mild. For a smaller group, however, such symptoms can be of sufficient severity to result in negative consequences for their home, social, and work lives.713 Of pronounced concern to many is the effect that the illness has on their family and social relationships,11 with some reporting feelings that life is not worth living.14 For approximately 15% of symptomatic women, such feelings result in suicide attempts.1517 Given the total length of time that women experience symptoms (seven days per month on average throughout their reproductive years), as well as the illness's prevalence, the illness burden of premenstrual dysphoric disorder (PMDD) is similar to that of dysthymic disorder and other common psychiatric conditions.18

Though the mix of mood, behavioral, and somatic symptoms that occur during the premenstrual phase has long been recognized, only recently have diagnostic criteria been specified and consensus guidelines formulated.19 Previously labeled premenstrual tension and premenstrual syndrome (PMS), the condition was described as a mix of clinically significant symptoms uncharacterized by specific criteria and accompanied by an attendant lack of diagnostic clarity, targeted research, or prescribing recommendations.19 This situation changed in 1980, when a multidisciplinary National Institute of Health consensus conference began the process of establishing clear-cut diagnostic criteria. Adopted by the Diagnostic and Statistical Manual of Mental Disorders (DSM III-R) as “late luteal phase dysphoric disorder” and subsequently termed “premenstrual dysphoric disorder” in the DSM-IV, the disorder is characterized by specific positive symptoms. The requirements for a DSM-IV diagnosis are presented in the text box.

Consistent with its focus on empirically grounded and field-test criteria, the DSM-IV required a minimum of five distinct symptoms.20,21 While the emergence of stipulated diagnostic criteria dispelled some of the ambiguity that existed prior to the formal recognition of the disorder, some women with clinically significant symptoms still may remain untreated due to failure to meet diagnostic criteria.22 Subthreshold rates of PMDD potentially affect an additional 18%–35% of women who experience up to four symptoms per month.15 In an attempt to address this problem, the American College of Obstetrics and Gynecology characterized a less severe condition, that of moderate to severe PMS. This condition is defined by the occurrence of at least one psychological or physical symptom resulting in significant impairment and substantiated by prospective symptom ratings.23 Though characterized by fewer absolute symptoms than PMDD, moderate to severe PMS may result in significant impairment due to symptom severity.

While differences in symptom burden between PMDD and moderate to severe PMS may be difficult to quantify, differences between mild PMS and moderate to severe PMS/PMDD translate into quality-of-life and economic costs. Women with moderate to severe PMS or PMDD experience greater quality-of-life detriments and work productivity losses, and incur greater health care costs, than do women with no or only mild symptoms.7 Nonetheless, almost 90% of women suffering from PMDD may be undiagnosed.18 Illness identification and appropriate treatment may be hindered by diagnostic inaccuracy and ambiguous research results—the product of differences in diagnostic instruments, methods, and criteria.19


Prior to the initiation of treatment for PMS/PMDD, adequate screening for conditions such as depression, dysthymic disorder, generalized anxiety disorder, and hypothyroidism is essential. Patients' social circumstances and life histories should be queried.24 The latter queries are especially important given the association of PMS/PMDD with trauma and sexual abuse.2429 Given that exacerbations of dysphoria and anxiety are linked to the use of alcohol and illegal drugs, patients' use of such substances should be evaluated during the clinical interview.

Diagnosis of PMS and PMDD requires two full monthly cycles of daily symptom charting.9,23 While this requirement may seem to impose an unnecessary delay in initiating treatment, it allows the clinician to differentiate between mild PMS and moderate to severe PMS and PMDD, as well as to exclude menstrual cycle exacerbation of underlying psychological conditions or disorders. The Daily Record of Severity of Problems,30,31 a 21-item measure, allows women to track 11 symptoms across the menstrual cycle. Other diagnostic measures include the Calendar of Premenstrual Experiences,32 the Moos Menstrual Distress Questionnaire,33 the Premenstrual Assessment Form,34 and the Prospective Record of the Impact and Severity of Menstruation.35 To meet diagnostic criteria for PMDD, five luteal-phase symptoms, including at least one mood symptom, must be reported together with impairment of social, emotional, or occupational functioning. For a diagnosis of moderate to severe PMS, a woman must report at least one psychological or physical symptom that results in significant impairment.23 Although there are no formal diagnostic criteria for a diagnosis of premenstrual exacerbation, it is to be considered in instances where a woman meets most of the diagnostic criteria for PMS or PMDD, while presenting with either a major psychiatric disorder or comorbid unstable medical condition.20

Definition of Search Strategy for This Review

For this review, we completed Medline and PubMed literature searches for the period of January 1950 through January 2008 using “premenstrual syndrome” and “premenstrual dypshoric disorder.” We will not discuss reviews and case reports in this article, although they were examined for background information and references. This article will discuss prevalence rates, symptom expression, and treatment recommendations. It will also consider the effect of PMDD and severe PMS in the exacerbation of mood disorders. This article tracks closely with a recently published review article by our group that was published in the Lancet.36

Prevalence Rates

Prevalence rates of premenstrual difficulties are derived primarily from retrospective reports.2,3,6,15,3739 While recall bias may affect such reports, the ratings are consistent with those of epidemiological studies using prospective ratings, which indicate between 2% and 8% of women in the United States and Europe experience moderate to severe symptoms.40,41 Slightly lower estimates (1.2% for moderate to severe PMS to 5.3% for PMDD) are projected for part of Asia based upon retrospective self-reports.42 In a European, community-based follow-up study using retrospective reports, approximately 5.8% of women were found to meet PMDD criteria, with another 18.6% reporting subthreshold symptom severity.15 The rates were found to remain relatively stable across a 48-month period.

Clinical Presentation

While some women experience symptoms for only a few days each cycle, others are affected for up to half of each month. For symptomatic women, the six days prior to menses commonly are marked by an increase in symptom levels, with the two days prior to menses resulting in the highest symptom reports,43 particularly involving mood symptoms of anger and irritability.43 While symptoms can carry over into the next menstrual cycle, a diagnosis of PMDD requires that women experience no symptoms during the pre-ovulatory period.43,44 Symptom expression tends to be consistent from month to month.13,45

Risk Factors and Etiology

Genetic vulnerabilities

Twin studies implicate heritable factors.4648 Recent association studies provide potential support for involvement of the gene coding for the serotonergic 5HT1A receptor49 as well as for the role of allelic variants of the estrogen receptor alpha gene (ESR1).50

Risk factors

High body mass index,51 stress,2,27 and experience of traumatic events25 may be risk factors for PMDD. Due to the experience of traumatic or stressful events, symptomatic women may have an impaired stress response;27,52 women with PMDD are thus more likely than controls to have histories of abuse.53


Mild premenstrual symptoms are common for many reproductive-aged women. Given their prevalence, such symptoms should be seen as physiological rather than pathological, and may have evolutionary implications.54 In lower species, sexual receptivity is enhanced and aggression reduced during the pre-ovulatory period (i.e., the period prior to ovulation), when estrogen is high.5560 Research conducted with female rodents suggests that cycle-dependent aggression may be related to greater sensitivity to changes in estrogen and progesterone levels.59,61 Other studies have attempted to model hormone-related depressive behavior in rodents using the forced swim test61,62 and by inhibiting allopregnanolone, the GABAergic neurosteroid.63

The Role of Steriods and Their Metabolites: Estrogen, Progesterone, Allopregnanolone

Noteworthy for the life course of presentday generations of women is the lack of the time involved in reproduction and childbearing. Historically, women experienced multiple pregnancies and lactation periods, with poor or inadequate nutrition often characterizing their diets. Extended periods of amenorrhea protected women from the long cyclic periods of fluctuating estrogen and progesterone levels linked to the appearance of premenstrual symptoms.64

Symptom expression during specific phases of the menstrual cycle led researchers to hypothesize the involvement of gonadal steroids in the pathophysiology of PMS.65 This hypothesis is supported by findings that symptoms are not present during nonovulatory cycles66 and disappear entirely with ovariectomy6771 or the use of ovulation inhibitors.7276

Exact mechanisms whereby gonadal steroid production may lead to symptom expression are not known but are theorized to involve both genomic and nongenomic effects of steroid hormones.77 Estrogen, perhaps through its influence on the serotonin system, is linked to positive mood and well-being, whereas the decline of progesterone characteristic of the late luteal phase has led some researchers to consider a link to CNS changes in GABA and progesterone metabolites that interact with the GABA-A receptor complex.7782

Since some women experience symptoms at the onset of ovulation and also during the early part of the luteal phase, an ebb in progesterone levels appears to be implicated. Arguing against this hypothesis, however, is that some women experience symptoms prior to the usual menstrual cycle–related decrease in progesterone. Treatment with a GnRH agonist (which abolishes menstrual cyclicity) followed by reexposure to progesterone can produce symptoms,83 whereas luteal-phase administration of progesterone has not been shown to be an effective treatment.84 In non-symptomatic women, administration of progesterone during the follicular phase has been found to enhance amygdala reactivity.85 In addition, in postmenopausal women, sequential hormone replacement results in reports of mood changes—with progesterone, rather than estrogen, linked to the experience of dysphoric moods.86,87

Rather than differences in the absolute level of progesterone, alterations in allopregnanolone, a metabolite of progesterone, may be related to PMS/PMDD pathophysiology. As with progesterone, levels of this metabolite fluctuate during the menstrual cycle.88 Some studies find that symptomatic women have lower levels than asymptomatic women,89,90 but not all studies agree.91 Progesterone metabolites and GABA-A receptors interact,7881 with symptomatic women showing less responsiveness than controls.92 Inhibitory responses to GABA-A receptor agonists are potentiated by allopregnanolone, possibly resulting in less sensitivity to GABA-A modulation.93 Symptomatic women are theorized to have an inadequate allopregnanolone response to stress due to reduced functional sensitivity of the GABA-A receptor.27 As additional support, rodent stress studies that involve social isolation find irregularities in GABA activity.94

Alternatively, differences in estrogen surge patterns,95 preovulatory estrogen peaks, or postovulatory rises in progesterone are posited as symptom triggers.83,96 Again, such theories fail to account fully for variability in timing of symptom onset. In perimenopausal women, estrogen has been found to have an antidepressant effect.97 However, the estrogen component of hormone replacement treatments also has the potential for increasing dysphoria, tentatively by enhancing progesterone receptor expression and hence progestational activity.98

Other Hormonal Differences

Greater variability in thyroid indices in PMS/PMDD susceptible women has been observed.99,100 However, PMDD should not be interpreted as masked hypothyroidism.99101 Circadian rhythm alterations, seen in anxiety and mood disorders, are also found.102,103 Studies of women with PMS reveal timing aberrations of hormone secretion; advanced timing rhythmicity for melatonin,104 cortisol, thyroid-stimulating hormone, and prolactin have thus been reported, in the absence of absolute changes in their levels.105 Differences in levels of relaxin—a reproduction-related peptide (e.g., in pregnancy-associated changes in the cervix and pubic symphysis)—also were reported, although levels were not linked to symptom expression.106

Calcium metabolism differences may result in reduced luteal-phase responsiveness to vitamin D metabolism. Among symptomatic women, declines in 1,25 (OH)2D may serve as a trigger for PMDD symptoms.107 Differences in bone and calcium metabolism and in IGF-1 levels between women with PMDD and controls may be indicative of genotypic differences.108

Intercellular differences of magnesium, in the presence of normal plasma levels, have been reported in women with PMS.109111 Such differences are not limited, however, to the luteal phase, which renders it difficult to interpret the role of magnesium in the pathophysiology of PMDD.111

Neurotransmitters in PMS/PMDD: Serotonin, GABA, Glutamate, and Beta Endorphins

Central neurotransmitters are clearly implicated in PMS/PMDD because of the mood and behavioral symptoms that are the hallmarks of the illness.112 Emotions and behavior are affected by levels of sex steroids, which easily pass the blood-brain barrier. Sex steroid receptors are plentiful—for example, in the amygdala and hypothalamus, brain regions that moderate emotions and behavior.


Serotonin is a brain neurotransmitter that is clearly involved in mood and behavior regulation, as evidenced by preclinical studies, by the antidepressant and anti-anxiety effects of drugs that increase serotonin availability, and by genetic113,114 and brain-imaging studies.115 Animal experiments aiming to shed light on the physiological role of serotonin have revealed that the most prominent behavioral effects of treatments causing serotonin depletion are enhanced aggression and sexual activity,59,117 pointing to a significant physiological role of serotonin in the modulation of sex steroid–driven behavior.116

Gonadal hormones may affect behavior through their effects upon serotonergic transmission, as shown in studies with rodents117121 and nonhuman primates.122,123 Given the role of serotonin in mood and aggression, as well the likely role of serotonin in sex steroid–driven behavior, this transmitter promises to be an important factor in PMS/PMDD pathophysiology. Premenstrual symptoms are diminished both by serotonin reuptake inhibitors (SRIs) and by other treatments that increase serotonin, such as releasing agents,124,125 a precursor,126 and a receptor agonist.127 In contrast, tryptophan-free diets128 and serotonin receptor antagonists129 can evoke PMS symptoms.

