The Premenstrual Syndrome: Pathophysiology, Causes, Clinical Manifestation and Therapies

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This article discusses the pathophysiology, causes, clinical manifestation and therapies for premenstrual syndrome (PMS). PMS is a condition characterized by behavioral, emotional and physical symptoms which tend to be more severe and acute during the luteal phase of the menstrual cycle and definitely end after menstruation. The article also highlights the difference between clinical manifestation of polycystic ovary syndrome and PMS.

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Title: The Premenstrual Syndrome

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Qn1. Pathophysiology of PMS
Premenstrual syndrome (PMS) is a condition characterized by behavioral, emotional
and physical symptoms which tend to be more severe and acute during the luteal phase of the
menstrual cycle and definitely end after menstruation (Walsh, Ismaili, Naheed, and O’Brien,
2015). Mostly affects women of the reproductive age and causes physical discomfort in some
weeks to menstruation. The symptoms could be mild but in other cases they are severe to
affect ones daily activities (Yonkers et al. 2008). According to O’Brien, Rapkin, Dennerstein,
and Nevatte (2011), its symptoms do not exceed 14 days before menses and has irritability
and anger as the long lasting and most severe symptoms. According to Mayo clinic (2018),
the behavioral and emotional sign and symptoms due to this syndrome include: depressed
mood, tension, anxiety, crying spells, mood swings, anger, change in appetite, irritability,
food cravings, insomnia, poor concentration, social withdrawal and change in libido.
The physical signs and symptoms are headache, fatigue, joint and muscle pains,
constipation, diarrhea, acne flare ups, weight gain, breast tenderness and alcohol intolerance.
Tracey experienced almost all these signs and symptoms. Earlier research linked this
syndrome with abnormal ovarian sex steroid levels but this has been dropped due to lack of
difference between asymptomatic and symptomatic women and also lack of enough study to
show the difference in progesterone levels. Research shows that almost 8 percent of
menstruating ladies are suffering from this syndrome. The International Society for
Premenstrual Disorder deviced a method for premenstrual disorder (PMD). They also divided
premenstrual syndrome into core and variant. Core PMD has spontaneous ovulatory
menstrual cycles and could be subdivided into predominantly physical, psychological or
mixed symptoms (Kedian & O’Brien, 2012). Variant PMD is subdivided into premenstrual
exacerbation, PMS with lack of menstruation, PMS with anovulatory ovarian activity and
progesterone induced PMS (Rapkin & Kou, 2008).
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Qn2. Causes of PMS
According to Moreno and Zuckerman (2016), the real causes of premenstrual
syndrome are unknown but several factors are thought to cause this condition. The signs and
symptoms of this syndrome change with hormonal change and cease with start of menopause
and pregnancy. It is therefore thought to be as a result of the cyclic change in hormones. It is
also thought to be caused by chemical changes in the brain and depression (Mayo clinic,
2018).
Earlier research linked this syndrome with abnormal ovarian sex steroid levels but this
has been dropped due to lack of difference between asymptomatic and symptomatic women
and also lack of enough study to show the difference in progesterone levels. Sex steroids
easily find their way past blood brain barriers, whose receptors are high in concentration in
the brain, including in the hypothalamus and amygdala. It is believed that progesterone is
metabolized in the brain to allopregnanolone and pregnanolone. These stimulate the gama-
aminobutryic acid (GABA) inhibitory neurotransmitter system. The GABA receptors are
responsible for the cognition and mood alteration (Rapkin & Akopians, 2012). Low
concentration of allopregnanolone causes aggression, anxiety and negative moods, like anger,
irritability and tiredness just as Tracey experienced. The GABA receptors sensitivity to
allopregnanolone decreases on high concentration which results to the worsening of the PMS
symptoms during luteal phase. Tracey’s case aggravated just before menstruation began.
Qn3. Difference between clinical manifestation of polycystic ovary syndrome and
PMS
According to Ramanand, Ghongane, Ramanand, Patwardhan, Ghanghas & Jain,
(2013), the diagnosis criteria for polycystic ovary syndrome (PCOS) were obesity, polycystic
ovary, oligomenorrhea and hirsutism. This disorder is now thought to be a heterogeneous
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defect resulting from over secretion of androgen in the ovaries and linked with insulin
resistance. Polycystic ovary syndrome presents itself with either amenorrhea, dyslipidemia,
infertility, signs of hyperandrogenemia and metabolic unrest like insulin resistance. This
could be due to the persistent anovulation for a long period of time. Different diseases of the
endocrine system can cause anovulation, thus occurrence of polycystic ovaries. PCOS is
therefore a functional derangement and makes women vulnerable to dyslipidemia,
endometrial carcinoma, type 2 diabetes and premature arteriosclerosis. Treatment of
polycystic ovarian syndrome should therefore focus on these defects too (Nidhi eta al. 2011,
McManus et al. 2013).
According to Freeman, Halberstadt, Rickels, Legler, Lin & Sammel (2011), 20
percent are suffering from PMS but the clinicians have not yet come up with an accepted
diagnosis for this syndrome. Clinical officer who manage this disorder just access a broad
array of symptoms to come up with the diagnostic guidelines. Limited health officers’ time
and diversity in diagnostic guidelines are the cause of poor diagnosis, leading to inadequate
treatment of this syndrome. PMS primary diagnosis method is therefore the use of the wide
range of its symptoms (Schmelzer, Ditzen, Weise, Andersson, Hiller and Kleinstauber, 2013).
It is not known which of the many symptoms of PMS give the accurate likelihood of the
disorder.
Qn4. Therapies for PMS
Mayo clinic (2018) recommends a lifestyle change to help in PMS treatment. They
also claim that the doctor could prescribe medication depending on the severity of the
syndrome. Therapy for this syndrome varies in different women but the most common
include: antidepressants- whereby selective serotonin reuptake inhibitors are used to reduce
the mood symptoms. Nonsteroidal anti-inflammatory drugs (NSAIDs), taken before the onset

