Author: Dr. Miles E. Drake Jr., MD













go

Premenstrual Dysphoric Disorder DSM-5 625.4 (N94.3)

DSM-5 Category: Depressive Disorders

Introduction

Premenstrual dysphoric disorder (PMDD) is an old condition but a new diagnosis in the Diagnostic and Statistical Manual of Mental Disorders. Diagnostic criteria for the disorder were suggested in the appendices of DSM-4 (“Criterion Sets and Axes provided for further study”) (American Psychiatric Association, 2000), and the criteria summarized below are included for the first time in DSM-5 (American Psychiatric Association, 2013). The new diagnosis has not been without controversy, as feminist writers have argued that this amounts to medicalization of some women’s normal bodily phenomena (Daw, 2002). The association of menstrual periods with mood disturbance, emotional changes and neurovegetative symptoms has been recognized since the time of Hippocrates, when menstrual bleeding was thought to purge melancholic and choleric humors (Stolberg, 2000). One of the first gynecologists, the woman physician Trotula of Salerno, observed in the 11th Century that “there are young women who are relieved when the menses are called forth” (Mason-Hohl, 1940). In 1931, Robert Frank described “premenstrual tension” and ascribed the mental and neurological symptoms to fluctuations in recently-characterized sex hormones (Frank, 1931), while Karen Horney observed “premenstrual mood swings” and attributed them to rejected fantasies of motherhood (Horney, 1931). The term “premenstrual syndrome” came to be applied to these symptoms, with assorted explanations proposed ranging from emotional conflict to biochemical disturbance (Greene & Dalton, 1953). An initial diagnostic rubric of “late luteal phase dysphoric disorder” was proposed in DSM-3-R, but was revised provisionally to the present title in DSM-4 as the occurrence of symptoms in the follicular phase of the menstrual cycle was recognized (Epperson, Steiner & Yonkers, 2012). The organic cause of PMDD is now generally accepted but not definitely established, and an association between hormonal fluctuations of the menstrual cycle and neurotransmitter disturbances involved in depression is suspected. Treatment focuses on regularization of menses, amelioration of symptoms and repair of disrupted social relationships.

Symptoms of Premenstrual Dysphoric Disorder

As many as 80 per cent of the women in the United States experience premenstrual emotional or physical symptoms (Boyle, Berkowitz & Kelsey, 1987). Between 3 and 8 per cent of women generally meet the criteria for PMDD, with a wide range according to geography and perhaps culture, from 3 per cent of women in Switzerland and 6 per cent in India to 36 per cent of female medical students in Nigeria) (Tschudin, Bertea, & Zemp, 2010). Symptoms occur principally during the late luteal phase of the menstrual cycle but in the first 2 or 3 days of the follicular phase in about one-third (Yonders et al., 2005). Symptoms last on average 6 days, and are most intense just before and after the start of menstrual flow. Feelings of sadness and despair, even including suicidality, anxiety and panic attacks, crying, irritability and anger, lack of interest in or attention to activities and relationships, fatigue and tiredness, difficulty focusing or thinking, food cravings and binge eating, and feeling out of control are common. Assorted somatic symptoms include breast tenderness, bloating, headache and pain. These symptoms resolve after the onset of menstruation Biggs & Demuth, 2011).

Diagnostic Criteria

The new DSM-5 criteria for PMDD require a combination of symptoms that began in the final week before menses, started to improve in the days after onset of menses and were absent in the postmenstrual weeks during the past year. At least one of 5 or more required symptoms must be marked lability of affect, irritability or anger or increased interpersonal conflict, depressed mood or hopelessness or self-deprecation, or marked anxiety or tension. Decreased interest in usual activities, subjective difficulty in concentrating, lethargy or fatigue or lack of energy, marked appetite change with overeating or food cravings, insomnia or hypersomnia, feelings of being out of control and somatic symptoms such as bloating, weight gain, breast tenderness, and joint or muscle pain may also be present (American Psychiatrica Association, 2013).

