Premenstrual dysphoric disorder

From Wikipedia, the free encyclopedia
Premenstrual dysphoric disorder
Other namesLate luteal phase dysphoric disorder
SpecialtyPsychiatry
SymptomsSevere mood swings, depression, irritability, agitation, uneasiness, change in appetite, severe fatigue, anxiety, anger, swelling, bruising, insomnia/hypersomnia, breast tenderness, decreased interest in usual /social activities, reduced interest in sexual activity, heart palpitations, difficulty in concentration.
Usual onsetearly teens
Duration6 days – 3 weeks of cycle
Causesunknown
Risk factorsFamily history
Diagnostic methodbased on symptoms & criteria
Differential diagnosisPremenstrual syndrome, depression, anxiety disorder
Treatmentmedication, counselling, lifestyle change, surgery
Medicationhormone treatment, SSRI’s,
Frequency1.8–5.8% of menstruating women

Premenstrual dysphoric disorder (PMDD) is a severe and disabling form of premenstrual syndrome affecting 1.8–5.8% of menstruating women.[1] The disorder consists of a variety of affective, behavioral and somatic symptoms that recur monthly during the luteal phase of the menstrual cycle.[2][3] PMDD affects patients from their early teens up until menopause, excluding those with hypothalamic amenorrhea or during pregnancy and breastfeeding.[4] Those with PMDD are at higher risk of suicide, with rates of suicidal thoughts 2.8 times higher, history of suicidal planning 4.15 times, and suicide attempts 3.3 times.[5]

The emotional effects of premenstrual dysphoric disorder are theorized to be the result of severe gonadal steroid fluctuations, as they cause dysregulation of serotonin uptake and transmission, and potentially calcium regulation, circadian rhythm, BDNF, the HPA-axis and immune function as well.[6]

In 2017, researchers at the National Institutes of Health discovered that people with PMDD have genetic changes that make their cells overreact to estrogen and progesterone. They believe this overreaction may be responsible for PMDD symptoms.[7]

Some studies have suggested that those with PMDD are more at risk of developing postpartum depression after pregnancy, but other evidence has been found to suggest against that notion.[8] PMDD was added to the list of depressive disorders in the Diagnostic and Statistical Manual of Mental Disorders in 2013.[1] It has 11 main symptoms, and a person has to exhibit at least five to qualify for PMDD.[6] Roughly 20% of women have some symptoms of PMDD, but either have less than five or do not have functional impairment.[9]

Treatment is often with antidepressants such as selective serotonin reuptake inhibitors (SSRIs) or hormone treatment (ovulation suppression) using birth control pills and GnRH analogues.[3] SSRIs are the most common treatment, as they tend to improve both the physical and emotional symptoms as well as the general behavior and functionality of the person, however the clinician must determine the best treatment based on the subjects criteria markers, only given that the subject doesn’t display markers outside the luteal phase or menses.[3]

Signs and symptoms[]

Premenstrual dysphoric disorder (PMDD) is a severe form of premenstrual syndrome (PMS). Like PMS, premenstrual dysphoric disorder follows a predictable, cyclic pattern. Symptoms begin in the late luteal phase of the menstrual cycle (after ovulation) and end shortly after menstruation begins.[10] On average, the symptoms last six days but can start up to two weeks before menses, meaning symptoms can be felt for up to three weeks out of a cycle. Severe symptoms can begin and worsen until the onset of menstruation, with many not feeling relief until a few days after menstruation ends. The most intense symptoms occurring in the week and days leading up to the first day of menstrual blood flow.[2] The symptoms usually cease shortly after the start of the menstrual period or a few days after it ending.[3][11] The onset of symptoms only during or around the luteal phase is key for diagnosing someone with PMDD rather than any other mood disorders.[4]

The symptoms can be physical or emotional, but mood symptoms must be present for the diagnosis.[10] Those with PMDD may have thoughts of suicide.[12] A mood log in which a person records mood patterns over time may help direct.[4]

The International Society for the Study of Premenstrual Disorders (ISPMD) defines two categories of premenstrual disorders: core PMD and variant PMD.[4]

Core PMD has six characteristics, all mainly focusing on the cyclical nature of PMDD and its typical onset pre-menses tracked over the course of more than two menstrual cycles. The four classified Variant PMDs involve more unexpected variables that cause the onset of premenstrual distress; such as, PMD with absent menstruation or premenstrual exacerbation, wherein the symptoms of another preexisting psychological disorder may be heightened as a result of PMDD onset.[4]

Associated conditions[]

Bipolar depression, anxiety disorders, and other Axis I disorders are more common in those with PMDD.[13] In those with PMDD, there is a 40% lifetime incidence of various psychiatric disorders such as generalized anxiety disorder, seasonal affective disorder, and major depressive disorder.[3]

Cause[]

PMDD mood symptoms are only present in menstruating people. Thus, symptoms do not occur during pregnancy and after menopause. Other mood disorders typically persist across all reproductive life events and are independent of a person's menstrual cycle or lack thereof.[14]

The most agreed-upon possibilities for what causes PMDD currently are heightened sensitivity to fluctuating levels of certain hormones (i.e. the reproductive hormones), environmental stress, and genetic predisposition.[4] The sex steroids—estrogen and progesterone—are neuroactive; they have been noted in rat models to be involved in serotonin pathways.[4] Serotonin is involved in mood regulation alongside estrogen, whose receptors are found in the prefrontal cortex and hippocampus—the regions most known for their involvement in regulating one's mood and cognition overall.[2][4]

While the timing of symptoms suggests hormonal fluctuations as the cause of PMDD, a demonstrable hormonal imbalance in people with PMDD has not been identified. In fact, levels of reproductive hormones and their metabolites in people with and without PMDD are indistinguishable.[15][16][17] It is instead hypothesized that people with PMDD are more sensitive to normal levels of hormone fluctuations, predominantly estrogen and progesterone, which produces biochemical events in the nervous system that cause the premenstrual symptoms.[17] These symptoms are more predominant in people who have a predisposition to the disorder.[10]