Aberrations in serotonergic transmission are found in women with PMS/PMDD.125,130140 Symptomatic women have lower density of serotonin transporter receptors than do controls.137,138 Luteal-phase PMDD symptoms can be provoked if levels of tryptophan, the serotonin precursor, are depleted or if a serotonin antagonist is administered.128,129 Moreover, administration of serotonergic probes (such as L-tryptophan, buspirone, m-CPP, and fenfluramine) results in abnormal prolactin or cortisol responses in women with PMS.125,131,133,136,139,140 Other differences include higher levels of serotonergic responsiveness in the follicular than in the luteal phase, a pattern different from that observed in controls.130 PET studies provide preliminary evidence of an association between premenstrual symptomatology and brain serotonergic transmission.132,141


Imaging studies, along with an observational study, point to the possible role of another neurotransmitter, GABA.92,142 Direct action, tolerance induction, and withdrawal effect are theorized to explain the possible influence of GABA in women with menstrual cycle phase disorders.82 Possible aberrations in GABA-A function as the pathophysiological trigger for the disorder is not uncontested,8991,143 however, and progesterone withdrawal as a mechanism in PMS/PMDD pathophysiology is also disputed. From a symptom-relief standpoint, GABA-A modulation may not be practical,144 but GABAergic and serotonergic neurons145147 do interact, making the role of GABA in PMS/PMDD pathophysiology theoretically consistent with the serotonin hypothesis. In addition, SRIs have been shown to affect the production of enzymes involved in progesterone metabolites that modulate GABA-A receptors.148,149


For both symptomatic and nonsymptomatic women, levels of the excitatory neurotransmitter glutamate fluctuate during the menstrual cycle. Luteal-phase levels of glutamate/creatine plus phosphocreatine in the medial prefrontal cortex are thus lower for all women. However, symptomatic women may have an increased sensitivity to such cyclical changes.150


Differences in beta-endorphin levels between the periovula-tory and premenstrual phases have been reported in women diagnosed with PMS.151153 The beta-endorphin withdrawal hypothesis proposed that decreased levels of endogenous opioids were linked to PMS symptom expression and pain sensitivity.154,155 A study comparing women with PMDD (n = 27) and healthy controls (n = 27) during both the follicular and luteal phases found that during both cycle phases, women with PMDD had lower levels of cortisol and beta-endorphins, shorter pain thresholds and tolerance times, and higher blood pressure levels at rest and during pain testing.156 These findings implicate the hypothalamicpituary-gonadal axis in PMDD pain sensitivity,156 which is consistent with findings of potential HPG-axis dysregulation in depressive and mood disorders.157,158

Reactivity and Stress Responses

Women with PMS differ from controls in their acoustic startle responses, with symptomatic women exhibiting an accentuated startle response indicative of increased physiological reactivity.159 Differences in luteal-phase reactivity are potentially indicative of increased stress responses among women with PMDD.160 In rodent models, an increased startle response was found to result from progesterone withdrawal,161,162 possibly indicating an upregulation of the alpha-4 unit of the GABA-A receptor complex.161 As discussed above, neurosteroid effects on GABA-A receptor function may have behavioral implications for PMDD.161

Menstrual Cycle Phase-Related Cognitive Biases,Negative Affective Processing, and Impulsivity

Late luteal phase–biased processing of information may increase symptomatic women's experience of negative mood states. Facial emotion discrimination tests administered to 28 PMDD patients and 27 controls found that women with PMDD demonstrated a luteal phase–dependent negative bias in nonverbal processing of affective content.163 This result is consistent with fMRI research,164 which shows increases in luteal-phase negative affect, and with phase-related negative perceptions reported by women with PMDD.163 Such cycle-related differences in affective processing and physiological reactivity may also be observable in measures of personality. In a study of major depressive disorder (MDD) and PMDD patients, women with either MDD or PMDD had higher harm avoidance scores than did controls.165 Women with PMDD also had higher novelty-seeking/impulsivity scores than did women with MDD, perhaps pointing to a loss of impulse control as a potential diagnostic feature of PMDD. In the cited study, impulsivity was measured by luteal-phase questionnaire report. It should be noted that such findings highlight the role of menstrual phase–specific abnormalities induced by cycle-related physiological changes, and do not suggest the existence of underlying trait differences in women with PMDD per se.

Somatic Symptom Pathophysiology

Somatic symptoms of breast tenderness, bloating, and joint and muscle pain are common among women with PMS. It is not known, however, whether such symptoms result from alterations in peripheral hormone-responsive tissues or, instead, are the effect of a lowered tolerance for physical discomfort. In women reporting symptoms of fluid retention and breast enlargement, studies have been unable to confirm tissue changes.166,167 SRIs, however, have shown some palliative effects.10 Prolactin-lowering agents, such as the dopamine D2 receptor agonist bromocriptine168,169 and chasteberry (Vitex Agnus Castus),170 effectively treat premenstrual mastalgia, as does luteal administration of danazol and estrogen receptor antagonists.171,172

Among women with PMDD, severe abdominal bloating often occurs in the absence of actual weight gain, with aldosterone, a progesterone metabolite173 and deoxycorticosterone, an aldosterone agonist,64,173 being the putative agents (either alone or together). Some recent evidence points to disturbed fluid-regulating mechanisms in symptomatic women during the luteal phase.174

Other common somatic complaints—for example, premenstrual headache, migraine, and epilepsy—may be constellations of other conditions, though women with migraines and comorbid endometriosis may be more likely to report PMDD symptoms.175 SRIs have been used to treat migraines prophylactically, though with little evidence to support their efficacy.176 Painful menses, dysmenorrhea, endometriosis, and menopausal symptoms often may present as PMS/PMDD.177 These are all separate conditions, however, and require specific treatment.


Two types of comorbidity potentially characterize PMDD symptomatic women: lifetime and concurrent, with premenstrual exacerbation functioning as an alternative diagnosis for some symptomatic women. Determination of true versus apparent comorbidity is complicated by symptom overlap. Lifetime comorbidity occurs when a woman has had prior experience with a psychiatric or medical condition. Concurrent morbidity occurs when a woman's premenstrual symptoms occur independently of any current psychiatric or medical condition. Premenstrual exacerbation is present when a current psychiatric or medical ailment is worsened during the premenstrual period.9,178

Women with PMDD, in particular, are more likely to have a past history of mood disorders and other psychiatric disorders,15,20,179 with lifetime estimates ranging from 30% to 70%.180188 PMDD may predict future MDD risk,189,190 and life-cycle factors associated with fluctuations in gonadal steroids—such as perimenopause191 and the postpartum period192—may place women with severe PMS/PMDD at greater risk for associated depressions.

Premenstrual exacerbation of PMDD symptoms generally refers to worsening of symptoms of MDD or bipolar disorder during the luteal phase193 but can refer to exacerbation of any existing condition, such as anxiety. Premenstrual exacerbation of depression in women with mood disorders is often reported.194197 Increased levels of neuroactive steroid concentrations (progesterone and allopregnanolone) are shown in the luteal phase by women diagnosed with mood disorders as compared to controls.198 In formerly stabilized patients with MDD, premenstrual breakthrough of depression is reported,194,199 as is mania.20,200 In a large study(n = 2,524) of women with mood disorders, 67.7% were found to have premenstrual symptoms, with women diagnosed with MDD particularly vulnerable.201 Associations with postpartum depression and perimenopausal symptoms were also found.201 The findings of this study on MDD and reproductive-cycle mood symptoms are consistent with those of other research.195,196

Women with PMS also tend to experience greater rates of anxiety disorders.202,203 Panic disorder and PMS may be characterized by common pathophysiological mechanisms since women with PMS and those with panic disorder both show a greater tendency to panic when exposed to lactate and CO2, as well as to other panicogenic agents.202,203 Premenstrual exacerbation of obsessive-compulsive disorder symptoms also may be associated with a higher prevalence of PMDD.204 In addition, women with seasonal affective disorder may be more likely to have PMDD than nondepressed women,188 and a higher rate of seasonal affective disorder has been reported in women with PMDD.187 Similarly, in a sample of young women, seasonal and premenstrual symptoms were found to be correlated.102

Other luteal-phase exacerbations of reported psychiatric illness include bulimia, substance abuse, mania, and psychosis.20 Medical conditions reportedly exacerbated during the luteal phase include migraine headaches, asthma, allergies, seizure disorders, and genital herpes.20 Common subjective reports of luteal-phase sleep disturbances were not substantiated, however, by polysomnographic measures and quantitative electroencephalographic analysis in a small study.205


In discussing treatment options, we will focus on the literature concerned with severe PMS and PMDD.

While a number of treatment options have been put forward to alleviate PMS symptoms, few are backed by clinical evidence. Importantly, even effective treatments do not reduce all symptoms equally. In addition, study results often are reported in terms of “responder” versus “nonresponder” status, and the use of summary symptom-change scales obscures the effect of treatment upon specific symptoms.206 Nonetheless, treatment should be targeted to meet individual symptom profiles.206

Serotonin Reuptake Inhibitors

SRIs have a demonstrated treatment efficacy for the management of PMS/PMDD symptoms,207 with response rates of 60%–90% reported for active treatment, as opposed to 30%–40% for placebo.208 Both mood and physical symptoms remitted with SRI use.10,209214 The serotonergric tricyclic antidepressant clomipramine,215,216 the selective SRIs (e.g., citalopram,217,218 escitalopram,219 fluoxetine,210212,220224 sertraline,225,226 and paroxetine),209,227230 and the serotonin and noradrenaline reuptake inhibitor venlafaxine231,232 all lessen both mood and somatic symptoms, while improving quality of life and social functioning.12,221,227,233 For PMS patients with severe mood symptoms, SRIs offer a strong first-treatment option.234,235

The beneficial effect of SRIs in PMS seems not to result from their antidepressant effect: antidepressants that primarily effect noradrenergic transmission thus prove less effective on PMS/PMDD symptoms,209,220,236 and SRIs' effects upon PMS/PMDD symptoms are rapid in comparison with their slower efficacy in MDD. The rapid action of SRIs in PMS/PMDD makes intermittent luteal-phase dosing—that is, dosing during the last 14 days of the cycle—an appealing alternative to continuous therapy.215,217,224,230,237240 Sertraline,237239,241,242 fluoxetine,214,224 citalopram,217 paroxetine,228,230 and clomipramine215 have all shown good efficacy in intermittent dosing during the luteal phase. Even briefer periods of active SRI treatment have been shown to be superior to placebo.229 Symptom-onset dosing—a newer dosing strategy that involves women taking medication when their symptoms begin (usually around 7 days prior to menses) and stopping at the onset of menses or within 3 days thereafter—has shown early promising results.229,243,244

In a recent randomized, controlled trial of continuous versus intermittent dosing of an SRI (paroxetine) in PMDD, continuous dosing was found to act quickly and to have a high response rate (85%–90%). Irritability symptoms, affect lability, and mood swings showed the greatest improvement, and fatigue the least.230 Intermittent dosing was equally effective as continuous treatment for irritability and mood swings, whereas depressed mood, tension, fatigue, and somatic issues were less remitted. For social functioning, continuous treatment was more effective than placebo. These findings are consistent with other studies, which found somatic symptoms less amenable to intermittent treatment than were mood symptoms.224 For somatic symptoms, continuous treatment may be warranted.230 Of the women on continuous therapy, 80% said they wanted to continue, versus 66% on intermittent treatment and 36% on placebo.230 Clinical experience suggests, however, that many, but not all, women with PMS may prefer half-cycle, intermittent dosing rather than continuous treatment.

Side effects of SRIs are usually tolerable. Nausea is common but typically abates after the first few days of treatment and does not return, even with intermittent treatment.230 Sexual side effects (reduced libido and anorgasmia) persist for the duration of treatment but do not carry over during the drug-free periods of intermittent treatment.245

Discontinuation symptoms may appear when medication is stopped abruptly,246248 although SRIs are not addictive. With intermittent treatment, discontinuation symptoms are not problematic, indicating that two weeks may not be sufficient time to provoke withdrawal symptoms.217,229 In summary, treatment efficacy of SRIs for PMDD is compelling.10,112,212,214,242

Other CNS-Acting Drugs

Lithium249 and nonserotonergic antidepressants209,220,250 have failed to show efficacy in dealing with PMS/PMDD symptoms. Buspirone,127,251 a serotonergic agonist, appears to have a weak beneficial effect. While alprazolam, the high-affinity benzodiazepine, presents conflicting reports of efficacy,144,252254 it may have merit as an adjunct for women with symptoms of premenstrual insomnia or extreme anxiety. Careful monitoring is necessary due to the risk of dependence and is especially warranted in cases of prior reported substance abuse.