Causes

The symptoms of PMDD have been ascribed to fluctuation of ovarian hormones, serotonin disturbance analogous to depression, somatic manifestations of unconscious feminine conflicts, maladaptive coping strategies for an aversive physical event, and culturally-determined expression of women’s discontent with their traditional roles in society (Klock, 1999). An imbalance between estrogen and progesterone with a relative progesterone deficiency led to the recommendation of progesterone suppositories for treatment of symptoms (Wyatt, Dimmock, and O’Brien, 2000). The current consensus is that normal hormonal fluctuations trigger pain, anxiety and depressive symptoms through interaction with serotonin systems (Steiner & Pearlstein, 2000). The cardinal symptoms of PMDD are generally alleviated by serotonin-augmenting drugs, while worsening of mood symptoms has been correlated with diminuition of serotonin receptors on positron tomography (Eriksson et al., 2006). Gamma-amino-butyric acid (GABA), adrenergic and opioid pathways have also been implicated in PMDD (Ling, 2000). PMDD has been linked to polymorphism of the estrogen alpha receptor gene ESR1, and women with this variant who have mood symptoms also share a polymorphism involving catechol-o-methyltransferase, which regulates mood chemistry in the prefrontal cortex (Huo et al., 2007). A prominent psychosocial component is suggested by the associations found between PMDD and history of sexual abuse, past or present domestic violence and perceived sexual discrimination (Pilver et al., 2011), as well as between PMDD and past unipolar depression, anxiety and other psychiatric disorders (Grady-Wellicky, 2003).

Treatment of Premenstrual Dysphoric Disorder

Pharmacological treatment initially relied on hormonal supplementation to redress apparent estrogen-progesterone imbalance: progesterone suppositories, medroxyprogesterone or dihydroprogesterone, drospirenone and ethinyl estradiol (Yaz®), the intrauterine levonorgesterol device, the synthetic steroid danazol, and gonadotropin-releasing hormone analogues are often attended by adverse effects, carry long-term risks of estrogen excess (endometrial carcinoma) or deficiency (osteoporosis) and have not found consistent support in controlled trials (Peralstein & Steiner, 2000). Diuretics have been used with some benefit in the belief that many premenstrual symptoms result from fluid retention (Werch & Krane, 1976), and naproxen and other nonsteroidal anti-inflammatory drugs have produced improvement compared to placebo (Werch & Krane, 1976). Buspirone has been given safely and effectively either throughout the menstrual cycle or just in the late luteal phase (Rickels, 1989). Essentially all SSRI antidepressants are demonstrably effective in controlled trials, but non-serotoninergic antidepressants, lithium and probably benzodiazepines are not (Brown et al., 2009). Worsening depression, suicidal ideation and serotonin syndrome need to be watched for with all serotoninergic agents (Mandour, 2012).

Alternative, complementary or integrative medicine treatments may be helpful for PMDD. Pyridoxine (vitamin B 6 ), calcium carbonate or magnesium during the luteal phase, evening primrose oil with the fatty acid gamma-linolenic acid, St. John’s wort (except when taking SSRIs), ginseng (Siberian and American more than Chinese), wild yam, pulsatilla, cayenne and dong quai (“female” ginseng) have been suggested to be of benefit. Among the homeopathic remedies, Folliculinum, Bovista, Calcarea carbonica, Chamomilla, Nux vomica, Pulsatilla and Sepia have been recommended (Stengler, 2010).

Nonpharmacologic treatments supported by some evidence include therapeutic exercise, which raises endorphin levels, relaxation techniques to decrease physiological tension, bright light exposure as for seasonal affective disorder and sleep deprivation, also effective for depression (Krasnik et al., 2005). Cognitive behavioral therapy, which seeks to examine and replace extreme or negative thought patterns in an adverse situation that have become habitual and unconscious, has been found effective for premenstrual anxiety, depression and disruption of activities (Busse et al., 2009).

References

American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental Disorders, ed. 4. Washington, DC: APA Press.

American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders, ed. 5.Washington, DC: APA Press.

Biggs, W.S. (2011). Demuth RH. Premenstrual syndrome and premenstrual dysphoric disorder. Am Fam Physic. 84(8), 918-924.

Boyle, C.A., Berkowitz, G.S., & Kelsey, J.L. (1987). Epidemiology of premenstrual symptoms. Am J Public Health. 77(3), 349-350.

Brown, J., O’Brien, P.M., Marjoribanks, J., & Wyatt, K. (2009). Selective serotonin reuptake inhibitors for premenstrual syndrome. Cochrane Database Syst Rev. CD001396.

Busse, J.W., Montori, V.M., Krasnik K et al. (2009). Psychological intervention for premenstrual syndrome: a meta-analysis of randomized controlled trials. Psychother Psychosom. 78(1), 6-15.