It is apparent that the premenstrual disorders are biologically driven and are not only psychological or cultural phenomena. PMDD has been reported by menstruating people worldwide, indicating a biological basis that is not geographically selective.[2] Most psychologists infer that this disorder is caused by both a reaction to hormone flux and also genetic components. There is evidence of heritability of (retrospectively-reported) premenstrual symptoms from several twin and family studies done in the 1990s, with the heritability of PMDD proving to be about 56%.[18][19][20]

Disorders of this nature are often caused by a mix of both environmental and biological factors. Environmental stressors have also been found to prospectively increase risk for PMDD symptoms.[21][22] Genetics do not operate in a vacuum: environmental components such as stress, hormonal fluctuation, and epigenetics play a key role in the pathology and onset of the disorder.[23] Some studies have noted evidence of interpersonal trauma (domestic violence, physical or emotional trauma, or substance abuse) or seasonal changes (making PMDD potentially comorbid with Seasonal Affective Disorder) having an impact on PMDD risk.[3][24] But the most common pre-existing disorder found in those diagnosed with PMDD is major depression, wherein they either actually had it or were misdiagnosed when they should have only been diagnosed with PMDD.[24] The last environmental factor is primarily sociological: the sociocultural aspects of being female, performing female gender roles, and stress from engaging in female sexual activity.[1]

Genetic Factors

While whether or not this disorder has a specific genetic basis is still being discussed in the academic community and the possible genetic factors contributing to PMDD have yet to be thoroughly researched, there has recently been multiple genetic factors identified that contribute to the moodiness, depression, irritability, increased appetite, trouble sleeping, acne, fluid retention, headaches, nausea, and other symptoms that are all associated with this disorder.

One case that has been identified of a gene that may be linked to PMDD is in a study in mice that has shown evidence that a polymorphism of the brain-derived neurotrophic factor gene (BDNF), a gene that helps support neurons in their function and survival in the brain by creating a protein that helps in the growth, maturation, and maintenance of these cells, may play a role in causing PMDD symptoms. This is because the result of this polymorphism mimics the hallmarks of PMDD: volatile moods, depression and irritability centered around the menstrual cycle. This gene has been studied extensively in its association with depression and, promisingly for PMDD research, mice homozygous for the BDNF polymorphism exhibited anxiety-like traits that fluctuated and changed around the mice’s estrus, analogous to the human’s menstruation, therefore mimicking some of the symptoms of PMDD.[25]

By comparing the genomes of lymphoblastoid cells in mice and people with and without PMDD, two common epigenetic biomarkers, which are both linked to postpartum depression were found that transcend both species and cell types. Two of these loci were HP1BP3 and TTC9B. The exact functions of these loci are currently unknown, however, bioinformatics analysis suggests that both loci may be involved in mediating synaptic plasticity as well as estrogen signaling.[26] These loci were most notable because they were able to correctly identify whether a person would develop PPMD with 87% accuracy based on differences in methylation. These biomarkers were also important in that they could be used to segregate postpartum depression status in people who became depressed during pregnancy and continued to be depressed after giving birth during the postpartum time period with 88% accuracy, meaning that the biomarkers may also be helpful in discovering the likelihood of a person developing postpartum depression.[27][25]

Another study has shown that people with PMDD have dysregulation of the ESC/E(Z) complex. This leads to the body having an abnormal response to ovarian steroids and to the person having some of the symptoms of PMDD.[27] The G/G genotype of HTR1A (rs6295), a serotonin receptor that plays a role in regulating dopamine levels in the brain, has been associated with poor working memory and worsened cognitive function during the premenstrual phase for people with PMDD as well, a less common symptom of the disorder. The G/G genotype specifically plays a role in PMDD because this genotype reduces serotonin neurotransmission and is more common in individuals with major depressive disorder. This gene may therefore give insight into the mechanism through which some people with PMDD experience their symptoms.[28]

Risk for PMDD is also associated with genetic variation of ESR1, the estrogen receptor alpha gene. Specifically, those with PMDD were observed to have four single nucleotide polymorphisms, a variation in a single nucleotide in a genetic sequence, in intron 4 of ESR1. This association was only observed in individuals with a Val/Val genotype of COMT, the gene that codes for an enzyme that degrades several catecholamines, which are hormones made by the adrenal gland. One such catecholamine that this enzyme degrades that is particularly important to PMDD is dopamine. The Val/Val genotype of COMT renders it over efficient, leading to dopamine deficiency. This provides a genetic basis to explain some of the symptoms of PMDD that affect mood such as depression, irritability, and mood swings.[29] Highly recurrent copy number variations, a phenomenon in which sections of the genome are repeated in numbers that vary among individuals, in GABRB2, a gene that codes for a brain receptor that plays a role in regulating stress responses, cognitive function, and energy regulation among other things, have also been found to be associated with both PMDD and schizophrenia. This is evidence that both of these neuropsychiatric disorders share some genetic basis.[30]

Relationship to pregnancy[]

People with PMDD usually see their symptoms disappear while they are pregnant. Premenstrual dysphoric disorder is primarily a mood disorder that is associated with onset of menstruation; pregnancy, menopause, and hysterectomies all cause menstruation to cease, thereby stopping the proposed sex steroid-/serotonin-caused symptoms from occurring.[31][32] Although one might expect a higher rate of postpartum depression among those with PMDD, a large study of women with prospectively-confirmed PMDD did not find a higher prevalence of postpartum depression than in controls.[8][32] If a person had experienced PPD beforehand, there was found to be a less-than 12% chance of PMDD pathology emerging—hardly any differentiation from the regular population of those who have never experienced postpartum depression.[32] However, PMDD symptoms can get worse following pregnancy, or other associated events such as birth and miscarriage.[12]

Menopause launches a person into an associated mood disorder called climacteric depression.[8] The permanent stopping of the menstrual cycle causes a myriad of physiological and psychological symptoms and issues, all associated with the natural estrogen deficiency post-menopause.[8]

Diagnosis[]

