Search tips
Search criteria 


Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Am J Psychiatry. Author manuscript; available in PMC 2012 October 2.
Published in final edited form as:
PMCID: PMC3462360

Premenstrual Dysphoric Disorder: Evidence for a New Category for DSM-5


Premenstrual dysphoric disorder, which affects 2%–5% of premenopausal women, was included in Appendix B of DSM-IV, “Criterion Sets and Axes Provided for Further Study.” Since then, aided by the inclusion of specific and rigorous criteria in DSM-IV, there has been an explosion of research on the epidemiology, phenomenology, pathogenesis, and treatment of the disorder. In 2009, the Mood Disorders Work Group for DSM-5 convened a group of experts to examine the literature on premenstrual dysphoric disorder and provide recommendations regarding the appropriate criteria and placement for the disorder in DSM-5. Based on thorough review and lengthy discussion, the work group proposed that the information on the diagnosis, treatment, and validation of the disorder has matured sufficiently for it to qualify as a full category in DSM-5. A move to the position of category, rather than a criterion set in need of further study, will provide greater legitimacy for the disorder and encourage the growth of evidence-based research, ultimately leading to new treatments.

Descriptions of a syndrome characterized by premenstrual psychological and physical distress have a long history, dating from the time of Hippocrates. At that time, a woman’s monthly bleed was purported to “purge her bad humors.” Trotula of Salerno, an 11th-century female gynecologist, remarked in The Diseases of Women, “There are young women who are relieved when the menses are called forth” (1). In modern times, a cluster of premenstrual symptoms has been variably referred to as premenstrual tension syndrome (2) or premenstrual syndrome (3, 4).

In DSM, a moderate to severe form of premenstrual distress was classified according to the type, timing, and severity of symptoms. The initial diagnostic criteria for “late luteal phase dysphoric disorder” in Appendix A of DSM-III-R (5) emphasized the timing and severity of symptoms by designating a minimum of five symptoms with predictable onset and offset in the late luteal and early follicular phases of the menstrual cycle, respectively. The DSM-IV work group on late luteal phase dysphoric disorder recommended the prospective use of standardized rating instruments to determine the true prevalence of the disorder in the general population of women, since previous studies suggested a prevalence ranging from 7% to 54%, depending on study methods and diagnostic algorithms (6). The work group proposed that prospective daily ratings would improve the accuracy of diagnosis by confirming the timing of symptom onset and offset with respect to menstrual cycle phase and limit the inappropriate inclusion of women with milder symptoms or premenstrual worsening of ongoing affective disorders. For DSM-IV, late luteal phase dysphoric disorder was renamed “premenstrual dysphoric disorder” and the diagnostic criteria were modified slightly. However, the category remained in an appendix, as the work group believed additional research was needed to confirm the distinctiveness of the diagnosis from other disorders, its true prevalence, and its specific criteria.

All diagnoses and categories of mental disorders are undergoing scrutiny and potential revision in the process of developing DSM-5 (7). The Mood Disorders Work Group for DSM-5 charged a panel of experts in women’s mental health to 1) evaluate the previous criteria for premenstrual dysphoric disorder, 2) assess whether there is sufficient empirical evidence to support its inclusion as a diagnostic category, and 3) comment on whether the previous diagnostic criteria are consistent with the additional data that have become available. The work group comprised eight individuals representative of various countries (United States, Canada, Sweden, United Kingdom), six of whom have specialty expertise in premenstrual dysphoric disorder or reproductive mood disorders. The literature was reviewed and thoroughly vetted by the panel, leading to the recommendation that premenstrual dysphoric disorder be moved from the appendix to reside as a diagnosis in the Mood Disorders section of the manual. In this review, we provide a summary of the literature and rationale behind this recommendation.

Before focusing specifically on the diagnosis of premenstrual dysphoric disorder, it is important to consider the general requirements for any disorder to be considered for inclusion in DSM-5. There must be sufficient empirical evidence that the disorder in question 1) is distinct from other disorders; 2) has antecedent validators, such as familial aggregation, presence in diverse populations, and environmental risk factors; 3) has concurrent validators, such as cognitive and temperament correlates, biological markers, and a certain comorbidity profile; and 4) has predictive validity with respect to diagnostic stability, predictability of course of illness, and response to treatment.

Addressing Requirements for Diagnostic Category

Evidence of Premenstrual Dysphoric Disorder as a Distinct Diagnosis

Epidemiological and clinical studies consistently show that some women experience a pattern of distressing symptoms beginning in the luteal phase of the menstrual cycle and terminating shortly after the onset of menses (617) (Table 1). While the prevalence of premenstrual dysphoric disorder varies depending on the population assessed and the study methods used, this pattern of symptom expression is distinct from that of other disorders in that the onset of symptoms occurs in the premenstrual phase (after midcycle) and has an on-off pattern that is recurrent and predictable (18).

Prevalence of Premenstrual Dysphoric Disorder in Treatment-Seeking and Non-Treatment-Seeking Populations

The DSM-IV criteria for premenstrual dysphoric disorder include symptoms most commonly endorsed by symptomatic women who have been surveyed in large clinical and community studies (6, 9, 19, 20). While the symptoms of premenstrual dysphoric disorder overlap with those of other mood disorders, the cluster proposed for diagnosis is clearly different from those of other mood disorders. For example, the psychological symptoms most commonly reported by women with significant premenstrual distress are mood lability and irritability, not depressed mood or diminished interest and pleasure, as seen with major depressive disorder. Although mood lability and irritability are commonly observed in bipolar disorder, the pattern of predictable symptom onset and offset with phases of the menstrual cycle remains a key feature distinguishing premenstrual dysphoric disorder from other cyclic mood disorders. Finally, physical symptoms such as bloating and breast tenderness are both unique and among the most frequently reported premenstrual symptoms in women suffering from premenstrual dysphoric disorder (20) (Table 2).