Daw, J. (2002). Is PMDD real? Amer Psychol Assoc Monitor. 33(9), 58.

Epperson, C.N., Steiner, E., & Yonkers, K.A. (2012). Premenstrual Dysphoric Disorder: Evidence for a new category of DSM-5. Amer J Psychiat. 169(5), 465-475.

Eriksson, O., Wall, A., Martinsdottir I, et al. (2006). Mood changes correlate to changes in brain serotonin precursor trapping in women with premenstrual dysphoria. Psychiatry Res. 146(2), 107-116.

Frank, R.T. (1931). The hormonal causes of premenstrual tension. Arch Neurol Psychiat, 26, 1053-1057.

Grady-Wellicky, T.A. (2003). Clinical practice. Premenstrual dysphoric disorder. New Engl J Med. 348(5), 433-438.

Greene, R., Dalton, K. (1953). The premenstrual syndrome. Br Med J. i: 1007-1014.

Horney, K. (1931). Die prämenstruellen Verstimmungen. Zeitschrift für psychoanalytische Pädagogik. 5(5/6), 1-7.

Huo, L., Straub, R.E., Roca, C. et al. (2007). Risk for premenstrual dysphoric disorder is associated with generic variation in ESR1, the estrogen receptor alpha gene. Biol Psychiat. 62(8), 925-933.

Klock, S.C. (1999). Premenstrual dysphoric disorder. In Ryan, K.J., Berkowitz, R.S., Barbieri, R.L., Dunaif, A.E. (eds). Kistner’s Gynecology and Women’s Health, ed. 7. Philadelphia, Mosby, 520-524.

Krasnik, C., Montori, V.M., Guyatt, G.H, et al. (2005). The effect of bright light therapy on depression associated with premenstrual dysphoric disorder. Am J Obstet Gynecol. 193(3 pt 1), 658-661.

Ling, F.W. (2000). Recognizing and treating premenstrual dysphoric disorder in the obstetric, gynecologic and primary care practices. J Clin Psychiat. 61(suppl 12), 9-16.

Mandour, R.A. (2012). Antidepressant medications and the relative risk of suicide attempt. Toxicology Int. 19(1), 42-46.

Mason-Hohl, E. (1940). (tr). The Diseases of Women (Passionibus Mulierum Curandorum). Los Angeles: Ward Ritchie Press.

Pearlstein, T., Steiner, M. (2000) Non-antidepressant treatment of premenstrual syndrome. J Clin Psychiat. 61(suppl 12), 21-27.

Pilver, C., Desai, S., Kasi, R., & Levy, B. (2011). Lifetime discrimination associated with greater likelihood of Premenstrual Dysphoric Disorder. J Womens Health. 20(6), 923-931.

Rickels, K., Freeman, E., Sondheimer, & S. Buspirone. (1989). In Treatment of Premenstrual Syndrome. Lancet. 1(8641), 777.

Steiner, M., & Pearlstein, T. (2000). Premenstrual dysphoria and the serotonin system: pathophysiology and treatment. J Clin Psychiat. 61(suppl 12), 17-21.

Stengler, M. (2010). The Natural Physician’s Healing Therapies, ed. 2. New York: Prentice-Hall.

Stolberg, M. (2000). The monthly malady: A history of premenstrual suffering. Med Hist, 44, 301-322.

Tschudin, S., Bertea, P.C., Zemp, E. (2010). Prevalence and predictors of premenstrual syndrome and premenstrual dysphoric disorder in a population-based sample. Arch Womens Mental Health. 13(6), 485-494.

Werch, A., Kane, R.E. (1976). Treatment of premenstrual tension with metolazone: a double-blind evaluation of a new diuretic. Curr Ther Res Clin Exp. 19(6), 565-572.

Wyatt, K., Dimmock, P., & O’Brien, PMS. Premenstrual syndrome. Clin Evid. 4, 1121-1123, 2000.

Yonkers, K.A., Pearlstein, T., Fayyad, R., Gillespie, J.A. (2005). Luteal phase treatment of premenstrual dysphoric disorder improves symptoms that continue into the postmenstrual phase. J Affect Dis. 85(3), 317-321.

Help Us Improve This Article

Did you find an inaccuracy? We work hard to provide accurate and scientifically reliable information. If you have found an error of any kind, please let us know by sending an email to contact@theravive.com, please reference the article title and the issue you found.

Share Therapedia With Others