Diagnostic criteria for PMDD are provided by a number of expert medical guides. Diagnosis can be supported by having people who are seeking treatment for PMDD use a daily charting method to record their symptoms.[4] Daily charting helps to distinguish when mood disturbances are experienced and allows PMDD to be more easily distinguished from other mood disorders. With PMDD, mood symptoms are present only during the luteal phase, or last two weeks, of the menstrual cycle.[10] While PMDD mood symptoms are of a cyclical nature, other mood disorders are variable or constant over time. Although there is a lack of consensus on the most efficient instrument by which to confirm a PMDD diagnosis, several validated scales for recording premenstrual symptoms include the Calendar of Premenstrual Experiences (COPE), Daily Record of Severity of Problems (DRSP), and Prospective Record of the Severity of Menstruation (PRISM).[33][34] In the context of research, standardized numerical cutoffs are often applied to verify the diagnosis.[33] The difficulty of diagnosing PMDD is one reason that it can be challenging for lawyers to cite the disorder as a defence of crime, in the very rare cases where PMDD is allegedly associated with criminal violence.[35]

DSM-5[]

The DSM-5 which established seven criteria (A through G) for the diagnosis of PMDD.[1] There is overlap between the criteria for PMDD in the DSM-5 and the criteria found in the Daily Record of Severity of Problems (DRSP).[33][34]

According to the DSM-5, a diagnosis of PMDD requires the presence of at least five of these symptoms with one of the symptoms being numbers 1-4.[1] These symptoms should occur during the week before menses and remit after initiation of menses. In order to meet criteria for the diagnosis, the symptoms should be charted prospectively for two consecutive ovulation cycles in order to confirm a temporal and cyclical nature of the symptoms. The symptoms should also be severe enough to affect normal work, school, social activities, and/or relationships with others.[1]

The symptoms of Criteria A-C must have been met for most menstrual cycles that occurred in the preceding year, and have to have affected normal functioning to some degree (Criterion D).

Timing

Criterion A: During most menstrual cycles throughout the past year, at least 5 of the symptoms outlined in Criterion B and Criterion C must be present in the final week before the onset of menses, must start to improve within a few days after the onset of menses, and become minimal or absent in the week post-menses. [1]

Symptoms

Criterion B: One (or more) of the following symptoms must be present:[1]

  1. Marked affective lability (e.g., mood swings, feeling suddenly sad or tearful, or increased sensitivity to rejection)
  2. Marked irritability or anger or increased interpersonal conflicts
  3. Marked depressed mood, feelings of hopelessness, or self-deprecating thoughts
  4. Marked anxiety, tension, and/or feelings of being keyed up or on edge

Criterion C: One (or more) of the following symptoms must be present additionally, to reach a total of 5 symptoms when combined with present symptoms from Criterion B above:[1]

  1. Decreased interest in usual activities (e.g., work, school, friends, hobbies).
  2. Subjective difficulty in concentration.
  3. Lethargy, easy fatigability, or marked lack of energy.
  4. Marked change in appetite; overeating; or specific food cravings.
  5. Hypersomnia or insomnia.
  6. A sense of being overwhelmed or out of control.
  7. Physical symptoms such as breast tenderness or swelling, joint or muscle pain, a sensation of "bloating," or weight gain.

Severity

Criterion D: The symptoms observed in Criteria A-C are associated with clinically significant distress or interference with work, school, usual social activities, or relationships with others (e.g., avoidance of social activities; decreased productivity and efficiency at work, school, or home).[1]

  • Clinically significant distress is not defined explicitly by the DSM-IV, where it has been critiqued by multiple scholars as being too vague, and potentially detrimental for those who have symptoms of depression, anxiety, or other mood disorders because they do not meet the clinical significance requirement.[36][37]

Consideration of Other Psychiatric Disorders

Criterion E: The disturbance is not merely an exacerbation of the symptoms of another disorder, such as major depressive disorder, panic disorder, persistent depressive disorder (Dysthymia), or a personality disorder—although it may co-occur with any of these disorders.[1]

Confirmation of the Disorder

Criterion F: Criterion A should be confirmed by prospective daily ratings during at least two symptomatic cycles. The diagnosis may be made provisionally prior to this confirmation.[1]

Criterion G: The symptoms are not attributable to the physiological effects of a substance (e.g., drug abuse, a medication, other treatments) or another medical condition (e.g., hyperthyroidism).[1]

ICD 11[]

Diagnostic criteria for PMDD are also provided by the 2016 World Health Organization's International Classification of Diseases (ICD-11-CM):[38][39]

GA34.41 Premenstrual dysphoric disorder

Description

During a majority of menstrual cycles within the past year, a pattern of mood symptoms (depressed mood, irritability), somatic symptoms (lethargy, joint pain, overeating), or cognitive symptoms (concentration difficulties, forgetfulness) that begin several days before the onset of menses, start to improve within a few days after the onset of menses, and then become minimal or absent within approximately 1 week following the onset of menses. The temporal relationship of the symptoms and luteal and menstrual phases of the cycle may be confirmed by a prospective symptom diary. The symptoms are severe enough to cause significant distress or significant impairment in personal, family, social, educational, occupational or other important areas of functioning and do not represent the exacerbation of a mental disorder.

Early drafts of the ICD did not recognize PMDD as a separate condition.[40] In the World Health Organisation's classification system, the International Classification of Diseases (ICD-11), PMDD is listed as a "disease of the genitourinary system".[41]

Other[]

Other organizations that have published diagnostic criteria for PMDD include the Royal College of Obstetricians and Gynecologists and the International Society for the Study of Premenstrual Disorders (ISPMD).[42][38] The ISPMD was a consensus group established by an international multidisciplinary group of experts. The group's diagnostic criteria for PMDD focuses on the cyclic nature of the symptoms occurring during the luteal phase of the menstrual cycle, as well as the symptoms being absent after menstruation and before ovulation and causing significant impairment. The ISPMD diagnostic criteria for PMDD do not specify symptom characteristics or number of symptoms.[42]

In 2003 the Committee for Proprietary Medicinal Products required the manufacturer of fluoxetine to remove PMDD from the list of indications in Europe.[43] In Australia, PMDD is recognized by the Therapeutic Goods Administration. However, antidepressants are not reimbursed for PMDD under the Pharmaceutical Benefits Scheme.[44]

Differential diagnosis[]

When considering a diagnosis of PMDD, it is important to also consider an underlying major psychiatric disorder that exhibits premenstrual exacerbation, the menopausal transition, hyperthyroidism, hypothyroidism, as well as other mood disorders. Furthermore, many medical disorders are worsened prior to ordering menses, but these typically do not present strictly during the luteal phase.