Comparison of Mean Effect Sizes and Symptom Ratings, by Premenstrual Dysphoric Disorder Symptom in Community and Clinical Samplesa

With respect to familial risk for premenstrual dysphoric disorder, data from the Virginia Twin Registry (21, 22), the Australian National Health and Medical Research Council Twin Register (23, 24), and studies conducted in the United Kingdom (25, 26) provide heritability estimates ranging from 30% to 80% for premenstrual symptoms. While each of these studies is based on retrospective reports of premenstrual symptoms, the Virginia Twin Registry study conducted two separate assessments, on average 72 months apart, in both members of 314 monozygotic and 181 dizygotic twin pairs. With a primary focus on psychological symptoms, the investigators found a remarkable stability of symptoms from the first to the second assessment. A best-fitting twin-measurement model estimated the heritability of the stable component of premenstrual symptoms at 56% and showed no impact of family environment factors (22). A study examining the genetic and familial factors that affect the liability to major depression and to premenstrual symptoms found that 86% of the genetic variance and 88% of the environmental variance for premenstrual symptoms were not shared with major depression (22). Likewise, other studies have found that a substantial portion of the genetic variance of premenstrual syndrome is not shared with major depression or with personality factors such as neuroticism (21, 24).

Treatment approaches to premenstrual dysphoric disorder are shared with other mood disorders but are also distinct in several important ways. In women with premenstrual dysphoric disorder, symptom response is better with serotonin reuptake inhibitors (SRIs) than with noradrenergic agents (27, 28). SRI treatment limited to the luteal phase appears to be as effective as daily administration (2937), indicating a much shorter onset of action of these drugs when used for premenstrual dysphoric disorder than when used for depression and anxiety disorders. There is also evidence that certain ovulation-inhibiting hormonal treatments (38, 39) and gonadotropin-releasing hormone (GnRH) agonists (4045) are efficacious in the treatment of premenstrual syndrome/premenstrual dysphoric disorder, and there is no reason to believe that these treatments would be effective in other mood disorders (41). While GnRH agonist treatment appears to be effective for both the behavioral and physical symptoms of premenstrual syndrome/premenstrual dysphoric disorder in the majority of cases, hormone add-back is required to reduce the adverse sequelae of long-term hypogonadism. Unfortunately, such add-back (estradiol, progesterone, or both) leads to a return of negative mood in some patients (46).

Antecedent Validators

As previously discussed, familial aggregation of premenstrual symptoms is due largely to genetic factors, with a very modest contribution, if any, from familial environment (22, 25). In addition, premenstrual dysphoric disorder is not a culture-bound syndrome and has been found in epidemiological cohorts in the United States (20), Canada (16, 17), Europe (8), India (12), and Japan (13). Rates are comparable in Caucasians and African Americans in the United States (47), and symptoms appear to be relatively stable over time (8, 22).

As in other psychiatric disorders, the possible relationship between environmental factors such as stress and the onset or expression of premenstrual dysphoric disorder symptoms, as well as psychological and physiological responses to stress, has been investigated (4850). A history of interpersonal trauma (5153) and seasonal changes have been suggested to have an impact on onset or expression of premenstrual dysphoric disorder (5456), although confirmatory studies are required. Studies examining prior psychiatric history in women presenting with premenstrual dysphoric disorder demonstrate that major depression is the most frequently reported previous disorder (5762). While this may be an accurate assessment, it is important to note that these frequency estimates are based primarily on clinical cohorts, which are more likely to have high rates of comorbidity. In addition, women with premenstrual dysphoric disorder may have been erroneously diagnosed with major depression, as the use of prospective ratings to confirm or rule out premenstrual dysphoric disorder would have been unlikely.

Concurrent Validators

Earlier work showed that women with premenstrual dysphoric disorder were hyperattentive to dysphoric stimuli. One study found that this negative attentional bias was limited to the luteal phase of the menstrual cycle (63), while another found it expressed during both phases of the cycle (64). Perception of the frequency and severity of stress has been reported to be greater during the luteal but not the follicular phase of the menstrual cycle in women with prospectively confirmed premenstrual dysphoric disorder compared with healthy comparison subjects (65). Personality disorders are typically more common in individuals with axis I disorders, although this has not been clearly shown in women with severe premenstrual syndrome or premenstrual dysphoric disorder when compared with the general population (62, 65). One report shows a greater odds of avoidant personality disorder in women with premenstrual dysphoric disorder, but only among those age 30 or older (66).

Similar to other psychiatric disorders, premenstrual dysphoric disorder is not clearly associated with particular biomarkers (7). Nevertheless, the timing of onset and offset of symptoms with ovulation has led numerous investigators to examine the role of hormones in the pathogenesis of the disorder. Although studies of peripheral levels of ovarian and stress hormones, neurosteroids, follicle-stimulating hormone, and luteinizing hormone have shown some positive findings, they have failed to consistently identify differences between women with and without premenstrual dysphoric disorder (6779). Several, but not all, studies suggest that among women with premenstrual dysphoric disorder, symptom severity is correlated with levels of estradiol, progesterone, or neurosteroids such as allopregnanolone and pregnenolone sulfate (7779).

One of the most compelling findings supporting the role of ovarian hormones in the pathogenesis of premenstrual dysphoric disorder comes from a study by Schmidt et al. (46) demonstrating that women with the disorder are more sensitive to both estradiol and progesterone than comparison subjects. In that study, women with premenstrual dysphoric disorder experienced significant improvement in core mood and physical symptoms with GnRH agonist treatment, only to have a return of negative affect when either estradiol or progesterone was reintroduced in a double-blind, placebo-controlled fashion. Notably, healthy comparison subjects pretreated with the GnRH agonist did not react negatively to administration of estradiol or progesterone.

Neuroimaging studies are in their infancy with regard to revealing the neural circuitry or neurochemistry of premenstrual dysphoric disorder. That said, functional MRI (80), positron emission tomography (81), and proton magnetic resonance spectroscopy (67) demonstrate specific CNS differences in neural network activation, glucose metabolism, and neurotransmitter concentration, respectively, between prospectively characterized women with premenstrual dysphoric disorder and healthy comparison subjects.

