Premenstrual syndrome

"PMS" redirects here. For other uses, see PMS (disambiguation).

Premenstrual syndrome
Classification and external resources
ICD-10	N94.3
ICD-9	625.4
DiseasesDB	10513
eMedicine	article/953696
MeSH	D011293

Premenstrual syndrome (PMS) (also called PMT or premenstrual tension) is a collection of physical and emotional symptoms related to a woman's menstrual cycle. While most women of child-bearing age (up to 85%) report having experienced physical symptoms related to normal ovulatory function, such as bloating or breast tenderness, medical definitions of PMS are limited to a consistent pattern of emotional and physical symptoms occurring only during the luteal phase of the menstrual cycle that are of "sufficient severity to interfere with some aspects of life".^[1] In particular, emotional symptoms must be present consistently to diagnose PMS. The specific emotional and physical symptoms attributable to PMS vary from woman to woman, but each individual woman's pattern of symptoms is predictable, occurs consistently during the ten days prior to menses, and vanishes either shortly before or shortly after the start of menstrual flow.

Only a small percentage of women (2 to 5%) have significant premenstrual symptoms that are separate from the normal discomfort associated with menstruation in healthy women.^[1][2]

Culturally, the abbreviation PMS is widely understood in English-speaking countries to refer to difficulties associated with menses, and the abbreviation is used frequently even in casual and colloquial settings, without regard to medical rigor. In these contexts, the syndrome is rarely referred to without abbreviation, and the connotations of the reference are frequently more broad than the clinical definition.

Premenstrual dysphoric disorder (PMDD) is a more severe condition, positioned as a psychiatric disorder similar to unipolar depression.

Symptoms

More than 200 different symptoms have been associated with PMS, but the three most prominent symptoms are irritability, tension, and dysphoria (unhappiness).^[1] Common emotional and non-specific symptoms include stress, anxiety, difficulty in falling asleep (insomnia), headache, fatigue, mood swings, increased emotional sensitivity, and changes in libido.^[3] Formal definitions absolutely require the presence of emotional symptoms as the chief complaint; the presence of exclusively physical symptoms associated with the menstrual cycle, such as bloating, abdominal cramps, constipation, swelling or tenderness in the breasts, cyclic acne, and joint or muscle pain.

The exact symptoms and their intensity vary from woman to woman and even from cycle to cycle. Most women with premenstrual syndrome experience only a few of the possible symptoms, in a relatively predictable pattern.^[4] Under typical definitions, symptoms must be present at some point during the ten days immediately before the onset of menses, and must not be present for at least one week between the onset of menses and ovulation.^[5] Although the intensity of symptoms may vary somewhat, most definitions require that the woman's unique constellation of symptoms be present in multiple, consecutive cycles.^[5]

Risk factors

• High caffeine intake^[5]
• Stress may precipitate condition
• Increasing age
• History of depression
• Family history
• Dietary factors^[6] (Low levels of certain vitamins and minerals, particularly magnesium, manganese, and vitamin E) and also Vitamin D

Family history is often a good predictor of the probability of premenstrual syndrome; studies have found that the concordance rate is two times higher among identical twins compared with fraternal twins.^[1] This means that if one twin has PMS, then the other twin is more likely than average to have PMS, and it suggests that the cause is partly genetic. Although the presence of premenstrual syndrome is high among women with affective disorders such as depression and bipolar disorder,^{[citation needed]} a causal relationship has not been established.

B vitamins, in particular vitamin B6, can also assist with PMS.^[7]

Diagnosis

There is no laboratory test or unique physical findings to verify the diagnosis of PMS. The three key features are:^[1]

• The woman's chief complaint is one or more of the emotional symptoms associated with PMS (most typically irritability, tension, and/or unhappiness).
• Symptoms appear predictably during the luteal (premenstrual) phase, reduce or disappear predictably shortly before or during menstruation, and remain absent during the follicular (pre-ovulatory) phase of the menstrual cycle.
• The symptoms must be severe enough to disrupt or interfere with the woman's everyday life.