Mood disorders – there is potential for patients to have psychiatric disorders with superimposed PMDD or psychiatric disorders. In order to distinguish the two, it is important to determine whether symptoms are in both the follicular and luteal phase or just the luteal phase. This can be determined through the use of a daily calendar tracking symptoms.

Menopausal transition – affective symptoms associated with the menopausal transition most commonly start when menstrual cycle starts to become irregular or anovulatory whereas PMDD symptoms occur during the luteal phase of ovulatory cycles.

Thyroid disorders—patients with both hyperthyroidism and hypothyroidism may present with affective symptoms, especially hyperthyroidism. Thyroid disorders can be ruled out by serum thyroid stimulating hormone (TSH).[45]

Treatment[]

Medication[]

Several medications have received empirical support for the treatment of PMDD. Selective serotonin reuptake inhibitors (SSRIs) are the first-line medication.[10][46][47] The U.S. Food and Drug Administration (FDA) has approved four SSRIs for the treatment of PMDD: Fluoxetine (available as generic or as Prozac or Sarafem), sertraline (Zoloft), paroxetine (Paxil), and escitalopram oxalate (Lexapro).[48] Unlike treatments for depressive disorders, SSRIs do not need to be taken daily but instead can be taken only in the luteal phase or during PMDD symptoms.[3] This is because those who respond to SSRIs usually experience symptoms relief within 1–2 days.[49] Studies in rats suggest this rapid response to SSRIs is due to the elevation of the neuroactive progesterone metabolite allopregnanolone in the brain, rather than serotonin.[50][51] Luteal phase dosing can be started 14 days before menses and subsequently discontinued after start of menstrual flow.[48] Women taking SSRIs to ease PMDD generally report >50% alleviation in symptoms, which was significant improvement compared to placebo.[49]

Although less studied, SNRIs have also shown benefits for those with PMDD. In a randomized, controlled clinical trial of women with PMDD, 60% of the subjects taking venlafaxine (Effexor) improved, versus 35% on placebo. Improvement was noticed during the first treatment cycle with 80% symptom reduction.[52]

Another FDA approved treatment for PMDD is the oral contraceptive with ethinylestradiol and drospirenone (a novel progestin) taken on a 24-4 schedule (24 active pills, 4 inactive pills).[48] It has been shown that hormonal birth control containing drospirenone and low levels of estrogen helps relieve severe PMDD symptoms, for at least the first three months that it is used.[53] The idea behind using oral contraceptives is to suppress ovulation, therefore suppressing sex hormone fluctuations.

Another treatment, typically used when other options have failed, is injection of a gonadotropin-releasing hormone agonist.[54] These drugs create a temporary, drug-induced menopause-like condition. Addback of estradiol is recommended to prevent bone loss long-term; this generally necessitates the concurrent addback of progesterone to prevent estradiol-induced endometrial hyperplasia. Two landmark studies have demonstrated that the addback of estradiol or progesterone on top of GnRH agonists can cause a resurgence of PMDD symptoms but that this resurgence of symptoms remits after one month of stable addback.[55][56][57]

Psychotherapy[]

Cognitive behavioral therapy (CBT) has been shown to be effective for reducing premenstrual symptoms in women with (retrospectively-reported) PMS.[58] CBT is an evidence-based approach for treating depression and focuses on the link between mood, thoughts, and actions to help people address current issues and symptoms. When CBT was compared to SSRI alone or in combination with SSRI, groups receiving CBT had significant improvement of PMS symptoms.[58] Through the practice of CBT, people are better able to recognize and modify recurrent issues as well as thought and behavior patterns that interfere with functioning well or that make depressive symptoms worse. However, a recent meta-analysis suggests that existing psychotherapies may be primarily useful for reducing impairment (rather than symptom severity) in PMDD.[58]

Surgery[]

When drug-based treatments are ineffective or produce significant side effects, then removing the ovaries through oophorectomy can produce an immediate and permanent cure.[31] Typically, the uterus is removed during the same surgery, and the patient is prescribed a low-dose estrogen patch to reduce the symptoms produced by surgically induced menopause.[31] There are five guidelines that should be considered before undergoing a surgical treatment. [59]

  • The diagnosis of PMDD must be confirmed
  • GnRH agonist therapy must be the only medical therapy that has been effective and it must have been effective continuously for a minimum of six months
  • Tolerance of estrogen replacement therapy has been tested
  • The person is done with childbearing
  • The person's age warrants several more years of therapy

Epidemiology[]

A majority of menstruating people have feelings of premenstrual symptoms to some degree, with 20-30% feeling enough symptoms to qualify for diagnosis of PMS and 3-8% of that group qualifying for the diagnosis of PMDD.[2][3] With only a small fraction feeling such intense distress linked to the onset of menstruation, any fear of social pathologizing of normal emotional and physical symptoms as a result of menstruation is unnecessary; PMDD is distinct, and having it included in the DSM-5 works to affirm that.[24]

History[]

In the 18th century, there were early accounts of weeping and other symptoms recurring almost every month,[60] and in 1822 Prichard gave this description: “Many women … display a degree of excitement and irritation … at the period of menstruation; these are chiefly females of very irritable habits. In such instances, … an unusual vehemence of feeling and expression is observed … or there is torpor and dejection of mind with a despondent disposition”. [61] In 1827 a German mother was acquitted of infanticide on the grounds of menstrual mood disorder.[62] Premenstrual tension was also described in the French literature of the early 19th century.[63] Nearly one hundred years later, there were American descriptions of a cyclic personality change appearing 10-14 days before, and ending dramatically at the menses.[64]

The diagnostic category was discussed in the DSM-IIIR (1987), in which the proposed condition was named "Late Luteal Phase Dysphoric Disorder" and was included in the appendix as a proposed diagnostic category needing further study.[65] Preparations for the DSM-IV led to debate about whether to keep the category at all, only keep it in the appendix, or remove it entirely; the reviewers determined that the condition was still too poorly studied and defined, so it was kept in the appendix but elaborated with diagnostic criteria to aid further study.[32][66]