Finally, several lines of evidence indicate altered cortical activity or physiological arousal in women with well-characterized premenstrual dysphoric disorder relative to healthy comparison subjects (8286). Using transcranial magnetic stimulation as a probe, Smith et al. (84) showed that women with premenstrual dysphoric disorder do not experience a normal increase in neuronal inhibition in the motor cortex when progesterone and allopregnanolone levels are elevated (during the luteal phase). Two studies have utilized the acoustic startle procedure to probe physiological arousal over the menstrual cycle. Women with premenstrual dysphoric disorder did not differ from healthy comparison subjects during the follicular phase but had greatly accentuated baseline startle during the symptomatic luteal phase (85). Using a slightly different paradigm, a second study (86) showed that arousal was accentuated across the menstrual cycle in women with premenstrual dysphoric disorder compared with healthy subjects, but particularly so in the luteal phase. In addition, the study found prepulse inhibition deficits in the luteal phase in women with premenstrual dysphoric disorder. Together, these data are consistent with the assertion that abnormal CNS response to menstrual cycle-related hormone fluctuations contributes to the pathophysiology of premenstrual dysphoric disorder.

Another aspect of concurrent validity is the relationship between a specific disorder and other psychiatric illnesses. As mentioned previously, it is crucial that a set of criteria describe a disorder that is distinct from other disorders, although there may be phenomenological similarities, including patterns of comorbidity. The diagnosis of premenstrual dysphoric disorder requires that symptoms of mood or anxiety be limited to the luteal phase of the menstrual cycle, even though many women with ongoing psychiatric disorders report exacerbation of their primary illness during the days leading up to menstruation. In an early study of women with major depression and premenstrual worsening (87), women who were treated with a tricyclic antidepressant improved in terms of depression but not premenstrual symptoms. These data are interesting in light of premenstrual dysphoric disorder’s preferential response to SRIs (28). Hartlage et al. (88) found that in the community, many women with major depression show premenstrual worsening that is not often addressed therapeutically.

Predictive Validators

The research criteria for premenstrual dysphoric disorder have demonstrated diagnostic stability in several ways. First, to meet criteria for premenstrual dysphoric disorder, women must experience the premenstrual pattern of symptoms in at least half of their menstrual cycles during the previous year. Although neither the criteria nor clinical practice requires women to prospectively chart their symptoms or cycles for 12 months, stability of symptom pattern from cycle to cycle has been documented in numerous studies using 2 to 3 months of prospective daily ratings (22, 89). In addition to the pattern of symptoms with respect to onset and offset across the menstrual cycle, the type of symptoms experienced by a given patient remains consistent between cycles.

Finally, the DSM-IV work group on premenstrual dysphoric disorder reanalyzed a large data set (N=670) from women with premenstrual complaints who completed daily ratings as part of their participation in clinical trials for premenstrual syndrome/premenstrual dysphoric disorder (6) and confirmed that the symptom criteria included in DSM-IV reflect the symptoms most frequently reported to fluctuate with the menstrual cycle. Likewise, several members of the DSM-5 work group conducted a secondary analysis of epidemiological and clinical cohorts (Table 2) whose members completed prospective daily ratings (20). The community sample was an area probability sample from the Midwest, and the clinical sample comprised women who responded to advertisements for women with premenstrual dysphoric disorder or premenstrual syndrome in Connecticut, New York, and Virginia. Each sample was roughly 65% white, 12%–15% Hispanic, 15%–17% black, and 5% other. Effect sizes were calculated according to the previous methods (6), allowing for a measure of change in symptom severity between postmenstrual and premenstrual periods that considers background variability across the cycle. For each symptom, the postmenstrual follicular score (average ratings on days 7–12 postmenses) was subtracted from the perimenstrual score (average over the various 6-day intervals near menses) and divided by the standard deviation of each symptom rating over the entire cycle. Table 2 highlights the symptoms that were similarly evaluated in the epidemiological and clinical samples. Peak symptom severity was greatest for physical symptoms in both cohorts. Peak severity for the most severe symptoms occurred either the day before or the day of onset of menstruation, although effect size calculations indicate that most symptoms were present 3 to 4 days prior to menstruation and continued through the first 2–3 days of menstruation. In addition, effect sizes revealed that physical symptoms such as bloating and low energy were common in both the general population and those seeking clinical care. Of the psychological symptoms, mood lability and irritability/anger ranked highest and were therefore listed first among the symptom clusters suggested for the DSM-5 criteria. In both cohort analyses, symptoms reflective of depressed mood or sadness demonstrated a lower effect size, further emphasizing the distinctiveness of premenstrual dysphoric disorder from major depressive disorder. Although the symptoms analyzed may be limited to those most queried with available daily rating scales, this body of research confirms the cluster of symptoms included in DSM-IV as well as diagnostic stability across time and among clinical and epidemiological cohorts with respect to types of symptoms endorsed.

Illness onset and trajectory of symptom severity should be relatively predictable over time for a given disorder. Treatment discontinuation studies show that women with premenstrual dysphoric disorder have a resurgence of the same symptoms when medication is openly (90, 91) or blindly (92) discontinued. Long-term follow-up studies conducted on two relatively small cohorts found that 8–12 years after initial assessment, menstruating women continued to have premenstrual symptoms (93, 94). For women in whom a diagnosis of premenstrual dysphoric disorder is established and who remain premenopausal, symptoms are likely to continue if they are not treated (95). As anticipated, cessation of ovarian cyclicity with menopause, be it surgical, medical, or natural, brings an end to symptoms of premenstrual dysphoric disorder in the majority of cases.

Finally, one of the most potent predictive validators of premenstrual dysphoric disorder as a disorder distinct from mood disorders is its preferential response to SRIs. A meta-analysis of the use of SRIs as treatment for premenstrual dysphoric disorder demonstrated uniformity of response (96). Furthermore, in no other psychiatric disorder do SRIs reduce symptoms with as short an onset of action as in premenstrual dysphoric disorder. Likewise, premenstrual dysphoric disorder is responsive to treatment with oral contraceptives containing the unique progestin drospirenone (38, 39) as well as to ovarian suppression with GnRH agonists (45, 46).