Hormonal Interventions: Estrogens, Anti-estrogens, Androgens, and Gonadotrophin-Releasing Hormone Agonists

Since sex steroids prompt the symptoms of PMS/PMDD, direct action upon these substances would seem the most direct treatment approach. Progesterone deficiency as the cause of symptoms, however, has little research support,255 and reports of luteal-phase treatment with either progesterone84 or estrogen256 are unpromising.

The goal of hormonal treatment of PMS/PMDD hence is to suppress the hypothalamus-gonadal cyclicity that triggers the symptoms. Long-acting GnRH agonists7276 interrupt this cycle and have strong evidence of efficacy. Since medical menopause results, however—with attendant problems of flushing and increased risk of osteoporosis—add-back therapy with estrogen and a gestagen (a hormone with progestational activity) is generally recommended; the gestagen component reduces the risk of endometrial hyperplasia caused by estrogen. A meta-analysis76 supports the feasibility of add-back therapy, although some patients report a recurrence of symptoms with add-back gestagen therapy.257 As an alternative, combining a GnRH agonist with continuous treatment with tibolone may prove efficacious.76,258

Danazol, a synthetic partial androgen antagonist/agonist and gonadotropin inhibitor, also prevents PMS symptoms when dosed to inhibit ovulation.259264 Its side effects of hirsutism and possible teratogenicity, however, argue against its use as an initial treatment. Low-dose administration during the luteal phase is not effective for PMS generally but does help with mastalgia.171 Reduction in mastalgia can also be accomplished by luteal administration of an estrogen receptor antagonist.172

A permanent, but more invasive, method is surgical bilateral oophorectomy, which effectively abolishes symptoms.67,68,71 It should be considered, however, only as a last resort when other, more conservative treatments have failed. Add-back therapy is required, as in the case with long-acting GnRH agonists. If a hysterectomy is performed, estrogen alone is required. Surgical approaches are too invasive for most patients, however, unless a concomitant gynecological condition necessitates hysterectomy. For younger patients, ovarian preservation is recommended unless the PMS/PMDD is severe and debilitating, in which case the patient may request a bilateral oophorectomy. Prior treatment of two to three months duration with a GnRH agonist is an effective way to simulate the effect of ovarian removal and may help identify whether oophorectomy is likely to be helpful.

Inhibition of ovulation through administration of estrogen at requisite doses265267 is a relatively straightforward and effective therapy. Transdermal patches267,268 or sub-cutaneous implants265 are recommended over oral therapy. Dosages range from 100 mg to 200 mg, which are higher than for hormone replacement therapy but less than for oral contraceptives. Again, a progestogen is necessary unless the patient has had a hysterectomy. In such instances, a levonorgestrel intra-uterine system can be used. While overall evidence for this treatment is limited, there is straightforward evidence that estrogen inhibits ovulation (and thus symptoms)267 and that the IUS protects against hyperplasia.269

Combined Oral Contraceptives

Oral contraceptive (OC) management of PMS/PMDD, while widespread in clinical practice, is not supported by strong evidence. Placebo-controlled trials have been limited, and the results primarily negative.270,271 OC treatment with fewer hormone-free days might be beneficial since women on OC report more hormone-related symptoms on the seven hormone-free days,272 while reducing the number of hormone-free days results in fewer symptom complaints.273 Use of a novel OC (drospirenone plus ethinyl estradiol) has shown promise.274276 Efficacy was found in reducing PMDD symptoms, including loss of productivity and impairment of social relationships, at least over a short time frame.275 Efficacy studies done with drospirenone and with only four hormone-free days also support this approach.277,278 The therapeutic benefit of these two options may be attributable to the antialdosterone and antiandrogenic effects of drospirenone, a gestagen.279 Androgenic hormones have thus been linked to increased symptoms of irritability in women with PMDD.280 In cases of premenstrual breakthrough of depression in women being treated with antidepressants, adding ethinyl estradiol and drospirenone has shown benefit.194

Other Treatments

Circadian rhythm abnormalities have been reported in women with PMS/PMDD.102,103,105 Trials using bright light-treatments provide support for this therapy.281283 However, no data exist on the duration of therapeutic efficacy. For the somatic symptoms of PMS—notably, bloating and breast pain—spironolactone, an aldosterone antagonist, has proved superior to placebo.173,284286

Methodological limitations, such as the lack of prospective ratings, have hampered studies assessing the impact of vitamin B-6 (pyridoxine) in PMS/PMDD treatment. Efficacy judgments cannot be conclusively made, but a quantitative review found vitamin B-6 superior to placebo.287 High doses of this vitamin, however, may result in neurotoxicity.287,288 While calcium supplements may be helpful,107,289291 results for magnesium treatments have been mixed, with some studies showing positive benefit292 and others not.293 In addition, supplemental magnesium may cause side effects, such as diarrhea or an upset stomach. Chasteberry, perhaps through its anti-prolactin effects, may show some benefit.170,294297 While the use of alternative treatments, such as oil of primrose, is popular, available evidence suggests they are ineffective, except possibly in the management of breast symptoms.298

No large-scale, randomized, control trials using St. John's Wort for PMDD or menstrual disorders have been completed,299 though a small pilot study did show efficacy in PMS.300 St. John's Wort has known interaction effects with SRIs and other medications, however, and may interfere with the effectiveness of oral contraceptives. In addition, while caffeine, sugar, and alcohol intake have been associated with increased PMS symptoms,301 dietary interventions—such as reducing the consumption of sugar and eating small, frequent meals—have little scientific evidence to support their efficacy. In contrast, increasing the intake of complex carbohydrates may be helpful, perhaps due to raising the levels of tryptophan, the dietary precursor of serotonin and other neurotransmitters.302,303 Aerobic exercise304 and cognitive-behavioral therapy305308 likewise may be helpful. Treatments that lack consistent, evidence-based support include nonsteroidal anti-inflammatories (NSAIDs), mefenamic acid,309 naproxen,310 and the opioid receptor blocker naltrexone.311 However, NSAIDs may prove useful in alleviating some physical symptoms, such as cramps, aches, and pain.

Future Research: Characterization of PMDD Subtypes

While SRIs offer a strong firstline treatment option, some women may be nonresponsive to current PMDD treatments.206 Re-analysis of existing data sets is warranted to define subgroups, to characterize treatment efficacy rates in order to further improve response rates, and to achieve greater understanding of the pathophysiology of PMDD.206


There is strong empirical support for the reality of a severe premenstrual condition that involves mood, behavioral, and somatic symptoms and impairments. Recent research in genetics, neuroendocrine challenge studies, and functional imaging add credence to the validity of PMDD as a diagnostic category.

PMDD affects an estimated 5% of women of child-bearing age.15 Key to effective management is clear diagnosis. PMS/PMDD must be distinguished from other diagnoses, notably depression, anxiety disorders, premenstrual exacerbation of another condition, or mild physiological symptoms. Prospective daily rating of symptoms over two menstrual cycles is warranted. Patients may chart their most severe symptoms or use a validated instrument, such as the Daily Record of Severity of Problems. To meet diagnostic criteria, five luteal-phase symptoms, including at least one mood symptom, must be present together with a reported impairment of social, emotional, or occupational functioning, albeit with the attendant disadvantage of excluding women who have a smaller number of severe symptoms. Key to diagnosis is the absence of symptoms within a few days following the onset of menstruation. In symptomatic women, premenstrual symptoms appear to be triggered by sensitivity to normal cyclical fluctuations in sex steroids following ovulation. Research thus suggests that the CNS responsiveness to sex steroids is enhanced, indicating that transmitters such as serotonin, GABA, and glutamate are of importance in this context.158,312 Inhibiting ovulation—through the use of GnRH analogues, estrogen, and new oral contraceptives—effectively eliminates symptoms. SRIs likewise reduce symptoms and are recommended for initial PMDD treatment. Treatments show different symptom efficacy. Whereas the suppression of ovulaton benefits both behavioral and physical symptoms, SRIs primarily alleviate irritability, depressed mood and anxiety, the lability of affect, and, with continuous use, some physical symptoms. GABAergic agents may be used to treat anxiety and anxious-depressive symptoms, whereas mastalgia is most effectively eased with dopamine agonists, such as bromocriptine.206

Requirements for Diagnosis of Premenstrual Dysphoric Disorder

  1. Symptoms must occur during the week before menses and remit a few days after onset of menses. Five of the following symptoms must be present and include at least one of 1–4.
    1. Depressed mood or dysphoria
    2. Anxiety or tension
    3. Affective lability
    4. Irritability
    5. Decreased interest in usual activities
    6. Concentration difficulties
    7. Marked lack of energy
    8. Marked change in appetite, overeating, or food cravings
    9. Hypersomnia or insomnia
    10. Feeling overwhelmed
    11. Other physical symptoms (e.g., breast tenderness, bloating)
  2. Symptoms must interfere with work, school, usual activities or relationships.
  3. Symptoms must not merely be an exacerbation of another disorder
  4. Criteria A, B, and C must be confirmed by prospective daily ratings for at least two consecutive menstrual cycles.

Adapted from the Diagnostic and Statistical Manual of Mental Disorders, 4th ed.9


Declaration of interest: In the past year Dr. Yonkers has received study medication for an NIMH grant trial from Pfizer and funds to support an investigator-initiated grant from Eli Lilly. Dr. O'Brien, in addition to being a member of the company's speakers' bureau, receives research funding, consulting fees, and lecture fees from Bayer Schering Pharma, Berlin on all matters related to PMS/PMDD, particularly in relation both to menstrual blood loss measurement and the company's contraceptive product Yaz.