As preparations were underway in 1998 for the DSM-IV-TR, the conversation changed, as Eli Lilly and Company paid for a large clinical trial of fluoxetine as a potential treatment for the condition that was then conducted by Canadian academics and published in the New England Journal of Medicine in 1995.[67] Other studies have been conducted as well, wherein all found that approximately 60% of women with PMDD in the trials improved with the drug; representatives from Lilly & Co. and the FDA participated in the discussion.[32][66]

Various strong stances were taken in said discussion. Sally Severino, a psychiatrist, argued that because symptoms were more prevalent in the United States, PMDD was a culture-bound syndrome and not a biological condition; she also claimed it unnecessarily pathologized the hormonal changes of the menstrual cycle.[32] Jean Endicott, another psychiatrist and chair of the committee, has argued that it was a valid condition from which women suffer and should be diagnosed and treated, and has claimed that if the symptoms were felt by males, far more effort and research would have been done by that moment. In the end the committee kept PMDD in the appendix.[32]

The decision has been criticized as being driven by Lilly's financial interests, and possibly by financial interests of members of the committee who had received funding from Lilly.[32] Paula Caplan, a psychologist who had served on the committee for the DSM-IV, noted at the time of the DSM-IV-TR decision that there was evidence that calcium supplements could treat PMDD but the committee gave it no attention. She had also claimed that the diagnostic category is harmful to women with PMDD, leading them to believe they are mentally ill, and potentially leading others to mistrust them in situations as important as job promotions or child custody cases.[32] She has called PMDD a fake disorder.[68] Nada Stotland has expressed concern that women with PMDD may actually have a more serious condition like major depressive disorder or may be facing difficult circumstances—such domestic abuse—and therefore may have their true issues remain undiagnosed and mismanaged if their gynecologist diagnoses them with PMDD and gives them drugs to treat it.[32]

The validity of PMDD was once more heavily debated when it came time to create the DSM-5 in 2008.[69][70] In the end it was moved out of the appendix and into the main text as a formal category. A review in the Journal of Clinical Psychiatry published in 2014 examined the arguments against inclusion, which it summarized as:

  1. the PMDD label will harm women economically, politically, legally, and domestically;
  2. there is no equivalent hormone-based medical label for males;
  3. the research on PMDD is faulty;
  4. PMDD is a culture-bound condition;
  5. PMDD is due to situational, rather than biological, factors; and
  6. PMDD was fabricated by pharmaceutical companies for financial gain.[71]

Each argument was addressed and researchers found:

  1. No evidence of harm;
  2. no equivalent hormone-driven disorder has been discovered in men despite research seeking it;
  3. the research base has matured and many more reputable studies have been performed;
  4. several cases of PMDD have been reported or identified;
  5. a small minority of women do have the condition; and
  6. while there has been financial conflict of interest, it has not made the available research unusable.[2][71]

It concluded that women have historically been under-treated and told that they were making their symptoms up, and that the formal diagnostic criteria would spur more funding, research, diagnosis and treatment for women with PMDD.[71]

References[]