Benefits of Inclusion as a Category in DSM-5

It is with this information in mind that the DSM-5 panel of experts proposed the inclusion of premenstrual dysphoric disorder as a full category in this next edition of DSM. The benefit of moving premenstrual dysphoric disorder from the research criterion stage to that of full-fledged diagnosis is considerable from both a scientific and a clinical perspective. The research criteria for the disorder have already led to more rigorous characterization of women participating in randomized clinical trials and studies focusing on pathophysiology. In addition, the Food and Drug Administration and similar authorities in other countries have approved several pharmacological agents for the treatment of premenstrual dysphoric disorder, making it a de facto diagnosis regardless of its position within DSM.

A category for premenstrual dysphoric disorder would describe individuals who are not well represented by other psychiatric diagnostic categories. Data from clinical as well as epidemiological cohorts show that many women experience symptoms that begin during the luteal phase of the menstrual cycle and terminate around the onset of menses. Prevalence rates vary considerably depending on study methods, particularly with respect to prospective or retrospective symptom reporting, consideration of symptom interference, and population sampling (Table 1). In the two studies conducted using probability sampling of the general population and using prospective daily ratings for two complete menstrual cycles and confirmed premenstrual interference in functioning, the mean prevalence of premenstrual dysphoric disorder was approximately 2% (14, 15). The mean prevalence is higher (5%) if all studies of the prevalence of premenstrual dysphoric disorder are included (Table 1).

A number of studies have found that women with premenstrual dysphoric disorder experience impaired functioning in various domains (9, 97100) and that functional impairment improves during treatment (99, 101). Such impairment among those affected argues for the need to detect and treat women who meet criteria for the disorder. Without clear diagnostic boundaries for premenstrual dysphoric disorder, symptoms may be dismissed and the diagnosis missed by providers. Clinicians may assume, for example, that the patient suffers from milder premenstrual syndrome or from an ongoing mood disorder such as major depression or dysthymic disorder. Because the treatments for these various conditions are distinct, accurate diagnosis is important. Moreover, the acceptance of strict diagnostic criteria may counteract unwarranted overdiagnosis of mild cases.

An additional reason for the suggested change is that it would promote accurate collection of data regarding the treatment need and delivery of services for premenstrual dysphoric disorder that could be obtained from epidemiological and treatment delivery studies. Such collection would thus benefit from premenstrual dysphoric disorder having a code of its own rather than being coded as depression not otherwise specified. Alternatively, it may today be coded as premenstrual tension syndrome according to ICD, which is also unfortunate given the lack of stringent criteria for this condition.

The inclusion of premenstrual dysphoric disorder as a diagnostic category may further facilitate the development of medications that are useful for treatment and may encourage additional biological research on the causes of the disorder. Finally, while the inclusion of criteria for premenstrual dysphoric disorder in the appendices of DSM-III-R and DSM-IV facilitated research, the work group felt that information on the diagnosis, treatment, and validators of the disorder has by now matured to the point that the disorder should qualify as a category in DSM-5. A move to the position of category, rather than a condition in need of further study, would provide greater legitimacy for the diagnosis (102, 103).

The DSM-5 work group recognizes that some stakeholders may be concerned about the inclusion of premenstrual dysphoric disorder as a new diagnostic category. Some individuals and groups assert that a disorder that focuses on the perimenstrual phase of the menstrual cycle may “pathologize” normal reproductive functioning in women. Likewise, there may be concerns that since only women are at risk for the condition, they may be subject to inappropriate stigmatization and insinuation that they are not able to perform needed activities during the premenstrual phase of the cycle. Our group reviewed this literature and considered these points of view. However, because the prevalence statistics clearly indicate that premenstrual dysphoric disorder is a condition that occurs in a small minority of women, it would be inappropriate to generalize any premenstrual disability to women as a group. On the contrary, the inclusion of the diagnosis as a DSM-5 category, with its specific criteria and accompanying text, would emphasize that only a minority of women experience severe symptoms with accompanying distress and impairment. Analogously, while most individuals experience the feeling of sadness at some point in their lives, not all individuals have experienced a mood disorder. The overall health benefit for women of having an empirically based diagnosis would thus outweigh the potential for unfounded stigmatization or demeaning remarks that some groups fear.

Suggested Criteria for Premenstrual Dysphoric Disorder

Figure 1 lists the criteria for premenstrual dysphoric disorder as worded in Appendix B of DSM-IV, and Figure 2 lists the criteria recommended by the sub-work group to be used in DSM-5 as premenstrual dysphoric disorder becomes a full diagnostic category. The suggested changes are relatively minor and serve to refine the language of the DMS-IV research criteria. In criterion A, the wording on the timing of symptom onset and offset has been altered to be more explicit with respect to menstruation. A recent analysis of the prevalence of symptoms in the perimenstruum (20) suggests that symptoms do not need to be present most of the week prior to menstruation, as indicated in the wording in DSM-IV, only present in the final week before onset of menses. Likewise, symptoms do not necessarily remit within a few days after onset of menstrual flow. They do, however, begin to improve within a few days after onset of menstruation and are minimal, if not absent, in the week postmenses.

Criteria for Premenstrual Dysphoric Disorder in Appendix B of DSM-IVa
Recommended Criteria for Premenstrual Dysphoric Disorder for DSM-5

As previously mentioned, recent analyses of daily ratings from epidemiological and clinical samples strongly suggest that mood lability and irritability should be emphasized as the prominent psychological symptoms of premenstrual dysphoric disorder (20). Hence, “marked affective lability” and “marked irritability or anger” have been moved to first and second in the symptom list. Criterion B now mentions “clinically significant distress” in addition to interference, as many highly symptomatic and distressed women muster coping skills to manage the impact of their symptoms on their work and interpersonal relationships. Also, criterion B now includes a reference to the impact of symptoms on productivity and efficiency at home and not just at work and school. Criterion C indicates that premenstrual dysphoric disorder may co-occur with, rather than be superimposed on, other disorders, maintaining the notion that women with other psychiatric disorders may also have premenstrual dysphoric disorder. The importance of prospective confirmation of the pattern and severity of symptoms with respect to functional impact has been retained in criterion D, although a provisional diagnosis may be made based on clinical history. Prospective daily ratings not only are helpful in confirming the diagnosis of premenstrual dysphoric disorder and ruling out premenstrual worsening of other conditions but also provide a baseline for comparison of the effectiveness of treatment interventions once they are initiated. While premenstrual exacerbation of depression and anxiety disorders is clinically relevant to this discussion, to date there are insufficient data to determine the prevalence of these conditions, and they must be excluded during the assessment of premenstrual dysphoric disorder, as there are distinct treatments for premenstrual dysphoric disorder that could worsen symptoms in women with premenstrual exacerbation of other disorders. Confirmation of criteria B and C is no longer considered necessary to the diagnosis, as distress or interference in functioning is typically ascertained during the psychiatric assessment. Finally, criterion E has been added to highlight the distinctiveness of premenstrual dysphoric disorder from an ongoing medical disorder or medication- or substance-induced conditions.