1. Borenstein J, Chiou CF, Dean B, Wong J, Wade S. Estimating direct and indirect costs of premenstrual syndrome. J Occup Environ Med. 2005;47:26–33. [PubMed]
2. Deuster P, Adera T, South-Paul J. Biological, social, and behavioral factors associated with premenstrual syndrome. Arch Fam Med. 1999;8:122–8. [PubMed]
3. Johnson S, McChesney C, Bean J. Epidemiology of premenstrual symptoms in a nonclinical sample. I. Prevalence, natural history and help-seeking behavior. J Reprod Med. 1988;33:340–6. [PubMed]
4. Meaden P, Hartlage S, Cook-Kerr J. Timing and severity of symptoms associated with the menstrual cycle in a community-based sample in the Midwestern United States. Psychiatry Res. 2005;134:27–36. [PubMed]
5. Wood C, Larsen L, Williams R. Menstrual characteristics of 2343 women attending the Shepherd Foundation. Aust N Z J Obstet Gynaecol. 1979;19:107–10. [PubMed]
6. Angst J, Sellaro R, Merikangas K, Endicott J. The epidemiology of perimenstrual psychological symptoms. Acta Psychiatr Scand. 2001;104:110–6. [PubMed]
7. Borenstein JE, Dean BB, Leifke E, Korner P, Yonkers KA. Differences in symptom scores and health outcomes in premenstrual syndrome. J Womens Health. 2007;16:1139–44. [PubMed]
8. Yang M, Wallenstein G, Hagan M, Guo A, Chang J, Kornstein S. Burden of premenstrual dysphoric disorder on health-related quality of life. J Womens Health. 2008;17:113–21. [PubMed]
9. American Psychiatric Association . Diagnostic and statistical manual of mental disorders. 4th ed. APA; Washington, DC: 1994.
10. Yonkers KA, Halbreich U, Freeman E, et al. Symptomatic improvement of premenstrual dysphoric disorder with sertraline treatment. A randomized controlled trial. Sertraline Premenstrual Dysphoric Collaborative Study Group. JAMA. 1997;278:983–8. comment 1024–5. [PubMed]
11. Hylan T, Sundell K, Judge R. The impact of premenstrual symptomatology on functioning and treatment-seeking behavior: experience from the United States, United Kingdom, and France. J Womens Health Gend Based Med. 1999;8:1043–52. [PubMed]
12. Pearlstein T, Halbreich U, Batzar E, et al. Psychosocial functioning in women with premenstrual dysphoric disorder before and after treatment with sertraline or placebo. J Clin Psychiatry. 2000;61:101–9. [PubMed]
13. Borenstein J, Dean B, Endicott J, et al. Health and economic impact of the premenstrual syndrome. J Reprod Med. 2003;48:515–24. [PubMed]
14. Campbell EM, Peterkin D, O'Grady K, Sanson-Fisher R. Premenstrual symptoms in general practice patients. Prevalence and treatment. J Reprod Med. 1997;42:637–46. [PubMed]
15. Wittchen HU, Becker E, Lieb R, Krause P. Prevalence, incidence and stability of premenstrual dysphoric disorder in the community. Psychol Med. 2002;32:119–32. [PubMed]
16. Chaturvedi SK, Chandra PS, Gururaj G, Pandian RD, Beena MB. Suicidal ideas during premenstrual phase. J Affect Disord. 1995;34:193–9. [PubMed]
17. Stout AL, Steege JF, Blazer DG, George LK. Comparison of lifetime psychiatric diagnoses in premenstrual syndrome clinic and community samples. J Nerv Ment Dis. 1986;174:517–22. [PubMed]
18. Halbreich U, Borenstein J, Pearlstein T, Kahn L. The prevalence, impairment, impact, and burden of premenstrual dysphoric disorder (PMS/PMDD) Psychoneuroendocrinology. 2003;28(suppl 3):1–23. [PubMed]
19. Halbreich U, Backstrom T, Eriksson E, et al. Clinical diagnostic criteria for premenstrual syndrome and guidelines for their quantification for research studies. Gynecol Endocrinol. 2007;23:123–30. [PubMed]
20. Yonkers K, Steiner M. Depression in women. Dunitz; London: 1999.
21. Hurt SW, Schnurr PP, Severino SK, et al. Late luteal phase dysphoric disorder in 670 women evaluated for premenstrual complaints. Am J Psychiatry. 1992;149:525–30. [PubMed]
22. Di Giulio G, Reissing ED. Premenstrual dysphoric disorder: prevalence, diagnostic considerations, and controversies. J Psychosom Obstet Gynaecol. 2006;27:201–10. [PubMed]
23. ACOG Committee on Practice Bulletins—Gynecology ACOG Practice Bulletin. Premenstrual syndrome. Number 15, April 2000. Int J Gynaecol Obstet. 2001;73:183–91.
24. Ross LE, Steiner M. A biopsychosocial approach to premenstrual dysphoric disorder. Psychiatr Clin North Am. 2003;26:529–46. [PubMed]
25. Perkonigg A, Yonkers K, Pfiste H, Lieb R, Wittchen HU. Risk factors for premenstrual dysphoric disorder in a community sample of young women: the role of traumatic events and posttraumatic stress disorder. J Clin Psychiatry. 2004;65:1314–22. [PubMed]
26. Girdler SS, Thompson KS, Light KC, Leserman J, Pedersen CA, Prange AJ., Jr. Historical sexual abuse and current thyroid axis profiles in women with premenstrual dysphoric disorder. Psychosom Med. 2004;66:403–10. [PubMed]
27. Girdler SS, Klatzkin R. Neurosteroids in the context of stress: implications for depressive disorders. Pharmacol Ther. 2007;116:125–39. [PMC free article] [PubMed]
28. Bunevicius R, Hinderliter AL, Light KC, Leserman J, Pedersen CA, Girdler SS. Histories of sexual abuse are associated with differential effects of clonidine on autonomic function in women with premenstrual dysphoric disorder. Biol Psychol. 2005;69:281–96. [PubMed]
29. Koci A, Strickland O. Relationship of adolescent physical and sexual abuse to perimenstrual symptoms (PMS) in adulthood. Issues Ment Health Nurs. 2007;28:75–87. [PubMed]
30. Endicott J, Nee J, Harrison W. Daily Record of Severity of Problems (DRSP): reliability and validity. Arch Womens Ment Health. 2006;9:41. [PubMed]
31. Borenstein JE, Dean BB, Yonkers KA, Endicott J. Using the daily record of severity of problems as a screening instrument for premenstrual syndrome. Obstet Gynecol. 2007;109:1068–75. [PubMed]
32. Mortola JF, Girton L, Beck L, Yen SS. Diagnosis of premenstrual syndrome by a simple, prospective, and reliable instrument: the calendar of premenstrual experiences. Obstet Gynecol. 1990;76:302–7. [PubMed]
33. Moos RH. The development of a menstrual distress questionnaire. Psychosom Med. 1968;30:853–67. [PubMed]
34. Endicott J, Halbreich U. Retrospective report of premenstrual depressive changes. Psychopharmacol Bull. 1982;18:109–12.
35. Reid R. Premenstrual syndrome. Curr Probl Obstet Gynecol Fertil. 1985;8:1.
36. Yonkers KA, O'Brien PMS, Eriksson E. Premenstrual syndrome. Lancet. 2008;371:1200–10. [PMC free article] [PubMed]
37. Woods N, Most A, Dery G. Prevalence of perimenstrual symptoms. Am J Public Health. 1982;72:1257–64. [PubMed]
38. Andersch B, Wendestam C, Hahn L, Ohman R. Premenstrual complaints. Prevalence of premenstrual symptoms in a Swedish urban population. J Psychosom Obstet Gynaecol. 1986;5:39–49.
39. Ramcharan S, Love EJ, Fick GH, Goldfien A. The epidemiology of premenstrual symptoms in a population based sample of 2650 urban women: attributable risk and risk factors. J Clin Epidemiol. 1992;45:377–81. [PubMed]
40. Rivera-Tovar AD, Frank E. Late luteal phase dysphoric disorder in young women. Am J Psychiatry. 1990;147:1634–6. [PubMed]
41. Soares CN, Cohen LS, Otto MW, Harlow BL. Characteristics of women with premenstrual dysphoric disorder (PMDD) who did or did not report history of depression: a preliminary report from the Harvard Study of Moods and Cycles. J Womens Health Gend Based Med. 2001;10:873–8. [PubMed]
42. Takeda T, Tasaka K, Sakata M, Murata Y. Prevalence of premenstrual syndrome and premenstrual dysphoric disorder in Japanese women. Arch Womens Ment Health. 2006;9:209–12. [PubMed]
43. Pearlstein T, Yonkers K, Fayyad R, Gillespie J. Pretreatment pattern of symptom expression in premenstrual dsyphoric disorder. J Affect Disord. 2005;85:275–82. [PubMed]
44. Sternfeld B, Swindle R, Chawla A, Long S, Kennedy S. Severity of premenstrual symptoms in a health maintenance organization population. Obstet Gynecol. 2002;99:1014–24. [PubMed]
45. Bloch M, Schmidt P, Rubinow D. Premenstrual syndrome: evidence for symptom stability across cycles. Am J Psychiatry. 1997;154:1741–6. [PubMed]
46. Condon JT. The premenstrual syndrome: a twin study. Br J Psychiatry. 1993;162:481–6. [PubMed]
47. Kendler K, Karkowski L, Corey L, Neale M. Longitudinal population-based study of retrospectively reported premenstrual symptoms and lifetime major depression. Am J Psychiatry. 1998;155:1234–40. [PubMed]
48. Treloar S, Heath AM, Martin NG. Genetic and environmental influences on premenstrual symptoms in an Australian twin sample. Psychol Med. 2002;32:25–38. [PubMed]
49. Dhingra V, Magnay JL, O'Brien PM, Chapman G, Fryer AA, Ismail KM. Serotonin receptor 1A C(−1019)G polymorphism associated with premenstrual dysphoric disorder. Obstet Gynecol. 2007;110:788–92. [PubMed]
50. Huo L, Straub RE, Roca C, et al. Risk for premenstrual dysphoric disorder is associated with genetic variation in ESR1, the estrogen receptor alpha gene. Biol Psychiatry. 2007;62:925–33. [PMC free article] [PubMed]
51. Masho SW, Adera T, South-Paul J. Obesity as a risk factor for premenstrual syndrome. J Psychosom Obstet Gynaecol. 2005;26:33–9. [PubMed]
52. Nakamoto Y, Sato M, Miwa M, Murakami M, Yoshii M. Impaired reactivity to mental stress in premenstrual dysphoric disorder [PMDD] patients. Neurosci Res. 2007;58(suppl 1):S165.
53. Girdler SS, Leserman J, Bunevicius R, Klatzkin R, Pedersen CA, Light KC. Persistent alterations in biological profiles in women with abuse histories: influence of premenstrual dysphoric disorder. Health Psychol. 2007;26:201–13. [PMC free article] [PubMed]
54. Rosseinsky D, Debonne lP. An evolutionary theory of premenstrual tension. Lancet. 1974;2:1024. [PubMed]
55. Castellanos F, Orihuela A, Galina CS. Aggressive behaviour in oestrus and dioestrus dairy cows and heifers. J Reprod Fertil. 1973;34:509–11. [PubMed]
56. Floody O, Pfaff D. Aggressive behaviour in female hamsters: the hormonal basis for fluctuations in female aggressiveness correlated with estrous state. J Comp Physiol Psychol. 1977;91:443–64. [PubMed]
57. Garcia-Castell E, Juarez Gonzalez J, Ervin F, Guzman-Flores C. Changes in the social dynamics associated to the menstrual cycle in the vervet monkey. Bol Estud Med Biol. 1989;37:11–6. [PubMed]
58. Rapkin A, Pollack D, Raleigh M, Stone B, McGuire MT. Menstrual cycle and social behavior in vervet monkeys. Psychoneuroendocrinology. 1995;20:289–97. [PubMed]
59. Ho H, Olsson M, Westberg L, Melke J, Eriksson E. The serotonin reuptake inhibitor fluoxetine reduces sex steroid-related aggression in female rats: an animal model of premenstrual irritability? Neuropsychopharmacology. 2001;24:502–10. [PubMed]
60. Hyde J, Sawyer T. Estrous cycle fluctuations in aggressiveness of house mice. Horm Behav. 1977;9:290–5. [PubMed]
61. Schneider T, Popik P. Increased depressive-like traits in an animal model of premenstrual irritability. Horm Behav. 2007;51:142–8. [PubMed]
62. Marvan ML, Chavez-Chavez L, Santana S. Clomipramine modifies fluctuations of forced swimming immobility in different phases of the rat estrous cycle. Arch Med Res. 1996;27:83–6. [PubMed]
63. Beckley EH, Finn DA. Inhibition of progesterone metabolism mimics the effect of progesterone withdrawal on forced swim test immobility. Pharmacol Biochem Behav. 2007;87:412–9. [PMC free article] [PubMed]
64. MacDonald P, Dombroski R, Casey M. Recurrent secretion of progesterone in large amounts: an endocrine/metabolic disorder unique to young women? Endocr Rev. 1991;12:372–401. [PubMed]
65. Frank R. The hormonal causes of premenstrual tension. Arch Neurol Psychiatry. 1931;26:1053–7.
66. Hammarback S, Ekholm U-B, Backstrom T. Spontaneous anovulation causing disappearance of cyclical symptoms in women with the premenstrual syndrome. Acta Endocrinol (Copenh) 1991;125:132–7. [PubMed]