  1. ^ Jump up to: a b c d e f g h i j k l m Diagnostic and Statistical Manual of Mental Disorders (5th ed.). Arlington, VA: American Psychiatric Association. 2013. p. 625.4. Code: 625.4 (N94.3)
  2. ^ Jump up to: a b c d e f Yonkers KA, O'Brien PM, Eriksson E (April 2008). "Premenstrual syndrome". Lancet. 371 (9619): 1200–10. doi:10.1016/S0140-6736(08)60527-9. PMC 3118460. PMID 18395582.
  3. ^ Jump up to: a b c d e f g h Rapkin AJ, Lewis EI (November 2013). "Treatment of premenstrual dysphoric disorder". Women's Health. 9 (6): 537–56. doi:10.2217/whe.13.62. PMID 24161307. S2CID 45517684.
  4. ^ Jump up to: a b c d e f g h i Reid RL, Soares CN (February 2018). "Premenstrual Dysphoric Disorder: Contemporary Diagnosis and Management". Journal of Obstetrics and Gynaecology Canada. 40 (2): 215–223. doi:10.1016/j.jogc.2017.05.018. PMID 29132964.
  5. ^ Pilver CE, Libby DJ, Hoff RA (March 2013). "Premenstrual dysphoric disorder as a correlate of suicidal ideation, plans, and attempts among a nationally representative sample". Social Psychiatry and Psychiatric Epidemiology. 48 (3): 437–46. doi:10.1007/s00127-012-0548-z. PMC 3774023. PMID 22752111.
  6. ^ Jump up to: a b Pearlstein T (April 2016). "Treatment of Premenstrual Dysphoric Disorder: Therapeutic Challenges". Expert Review of Clinical Pharmacology. 9 (4): 493–496. doi:10.1586/17512433.2016.1142371. PMID 26766596. S2CID 12172042.
  7. ^ Dubey N, Hoffman JF, Schuebel K, Yuan Q, Martinez PE, Nieman LK, et al. (August 2017). "The ESC/E(Z) complex, an effector of response to ovarian steroids, manifests an intrinsic difference in cells from women with premenstrual dysphoric disorder". Molecular Psychiatry. 22 (8): 1172–1184. doi:10.1038/mp.2016.229. PMC 5495630. PMID 28044059.
  8. ^ Jump up to: a b c d Studd J, Nappi RE (March 2012). "Reproductive depression". Gynecological Endocrinology. 28 Suppl 1 (s1): 42–5. doi:10.3109/09513590.2012.651932. PMID 22394303. S2CID 41778636.
  9. ^ Steiner M, Macdougall M, Brown E (August 2003). "The premenstrual symptoms screening tool (PSST) for clinicians". Archives of Women's Mental Health. 6 (3): 203–9. doi:10.1007/s00737-003-0018-4. PMID 12920618. S2CID 24822881.
  10. ^ Jump up to: a b c d e Steiner M, Pearlstein T, Cohen LS, Endicott J, Kornstein SG, Roberts C, et al. (2006). "Expert guidelines for the treatment of severe PMS, PMDD, and comorbidities: the role of SSRIs". Journal of Women's Health. 15 (1): 57–69. doi:10.1089/jwh.2006.15.57. PMID 16417420.
  11. ^ Biggs WS, Demuth RH (October 2011). "Premenstrual syndrome and premenstrual dysphoric disorder". American Family Physician. 84 (8): 918–24. PMID 22010771.
  12. ^ Jump up to: a b Liisa H (14 January 2019). "What is PMDD?". IAPMD. Retrieved 29 April 2019.
  13. ^ Kim DR, Gyulai L, Freeman EW, Morrison MF, Baldassano C, Dubé B (February 2004). "Premenstrual dysphoric disorder and psychiatric co-morbidity". Archives of Women's Mental Health. 7 (1): 37–47. doi:10.1007/s00737-003-0027-3. PMID 14963731. S2CID 2977103.
  14. ^ Douma SL, Husband C, O'Donnell ME, Barwin BN, Woodend AK (October 2005). "Estrogen-related mood disorders: reproductive life cycle factors". ANS. Advances in Nursing Science. 28 (4): 364–75. doi:10.1097/00012272-200510000-00008. PMID 16292022. S2CID 9172877.
  15. ^ Rubinow DR, Schmidt PJ (July 2006). "Gonadal steroid regulation of mood: the lessons of premenstrual syndrome". Frontiers in Neuroendocrinology. 27 (2): 210–6. doi:10.1016/j.yfrne.2006.02.003. PMID 16650465. S2CID 8268435.
  16. ^ Nguyen TV, Reuter JM, Gaikwad NW, Rotroff DM, Kucera HR, Motsinger-Reif A, et al. (August 2017). "The steroid metabolome in people with premenstrual dysphoric disorder during GnRH agonist-induced ovarian suppression: effects of estradiol and progesterone addback". Translational Psychiatry. 7 (8): e1193. doi:10.1038/tp.2017.146. PMC 5611719. PMID 28786978.
  17. ^ Jump up to: a b Hantsoo L, Epperson CN (November 2015). "Premenstrual Dysphoric Disorder: Epidemiology and Treatment". Current Psychiatry Reports. 17 (11): 87. doi:10.1007/s11920-015-0628-3. PMC 4890701. PMID 26377947.
  18. ^ Kendler KS, Karkowski LM, Corey LA, Neale MC (September 1998). "Longitudinal population-based twin study of retrospectively reported premenstrual symptoms and lifetime major depression". The American Journal of Psychiatry. 155 (9): 1234–40. doi:10.1176/ajp.155.9.1234. PMID 9734548. S2CID 2048753.
  19. ^ Condon JT (April 1993). "The premenstrual syndrome: a twin study". The British Journal of Psychiatry. Cambridge University Press. 162 (4): 481–6. doi:10.1192/bjp.162.4.481. PMID 8481739.
  20. ^ Wilson CA, Turner CW, Keye WR (March 1991). "Firstborn adolescent daughters and mothers with and without premenstrual syndrome: a comparison". The Journal of Adolescent Health. 12 (2): 130–7. doi:10.1016/0197-0070(91)90455-U. PMID 2015237.
  21. ^ Namavar Jahromi B, Pakmehr S, Hagh-Shenas H (March 2011). "Work stress, premenstrual syndrome and dysphoric disorder: are there any associations?". Iranian Red Crescent Medical Journal. 13 (3): 199–202. PMC 3371938. PMID 22737463.
  22. ^ Gollenberg AL, Hediger ML, Mumford SL, Whitcomb BW, Hovey KM, Wactawski-Wende J, Schisterman EF (May 2010). "Perceived stress and severity of perimenstrual symptoms: the BioCycle Study". Journal of Women's Health. 19 (5): 959–67. doi:10.1089/jwh.2009.1717. PMC 2875955. PMID 20384452.
  23. ^ Dubey N, Hoffman JF, Schuebel K, Yuan Q, Martinez PE, Nieman LK, et al. (August 2017). "The ESC/E(Z) complex, an effector of response to ovarian steroids, manifests an intrinsic difference in cells from women with premenstrual dysphoric disorder". Molecular Psychiatry. 22 (8): 1172–1184. doi:10.1038/mp.2016.229. PMC 5495630. PMID 28044059.