To establish a pattern, a woman's physician may ask her to keep a prospective record of her symptoms on a calendar for at least two menstrual cycles.^[4] This will help to establish if the symptoms are, indeed, limited to the premenstrual time and are predictably recurring. A number of standardized instruments have been developed to describe PMS, including the Calendar of Premenstrual syndrome Experiences (COPE), the Prospective Record of the Impact and Severity of Menstruation (PRISM), and the Visual Analogue Scales (VAS).^[1] . In addition, other conditions that may better explain symptoms must be excluded.^[1] A number of medical conditions are subject to exacerbation at menstruation, a process called menstrual magnification. These conditions may lead the patient to believe that she has PMS, when the underlying disorder may be some other problem, such as anemia, hypothyroidism, eating disorders and substance abuse.^[1] A key feature is that these conditions may also be present outside of the luteal phase. Conditions that can be magnified perimenstrually include depression or other affective disorders, migraine, seizure disorders, fatigue, irritable bowel syndrome, asthma, and allergies.^[1] Also, problems with other aspects of the female reproductive system must be excluded, including dysmenorrhea (pain during menses, rather than before it), endometriosis, perimenopause, and adverse effects produced by oral contraceptive pills.^[1]

Although there is no universal agreement about what qualifies as PMS, two definitions are commonly used in research programs:

• The National Institute of Mental Health research compares the intensity of symptoms from cycle days 5 to 10 to the six-day interval before the onset of menses.^[1] To qualify as PMS, symptom intensity must increase at least 30% in the six days before menstruation. Additionally, this pattern must be documented for at least two consecutive cycles.
• The definition formulated at the University of California at San Diego requires both affective (emotional) and somatic (physical) symptoms during the five days before menses in each of three consecutive cycles, and must not be present during the pre-ovulatory part of the cycle (days 4 through 13).^[1] For this definition, affective symptoms include symptoms like depression, angry outbursts, irritability, anxiety, confusion, and social withdrawal. Somatic symptoms include symptoms like breast tenderness, abdominal bloating, headache, and swelling of hands and feet.

Cause

The exact causes of PMS are not fully understood. While PMS is linked to the luteal phase, measurements of sex hormone levels are within normal levels. In twin studies, the concordance of PMS is twice as high in monozygotic twins as in dizygotic twins, suggesting the possibility of some genetic component.^[1][8] Current thinking suspects that central-nervous-system neurotransmitter interactions with sex hormones are affected.^[1] It is thought to be linked to activity of serotonin (a neurotransmitter) in the brain.^[3][9][10]

Preliminary studies suggest that up to 40% of women with symptoms of PMS have a significant decline in their circulating serum levels of beta-endorphin. Beta endorphin is a naturally occurring opioid neurotransmitter which has an affinity for the same receptor that is accessed by heroin and other opiates. Some researchers have noted similarities in symptom presentation between PMS symptoms and opiate withdrawal symptoms.^[11]

In one study of 71 women with PMS ,elevated levels of serum pseudocholinesterase were found. This enzyme is considered a possible marker for trait-anxiety ^[12].

A variety of evolutionary rationales for the syndrome have been offered, including that it is an epiphenomenon due to the selective advantage accruing to other phases of the hormonal cycle,^[13] that it leads to "intensification of male ardour during the next onset of fertility",^[14] and that it prompts females to reject infertile males (who cause PMS due to not impregnating the female). "… an infertile male/potentially fertile female partnership would tend to break down, thus allowing a new pair-bond to be formed. The greater the degree of premenstrual hostility of the female, the sooner a fertile mating could ensue."^[15] Any theory would have to account for the persistence of PMS over substantial evolutionary time, as it appears to afflict baboons as well.^[16]

Management

Many treatments have been suggested for PMS, including diet or lifestyle changes, and other supportive means. Medical interventions are primarily concerned with hormonal intervention and use of selective serotonin reuptake inhibitors (SSRIs).

• Supportive therapy includes evaluation, reassurance, and informational counseling, and is an important part of therapy in an attempt to help the patient regain control over her life. In addition, aerobic exercise has been found in some studies to be helpful.^[1] Some PMS symptoms may be relieved by leading a healthy lifestyle: Reduction of caffeine, sugar, and sodium intake and increase of fiber, and adequate rest and sleep.^[17]
• Dietary intervention studies indicate that calcium supplementation (1200 mg/d) may be useful. Also vitamin E (400 IU/d) has shown some effectiveness.^[1] A number of other treatments have been suggested, although research on these treatments is inconclusive so far: Vitamin B6,^[7] magnesium, manganese and tryptophan.^[17]
• SSRIs can be used to treat severe PMS.^[18] Women with PMS may be able to take medication only on the days when symptoms are expected to occur.^[19] Although intermittent therapy might be more acceptable to some women, this might be less effective than continuous regimens.^[18]
• Hormonal intervention may take many forms:
  • Hormonal contraception is commonly used; common forms include the combined oral contraceptive pill and the contraceptive patch. This class of medication may cause PMS-related symptoms in some women, and may reduce physical symptoms in other women.^[1] They do not relieve emotional symptoms.^[1]
  • Progesterone support has been used for many years but evidence of its efficacy is inadequate.
  • Gonadotropin-releasing hormone agonists can be useful in severe forms of PMS but have their own set of significant potential side effects.
• Diuretics have been used to handle water retention. Spironolactone has been shown in some studies to be useful.^[1]
• Non-steroidal anti-inflammatory drugs (NSAIDs; e.g., ibuprofen) have been used to treat pain.
• Evening primrose oil, which contains gamma-Linolenic acid (GLA), has been advocated but lacks scientific support.
• Clonidine has been reported to successfully treat a significant number of women whose PMS symptoms coincide with a steep decline in serum beta-endorphin on a monthly basis.^[20]
• Chasteberry has been used by women for thousands of years to ease symptoms related to menstrual problems.^[21] It is believed some of the compounds found within Chasteberry work on the pituitary gland to balance hormone levels.
• DL phenylalanine can reduce or prevent symptoms of PMS in some women. It is only effective when the PMS is associated with an abrupt decline in circulating serum beta-endorphin levels.^[22]
• Recent evidence suggests that daily treatment with St. Johns wort (Hypericum perforatum) may improve the most common physical and emotional symptoms associated with PMS.^[23]