67. Casper R, Hearn M. The effect of hysterectomy and bilateral oophorectomy in women with severe premenstrual syndrome. Am J Obstet Gynecol. 1990;162:105–9. [PubMed]
68. Casson P, Hahn P, Van Vugt D, Reid R. Lasting response to ovariectomy in severe intractable premenstrual syndrome. Am J Obstet Gynecol. 1990;162:99–105. [PubMed]
69. Studd J, Panay N. Hormones and depression in women. Climacteric. 2004;7:338–46. [PubMed]
70. Studd J, Smith R. Estrogens and depression in women. Menopause. 1994;1:33–7.
71. Cronje WH, Vashisht A, Studd JWW. Hysterectomy and bilateral oophorectomy for severe premenstrual syndrome. Hum Reprod. 2004;19:2152–5. [PubMed]
72. Muse K, Cetel N, Futterman L, Yen S. The premenstrual syndrome: effects of “medical ovariectomy.” N Engl J Med. 1984;311:1345–9. [PubMed]
73. Bancroft J, Boyle H, Warner P, Fraser HM. The use of an LHRH agonist, buserelin, in the long-term management of premenstrual syndromes. Clin Endocrinol (Oxf) 1987;27:171–82. [PubMed]
74. Hammarback S, Backstrom T. Induced anovulation as treatment of premenstrual tension syndrome. A double-blind crossover study with GnRH-agonist versus placebo. Acta Obstet Gynecol Scand. 1988;67:159–66. [PubMed]
75. Sundstrom I, Nyberg S, Bixo M, S H, Backstrom T. Treatment of premenstrual syndrome with gonadotropin-releasing hormone agonist in a low dose regimen. Acta Obstet Gynecol Scand. 1999;78:891–9. [PubMed]
76. Wyatt K, Dimmock P, Ismail K, Jones P, O'Brien P. The effectiveness of GnRHa with and without `add-back' therapy in treating premenstrual syndrome: a meta analysis. BJOG. 2004;6:585–93. [PubMed]
77. Birzniece V, Backstrom T, Johansson IM, et al. Neuroactive steroid effects on cognitive functions with a focus on the serotonin and GABA systems. Brain Res Rev. 2006;51:212–39. [PubMed]
78. Smith S, Gong Q, Hsu F, Markowitz R, French-Mullen J, Li X. GABA A receptor alpha-4 subunit suppression prevents withdrawal properties of an endogenous steroid. Nature. 1998;392:926–30. [PubMed]
79. Smith S, Ruderman Y, Frye C, Homanics G, Yuan M. Steroid withdrawal in the mouse results in anxiogenic effects of 3alpha, 5beta-THP: a possible model of premenstrual dysphoric disorder. Psychopharmacology (Berl) 2006;186:323–33. [PMC free article] [PubMed]
80. Sundstrom Poromaa I, Smith S, Gulinello M. GABA receptors, progesterone and premenstrual dysphoric disorder. Arch Womens Ment Health. 2003;6:23–41. [PubMed]
81. Griffiths J, Lovick T. Withdrawal from progesterone increases expression of alpha4, beta1, and delta GABA(A) receptor subunits in neurons in the periaqueductal gray matter in female Wistar rats. J Comp Neurol. 2005;486:89–97. [PubMed]
82. Backstrom T, Andersson A, Andree L, et al. Pathogenesis in menstrual cycle-linked CNS disorders. Ann N Y Acad Sci. 2003;1007:42–53. [PubMed]
83. Schmidt P, Nieman L, Danaceau M, Adams L, Rubinow D. Differential behavioral effects of gonadal steriods in women with and in those without premenstrual syndrome. N Engl J Med. 1998;338:209–16. [PubMed]
84. Wyatt K, Dimmock P, Jones P, Obhrai M, O'Brien S. Efficacy of progesterone and progestogens in management of premenstrual syndrome: systematic review. BMJ. 2001;323:776–80. [PMC free article] [PubMed]
85. van Wingen G, van Broekhoven F, Verkes R, et al. Progesterone selectively increases amygdala reactivity in women. Mol Psychiatry. 2008;13:325–33. [PubMed]
86. Magos A, Brewster E, Singh R, O'Dowd T, Brincat M, Studd J. The effects of norethisterone in postmenopausal women on oestrogen replacement therapy: a model for the premenstrual syndrome. Br J Obstet Gynaecol. 1986;93:1290–6. [PubMed]
87. Hammarback S, Backstrom T, Holst J, von Schoultz B, Lyrenas S. Cyclical mood changes as in the premenstrual tension syndrome during sequential estrogen-progestagen postmenopausal replacement therapy. Acta Obstet Gynecol Scand. 1985;64:393–7. [PubMed]
88. Genazzani AR, Petraglia F, Bernardi F, et al. Circulating levels of allopregnanolone in humans: gender, age, and endocrine influences. J Clin Endocrinol Metab. 1998;83:2099–103. [PubMed]
89. Bicikova M, Dibbelt L, Hill M, Hampl R, Starka L. Allopregnanolone in women with premenstrual syndrome. Horm Metab Res. 1998;30:227–30. [PubMed]
90. Rapkin A, Morgan M, Goldman L, Brann D, Simone D, Mahesh V. Progesterone metabolite allopregnanolone in women with premenstrual syndrome. Obstet Gynecol. 1997;90:709–14. [PubMed]
91. Schmidt P, Purdy R, Moore P, Paul S, Rubinow D. Circulating levels of anxiolytic steroids in the luteal phase in women with premenstrual syndrome and in control subjects. J Clin Endocrinol Metab. 1994;79:1256–60. [PubMed]
92. Sundstrom I, Ashbrook D, Backstrom T. Reduced benzodiazepine sensitivity in patients with premenstrual syndrome: a pilot study. Psychoneuroendocrinology. 1997;22:25–38. [PubMed]
93. Kaura V, Ingram CD, Gartside SE, Young AH, Judge SJ. The progesterone metabolite allopregnanolone potentiates GABA(A) receptor-mediated inhibition of 5-HT neuronal activity. Eur Neuropsychopharmacol. 2007;17:108–15. [PubMed]
94. Matsumoto K, Puia G, Dong E, Pinna G. GABA(A) receptor neurotransmission dysfunction in a mouse model of social isolation-induced stress: possible insights into a nonserotonergic mechanism of action of SSRIs in mood and anxiety disorders. Stress. 2007;10:3–12. [PubMed]
95. Thys-Jacobs S, McMahon D, Bilezikian JP. Differences in free estradiol and sex hormone-binding globulin in women with and without premenstrual dysphoric disorder. J Clin Endocrinol Metab. 2008;93:96–102. [PubMed]
96. Schmidt P, Nieman L, Grover G, Muller K, Merriam G, Rubinow D. Lack of effect of induced menses on symptoms in women with premenstrual syndrome. N Engl J Med. 1991;324:1174–9. [PubMed]
97. Schmidt P. Depression, the perimenopause, and estrogen therapy. Ann N Y Acad Sci. 2005;1052:27–40. [PubMed]
98. Bjorn I, Sundstrom-Poromaa I, Bixo M, Nyberg S, Backstrom G, Backstrom T. Increase of estrogen dose deteriorates mood during progestin phase in sequential hormonal therapy. J Clin Endocrinol Metab. 2003;88:2026–30. [PubMed]
99. Schmidt P, Grover G, Roy-Byrne P, Rubinow D. Thyroid function in women with premenstrual syndrome. J Clin Endocrinol Metab. 1993;76:671–4. [PubMed]
100. Girdler S, Pedersen C, Light K. Thyroid axis function during the menstral cycle in women with premenstrual syndrome. Psychoneuroendocrinology. 1995;20:395–403. [PubMed]
101. Korzekwa MI, Lamont JA, Steiner M. Late luteal phase dysphoric disorder and the thyroid axis revisited. J Clin Endocrinol Metab. 1996;81:2280–4. [PubMed]
102. Portella AT, Haaga DA, Rohan KJ. The association between seasonal and premenstrual symptoms is continuous and is not fully accounted for by depressive symptoms. J Nerv Ment Dis. 2006;194:833–7. [PubMed]
103. Dalgleish T, Rosen K, Marks M. Rhythm and blues: the theory and treatment of seasonal affective disorder. Br J Clin Psychol. 1996;35:163–82. [PubMed]
104. Parry BL, Berga SL, Kripke DF, et al. Altered waveform of plasma nocturnal melatonin secretion in premenstrual depression. Arch Gen Psychiatry. 1990;47:1139–46. [PubMed]
105. Parry BL, Newton RP. Chronobiological basis of female-specific mood disorders. Neuropsychopharmacology. 2001;25(5 suppl):S102–8. [PubMed]
106. Pehrsson M, Westberg L, Landén M, Ekman A. Stable serum levels of relaxin throughout the menstrual cycle: a preliminary comparison of women with premenstrual dysphoria and controls. Arch Womens Ment Health. 2007;10:147–53. [PubMed]
107. Thys-Jacobs S, McMahon D, Bilezikian JP. Cyclical changes in calcium metabolism across the menstrual cycle in women with premenstrual dysphoric disorder. J Clin Endocrinol Metab. 2007;92:2952–9. [PubMed]
108. Thys-Jacobs S, McMahon D, Bilezikian JP. Lower insulin-like growth factor-1 concentrations in women with premenstrual dysphoric disorder. Am J Obstet Gynecol. 2008;198:506. [PubMed]
109. Sherwood R, Rocks B, Stewart A, Saxton R. Magnesium and the premenstrual syndrome. Ann Clin Biochem. 1986;23:667–70. [PubMed]
110. Facchinetti F, Borella P, Fioroni L, et al. Reduction of monocyte's magnesium in patients affected by premenstrual syndrome. J Psychosom Obstet Gynaecol. 1990;11:221.
111. Rosenstein D, Elin R, Hosseini J, Grover G, Rubinow D. Magnesium measures across the menstrual cycle in premenstrual syndrome. Biol Psychiatry. 1994;35:557–61. [PubMed]
112. Steiner M, Pearlstein T. Premenstrual dysphoria and the serotonin system: pathophysiology and treatment. J Clin Psychiatry. 2000;61(suppl 12):17–21. [PubMed]
113. Lesch K, Bengel D, Heils A, et al. Association of anxiety-related traits with a polymorphism in the serotonin transporter gene regulatory region. Science. 1996;274:1527–31. [PubMed]
114. Hariri A, Mattay V, Tessitore A, et al. Serotonin transporter genetic variation and the response of the human amygdala. Science. 2002;297:400–3. [PubMed]
115. Parsey R, Hastings R, Oquendo M, et al. Lower serotonin transporter binding potential in the human brain during major depressive episodes. Am J Psychiatry. 2006;163:52–8. [PubMed]
116. Eriksson E, Andersch B, Ho H, Landen M, Sundblad C. Diagnosis and treatment of premenstrual dysphoria. J Clin Psychiatry. 2002;63(suppl 7):16–23. [PubMed]
117. Schneider T, Popik P. Attenuation of estrous cycle-dependent marble burying in female rats by acute treatment with progesterone and antidepressants. Psychoneuroendocrinology. 2007;32:651–9. [PubMed]
118. Carlsson M, Carlsson A. A regional study of sex differences in rat brain serotonin. Prog Neuropsychopharmacol Biol Psychiatry. 1988;12:53–61. [PubMed]
119. Hiroi R, McDevitt R, Neumaier J. Estrogen selectively increases tryptophan hydroxylase-2 mRNA expression in distinct subregions of rat midbrain raphe nucleus: association between gene expression and anxiety behavior in the open field. Biol Psychiatry. 2006;60:288–95. [PubMed]
120. Rubinow D, Schmidt P, Roca C. Estrogen-serotonin interactions: implications for affective regulation. Biol Psychiatry. 1998;44:839–50. [PubMed]
121. Zhang L, Ma W, Barker J, Rubinow D. Sex differences in expression of serotonin receptors (subtypes 1A and 2A) in rat brain: a possible role of testosterone. Neuroscience. 1999;94:251–9. [PubMed]
122. Bethea C, Lu N, Gundlah C, Streicher J. Diverse actions of ovarian steroids in the serotonin neural system. Front Neuroendocrinol. 2002;23:41–100. [PubMed]
123. Qiao M, Zhao Q, Zhang H, Wang H, Xue L, Wei S. Isolating with physical restraint low status female monkeys during luteal phase might make an appropriate premenstrual depression syndrome model. J Affect Disord. 2007;102:81–91. [PubMed]
124. Brzezinski A, Wurtman J, Wurtman R, Gleason R, Greenfield J, Nader T. d-Fenfluramine suppresses the increased calorie and carbohydrate intakes and improves the mood of women with premenstrual depression. Obstet Gynecol. 1990;76:296–300. [PubMed]
125. Su T-P, Schmidt P, Danaceau M, Murphy D, Rubinow D. Effect of menstrual cycle phase on neuroendocrine and behavioral responses to the serotonin agonist m-chlorophenylpiperazine in women with premenstrual syndrome and controls. J Clin Endocrinol Metab. 1997;82:1220–8. [PubMed]
126. Steinberg S, Annable L, Young S, Liyanage N. A placebo-controlled clinical trial of L-tryptophan in premenstrual dysphoria. Biol Psychiatry. 1999;45:313–20. [PubMed]
127. Landen M, Eriksson O, Sundblad C, Andersch B, Naessen T, Erikkson E. Compounds with affinity for serotonergic receptors in the treatment of premenstrual dysphoria: a comparison of buspirone, nefazodone and placebo. Psychopharmacology (Berl) 2001;155:292–8. [PubMed]
128. Menkes DB, Coates DC, Fawcett JP. Acute tryptophan depletion aggravates premenstrual syndrome. J Affect Disord. 1994;32:37–44. [PubMed]