Current data support the criteria listed in Appendix B of DSM-IV for premenstrual dysphoric disorder. Recent analysis of clinical and epidemiological samples has helped clarify the timing of peak symptom severity and the types of symptoms most frequently experienced by women with premenstrual complaints. It is clear that only a minority of premenopausal women—far less than 10%—will experience premenstrual distress of the type and severity that would meet the proposed DSM-5 diagnostic criteria for premenstrual dysphoric disorder. Thus, the normal menstrual fluctuations in physical and emotional symptoms experienced by the majority of women would not be considered pathological if premenstrual dysphoric disorder becomes a distinct category in the Mood Disorders section of DSM-5. The benefits of including premenstrual dysphoric disorder in DSM-5 will be substantial, as it will enhance not only research and clinical care but also the credibility of women who experience significant monthly distress.


Dr. Epperson has received research support from Shire for an investigator-initiated study, has received donation of products for research purposes from Novartis, and holds equity in Johnson & Johnson and Merck. Dr. Steiner has served as a consultant for AstraZeneca, Azevan, Bayer Canada, and Servier, has received research grants from the Canadian Institutes of Health Research, and has received honoraria from AstraZeneca and the Society for Women’s Health Research. Dr. Hartlage received funding from APA to conduct secondary analyses of data sets on premenstrual dysphoric disorder. Dr. Eriksson has served on advisory boards for Lundbeck and Schering-Bayer and has received consultancy fees and research grants from Lundbeck. Dr. Schmidt reports no financial relationships with commercial interests. Dr. Jones has received honoraria or consultancy fees from AstraZeneca, Eli Lilly, GlaxoSmithKline, Janssen-Cilag, Lundbeck, and Sanofi-Aventis and has received research funding from GlaxoSmith-Kline. Dr. Yonkers has received research support from Eli Lilly, NIMH, and the National Institute on Drug Abuse, study medication from Pfizer for an NIMH-funded trial, and royalties from UpToDate; she also received funding from APA to conduct secondary analyses of data sets on premenstrual dysphoric disorder.