Prognosis

PMS is generally a stable diagnosis, with susceptible women experiencing the same symptoms at the same intensity near the end of each cycle for years.^[24]

Treatment for specific symptoms is usually effective at controlling the symptoms. Even without treatment, symptoms tend to decrease in perimenopausal women, and disappear at menopause.^[25]

Women who have PMS have an increased risk for clinical depression.

Epidemiology

The number of women who experience PMS depends entirely on the stringency of the definition of PMS.^[26] While 80% of menstruating women have experienced at least one symptom that could be attributed to PMS, estimates of prevalence range from as low as 3%^[27] to as high as 30%.^[26]

Mood symptoms such as emotional lability are both more consistent and more disabling than somatic symptoms such as bloating.^[28] A woman who experiences mood symptoms is likely to experience these symptoms consistently and predictably, whereas physical symptoms may come and go. Most women find that physical symptoms related to PMS are less disruptive than emotional symptoms

History

PMS was originally seen as an imagined disease.^{[citation needed]} When women first started reporting these symptoms, they were often told it was "all in their head". Interest in PMS began to increase after it was used as a criminal defense in Britain during the early 1980s.^[29]

The study of PMS was brought about by many characters in society. Physicians and researchers study and treat recognized medical conditions. In order to have an impact, the existence, and importance of a disease needs to be socially accepted. Women have contributed to the rise of interest in PMS and society's acceptance of it as an illness. It is argued that women are partially responsible for the medicalization of PMS.^[30] By legitimizing this disorder, women have contributed to the social construction of PMS as an illness. It has also been suggested that the public debate over PMS and PMDD was impacted by organizations who had a stake in the outcome including feminists, the APA, physicians and scientists.^[31]

The study of PMS symptoms is not a new development. Debates about the definition and validity of this syndrome have a long history. As stated above, growing public attention was given to PMS starting in the 1980s.^[32] Up until this point, there was little research done surrounding PMS and it was not seen as a social problem. Through clinical trials and the work of feminists, viewing PMS in a social context had begun to take place.

Alternative views

Some medical professionals suggest that PMS might be a socially constructed disorder.^[33]

Supporters of PMS' medical validity claim support from work on the similar problem, premenstrual dysphoric disorder ("PMDD"). In women with PMDD, studies have shown a correlation between self-reported emotional distress and levels of a serotonin precursor as measured by positron emission tomography (PET).^[34] PMDD also has a consistent treatment record with SSRIs, when compared with placebos.^[35] However, the diagnosis has been controversial (including in regard to the pharmaceutical company influence, see below) and questioned on scientific grounds as medicalization.^[36]

However, most supporters of PMS as a social construct do not dispute PMDD's medical status. Rather, they believe PMDD and PMS to be unrelated issues: one a product of brain chemistry, the other a product of a hypochondriatic culture. Many Western studies on PMS rely solely on self-reporting. According to Carol Tavris, Western women are socially conditioned to expect PMS or to at least know of its purported existence, and therefore they report their symptoms accordingly.^[37]

Another view holds that PMS is too frequently or wrongly diagnosed in many cases. A variety of problems, such as chronic depression, infections, and outbursts of frustration can be mis-diagnosed as PMS if they happen to coincide with the premenstrual period. Often, says this theory, PMS is used as an explanation for outbursts of rage or sadness, even when it is not the primary cause.^[38][39]