129. Roca C, Schmidt P, Smith M, Danaceau MA, Murphy DL, Rubinow D. Effects of metergoline on symptoms in women with premenstrual dysphoric disorder. Am J Psychiatry. 2002;159:1876–81. [PubMed]
130. Inoue Y, Terao T, Iwata N, et al. Fluctuating serotonergic function in premenstrual dysphoric disorder and premenstrual syndrome: findings from neuroendocrine challenge tests. Psychopharmacology (Berl) 2007;190:213–9. [PubMed]
131. Bancroft J, Cook A, Davidson D, Bennie J, Goodwin G. Blunting of neuroendocrine responses to infusion of L-tryptophan in women with perimenstrual mood change. Psychol Med. 1991;21:305–12. [PubMed]
132. Eriksson O, Wall A, Marteinsdottir I, et al. Mood changes correlate to changes in brain serotonin precursor trapping in women with premenstrual dysphoria. Psychiatry Res. 2006;146:107–16. [PubMed]
133. Fitzgerald M, Malone K, Li S, et al. Blunted serotonin response to fenfluramine challenge in premenstrual dysphoric disorder. Am J Psychiatry. 1997;154:556. [PubMed]
134. Halbreich U, Tworek H. Altered serotonergic activity in women with dysphoric premenstrual syndromes. Int J Psychiatry Med. 1993;23:1–27. [PubMed]
135. Melke J, Westberg L, Landen M, et al. Serotonin transporter gene polymorphisms and platelet [3H] paroxetine binding in premenstrual dysphoria. Psychoneuroendocrinology. 2003;28:446–58. [PubMed]
136. Rasgon N, McGuire M, Tanavoli S, Fairbanks L, Rapkin A. Neuroendocrine response to an intravenous L-tryptophan challenge in women with premenstrual syndrome. Fertil Steril. 2000;73:144–9. [PubMed]
137. Rojansky N, Halbreich U, Zander K, Barkai A, Goldstein S. Imipramine receptor binding and serotonin uptake in platelets of women with premenstrual changes. Gynecol Obstet Invest. 1991;31:146–52. [PubMed]
138. Steege JF, Stout AL, Knight BS, Nemeroff CB. Reduced platelet tritium-labeled imipramine binding sites in women with premenstrual syndrome. Am J Obstet Gynecol. 1992;167:168–72. [PubMed]
139. Steiner M, Yatham LN, Coote M, Wilkins A, Lepage P. Serotonergic dysfunction in women with pure premenstrual dysphoric disorder: is the fenfluramine challenge test still relevant. Psychiatry Res. 1999;87:107–15. [PubMed]
140. Yatham L, Barry S, Dinan T. Serotonin receptors, buspirone, and premenstrual syndrome. Lancet. 1989;1:1447–8. [PubMed]
141. Jovanovic H, Cerin A, Karlsson P, Lundberg J, Halldin C, Nordstrom AL. A PET study of 5-HT1A receptors at different phases of the menstrual cycle in women with premenstrual dysphoria. Psychiatry Res. 2006;148:185–93. [PubMed]
142. Epperson C, Haga K, Mason G, et al. Cortical gamma-aminobutyric acid levels across the menstrual cycle in healthy women and those with premenstrual dysphoric disorder: a proton magnetic resonance spectroscopy study. Arch Gen Psychiatry. 2002;59:851–8. [PubMed]
143. Girdler S, Straneva P, Light K, Pederson C, Morrow A. Allopregnanolone levels and reactivity to mental stress in premenstrual dysphoric disorder. Biol Psychiatry. 2001;49:788–97. [PubMed]
144. Schmidt P, Grover G, Rubinow D. Alprazolam in the treatment of premenstrual syndrome. A double-blind, placebo-controlled trial. Arch Gen Psychiatry. 1993;50:467–73. [PubMed]
145. Bhagwagar Z, Wylezinska M, Taylor M, Jezzard P, Matthews P, Cowen P. Increased brain GABA concentrations following acute administration of a selective serotonin reuptake inhibitor. Am J Psychiatry. 2004;161:368–70. [PubMed]
146. Soderpalm B, Engel J. Involvement of the GABA A/benzodiazepine chloride ionophore receptor complex in the 5,7-DHT Induced anticonflict effect. Life Sci. 1991;49:139–53. [PubMed]
147. Sundstrom I, Backstrom T. Citalopram increases pregnanolone sensitivity in patients with premenstrual syndrome: an open trial. Psychoneuroendocrinology. 1998;23:73–88. [PubMed]
148. Pinna G, Costa E, Guidotti A. Fluoxetine and norfluoxetine stereospecifically and selectively increase brain neurosteroid content at doses that are inactive on 5-HT reuptake. Psychopharmacology (Berl) 2006;186:362–72. [PubMed]
149. Griffin L, Mellon S. Selective serotonin reuptake inhibitors directly alter activity of neurosteroidogenic enzymes. Proc Natl Acad Sci U S A. 1999;96:13512–7. [PubMed]
150. Batra M, Seres-Mailo J, Hanstock C, et al. Proton magnetic resonance spectroscopy measurement of brain glutamate levels in premenstrual dysphoric disorder. Biol Psychiatry. 2007;63:1178–84. [PubMed]
151. Chuong C, Hsi B, Gibbons W. Periovulatory beta-endorphin levels in premenstrual syndrome. Obstet Gynecol. 1994;83:755–60. [PubMed]
152. Chuong C, Coulam C, Kao P, Bergstralh E, Go V. Neuropeptide levels in premenstrual syndrome. Fertil Steril. 1985;44:760–5. [PubMed]
153. Giannini A, Martin D, Turner C. Beta-endorphin decline in late luteal phase dysphoric disorder. Int J Psychiatry Med. 1990;20:279–84. [PubMed]
154. Halbreich U, Endicott J. Possible involvement of endorphin withdrawal or imbalance in specific premenstrual syndromes and postpartum depression. Med Hypotheses. 1981;7:1045–58. [PubMed]
155. Reid R, Yen S. Premenstrual syndrome. Am J Obstet Gynecol. 1981;139:85–104. [PubMed]
156. Straneva PA, Maixner W, Light KC, Pedersen CA, Costello NL, Girdler SS. Menstrual cycle, beta-endorphins, and pain sensitivity in premenstrual dysphoric disorder. Health Psychol. 2002;21:358–67. [PubMed]
157. Joffe H, Kim DR, Foris JM, et al. Menstrual dysfunction prior to onset of psychiatric illness is reported more commonly by women with bipolar disorder than by women with unipolar depression and healthy controls. J Clin Psychiatry. 2006;67:297–304. [PubMed]
158. Young EA, Korszun A. The hypothalamic-pituitary-gonadal axis in mood disorders. Endocrinol Metab Clin North Am. 2002;31:63–78. [PubMed]
159. Kask K, Gulinello M, Backstrom T, Geyer MA, Sundstrom-Poromaa I. Patients with premenstrual dysphoric disorder have increased startle response across both cycle phases and lower levels of prepulse inhibition during the late luteal phase of the menstrual cycle. Neuropsychopharmacology. 2008;33:2283–90. [PubMed]
160. Epperson CN, Pittman B, Czarkowski KA, Stiklus S, Krystal JH, Grillon C. Luteal-phase accentuation of acoustic startle response in women with premenstrual dysphoric disorder. Neuropsychopharmacology. 2007;32:2190–8. [PMC free article] [PubMed]
161. Smith SS, Shen H, Gong QH, Zhou X. Neurosteroid regulation of GABA(A) receptors: focus on the alpha4 and delta subunits. Pharmacol Ther. 2007;116:58–76. [PMC free article] [PubMed]
162. Gulinello M, Gong Q, Smith S. Progesterone withdrawal increases the α4 subunit of the GABA(A) receptor in male rats in association with anxiety and altered pharmacology: a comparison with female rats. Neuropharmacology. 2002;43:701–14. [PMC free article] [PubMed]
163. Rubinow DR, Smith MJ, Schenkel LA, Schmidt PJ, Dancer K. Facial emotion discrimination across the menstrual cycle in women with premenstrual dysphoric disorder (PMDD) and controls. J Affect Disord. 2007;104:37–44. [PMC free article] [PubMed]
164. Protopopescu X, Tuescher O, Pan H, et al. Toward a functional neuroanatomy of premenstrual dysphoric disorder. J Affect Disord. 2008;108:87–94. [PubMed]
165. Hsu SC, Liu CY, Hsiao MC. A comparison of the Tridimensional Personality Questionnaire in premenstrual dysphoric disorder and major depressive disorder. Compr Psychiatry. 2007;48:366–70. [PubMed]
166. Faratian B, Gaspar A, O'Brien P, Johnson I, Filshie G, Prescott P. Premenstrual syndrome: weight, abdominal swelling, and perceived body image. Am J Obstet Gynecol. 1984;150:200–4. [PubMed]
167. Andersch B, Hahn L, Andersson M, Isaksson B. Body water and weight in patients with premenstrual tension. Br J Obstet Gynaecol. 1978;85:546–50. [PubMed]
168. Andersch B. Bromocriptine and premenstrual symptoms: a survey of double blind trials. Obstet Gynecol Surv. 1983;38:643–6. [PubMed]
169. Ylostalo P, Kauppila A, Puolakka J, Ronnberg L, Janne O. Bromocriptine and norethisterone in the treatment of premenstrual syndrome. Obstet Gynecol. 1982;59:292–8. [PubMed]
170. Wuttke W, Jarry H, Christoffel V, Spengler B, Seidlova-Wuttke D. Chaste tree (Vitex agnus-castus)—pharmacology and clinical indications. Phytomedicine. 2003;10:348–57. [PubMed]
171. O'Brien P, Abukhalil I. Randomized controlled trial of the management of premenstrual syndrome and premenstrual mastalgia using luteal phase–only danazol. Am J Obstet Gynecol. 1999;180:18–23. [PubMed]
172. Oksa S, Luukkaala T, Maenpaa J. Toremifene for premenstrual mastalia: a randomised, placebo-controlled crossover study. BJOG. 2006;113:713–8. [PubMed]
173. O'Brien P, Craven D, Selby C, et al. Treatment of premenstrual syndrome by spironolactone. Br J Obstet Gynaecol. 1979;86:142–7. [PubMed]
174. Rosenfeld R, Livne D, Nevo O, et al. Hormonal and volume dysregulation in women with premenstrual syndrome. Hypertension. 2008;51:1225–30. [PubMed]
175. Tietjen GE, Bushnell CD, Herial NA, Utley C, White L, Hafeez F. Endometriosis is associated with prevalence of comorbid conditions in migraine. Headache. 2007;47:1069–78. [PubMed]
176. Moja P, Cusi C, Sterzi R, Canepari C. Selective serotonin re-uptake inhibitors (SSRIs) for preventing migraine and tension-type headaches. Cochrane Database Syst Rev. 2005 Jul 20;(3):CD002919. [PubMed]
177. Bancroft J, Rennie D. Perimenstrual depression: its relationship to pain, bleeding, and previous history of depression. Psychosom Med. 1995;57:445–52. [PubMed]
178. Steiner M, Born L. Diagnosis and treatment of premenstrual dysphoric disorder: an update. Int Clin Psychopharmacol. 2000;15(suppl 3):S5–17. [PubMed]
179. Kim DR, Gyulai L, Freeman EW, Morrison MF, Baldassano C, Dube B. Premenstrual dysphoric disorder and psychiatric co-morbidity. Arch Womens Ment Health. 2004;7:37–47. [PubMed]
180. Pearlstein TB, Frank E, Rivera-Tovar A, Thoft JS, Jacobs E, Mieczkowski TA. Prevalence of Axis I and Axis II disorders in women with late luteal phase dysphoric disorder. J Affect Disord. 1990;20:129–34. [PubMed]
181. Halbreich U, Endicott J. Relationship of dysphoric premenstrual changes to depressive disorders. Acta Psychiatr Scand. 1985;71:331–8. [PubMed]
182. Endicott J, Halbreich U, Schacht S, Nee J. Premenstrual changes and affective disorders. Psychosom Med. 1981;43:519–29. [PubMed]
183. Mackenzie TB, Wilcox K, Baron H. Lifetime prevalence of psychiatric disorders in women with perimenstrual difficulties. J Affect Disord. 1986;10:15–9. [PubMed]
184. Fava M, Pedrazzi F, Guaraldi GP, Giovanni R, Genazzani AR, Facchinetti F. Comorbid anxiety and depression among patients with late luteal phase dysphoric disorder. J Anxiety Disord. 1992;6:325–35.
185. Critchlow D, Bond AJ, Wingrove J. Mood disorder history and personality assessment in premenstrual dysphoric disorder. J Clin Psychiatry. 2001;62:688–93. [PubMed]
186. De Ronchi D, Muro A, Marziani A, Rucci P. Personality disorders and depressive symptoms in late luteal phase dysphoric disorder. Psychother Psychosom. 2000;69:27–34. [PubMed]
187. Maskall DD, Lam RW, Misri S, et al. Seasonality of symptoms in women with late luteal phase dysphoric disorder. Am J Psychiatry. 1997;154:1436–41. [PubMed]
188. Praschak-Rieder N, Willeit M, Neumeister A, et al. Prevalence of premenstrual dysphoric disorder in female patients with seasonal affective disorder. J Affect Disord. 2001;63:239–42. [PubMed]
189. Graze KK, Nee J, Endicott J. Premenstrual depression predicts future major depressive disorder. Acta Psychiatr Scand. 1990;81:201–5. [PubMed]
190. Hartlage SA, Arduino KE, Gehlert S. Premenstrual dysphoric disorder and risk for major depressive disorder: a preliminary study. J Clin Psychol. 2001;57:1571–8. [PubMed]
