Easing the burden of premenstrual dysphoric disorder

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Applied Evidence

Easing the burden of premenstrual dysphoric disorder

J Fam Pract. 2013 January;62(1):E1-E7

By

Folashade Omole, MD

Yolanda Hacker, MD

Eltanya Patterson, MD

Mercy Isang, MD, MPH

Denise Bell-Carter, MD

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References

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10. Halbreich U, Petty F, Yonkers K, et al. Low plasma gamma-aminobutyric acid levels during the late luteal phase of women with premenstrual dysphoric disorder. Am J Psychiatry. 1996;153:718-720.

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13. Girdler SS, Straneva PA, Light KC, et al. Allopregnanolone levels and reactivity to mental stress in premenstrual dysphoric disorder. Biol Psychiatry. 2001;49:788-797.

14. Klatzkin RR, Lindgren ME, Forneris CA, et al. Histories of major depression and premenstrual dysphoric disorder: Evidence for phenotypic differences. Biol Psychol. 2010;84:235-247.

15. Girdler SS, Klatzkin R. Neurosteroids in the context of stress: implications for depressive disorders. Pharmacol Ther. 2007;116:125-139.

16. Perkonigg A, Yonkers KA, Pfister H, et al. Risk factors for premenstrual dysphoric disorder in a community sample of young women: the role of traumatic events and posttraumatic stress disorder. J Clin Psychiatry. 2004;65:1314-1322.

17. Tschudin S, Bertea PC, Zemp E. Prevalence and predictors of premenstrual syndrome and premenstrual dysphoric disorder in a population-based sample. Arch Womens Ment Health. 2010;13:485-494.

18. Girdler SS, Leserman J, Bunevicius R, et al. Persistent alterations in biological profiles in women with abuse histories: influence of premenstrual dysphoric disorder. Health Psychol. 2007;26:201-213.

19. Girdler SS, Sherwood A, Hinderliter AL, et al. Biological correlates of abuse in women with premenstrual dysphoric disorder and healthy controls. Psychosom Med. 2003;65:849-856.

20. Miyaoka Y, Akimoto Y, Ueda K, et al. Fulfillment of the premenstrual dysphoric disorder criteria confirmed using a self-rating questionnaire among Japanese women with depressive disorders. Biopsychosoc Med. 2011;5:5.-

21. Rapkin A, Winer S. Premenstrual syndrome and premenstrual dysphoric disorder: quality of life and burden of illness. Expert Rev Pharmacoecon Outcomes Res. 2009;9:157-170.

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25. Halbreich U, O’Brien PM, Eriksson E, et al. Are there differential symptom profiles that improve in response to different pharmacological treatments of premenstrual syndrome/premenstrual dysphoric disorder? CNS Drugs. 2006;20:523-547.

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34. Eriksson E, Ekman A, Sinclair S, et al. Escitalopram administered in the luteal phase exerts a marked and dose-dependent effect in premenstrual dysphoric disorder. J Clin Psychopharmacol. 2008;28:195-202.

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PRACTICE RECOMMENDATIONS

• Consider low doses of selective serotonin reuptake inhibitors such as fluoxetine, sertraline, or paroxetine as first-line therapy for premenstrual dysphoric disorder. A

• Consider other treatment options, including diet and lifestyle changes and hormonal therapy. A

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence

B Inconsistent or limited-quality patient-oriented evidence

C Consensus, usual practice, opinion, disease-oriented evidence, case series

CASE Carol J, 25, comes to your office and tells you that for the past year, she has been suffering from severe discomfort during her menstrual periods. She says that shortly before her period begins, she experiences headaches, breast tenderness, pain in her joints, and a “bloated feeling.” She has trouble sleeping and feels irritable and “on edge.” She is often too depressed or tired to go to work or go out with her friends. Although the symptoms go away within a few days after her period starts, Ms. J is miserable while they last and worried about the toll they are taking on her job and her relationships. How would you address Ms. J’s complaints?

FAST TRACK

Symptoms must be severe enough to cause psychological impairment that interferes with relationships and the patient’s work life.

Premenstrual dysphoric disorder (PMDD), the most severe type of premenstrual syndrome (PMS), is a chronic debilitating condition characterized by a constellation of somatic and behavioral symptoms that cause significant functional impairment and greatly diminish quality of life.¹ Although PMDD has a prevalence of only 3% to 8%, compared with a prevalence as high as 75% for PMS, it carries a substantial health and economic burden.^1,2 Diagnosing and managing it can present a clinical challenge.¹

The diagnostic criteria for PMDD outlined in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), which classifies the condition as a depressive disorder not otherwise specified, help to differentiate PMDD from PMS.³ The diagnosis requires regular occurrence of at least 5 of 11 mood and physical symptoms during the last week of the luteal phase of the menstrual cycle and remission of symptoms within 4 days of the onset of menses (TABLE 1).³ One of the 5 symptoms must be a mood symptom: depression, anxiety, mood lability, or irritability.⁴

TABLE 1
Research criteria for premenstrual dysphoric disorder

In most menstrual cycles during the past year, 5 (or more) of the following symptoms were present for most of the time during the last week of the luteal phase, began to remit within a few days after the onset of the follicular phase, and were absent in the week post-menses, with at least one of the symptoms being either 1, 2, 3, or 4:
The disturbance markedly interferes with work or school or with usual social activities and relationships with others (eg, avoidance of social activities, decreased productivity and efficiency at work or school).
The disturbance is not merely an exacerbation of the symptoms of another disorder, such as major depressive disorder, panic disorder, dysthymic disorder, or a personality disorder (although it may be superimposed on any of these disorders).
Criteria A, B, and C must be confirmed by prospective daily ratings during at least 2 consecutive symptomatic cycles. (The diagnosis may be made provisionally prior to this confirmation).

Source: American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders DSM-IV-TR. 4th ed. text revision. 2000.³

What causes PMDD?

Although the etiology of PMDD is unknown, neuroendocrine and psychological factors have been implicated. Because PMDD is cyclical, the cyclic fluctuations of normal ovarian function, not hormonal imbalance, are thought to trigger PMDD-related biochemical events within the central nervous system and other target tissues.^5,6

Serotonergic dysregulation. Women with PMDD have increased sensitivity to central nervous system neurotransmitters, including serotonin, which is down-regulated by the cyclical change of the ovarian hormones estradiol and progesterone.^7,8 Several clinical studies have shown strong correlation between serotonergic dysfunction and PMDD based on the proven efficacy of selective serotonin reuptake inhibitors (SSRIs) in controlling symptoms. A randomized, double-blind, placebo-controlled trial conducted at 47 outpatient centers in the United States and Canada is one of many studies that implicate serotonergic down-regulation by demonstrating that PMDD responds to the SSRI paroxetine.⁹

Gamma aminobutyric acid (GABA), the inhibitory neurotransmitter, also plays a role in PMDD. Low levels of GABA diminish its inhibitory effect, resulting in mood disorders. A small clinical trial comparing plasma GABA levels in healthy women and women with PMDD with and without major depression demonstrated this effect.¹⁰ The study found that plasma GABA levels decreased from the midfollicular to the late luteal phase in women with PMDD, whereas they increased in healthy women; in women with PMDD and depression, GABA levels were low during both phases.