1. Mason-Hohl E. The Diseases of Women, by Trotula of Salerno: A Translation of Passionibus Mulierum Curandorum by Elizabeth Mason-Hohl, MD. Los Angeles: Ward Ritchie Press; 1940.
2. Frank RT. The hormonal causes of premenstrual tension. Arch Neurol Psychiatry. 1931;26:1053–1057.
3. Greene R, Dalton K. The premenstrual syndrome. Br Med J. 1953;1:1007–1014. [PMC free article] [PubMed]
4. Endicott J. History, evolution, and diagnosis of premenstrual dysphoric disorder. J Clin Psychiatry. 2000;61(suppl 12):5–8. [PubMed]
5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 3. Washington, DC: American Psychiatric Association; 1987. revised (DSM-III-R)
6. Hurt SW, Schnurr PP, Severino SK, Freeman EW, Gise LH, Rivera-Tovar A, Steege JF. Late luteal phase dysphoric disorder in 670 women evaluated for premenstrual complaints. Am J Psychiatry. 1992;149:525–530. [PubMed]
7. Stein DJ, Phillips KA, Fulford KWM, Sadler JZ, Kendler KS. What is a mental/psychiatric disorder? from DSM-IV to DSM-V. Psychol Med. 2010;40:1759–1765. [PMC free article] [PubMed]
8. Wittchen H, Becker E, Lieb R, Krause P. Prevalence, incidence, and stability of premenstrual dysphoric disorder in the community. Psychol Med. 2002;32:119–132. [PubMed]
9. Rivera-Tovar A, Pilkonis P, Frank E. Symptom patterns in late luteal-phase dysphoric disorder. J Psychopathol Behav Assess. 1992;14:189–199.
10. Cohen LS, Soares CN, Otto MW, Sweeney BH, Liberman RF, Harlow BL. Prevalence and predictors of premenstrual dysphoric disorder (PMDD) in older premenopausal women: the Harvard Study of Moods and Cycles. J Affect Disord. 2002;70:125–132. [PubMed]
11. Endicott J, Amsterdam J, Eriksson E, Frank E, Freeman E, Hirschfeld R, Ling F, Parry B, Pearlstein T, Rosenblum J, Rubinow D, Schmidt P, Serverino S, Steiner M, Stewart DE, Thys-Jacobs S. Is premenstrual dysphoric disorder a distinct clinical entity? J Womens Health Gend Based Med. 1999;8:663–679. [PubMed]
12. Banerjee N, Roy K, Takkar D. Premenstrual dysphoric disorder: a study from India. Int J Fertil Womens Med. 2000;45:342–344. [PubMed]
13. Takeda T, Tasaka K, Sakata M, Murata Y. Prevalence of premenstrual syndrome and premenstrual dysphoric disorder in Japanese women. Arch Womens Ment Health. 2006;9:209–212. [PubMed]
14. Sveinsdóttir H, Bäckström T. Menstrual cycle symptom variation in a community sample of women using and not using oral contraceptives. Acta Obstet Gynecol Scand. 2000;79:757–764. [PubMed]
15. Gehlert S, Song IH, Chang CH, Hartlage SA. The prevalence of premenstrual dysphoric disorder in a randomly selected group of urban and rural women. Psychol Med. 2009;39:129–136. [PMC free article] [PubMed]
16. Steiner M, Macdougall M, Brown E. The Premenstrual Symptoms Screening Tool (PSST) for clinicians. Archives Womens Ment Health. 2003;6:203–209. [PubMed]
17. Steiner M, Peer M, Palova E, Freeman E, Macdougall M, Soares CN. The Premenstrual Symptoms Screening Tool revised for adolescents (PSST-A): prevalence of severe PMS and premenstrual dysphoric disorder in adolescents. Arch Womens Ment Health. 2011;14:77–81. [PubMed]
18. Steiner M, Wilkins A. Diagnosis and assessment of premenstrual dysphoria. Psychiatr Ann. 1996;26:571–575.
19. Meaden PM, Hartlage SA, Cook-Karr 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]
20. Hartlage SA, Freels A, Gotman N, Yonkers KA. Criteria for premenstrual dysphoric disorder: secondary analyses of relevant data sets. Arch Gen Psychiatry. 2012;69:300–305. [PMC free article] [PubMed]
21. Kendler KS, Silberg JL, Neale MC, Kessler RC, Heath AC, Eaves LJ. Genetic and environmental factors in the aetiology of menstrual, premenstrual, and neurotic symptoms: a population-based twin study. Psychol Med. 1992;22:85–100. [PubMed]
22. Kendler KS, Karkowski LM, Corey LA, Neale MC. Longitudinal population-based twin study of retrospectively reported premenstrual symptoms and lifetime major depression. Am J Psychiatry. 1998;155:1234–1240. [PubMed]
23. Condon JT. The premenstrual syndrome: a twin study. Br J Psychiatry. 1993;162:481–486. [PubMed]
24. Treloar SE, Heath AC, Martin NG. Genetic and environmental influences on premenstrual symptoms in an Australian twin sample. Psychol Med. 2002;32:25–38. [PubMed]
25. van den Akker OB, Stein GS, Neale MC, Murray RM. Genetic and environmental variation in menstrual cycle: histories of two British twin samples. Acta Genet Med Gemellol (Roma) 1987;36:541–548. [PubMed]
26. van den Akker OB, Eves FF, Stein GS, Murray RM. Genetic and environmental factors in premenstrual symptom reporting and its relationship to depression and a general neuroticism trait. J Psychosom Res. 1995;39:477–487. [PubMed]
27. Eriksson E, Hedberg MA, 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;12:167–176. [PubMed]
28. Freeman EW, Rickels K, Sondheimer SJ, Wittmaack FM. Sertraline versus desipramine in the treatment of premenstrual syndrome: an open-label trial. J Clin Psychiatry. 1996;57:7–11. [PubMed]
29. Sundblad C, Modigh K, Andersch B, Eriksson E. Clomipramine effectively reduces premenstrual irritability and dysphoria: a placebo-controlled trial. Acta Psychiatr Scand. 1992;85:39–47. [PubMed]
30. Steiner M, Korzekwa M, Lamont J, Wilkins A. Intermittent fluoxetine dosing in the treatment of women with premenstrual dysphoria. Psychopharmacol Bull. 1997;33:771–774. [PubMed]
31. Jermain DM, Preece CK, Sykes RL, Kuehl TJ, Sulak PJ. Luteal phase sertraline treatment for premenstrual dysphoric disorder: results of a double-blind, placebo-controlled, crossover study. Arch Fam Med. 1999;8:328–332. [PubMed]
32. 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;161:343–351. [PubMed]
33. Halbreich U, Bergeron R, Yonkers KA, Freeman E, Stout AL, Cohen L. Efficacy of intermittent luteal phase sertraline treatment of premenstrual dysphoric disorder. Obstet Gynecol. 2002;100:1219–1229. [PubMed]
34. Cohen LS, Miner C, Brown EW, Freeman E, Halbreich U, Sundell K, McCray S. Premenstrual daily fluoxetine for premenstrual dysphoric disorder: a placebo-controlled clinical trial using computerized diaries. Obstet Gynecol. 2002;100:435–444. [PubMed]
35. Yonkers KA, Holthausen GA, Poschman K, Howell HB. Symptom-onset treatment for women with premenstrual dysphoric disorder. J Clin Psychopharmacol. 2006;26:198–202. [PubMed]