The use of multiple SSRI's to treat PMS has caused some controversy. The makers of Prozac began marketing the generic form, fluoxetine, under the name Sarafem to treat PMS. This coincided with their loss of patent on Prozac, which has led to suggestions that their motivations are not completely benign.^[40] Recently an oral contraceptive named Drospirenone (Yaz) has become the only birth control pill approved to treat PMDD. The marketing of Yaz centers on this aspect of the drug.^[41]

References

1. ^ ^{a b c d e f g h i j k l m n o p q r s} Dickerson, Lori M., Pamela J. Mazyck and Melissa H. Hunter (April 2003). "Premenstrual Syndrome". Am Fam Physician (American Academy of Family Physicians) 67 (8): 1743–52. PMID 12725453. http://www.aafp.org/afp/20030415/1743.html. 
2. ^ Matlin, Margaret W., The Psychology of Women: Sixth Edition 2008.
3. ^ ^{a b} "Merck Manual Professional - Menstrual Abnormalities". 2005-11. http://www.merck.com/mmpe/sec18/ch244/ch244g.html. Retrieved 2007-02-02. 
4. ^ ^{a b} "MayoClinic.com: Premenstrual syndrome syndrome (PMS): Signs and symptoms". MayoClinic.com. 2006-10-27. http://www.mayoclinic.com/health/premenstrual-syndrome/DS00134/DSECTION=2. Retrieved 2007-02-02. 
5. ^ ^{a b c} Johnson S, PHD. "Premenstrual Syndrome (Premenstrual Tension)". Menstrual Abnormalities and Abnormal Uterine Bleeding. Armenian Health Network, Health.am. http://www.health.am/gyneco/more/premenstrual-syndroma-premenstrual-tension/. Retrieved 2008-01-10. 
6. ^ Amy Scholten, MPH. "What are the risk factors for premenstrual syndrome?". Premenstrual Syndrome (PMS). Harvard Medical school. http://healthgate.partners.org/browsing/browseContent.asp?fileName=19962.xml&title=Conditions%20InDepth:%20Premenstrual%20Syndrome%20(PMS). Retrieved 2008-01-10. 
7. ^ ^{a b} "Controversial vitamin may beat PMS", BBC News. Friday, May 21, 1999.
8. ^ Kendler KS, Karkowski LM, Corey LA, Neale MC (September 1998). "Longitudinal population-based twin study of retrospectively reported premenstrual symptoms and lifetime major depression". Am J Psychiatry 155 (9): 1234–40. PMID 9734548. http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=9734548. 
9. ^ "NHS Direct: Premenstrual syndrome - Causes". NHS Direct. 2005-11-09. Archived from the original on 2007-02-23. http://web.archive.org/web/20070223153342/http://www.nhsdirect.nhs.uk/articles/article.aspx?articleId=295&sectionId=1690. Retrieved 2007-02-02. 
10. ^ "Causes of PMS". Always. 2007. http://www.always.com/period/pmscauses.jsp. Retrieved 2007-02-11. 
11. ^ Giannini AJ, Martin DM, Turner CE (1990). "Beta-endorphin decline in late luteal phase dysphoric disorder". Int J Psychiatry Med 20 (3): 279–84. doi:10.2190/JRQJ-XTX9-CQPF-HD70. PMID 2265889. 
12. ^ Giannini AJ, Price WA, Loiselle RH, Giannini MC (April 1985). "Pseudocholinesterase and trait anxiety in premenstrual tension syndrome". J Clin Psychiatry 46 (4): 139–40. PMID 4038979. 
13. ^ Reiber C (2008). "An evolutionary model of premenstrual syndrome". Med Hypotheses 70 (5): 158–65. doi:10.1016/j.mehy.2007.08.031. PMID 18053655. 
14. ^ Rosseinsky DR, Hall PG (1974). "Letter: An evolutionary theory of premenstrual tension.". Lancet 7887 (2): 1024. doi:10.1016/S0140-6736(74)92132-1. PMID 4138262. 
15. ^ Morriss GM, Keverne, EB (1974). "Letter: Premenstrual tension.". Lancet 2 (7892): 1317–8. PMID 4139547. 
16. ^ Erik Eckholm (1985-06-04). "Premenstrual Problems Seem To Beset Baboons". The New York Times. http://query.nytimes.com/gst/fullpage.html?sec=health&res=9F07E2DA1439F937A35755C0A963948260. Retrieved 2009-01-05. 
17. ^ ^{a b} "familydoctor.org: PMS: What you can do to ease your symptoms?". familydoctor.org. 2005. http://familydoctor.org/141.xml. Retrieved 2007-02-02. 