  24. ^ Jump up to: a b c Epperson CN, Steiner M, Hartlage SA, Eriksson E, Schmidt PJ, Jones I, Yonkers KA (May 2012). "Premenstrual dysphoric disorder: evidence for a new category for DSM-5". The American Journal of Psychiatry. 169 (5): 465–75. doi:10.1176/appi.ajp.2012.11081302. PMC 3462360. PMID 22764360.
  25. ^ Jump up to: a b McEvoy K, Osborne LM, Nanavati J, Payne JL (October 2017). "Reproductive Affective Disorders: a Review of the Genetic Evidence for Premenstrual Dysphoric Disorder and Postpartum Depression". Current Psychiatry Reports. 19 (12): 94. doi:10.1007/s11920-017-0852-0. PMID 29082433. S2CID 21658798.
  26. ^ Guintivano J, Arad M, Gould TD, Payne JL, Kaminsky ZA (May 2014). "Antenatal prediction of postpartum depression with blood DNA methylation biomarkers". Molecular Psychiatry. 19 (5): 560–7. doi:10.1038/mp.2013.62. PMC 7039252. PMID 23689534.
  27. ^ Jump up to: a b Goff A, Hoffman J, Dubey N, Schuebel K, Marrieta C, Yuan Q, et al. (2017-05-15). "505. Lymphoblastoid Cell Lines from Women with Premenstrual Dysphoric Disorder Differ in Genetic, mRNA, and Protein Expression Profiles Compared with Asymptomatic Controls". Biological Psychiatry. 81 (10): S205. doi:10.1016/j.biopsych.2017.02.1113. ISSN 0006-3223. S2CID 54278207.
  28. ^ Yen JY, Tu HP, Chen CS, Yen CF, Long CY, Ko CH (December 2014). "The effect of serotonin 1A receptor polymorphism on the cognitive function of premenstrual dysphoric disorder". European Archives of Psychiatry and Clinical Neuroscience. 264 (8): 729–39. doi:10.1007/s00406-013-0466-4. PMID 24158751. S2CID 27834770.
  29. ^ Huo L, Straub RE, Roca C, Schmidt PJ, Shi K, Vakkalanka R, et al. (October 2007). "Risk for premenstrual dysphoric disorder is associated with genetic variation in ESR1, the estrogen receptor alpha gene". Biological Psychiatry. 62 (8): 925–33. doi:10.1016/j.biopsych.2006.12.019. PMC 2762203. PMID 17599809.
  30. ^ Ullah A, Long X, Mat WK, Hu T, Khan MI, Hui L, et al. (2020). "Highly Recurrent Copy Number Variations in GABRB2 Associated With Schizophrenia and Premenstrual Dysphoric Disorder". Frontiers in Psychiatry. 11: 572. doi:10.3389/fpsyt.2020.00572. PMC 7338560. PMID 32695026.
  31. ^ Jump up to: a b c Reid RL (June 2012). "When should surgical treatment be considered for premenstrual dysphoric disorder?". Menopause International. 18 (2): 77–81. doi:10.1258/mi.2012.012009. PMID 22611227. S2CID 21181483.
  32. ^ Jump up to: a b c d e f g h i j Kepple AL, Lee EE, Haq N, Rubinow DR, Schmidt PJ (April 2016). "History of postpartum depression in a clinic-based sample of women with premenstrual dysphoric disorder". The Journal of Clinical Psychiatry. 77 (4): e415-20. doi:10.4088/JCP.15m09779. PMC 6328311. PMID 27035701.
  33. ^ Jump up to: a b c Eisenlohr-Moul TA, Girdler SS, Schmalenberger KM, Dawson DN, Surana P, Johnson JL, Rubinow DR (January 2017). "Toward the Reliable Diagnosis of DSM-5 Premenstrual Dysphoric Disorder: The Carolina Premenstrual Assessment Scoring System (C-PASS)". The American Journal of Psychiatry. 174 (1): 51–59. doi:10.1176/appi.ajp.2016.15121510. PMC 5205545. PMID 27523500.
  34. ^ Jump up to: a b Endicott J, Nee J, Harrison W (January 2006). "Daily Record of Severity of Problems (DRSP): reliability and validity". Archives of Women's Mental Health. 9 (1): 41–9. doi:10.1007/s00737-005-0103-y. PMID 16172836. S2CID 25479566.
  35. ^ Ro C. "The overlooked condition that can trigger extreme behaviour". www.bbc.com. Retrieved 2020-01-04.
  36. ^ Spitzer RL, Wakefield JC (December 1999). "DSM-IV diagnostic criterion for clinical significance: does it help solve the false positives problem?". The American Journal of Psychiatry. 156 (12): 1856–64. doi:10.1176/ajp.156.12.1856 (inactive 31 May 2021). PMID 10588397.CS1 maint: DOI inactive as of May 2021 (link)
  37. ^ Grenier S, Préville M, Boyer R, O'Connor K, Béland SG, Potvin O, et al. (April 2011). "The impact of DSM-IV symptom and clinical significance criteria on the prevalence estimates of subthreshold and threshold anxiety in the older adult population". The American Journal of Geriatric Psychiatry. 19 (4): 316–26. doi:10.1097/JGP.0b013e3181ff416c. PMC 3682986. PMID 21427640.
  38. ^ Jump up to: a b "Premenstrual Syndrome, Management (Green-top Guideline No. 48)". Royal College of Obstetricians and Gynaecologists. December 2016.
  39. ^ ICD-11: GA34.41 Premenstrual dysphoric disorder
  40. ^ Worcester N, Whatley MN (2000). Women's Health: Readings on Social, Economic, and Political Issues. Sage Publications. p. 613.
  41. ^ "ICD-11 - Mortality and Morbidity Statistics". icd.who.int. Retrieved 2019-08-26.
  42. ^ Jump up to: a b O'Brien PM, Bäckström T, Brown C, Dennerstein L, Endicott J, Epperson CN, et al. (February 2011). "Towards a consensus on diagnostic criteria, measurement and trial design of the premenstrual disorders: the ISPMD Montreal consensus". Archives of Women's Mental Health. 14 (1): 13–21. doi:10.1007/s00737-010-0201-3. PMC 4134928. PMID 21225438.
  43. ^ Moynihan R (February 2004). "Controversial disease dropped from Prozac product information". BMJ. 328 (7436): 365. doi:10.1136/bmj.328.7436.365. PMC 341379. PMID 14962861.
  44. ^ "Sertraline (Zoloft), fluoxetine (Lovan, Prozac) for premenstrual dysphoric disorder (PMDD)". National Prescribing Service Limited.
  45. ^ "UpToDate". www.uptodate.com. Retrieved 2021-09-09.
  46. ^ Agyemang AA (2018). Kreutzer JS, DeLuca J, Caplan B (eds.). Encyclopedia of Clinical Neuropsychology. Switzerland: Springer, Cham. doi:10.1007/978-3-319-57111-9. ISBN 978-3-319-57111-9.
  47. ^ Eriksson E, Endicott J, Andersch B, Angst J, Demyttenaere K, Facchinetti F, et al. (2002). "New perspectives on the treatment of premenstrual syndrome and premenstrual dysphoric disorder". Archives of Women's Mental Health. 4 (4): 111–119. doi:10.1007/s007370200009. S2CID 10427915.