36. Steiner M, Hirschberg AL, Bergeron R, Holland F, Gee M, van Erp E. Luteal phase dosing with paroxetine controlled-release in the treatment of premenstrual dysphoric disorder. Am J Obstet Gynecol. 2005;193:352–360. [PubMed]
37. Steiner M, Ravindran A, LeMelledo JM, Carter D, Huang J, Anonychuk A, Simpson S. Luteal-phase administration of paroxetine for the treatment of premenstrual dysphoric disorder: a randomized, double-blind, placebo controlled trial in Canadian women. J Clin Psychiatry. 2008;69:991–998. [PubMed]
38. Pearlstein TB, Bachmann GA, Zacur HA, Yonkers KA. Treatment of premenstrual dysphoric disorder with a new drospirenone-containing oral contraceptive formulation. Contraception. 2005;72:414–421. [PubMed]
39. Yonkers K, Foegh M. A new low-dose, drospirenone-containing oral contraceptive (OC) with a new dosing regimen is effective in reducing premenstrual dysphoric disorder (PMDD) Fertil Steril. 2004;82(suppl 2):S102–S103. [PubMed]
40. Muse KN, Cetel NS, Futterman LA, Yen SC. The premenstrual syndrome: effects of “medical ovariectomy. N Engl J Med. 1984;311:1345–1349. [PubMed]
41. Freeman EW, Sondheimer SJ, Rickels K. Gonadotropin-releasing hormone agonist in the treatment of premenstrual symptoms with and without ongoing dysphoria: a controlled study. Psychopharmacol Bull. 1997;33:303–309. [PubMed]
42. Brown CS, Ling FW, Anderson RN, Falmer RG, Arheart KL. Efficacy of depot leuprolide in premenstrual syndrome: effect of symptom severity and type in a controlled trial. Obstet Gynecol. 1994;84:779–786. [PubMed]
43. Leather AT, Studd JWW, Watson NR, Holland EFN. 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]
44. 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;27:171–182. [PubMed]
45. Wyatt KM, Dimmock PW, Ismail KM, Jones PW, O’Brien PM. The effectiveness of GnRHa with and without “add-back” therapy in treating premenstrual syndrome: a meta-analysis. BJOG. 2004;111:585–593. [PubMed]
46. Schmidt PJ, Nieman LK, Danaceau MA, Adams LF, Rubinow DR. Differential behavioral effects of gonadal steriods in women with and in those without premenstrual syndrome. N Engl J Med. 1998;338:209–216. [PubMed]
47. Stout AL, Grady TA, Steege JF, Blazer DG, George LK, Melville ML. Premenstrual symptoms in black and white community samples. Am J Psychiatry. 1986;143:1436–1439. [PubMed]
48. Fontana AM, Palfai TG. Psychosocial factors in premenstrual dysphoria: stressors, appraisal, and coping processes. J Psychosom Res. 1994;38:557–567. [PubMed]
49. Girdler S, Straneva P, Light K, Pederson C, Morrow A. Allopregnanolone levels and reactivity to mental stress in premenstrual dysphoric disorder. Biol Psychiatry. 2001;49:788–797. [PubMed]
50. Deuster P, Adera T, South-Paul J. Biological, social, and behavioral factors associated with premenstrual syndrome. Arch Fam Med. 1999;8:122–128. [PubMed]
51. Pilver CE, Levy BR, Libby DJ, Desai RA. Posttraumatic stress disorder and trauma characteristics are correlates of premenstrual dysphoric disorder. Arch Womens Ment Health. 2011;14:383–393. [PMC free article] [PubMed]
52. Golding J, Taylor D, Menard L, King M. Prevalence of sexual abuse history in a sample of women seeking treatment for premenstrual syndrome. J Psychsom Obstet Gynaecol. 2000;21:69–80. [PubMed]
53. Perkonigg A, Yonkers K, Pfister H, Lieb R, Wittchen HU. Risk factors for premenstrual dysphoric disorder in a community sample of young women: the role of traumatic events and post-traumatic stress disorder. J Clin Psychiatry. 2004;65:1314–1322. [PubMed]
54. Maskall DD, Lam RW, Misri S, Carter D, Kuan AJ, Yatham LN, Zis AP. Seasonality of symptoms in women with late luteal phase dysphoric disorder. Am J Psychiatry. 1997;154:1436–1441. [PubMed]
55. Praschak-Rieder N, Willeit M, Neumeister A, Hilger E, Stastny J, Thierry N, Lenzinger E, Kasper S. Prevalence of premenstrual dysphoric disorder in female patients with seasonal affective disorder. J Affect Disord. 2001;63:239–242. [PubMed]
56. Kim DR, Czarkowski KA, Epperson CN. The relationship between bipolar disorder, seasonality, and premenstrual symptoms. Curr Psychiatry Rep. 2011;13:500–503. [PubMed]
57. De Ronchi D, Ujkaj M, Boaron F, Muro A, Piselli M, Quartesan R. Symptoms of depression in late luteal phase dysphoric disorder: a variant of mood disorder? J Affect Disord. 2005;86:169–174. [PubMed]
58. Kim D, Gyulai L, Freeman E, Morrison M, Baldassano C, Dube B. Premenstrual dysphoric disorder and psychiatric co-morbidity. Arch Womens Ment Health. 2004;7:37–47. [PubMed]
59. Halbreich U, Endicott J. Relationship of dysphoric premenstrual changes to depressive disorder. Acta Psychiatr Scand. 1985;71:331–338. [PubMed]
60. Mackenzie TB, Wilcox K, Baron H. Lifetime prevalence of psychiatric disorders in women with perimenstrual difficulties. J Affect Disord. 1986;10:15–19. [PubMed]
61. Fava M, Pedrazzi F, Guaraldi GP, Romano G, Genazzani AR, Facchinetti F. Comorbid anxiety and depression among patients with late luteal phase dysphoric disorder. J Anxiety Disord. 1992;6:325–335.
62. 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;20:129–134. [PubMed]
63. 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]
64. Keenan PA, Lindamer LA, Jong SK. Menstrual phase-independent retrieval deficit in women with PMS. Biol Psychiatry. 1995;38:369–377. [PubMed]
65. Critchlow DG, Bond AJ, Wingrove J. Mood disorder history and personality assessment in premenstrual dysphoric disorder. J Clin Psychiatry. 2001;62:688–693. [PubMed]
66. 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]
67. Epperson CN, Haga K, Mason GF, Sellers E, Gueorguieva R, Zhang W, Weiss E, Rothman DL, Krystal JH. 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;59:851–858. [PubMed]
68. Backstrom T, Sanders D, Leask R, Davidson D, Warner P, Bancroft J. Mood, sexuality, hormones, and the menstrual cycle, II: hormone levels and their relationship to the premenstrual syndrome. Psychosom Med. 1983;45:503–506. [PubMed]
69. Bloch M, Schmidt PJ, Su T-P, Tobin MB, Rubinow DR. Pituitary-adrenal hormones and testosterone across the menstrual cycle in women with premenstrual syndrome and controls. Biol Psychiatry. 1998;43:897–903. [PubMed]