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of menses are used ease breast discomfort and cramping. These drugs are mostly taken by
women who experience headache and abdominal pains before their periods and also help to
reduce inflammation and secretion of prostaglandin. Diuretics are recommended to help shed
excess fluids through the kidneys and hormonal contraceptives are prescribed to stop
ovulation (PubMed Health, 2017). Though not an approved treatment of PMS, some women
would take progesterone hormone as their periods approach. This prevents the symptoms
caused by reduced levels of progesterone.
PMS symptoms could also be managed by changing one’s eating habits and other life
style activities. Some modifications to the diet include: eating smaller and more frequent
meals reduce bloating and fullness; limiting salty meals to reduce fluid retention and
bloating; eating foods with a high concentration of complex carbohydrates, eating foods rich
in calcium and avoiding alcohol and caffeine. One should also engage in daily physical
exercise, reduce stress, gen enough sleep and try yoga or massage (Mayo clinic, 2018).
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References
Freeman, E. W., Halberstadt, S. M., Rickels, K., Legler, J. M., Lin, H., & Sammel, M. D.
(2011). Core Symptoms That Discriminate Premenstrual Syndrome. Journal of
Women’s Health, 20(1), 29–35. http://doi.org/10.1089/jwh.2010.2161
Kadian, S. and O’Brien, S. (2012). Classification of premenstrual disorders as proposed by
the International Society for Premenstrual Disorders. Menopause Int., Vol. 18, pp.
43–47
Mayo clinic. (2018). Premenstrual syndrome (PMS). Retrieved from:
https://www.mayoclinic.org/diseases-conditions/premenstrual-syndrome/diagnosis-
treatment/drc-20376787
Moreno, M. A. and Zuckerman, A. L. (2016). Premenstrual Syndrome. Retrieved from:
https://emedicine.medscape.com/article/953696-overview
Nidhi, R., Padmalata V, Nagarathna, R. and Amritanshu, R. (2011). Prevalence of polycystic
ovarian syndrome in Indian adolescents. J Pediatr Adolesc Gynecol, Vol. 24, pp. 223–
227.
PubMed Health. (2017). Premenstrual Syndrome: Treatment of PMS. Retrieved from:
https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0072448/
O’Brien P. M., Backstrom, T., Brown, C., Dennerstein, L., Endicott, J. and Epperson, C. N.
(2011). Towards a consensus on diagnostic criteria, measurement and trial design of
the premenstrual disorders: The ISPMD Montreal consensus. Arch Women’s Ment.
Health, Vol.14, pp.13–21.
O’Brien, S., Rapkin, A., Dennerstein, L. and Nevatte, T. (2011). Diagnosis and management
of premenstrual disorders.BMJ, Vol. 34, No. 2, pp. 2994-3010.
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Rapkin, A. J. and Kuo, J. (2017). Neurotransmitter physiology: the basics for understanding
premenstrual syndrome. In: O’Brien PMS, Rapkin A, Schmidt P, editors. The
Premenstrual Syndromes: PMS and PMDD. London: Informa. Healthcare, p. 69–71.
Ramanand, S. J., Ghongane, B. B., Ramanand, J. B., Patwardhan, M. H., Ghanghas, R. R., &
Jain, S. S. (2013). Clinical characteristics of polycystic ovary syndrome in Indian
women. Indian Journal of Endocrinology and Metabolism, 17(1), 138–145.
http://doi.org/10.4103/2230-8210.107858
Rapkin, A. J. and Akopians, A. L. (2012). Pathophysiology of premenstrual syndrome and
premenstrual dysphoric disorder. Post Reproductive Health, Vol. 18, No. 2, pp. 52-59.
Doi: 10.1258/mi.2012.012014
Schmelzer, K., Ditzen, B., Weise, C., Andersson, G., Hiller, W. and Kleinstauber, M. (2015).
Clinical Profiles of Premenstrual Experiences Among Women Having Premenstrual
Syndrome (PMS): Affective Changes Predominate and Relate to Social and
Occupational Functioning. Health Care for Women International, Vol. 36, No. 10, pp.
1104-1123. Doi: 10.1080/07399332.2014.954701
Walsh, S., Ismaili, E., Naheed, B. and O’Brien, S. (2015). Diagnosis, pathophysiology and
management of premenstrual syndrome. The Obstetrician & Gynaecologist, Vol. 17,
No. 2015, pp. 99-104. Doi: 10.1111/tog.12180
Yonkers, K. A., O’Brien, P. S. and Eriksson, E. (2008). Premenstrual syndrome. The Lancet,
Vol. 371, No. 9619, pp. 1200-1210. Doi: 10.1016/S0140-6736(08)60527-9
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