191. Richards M, Rubinow D, Daly R, Schmidt P. Premenstrual symptoms and perimenopausal depression. Am J Psychiatry. 2006;163:133–7. [PubMed]
192. Bloch M, Schmidt P, Danaceau M, Murphy J, Nieman L, Rubinow D. Effects of gonadal steroids in women with a history of postpartum depression. Am J Psychiatry. 2000;157:924–30. [PubMed]
193. Miller MN, Miller BE. Premenstrual exacerbations of mood disorders. Psychopharmacol Bull. 2001;35:135–49. [PubMed]
194. Joffe H, Petrillo LF, Viguera AC, et al. Treatment of premenstrual worsening of depression with adjunctive oral contraceptive pills: a preliminary report. J Clin Psychiatry. 2007;68:1954–62. [PubMed]
195. Harvey AT, Silkey BS, Kornstein SG, Clary CM. Acute worsening of chronic depression during a double-blind, randomized clinical trial of antidepressant efficacy: differences by sex and menopausal status. J Clin Psychiatry. 2007;68:951–8. [PubMed]
196. Kornstein SG, Harvey AT, Rush AJ, et al. Self-reported premenstrual exacerbation of depressive symptoms in patients seeking treatment for major depression. Psychol Med. 2005;35:683–92. [PubMed]
197. Yonkers KA, White K. Premenstrual exacerbation of depression: one process or two? J Clin Psychiatry. 1992;53:289–92. [PubMed]
198. Hardoy MC, Serra M, Carta MG, Contu P, Pisu MG, Biggio G. Increased neuroactive steroid concentrations in women with bipolar disorder or major depressive disorder. J Clin Psychopharmacol. 2006;26:379–84. [PubMed]
199. Hartlage SA, Brandenburg DL, Kravitz HM. Premenstrual exacerbation of depressive disorders in a community-based sample in the United States. Psychosom Med. 2004;66:698–706. [PubMed]
200. Hsiao MC, Liu CY, Chen KC, Hsieh TT. Characteristics of women using a mental health clinic in a gynecologic out-patient setting. Psychiatry Clin Neurosci. 2002;56:459–63. [PubMed]
201. Payne JL, Roy PS, Murphy-Eberenz K, et al. Reproductive cycle-associated mood symptoms in women with major depression and bipolar disorder. J Affect Disord. 2007;99:221–9. [PubMed]
202. Landen M, Eriksson E. How does premenstrual dysphoric disorder relate to depression and anxiety disorders? Depress Anxiety. 2003;17:122–9. [PubMed]
203. Yonkers KA. Anxiety symptoms and anxiety disorders: how are they related to premenstrual disorders. J Clin Psychiatry. 1997;58:62–7. [PubMed]
204. Vulink NC, Denys D, Bus L, Westenberg HG. Female hormones affect symptom severity in obsessive-compulsive disorder. Int Clin Psychopharmacol. 2006;21:171–5. [PubMed]
205. Baker FC, Kahan TL, Trinder J, Colrain IM. Sleep quality and the sleep electroencephalogram in women with severe premenstrual syndrome. Sleep. 2007;30:1283–91. [PubMed]
206. Halbreich U, O'Brien PM, Eriksson E, Backstrom T, Yonkers KA, Freeman EW. Are there differential symptom profiles that improve in response to different pharmacological treatments of premenstrual syndrome/premenstrual dysphoric disorder? CNS Drugs. 2006;20:523–47. [PubMed]
207. Wyatt K, Dimmock P, O'Brien P. Selective serotonin reuptake inhibitors for premenstrual syndrome. Cochrane Database Syst Rev. 2002;(4):CD001396. [PubMed]
208. Yonkers K, Clark R, Trivedi M. The psychopharmacological treatment of nonmajor mood disorders. Karger; Basel: 1997. [PubMed]
209. Eriksson E, Hedberg M, Andersch B, Sundblad C. The serotonin reuptake inhibitor paroxetine is superior to the noradrenaline reuptake inhibitor maprotiline in the treatment of premenstrual syndrome. Neuropsychopharmacology. 1995;12:167–76. [PubMed]
210. Ozeren S, Corakci A, Yucesoy I, Mercan R, Ethan G. Fluoxetine in the treatment of premenstrual syndrome. Eur J Obstet Gynecol Reprod Biol. 1997;73:167–70. [PubMed]
211. Menkes DB, Taghavi E, Mason PA, Spears GFS, Howard RC. Fluoxetine treatment of severe premenstrual syndrome. Br Med J. 1992;305:346–7. [PMC free article] [PubMed]
212. Su T-P, Schmidt P, Danaceau M, et al. Fluoxetine in the treatment of premenstrual dysphoria. Neuropsychopharmacology. 1997;16:346–56. [PubMed]
213. Wood SH, Mortola JF, Chan YF, Moossazadeh F, Yen SS. Treatment of premenstrual syndrome with fluoxetine: a double-blind, placebo-controlled, crossover study. Obstet Gynecol. 1992;80:339–44. [PubMed]
214. Steiner M, Korzekwa M, Lamont J, Wilkins A. Intermittent fluoxetine dosing in the treatment of women with premenstrual dysphoria. Psychopharmacol Bull. 1997;33:771–4. [PubMed]
215. Sundblad C, Hedberg M, Eriksson E. Clomipramine administered during the luteal phase reduces the symptoms of premenstrual syndrome: a placebo-controlled trial. Neuropsychopharmacology. 1993;9:133–45. [PubMed]
216. Sundblad C, Modigh K, Andersch B, Eriksson E. Clomipraine effectively reduces premenstrual irritability and dysphoria: a placebo-controlled trial. Acta Psychiatr Scand. 1992;85:39–47. [PubMed]
217. Wikander I, Sundblad C, Andersch B, et al. Citalopram in premenstrual dysphoria: is intermittent treatment during luteal phases more effective than continuous medication throughout the menstrual cycle? J Clin Psychopharmacol. 1998;18:390–8. [PubMed]
218. Ravindran LN, Woods SA, Steiner M, Ravindran AV. Symptom-onset dosing with citalopram in the treatment of premenstrual dysphoric disorder (PMDD): a case series. Arch Womens Ment Health. 2007;10:125–7. [PubMed]
219. Eriksson EMD, Ekman AP, Sinclair SMD, et al. Escitalopram administered in the luteal phase exerts a marked and dose-dependent effect in premenstrual dysphoric disorder. J Clin Psychopharmacol. 2008;28:195–202. [PubMed]
220. Pearlstein T, Stone A, Lund S, Scheft H, Zlotnick C, Brown W. Comparison of fluoxetine, buproprion, and placebo in the treatment of premenstrual dysphoric disorder. J Clin Psychopharmacol. 1997;17:261–5. [PubMed]
221. Steiner M, Brown E, Trzepacz P, et al. Fluoxetine improves functional work capacity in women with premenstrual dysphoric disorder. Arch Womens Ment Health. 2003;6:71–7. [PubMed]
222. Stone A, Pearlstein T, Brown W. Fluoxetine in the treatment of late luteal phase dysphoric disorder. J Clin Psychiatry. 1991;52:290–3. [PubMed]
223. Cohen L, Miner C, Brown E, et al. Premenstrual daily fluoxetine for premenstrual dysphoric disorder: a placebo-controlled, clinical trial using computerized diaries. Obstet Gynecol. 2002;100:435–44. [PubMed]
224. Miner C, Brown E, McCray S, Gonzales J, Wohlreich M. Weekly luteal phase dosing with enteric-coated fluoxetine 90 mg in premenstrual dysphoric disorder: a randomized, double-blind, placebo-controlled clinical trial. Clin Ther. 2002;24:417–33. [PubMed]
225. Yonkers KA, Halbreich U, Freeman EW, Brown CS, Pearlstein TB. Sertraline in the treatment of premenstrual dysphoric disorder. Psychopharmacol Bull. 1996;32:41–6. [PubMed]
226. Freeman E, Sondheimer S, Polansky M, Garcia-Espagna B. Predictors of response to sertraline treatment of severe premenstrual syndromes. J Clin Psychiatry. 2000;61:579–84. [PubMed]
227. Cohen L, Soares C, Yonkers K, Bellew K, Bridges I, Steiner M. Paroxetine controlled release for premenstrual dysphoric disorder: a double-blind, placebo-controlled trial. Psychosom Med. 2004;66:707–13. [PubMed]
228. Steiner M, Hirschberg A, Bergeron R, Holland F, Gee M, Van-Erp E. Luteal phase dosing with paroxetine controlled release (CR) in the treatment of premenstrual dysphoric disorder. Am J Obstet Gynecol. 2005;193:352–60. [PubMed]
229. Yonkers K, Holthausen G, Poschman K, Howell H. Symptom-onset treatment for women with premenstrual dysphoric disorder. J Clin Psychopharmacol. 2006;26:198–202. [PubMed]
230. Landen M, Nissbrandt H, Allgulander C, Sorvik K, Ysander C, Eriksson E. Placebo-controlled trial comparing intermittent and continuous paroxetine in premenstrual dysphoric disorder. Neuropsychopharmacology. 2007;32:153–61. [PubMed]
231. Freeman E, Rickels K, Yonkers K, et al. Venlafaxine in the treatment of premenstrual dysphoric disorder. Obstet Gynecol. 2001;98:737–44. [PubMed]
232. Cohen L, Soares C, Lyster A, Cassano P, Brandes M, Leblanc G. Efficacy and tolerability of premenstrual use of venlafaxine (flexible dose) in the treatment of premenstrual dysphoric disorder. J Clin Psychopharmacol. 2004;24:540–3. [PubMed]
233. Freeman E, Rickels K, Sondheimer S, Polansky M, Xiao S. Continuous or intermittent dosing with sertraline for patients with severe premenstrual syndrome or premenstrual dysphoric disorder. Am J Psychiatry. 2004;161:343–51. [PubMed]
234. Eriksson E, Endicott J, Andersch B, et al. New perspectives on the treatment of premenstrual syndrome and premenstrual dysphoric disorder. Arch Womens Ment Health. 2002;4:111–9.
235. Steiner M, Pearlstein T, Cohen LS, et al. Expert guidelines for the treatment of severe PMS, PMDD, and comorbidities: the role of SSRIs. J Womens Health (Larchmt) 2006;15:57–69. [PubMed]
236. Freeman E, Rickels K, Sondheimer S, Polansky M. Differential response to antidepressants in women with premenstrual syndrome/premenstrual dysphonic disorder: a randomised controlled trial. Arch Gen Psychiatry. 1999;56:932–9. [PubMed]
237. Halbreich U, Kahn L. Treatment of premenstrual dysphoric disorder with luteal phase dosing of sertraline. Expert Opin Pharmacother. 2003;4:2065–78. [PubMed]
238. Jermain D, Preece C, Sykes R, Kuehl T, Sulak P. Luteal phase sertraline treatment for premenstrual dysphoric disorder: results of a double-blind, placebo-controlled, crossover study. Arch Fam Med. 1999;8:328–32. [PubMed]
239. Young S, Hurt P, Benedeck D, Howard R. Treatment of premenstrual dysphoric disorder with sertraline during the luteal phase: a randomised, double-blind, placebo controlled crossover trial. J Clin Psychiatry. 1998;59:76–80. [PubMed]
240. Yonkers KA, Pearlstein T, Fayyad R, Gillespie JA. Luteal phase treatment of premenstrual dysphoric disorder improves symptoms that continue into the postmenstrual phase. J Affect Disord. 2005;85:317–21. [PubMed]
241. Halbreich U, Smoller JW. Intermittent luteal phase sertraline treatment of dysphoric premenstrual syndrome. J Clin Psychiatry. 1997;58:399–402. [PubMed]
242. Halbreich U, Bergeron R, Yonkers K, Freeman E, Stout A, Cohen L. Efficacy of intermittent, luteal phase sertraline treatment of premenstrual dysphoric disorder. Obstet Gynecol. 2002;100:1219–29. [PubMed]
243. Freeman EW, Sondheimer SJ, Sammel MD, Ferdousi T, Lin H. A preliminary study of luteal phase versus symptom-onset dosing with escitalopram for premenstrual dysphoric disorder. J Clin Psychiatry. 2005;66:769–73. [PubMed]
244. Kornstein SG, Pearlstein TB, Fayyad R, Farfel GM, Gillespie JA. Low-dose sertraline in the treatment of moderate-to-severe premenstrual syndrome: efficacy of 3 dosing strategies. J Clin Psychiatry. 2006;67:1624–32. [PubMed]
245. Sundblad C, Wikander I, Andersch B, Eriksson E. A naturalistic study of paroxetine in premenstrual syndrome: efficacy and side effects during ten cycles of treatment. Eur Neuropsychopharmacol. 1997;7:201–6. [PubMed]
246. Michelson D, Fava M, Amsterdam J, et al. Interruption of selective serotonin reuptake inhibitor treatment: double-blind placebo-controlled trial. Br J Psychiatry. 2000;176:363–8. [PubMed]
247. Rosenbaum J, Fava M, Hoog S, Ascroft R, Krebs W. Selective serotonin reuptake inhibitor discontinuation syndrome: a randomized clinical trial. Biol Psychiatry. 1998;44:77–87. [PubMed]
248. Judge R, Parry M, Quail D, Jacobson J. Discontinuation symptoms: comparison of brief interruption in fluoxetine and paroxetine treatment. Int Clin Psychopharmacol. 2002;17:217–25. [PubMed]
249. Steiner M, Haskett R, Osmun J, Carroll B. Treatment of premenstrual tension with lithium carbonate. A pilot study. Acta Psychiatr Scand. 1980;61:96–102. [PubMed]