18. ^ ^{a b} Shah NR, Jones JB, Aperi J, Shemtov R, Karne A, Borenstein J (May 2008). "Selective serotonin reuptake inhibitors for premenstrual syndrome and premenstrual dysphoric disorder: a meta-analysis". Obstet Gynecol 111 (5): 1175–82. doi:10.1097/AOG.0b013e31816fd73b. PMC 2670364. PMID 18448752. http://journals.lww.com/greenjournal/Fulltext/2008/05000/Selective_Serotonin_Reuptake_Inhibitors_for.24.aspx. 
19. ^ http://www.sciencedaily.com/releases/2006/10/061013202144.htm
20. ^ Giannini AJ, Sullivan B, Sarachene J, Loiselle RH (February 1988). "Clonidine in the treatment of premenstrual syndrome: a subgroup study". J Clin Psychiatry 49 (2): 62–3. PMID 2962993. 
21. ^ "NCCAM Herbs at a Glance: Chasteberry". National Institutes of Health. 2005. http://nccam.nih.gov/health/chasteberry. Retrieved 2009-08-28. 
22. ^ AJ Giannini, DE Sternberg, DM Martin, K. Tipton. Prevention of late luteal phase dysphoric disorder symptoms by DL-phenylalanine in women with abrupt beta-endorphin decline. Annals of Clinical Psychiatry,1:259-261,1989.
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26. ^ ^{a b} Dean BB, Borenstein JE, Knight K, Yonkers K (2006). "Evaluating the criteria used for identification of PMS". J Womens Health (Larchmt) 15 (5): 546–55. doi:10.1089/jwh.2006.15.546. PMID 16796482. 
27. ^ "NIH Press Release-Hormones Trigger PMS Symptoms - 01/21/1998". http://www.nih.gov/news/pr/jan98/nimh-21.htm. Retrieved 2008-02-28. 
28. ^ Bloch M, Schmidt PJ, Rubinow DR (1997). "Premenstrual syndrome: evidence for symptom stability across cycles". Am J Psychiatry 154 (12): 1741–6. PMID 9396955. http://ajp.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=9396955. 
29. ^ Apodaca, Lillian; Fink, Lori (1984). "Criminal Law: Premenstrual Syndrome in the Courts?". http://heinonline.org/HOL/LandingPage?collection=journals&handle=hein.journals/wasbur24&div=13&id=&page=. Retrieved 2010-04-04. 
30. ^ Markens, Susan. “The Problematic of ‘Experience’ A Political and Cultural Critique of PMS.” Gender & Society. 10.1 (February 1996): 42-58.
31. ^ Figert, Anne E. “The Three Faces of PMS: The Professional, Gendered, and Scientific Structuring of a Psychiatric Disorder.” Social Problems. 42.1 (February 1995): 56-73.
32. ^ Nadine Brozan (1982-07-12). "Premenstrual Syndrome: A Complex Issue". The New York Times. http://www.nytimes.com/1982/07/12/style/premenstrual-syndrome-a-complex-issue.html. Retrieved 2010-04-04. 
33. ^ Rodin M (1992). "The social construction of premenstrual syndrome". Soc Sci Med 35 (1): 49–56. doi:10.1016/0277-9536(92)90118-A. PMID 1496412. 
34. ^ Eriksson O, Wall A, Marteinsdottir I, et al. (2006). "Mood changes correlate to changes in brain serotonin precursor trapping in women with premenstrual dysphoria". Psychiatry Res 146 (2): 107–16. doi:10.1016/j.pscychresns.2005.02.012. PMID 16515859. http://linkinghub.elsevier.com/retrieve/pii/S0925-4927(05)00215-5. 
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36. ^ Does PMDD Belong in the DSM? Challenging the Medicalization of Women's Bodies Journal article by Alia Offman, Peggy J. Kleinplatz; The Canadian Journal of Human Sexuality, Vol. 13, 2004
37. ^ Carol Tavris, The Mismeasure of Woman (New York: Simon & Schuster, 1992), 144.
38. ^ "UNC Center for Women's Mood Disorders" http://www.med.unc.edu/psych/wmd/research/pmdd
39. ^ Carol Tavris, The Mismeasure of Woman (New York: Simon & Schuster, 1992), 142.
40. ^ Lorber, Judith and Lisa Jean Moore. Gender and the Social Construction of Illness. 2nd ed. Walnut Creek, CA: Altamira Press, 2002.
41. ^ http://www.yaz.com/html/index.html

External links

• National Association for Premenstrual Syndrome
• U.S. Department of Health & Human Services
• familydoctor.org
• MayoClinic.com at Mayo clinic
• Direct Online Health Encyclopaedia: Premenstrual syndrome (UK) at NHS
• "Premenstrual Syndrome (PMS) (Premenstrual Tension)" at Merck Manual