70. Eriksson E, Sundblad C, Lisjö 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]
71. Facchinetti F, Genazzani AD, Martignoni E, Fioroni L, Nappi G, Genazzani AR. Neuroendocrine changes in luteal function in patients with premenstrual syndrome. J Clin Endocrinol Metab. 1993;76:1123–1127. [PubMed]
72. Reame NE, Marshall JC, Kelch RP. Pulsatile LH secretion in women with premenstrual syndrome (PMS): evidence for normal neuroregulation of the menstrual cycle. Psychoneuroendocrinology. 1992;17:205–213. [PubMed]
73. Redei E, Freeman EW. Preliminary evidence for plasma adrenocorticotropin levels as biological correlates of premenstrual symptoms. Acta Endocrinol. 1993;128:536–542. [PubMed]
74. Rubinow DR, Hoban MC, Grover GN, Galloway DS, Roy-Byrne P, Andersen R, Merriam GR. Changes in plasma hormones across the menstrual cycle in patients with menstrually related mood disorder and in control subjects. Am J Obstet Gynecol. 1988;158:5–11. [PubMed]
75. Steiner M, Haskett RF, Carroll BJ, Hays SE, Rubin RT. Circadian hormone secretory profiles in women with severe premenstrual tension syndrome. Br J Obstet Gynaecol. 1984;91:466–471. [PubMed]
76. 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]
77. Wang M, Seippel L, Purdy RH, Bäckström T. Relationship between symptom severity and steroid variation in women with premenstrual syndrome: study on serum pregnenolone, pregnenolone sulfate, 5 alpha-pregnane-3,20-dione and 3 alpha-hydroxy-5 alpha-pregnan-20-one. J Clin Endocrinol Metab. 1996;81:1076–1082. [PubMed]
78. Rapkin AJ, Morgan M, Goldman L, Brann DW, Simone D, Mahesh VB. Progesterone metabolite allopregnanolone in women with premenstrual syndrome. Obstet Gynecol. 1997;90:709–714. [PubMed]
79. Seippel L, Bäckström T. Luteal-phase estradiol relates to symptom severity in patients with premenstrual syndrome. J Clin Endocrinol Metab. 1998;83:1988–1992. [PubMed]
80. Protopopescu X, Tuescher O, Pan H, Epstein J, Root J, Chang L, Altemus M, Polanecsky M, McEwen B, Stern E, Silbersweig D. Toward a functional neuroanatomy of premenstrual dysphoric disorder. J Affect Disord. 2008;108:87–94. [PubMed]
81. Rapkin AJ, Berman SM, Mandelkern MA, Silverman DH, Morgan M, London ED. Neuroimaging evidence of cerebellar involvement in premenstrual dysphoric disorder. Biol Psychiatry. 2011;69:374–380. [PMC free article] [PubMed]
82. Sundström I, Bäckström T. Patients with premenstrual syndrome have decreased saccadic eye velocity compared to control subjects. Biol Psychiatry. 1998;44:755–764. [PubMed]
83. Sundström I, Andersson A, Nyberg S, Ashbrook D, Purdy RH, Bäckström T. Patients with premenstrual syndrome have a different sensitivity to a neuroactive steroid during the menstrual cycle compared to control subjects. Neuroendocrinology. 1998;67:126–138. [PubMed]
84. Smith MJ, Adams LF, Schmidt PJ, Rubinow DR, Wassermann EM. Abnormal luteal phase excitability of the motor cortex in women with premenstrual syndrome. Biol Psychiatry. 2003;54:757–762. [PubMed]
85. 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;32:2190–2198. [PMC free article] [PubMed]
86. Kask K, Gulinello M, Bäckström T, Geyer MA, Sundström-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;33:2283–2290. [PubMed]
87. Yonkers KA, White K. Premenstrual exacerbation of depression: one process or two? J Clin Psychiatry. 1992;53:289–292. [PubMed]
88. Hartlage S, Brandenburg D, Kravitz H. Premenstrual exacerbation of depressive disorders in a community-based sample in the United States. Psychosom Med. 2004;66:698–706. [PubMed]
89. Bloch M, Schmidt PJ, Rubinow DR. Premenstrual syndrome: evidence for symptom stability across cycles. Am J Psychiatry. 1997;154:1741–1746. [PubMed]
90. de la Gándara Martín JJ. Premenstrual dysphoric disorder: long-term treatment with fluoxetine and discontinuation. Actas Luso Esp Neurol Psiquiatr Cienc Afines. 1997;25:235–242. (Spanish) [PubMed]
91. 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;7:201–206. [PubMed]
92. Freeman EW, Rickels K, Sammel MD, Lin H, Sondheimer SJ. Time to relapse after short- or long-term treatment of severe premenstrual syndrome with sertraline. Arch Gen Psychiatry. 2009;66:537–544. [PMC free article] [PubMed]
93. Metcalf MG, Braiden V, Livesey JH. Symptom cyclicity in women with the premenstrual syndrome: an 8-year follow-up study. J Psychosom Res. 1992;36:237–241. [PubMed]
94. Roca CA, Schmidt PJ, Rubinow DR. A follow-up study of premenstrual syndrome. J Clin Psychiatry. 1999;60:763–766. [PubMed]
95. Freeman EW, Rickels K, Sondheimer SJ. Course of premenstrual syndrome symptom severity after treatment. Am J Psychiatry. 1992;149:531–533. [PubMed]
96. Dimmock P, Wyatt K, Jones P, O’Brien S. Efficacy of selective serotonin-reuptake inhibitors in premenstrual syndrome: a systematic review. Lancet. 2000;356:1131–1136. [PubMed]
97. 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;85:317–321. [PubMed]
98. 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 (Larchmt) 2008;17:113–121. [PubMed]
99. Pearlstein T, Halbreich U, Batzar E, Brown C, Endicott J, Frank E, Freeman EW, Harrison WM, Haskett RF, Stout AL, Yonkers KA. Psychosocial functioning in women with premenstrual dysphoric disorder before and after treatment with sertraline or placebo. J Clin Psychiatry. 2000;61:101–109. [PubMed]
100. Halbreich U, Borenstein J, Pearlstein T, Kahn LS. The prevalence, impairment, impact, and burden of premenstrual dysphoric disorder (PMS/PMDD) Psychoneuroendocrinology. 2003;28(suppl 3):1–23. [PubMed]
101. Steiner M, Brown E, Trzepacz P, Dillon J, Berger C, Carter D, Reid R, Stewart D. Fluoxetine improves functional work capacity in women with premenstrual dysphoric disorder. Arch Womens Ment Health. 2003;6:71–77. [PubMed]
102. Pearlstein T. Premenstrual dysphoric disorder: out of the appendix. Arch Womens Ment Health. 2010;13:21–23. [PubMed]
103. O’Brien PM, Bäckström T, Brown C, Dennerstein L, Endicott J, Epperson CN, Eriksson E, Freeman E, Halbreich U, Ismail KM, Panay N, Pearlstein T, Rapkin A, Reid R, Schmidt P, Steiner M, Studd J, Yonkers K. Towards a consensus on diagnostic criteria, measurement, and trial design of the premenstrual disorders: the ISPMD Montreal consensus. Arch Womens Ment Health. 2011;14:13–21. [PubMed]