250. Freeman EW, Rickels K, Sondheimer SJ, Polansky M. Differential response to antidepressants in women with premenstrual syndrome/premenstrual dysphoric disorder: a randomized controlled trial. Arch Gen Psychiatry. 1999;56:932–9. [PubMed]
251. Rickels K, Freeman E, Sondheimer S. Buspirone in treatment of premenstrual syndrome. Lancet. 1989;4:777. [PubMed]
252. Smith S, Rinehart J, Ruddock V, Schiff I. Treatment of premenstrual syndrome with alprazolam: results of a double-blind, placebo-controlled, randomized crossover clinical trial. Obstet Gynecol. 1987;70:37–43. [PubMed]
253. Harrison W, Endicott J, Nee J. Treatment of premenstrual dysphoria with alprazolam. Arch Gen Psychiatry. 1990;47:270–5. [PubMed]
254. Freeman E, Rickels K, Sondheimer S, Polansky M. A double-blind trail of oral progesterone, alprazolam, and placebo in treatment of severe premenstrual syndrome. JAMA. 1995;274:51–7. [PubMed]
255. Usman S, Indusekhar R, O'Brien S. Hormonal management of premenstrual syndrome. Best Pract Res Clin Obstet Gynaecol. 2008;22:251–60. [PubMed]
256. Dhar V, Murphy B. Double-blind randomized crossover trial of luteal phase estrogens (Premarin) in the premenstrual syndrome (PMS) Psychoneuroendocrinology. 1990;15:489–93. [PubMed]
257. Leather A, Studd J, Watson N, Holland E. The treatment of severe premenstrual syndrome with goserelin with and without “add-back” estrogen therapy: a placebo-controlled study. Gynecol Endocrinol. 1999;13:48–55. [PubMed]
258. Di Carlo C, Palomba S, Tommaselli G, Guida M, Sardo A, Nappi C. Use of leuprolide acetate plus tibolone in the treatment of severe premenstrual syndrome. Fertil Steril. 2001;75:380–4. [PubMed]
259. Halbreich U, Rojansky N, Palter S. Elimination of ovulation and menstrual cyclicity (with danazol) improves dysphoric premenstrual syndromes. Fertil Steril. 1991;56:1066–9. [PubMed]
260. Deeny M, Hawthorn R, McKay-Hart D. Low dose danazol in the treatment of the premenstrual syndrome. Postgrad Med J. 1991;67:450–4. [PMC free article] [PubMed]
261. Sarno A, Miller E, Lundblad E. Premenstrual syndrome: beneficial effects of periodic, low-dose danazol. Obstet Gynecol. 1987;70:33–6. [PubMed]
262. Day J. Danazol and premenstrual syndrome. Postgrad Med J. 1979;55:87–9. [PubMed]
263. Watts J, Butt W, Edwards R. A clinical trial using danazol for the treatment of premenstrual tension. Br J Obstet Gynaecol. 1987;94:30–4. [PubMed]
264. Hahn PM, Van Vugt DA, Reid RL. A randomized, placebo-controlled, crossover trial of danazol for the treatment of premenstrual syndrome. Psychoneuroendocrinology. 1995;20:193–209. [PubMed]
265. Magos A, Brincat M, Studd J. Treatment of the premenstrual syndrome by subcutaneous estradiol implants and cyclical oral norethisterone: placebo-controlled study. Br Med J (Clin Res Ed) 1986;292:1629. [PMC free article] [PubMed]
266. Watson NR, Studd JW, Savvas M, Baber RJ. The long-term effects of estradiol implant therapy for the treatment of premenstrual syndrome. Gynecol Endocrinol. 1990;4:99–107. [PubMed]
267. Watson N, Studd J, Savvas M, Garnett T, Baber R. Treatment of severe premenstrual syndrome with oestradiol patches and cyclical oral norethisterone. Lancet. 1989;2:730–2. [PubMed]
268. Domoney C, Panay N, Hawkins A, Studd J. Treatment of premenstrual syndrome with transdermal oestrogen. Int J Gynaecol Obstet. 2003;83(suppl 3):37. [PubMed]
269. Wildemeersch D, Dhont M. Treatment of nonatypical and atypical endometrial hyperplasia with a levonorgestrel-releasing intrauterine system. Am J Obstet Gynecol. 2003;188:1297–8. [PubMed]
270. Bancroft J, Rennie D. The impact of oral contraceptives on the experience of perimenstrual mood, clumsiness, food craving and other symptoms. J Psychosom Res. 1993;37:195–202. [PubMed]
271. Graham CA, Sherwin BB. A prospective treatment study of premenstrual symptoms using a triphasic oral contraceptive. J Psychosom Res. 1992;36:257–66. [PubMed]
272. Sulak P, Scow R, Preece C, Riggs M, Kuehl T. Hormone withdrawal symptoms in oral contraceptive users. Obstet Gynecol. 2000;95:261–6. [PubMed]
273. Sulak P, Kuehl T, Ortiz M, Schull B. Acceptance of altering the standard 21-day/7-day oral contraceptive regimen to delay menses and reduce hormone withdrawal symptoms. Am J Obstet Gynecol. 2002;186:1142–9. [PubMed]
274. Freeman EW. Evaluation of a unique oral contraceptive (Yasmin) in the management of premenstrual dysphoric disorder. Eur J Contracept Reprod Health Care. 2002;7(suppl 3):27–34. [PubMed]
275. Lopez L, Kaptein A, Helmerhorst F. Oral contraceptives containing drospirenone for premenstrual syndrome. Cochrane Database Syst Rev. 2008 Jan 23;(1):CD006586. [PubMed]
276. Rapkin AJ, Winer SA. Drospirenone: a novel progestin. Exp Opin Pharmacother. 2007;8:989–99. [PubMed]
277. Yonkers K, Brown C, Pearlstein T, Foegh M, Sampson-Landers C, Rapkin A. Efficacy of a new low-dose oral contraceptive with drospirenone in premenstrual dysphoric disorder. Obstet Gynecol. 2005;106:492–501. [PubMed]
278. Pearlstein T, Bachmann G, Zacur H, Yonkers K. Treatment of premenstrual dysphoric disorder with a new drospirenone-containing oral contraceptive formulation. Contraception. 2005;72:414–21. [PubMed]
279. Rubig A. Drospirenone: a new cardiovascular-active progestin with antialdosterone and antiandrogenic properties. Climateric. 2003;6:49–54. [PubMed]
280. Eriksson E, Sundblad C, Lisjo P, Modigh K, Andersch B. Serum levels of androgens are higher in women with premenstrual irritability and dysphoria than in controls. Psychoneuroendocrinology. 1992;17:195–204. [PubMed]
281. Krasnik C, Montori VM, Guyatt GH, Heels-Ansdell D, Busse JW. The effect of bright light therapy on depression associated with premenstrual dysphoric disorder. Am J Obstet Gynecol. 2005;193:658–61. [PubMed]
282. Lam RW, Carter D, Misri S, Kuan AJ, Yatham LN, Zis AP. A controlled study of light therapy in women with late luteal phase dysphoric disorder. Psychiatry Res. 1999;86:185–92. [PubMed]
283. Parry BL, Berga SL, Mostofi N, Sependa PA, Kripke DF, Gillin JC. Morning versus evening bright light treatment of late luteal phase dysphoric disorder. Am J Psychiatry. 1989;146:1215–7. [PubMed]
284. Vellacott I, Shroff N, Pearce M, Stratford M, Akbar F. A double-blind, placebo-controlled evaluation of spironolactone in the premenstrual syndrome. Curr Med Res Opin. 1987;10:450–6. [PubMed]
285. Aslaksen K, Falk V. Spironolactone in the treatment of premenstrual tension: a double-blind study of spironolactone vs. bendroflumethiazide and placebo. Curr Ther Res Clin Exp. 1991;49:120–30.
286. Wang M, Hammarback S, Lindhe BA, Backstrom T. Treatment of premenstrual syndrome by spironolactone: a double-blind, placebo-controlled study. Acta Obstet Gynecol Scand. 1995;74:803–8. [PubMed]
287. Wyatt KM, Dimmock PW, Jones PW, Shaughn O'Brien PM. Efficacy of vitamin B-6 in the treatment of premenstrual syndrome: systematic review. BMJ. 1999;318:1375–81. [PMC free article] [PubMed]
288. London R, Bradley L, Chiamori N. Effect of nutritional supplement on premenstrual symptomatology in women with premenstrual syndrome: a double-blind longitudinal study. J Am Coll Nutr. 1991;10:494–9. [PubMed]
289. Thys-Jacobs S. Micronutrients and the premenstrual syndrome: the case for calcium. J Am Coll Nutr. 2000;19:220–7. [PubMed]
290. Thys-Jacobs S, Ceccarelli S, Bierman A, Weisman H, Cohen M, Alvir J. Calcium supplementation in premenstrual syndrome: a randomized crossover trial. J Gen Intern Med. 1989;4:183–9. [PubMed]
291. Thys-Jacobs S, Starkey P, Bernstein D, Tian J. Calcium carbonate and the premenstrual syndrome: effects on premenstrual and menstrual symptoms. Premenstrual Syndrome Study Group. Am J Obstet Gynecol. 1998;179:444–52. [PubMed]
292. Walker AF, De Souza MC, Vickers MF, Abeyasekera S, Collins ML, Trinca LA. Magnesium supplementation alleviates premenstrual symptoms of fluid retention. J Womens Health. 1998;7:1157–65. [PubMed]
293. Khine K, Rosenstein DL, Elin RJ, Niemela JE, Schmidt PJ, Rubinow DR. Magnesium (Mg) retention and mood effects after intravenous Mg infusion in premenstrual dysphoric disorder. Biol Psychiatry. 2006;59:327–33. [PMC free article] [PubMed]
294. Schellenberg R. Treatment for the premenstrual syndrome with agnus castus fruit extract: prospective, randomised, placebo controlled study. BMJ. 2001;322:134–7. [PMC free article] [PubMed]
295. Berger D, Schaffner W, Schrader E, Meier B, Brattstrom A. Efficacy of Vitex agnus castus L. extract Ze 440 in patients with pre-menstrual syndrome (PMS) Arch Gynecol Obstet. 2000;264:150–3. [PubMed]
296. Atmaca M, Kumru S, Tezcan E. Fluoxetine versus Vitex agnus castus extract in the treatment of premenstrual dysphoric disorder. Hum Psychopharmacol. 2003;18:191–5. [PubMed]
297. Loch EG, Selle H, Boblitz N. Treatment of premenstrual syndrome with a phytopharmaceutical formulation containing Vitex agnus castus. J Womens Health Gend Based Med. 2000;9:315–20. [PubMed]
298. Budeiri D, Li Wan Po A, Dornan J. Is evening primrose oil of value in the treatment of premenstrual syndrome? Control Clin Trials. 1996;17:60–8. [PubMed]
299. Tesch BJ. Herbs commonly used by women: an evidence-based review. Am J Obstet Gynecol. 2003;188(5 suppl):S44–55. [PubMed]
300. Stevinson C, Ernst E. A pilot study of Hypericum perforatum for the treatment of premenstrual syndrome. BJOG. 2000;107:870–6. [PubMed]
301. Rossignol AM, Bonnlander H. Caffeine-containing beverages, total fluid consumption, and premenstrual syndrome. Am J Public Health. 1990;80:1106–10. [PubMed]
302. Sayegh R, Schiff I, Wurtman J, Spiers P, McDermott J, Wurtman R. The effect of a carbohydrate-rich beverage on mood, appetite, and cognitive function in women with premenstrual syndrome. Obstet Gynecol. 1995;86:520–8. [PubMed]
303. Freeman E, Stout A, Endicott J, Spiers P. Treatment of premenstrual syndrome with a carbohydrate-rich beverage. Int J Gynecol Obstet. 2002;77:253–4. [PubMed]
304. Steege J, Blumenthal J. The effects of aerobic exercise on premenstrual symptoms in middle-aged women: a preliminary study. J Psychosom Res. 1993;37:127–33. [PubMed]
305. Hunter M, Ussher J, Browne S, Cariss M, Jelley R, Katz M. A randomized comparison of psychological (cognitive behavior therapy), medical (fluoxetine) and combined treatment for women with premenstrual dysphoric disorder. J Psychosom Obstet Gynaecol. 2002;23:193–9. [PubMed]
306. Hunter MS, Ussher JM, Cariss M, Browne S, Jelley R, Katz M. Medical (fluoxetine) and psychological (cognitive-behavioural therapy) treatment for premenstrual dysphoric disorder: a study of treatment processes. J Psychosom Res. 2002;53:811–7. [PubMed]
307. Blake F, Salkovskis P, Gath D, Day A, Garrod A. Cognitive therapy for premenstrual syndrome: a controlled trial. J Psychosom Res. 1998;45:307–18. [PubMed]
308. Christensen AP, Oei TP. The efficacy of cognitive behaviour therapy in treating premenstrual dysphoric changes. J Affect Disord. 1995;33:57–63. [PubMed]
309. Mira M, McNeil D, Fraser I, Vizzard J, Abraham S. Mefenamic acid in the treatment of premenstrual syndrome. Obstet Gynecol. 1986;68:395–8. [PubMed]
310. Facchinetti F, Fioroni L, Sances G, Romano G, Nappi G, Genazzani A. Naproxen sodium in the treatment of premenstrual symptoms. A placebo-controlled study. Gynecol Obstet Invest. 1989;28:205–8. [PubMed]
311. Chuong C, Hsi P. Effect of naloxone on luteinizing hormone secretion in premenstrual syndrome. Fertil Steril. 1994;61:1039–44. [PubMed]
312. Young E, Korszun A. Psychoneuroendocrinology of depression. Hypothalamic pituitary-gonadal axis. Psychiatr Clin North Am. 1998;21:309–23. [PubMed]