  48. ^ Jump up to: a b c Ward S (2016). Maternal-Child Nursing Care. Philadelphia, PA, USA: F.A. Davis Company. p. 32. ISBN 978-0-8036-3665-1.
  49. ^ Jump up to: a b Rapkin AJ, Winer SA (February 2008). "The pharmacologic management of premenstrual dysphoric disorder". Expert Opinion on Pharmacotherapy. 9 (3): 429–45. doi:10.1517/14656566.9.3.429. PMID 18220493. S2CID 72888643.
  50. ^ Fry JP, Li KY, Devall AJ, Cockcroft S, Honour JW, Lovick TA (December 2014). "Fluoxetine elevates allopregnanolone in female rat brain but inhibits a steroid microsomal dehydrogenase rather than activating an aldo-keto reductase". British Journal of Pharmacology. 171 (24): 5870–80. doi:10.1111/bph.12891. PMC 4290723. PMID 25161074.
  51. ^ Devall AJ, Santos JM, Fry JP, Honour JW, Brandão ML, Lovick TA (January 2015). "Elevation of brain allopregnanolone rather than 5-HT release by short term, low dose fluoxetine treatment prevents the estrous cycle-linked increase in stress sensitivity in female rats" (PDF). European Neuropsychopharmacology. 25 (1): 113–23. doi:10.1016/j.euroneuro.2014.11.017. PMID 25498416. S2CID 21493779.
  52. ^ Freeman EW, Rickels K, Yonkers KA, Kunz NR, McPherson M, Upton GV (November 2001). "Venlafaxine in the treatment of premenstrual dysphoric disorder". Obstetrics and Gynecology. 98 (5 Pt 1): 737–44. doi:10.1016/s0029-7844(01)01530-7. PMID 11704162. S2CID 42597741.
  53. ^ Lopez LM, Kaptein AA, Helmerhorst FM (February 2012). "Oral contraceptives containing drospirenone for premenstrual syndrome". The Cochrane Database of Systematic Reviews. 2 (2): CD006586. doi:10.1002/14651858.CD006586.pub4. PMID 22336820.
  54. ^ Yonkers KA, Simoni MK (January 2018). "Premenstrual disorders". American Journal of Obstetrics and Gynecology. 218 (1): 68–74. doi:10.1016/j.ajog.2017.05.045. PMID 28571724. S2CID 21125434.
  55. ^ Yonkers KA, Simoni MK (January 2018). "Premenstrual disorders". American Journal of Obstetrics and Gynecology. 218 (1): 68–74. doi:10.1016/j.ajog.2017.05.045. PMID 28571724. S2CID 21125434.
  56. ^ Schmidt PJ, Nieman LK, Danaceau MA, Adams LF, Rubinow DR (January 1998). "Differential behavioral effects of gonadal steroids in women with and in those without premenstrual syndrome". The New England Journal of Medicine. 338 (4): 209–16. doi:10.1056/NEJM199801223380401. PMID 9435325.
  57. ^ Schmidt PJ, Martinez PE, Nieman LK, Koziol DE, Thompson KD, Schenkel L, et al. (October 2017). "Premenstrual Dysphoric Disorder Symptoms Following Ovarian Suppression: Triggered by Change in Ovarian Steroid Levels But Not Continuous Stable Levels". The American Journal of Psychiatry. 174 (10): 980–989. doi:10.1176/appi.ajp.2017.16101113. PMC 5624833. PMID 28427285.
  58. ^ Jump up to: a b c Kleinstäuber M, Witthöft M, Hiller W (September 2012). "Cognitive-behavioral and pharmacological interventions for premenstrual syndrome or premenstrual dysphoric disorder: a meta-analysis". Journal of Clinical Psychology in Medical Settings. 19 (3): 308–19. doi:10.1007/s10880-012-9299-y. PMID 22426857. S2CID 28720541.
  59. ^ Johnson, Susan R. (October 2004). "Premenstrual syndrome, premenstrual dysphoric disorder, and beyond: a clinical primer for practitioners". Obstetrics and Gynecology. 104 (4): 845–859. doi:10.1097/01.AOG.0000140686.66212.1e. ISSN 0029-7844. PMID 15458909. Retrieved September 7, 2021.
  60. ^ Stolberg M (July 2000). "The monthly malady: a history of premenstrual suffering". Medical History. 44 (3): 301–22. doi:10.1017/S0025727300066722. PMC 1044286. PMID 10954967.
  61. ^ Prichard JC (1822). A Treatise on Diseases of the Nervous System. 1. London: Underwood. p. 195.
  62. ^ Hitzig JE (1827). "Mord in einem durch Eintreten des Monatsflusses herbeigeführten unfreien Zustande". Zeitschrift für Criminal-rechts-pflege in den Preussischen Staaten. 12: 239–331.
  63. ^ Brière de Boisment A (1842). De la Menstruation considerée dans ses Rapports Physiologiques et Pathologiques. Paris: Baillière. p. 37.
  64. ^ Israel SL (May 1938). "Premenstrual tension". Journal of the American Medical Association. 110 (21): 1721–3. doi:10.1001/jama.1938.02790210001001.
  65. ^ Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition Revised. American Psychiatric Association. 1987. doi:10.1176/appi.books.9780890420188.dsm-iii-r (inactive 31 May 2021).CS1 maint: DOI inactive as of May 2021 (link)
  66. ^ Jump up to: a b Spartos C (December 5, 2000). "Sarafem Nation". Village Voice. Archived from the original on 2018-06-17.
  67. ^ Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. American Psychiatric Association. 2000. doi:10.1176/appi.books.9780890420249.dsm-iv-tr (inactive 31 May 2021).CS1 maint: DOI inactive as of May 2021 (link)
  68. ^ Steiner M, Steinberg S, Stewart D, Carter D, Berger C, Reid R, et al. (June 1995). "Fluoxetine in the treatment of premenstrual dysphoria. Canadian Fluoxetine/Premenstrual Dysphoria Collaborative Study Group". The New England Journal of Medicine. 332 (23): 1529–34. doi:10.1056/NEJM199506083322301. PMID 7739706.
  69. ^ Caplan PJ (2004). "The Debate About PMDD and Sarafem". Women & Therapy. 27 (3–4): 55–67. doi:10.1300/J015v27n03_05. S2CID 141754567.
  70. ^ Chen I (18 December 2008). "A Clash of Science and Politics Over PMS". The New York Times. Archived from the original on 2011-01-23. Retrieved 27 April 2019.
  71. ^ Jump up to: a b c Hartlage SA, Breaux CA, Yonkers KA (January 2014). "Addressing concerns about the inclusion of premenstrual dysphoric disorder in DSM-5". The Journal of Clinical Psychiatry. 75 (1): 70–6. doi:10.4088/JCP.13cs08368. PMID 24345853.

External links[]

Classification
External resources
Retrieved from ""