Abstract
Premenstrual syndrome (PMS) is a condition characterized by psychological, physical and behavioural symptoms occurring in the luteal phase of the normal menstrual cycle but resolves shortly after menstruation. Around 40% of women experience symptoms of PMS and of these 5–8% suffer from severe PMS including premenstrual dysphoric disorder (PMDD), a debilitating condition with severe emotional and physical symptoms and functional impairment. Premenstrual syndrome is effectively related to hormonal changes in the menstrual cycle, supported by the absence of PMS prior to puberty, during pregnancy, and after the menopause. Diagnosis is aided by reviewing symptoms in the Daily Record of Severity of Problems (DRSP) questionnaire. Management is centred around lifestyle modifications, cognitive behavioural therapy and pharmacological treatment. This article is a review of the clinical impact of premenstrual syndrome and its management strategies.
Introduction
Premenstrual syndrome (PMS) is a condition characterized by psychological, physical and behavioural symptoms which occur in the luteal phase of the normal menstrual cycle but resolve shortly after menstruation. The most common psychological symptoms include depression, anxiety, irritability, loss of confidence, and mood swings. Abdominal bloating and breast tenderness are invariably present as physical symptoms. Behavioural symptoms include reduced cognitive ability and aggression. A diagnosis of PMS is supported by the timing of these symptoms and their impact on daily functionality. Physiological symptoms of menstruation can be differentiated from PMS by the significant impairment in the personal, professional and social life of the woman in the latter.
Prevalence
About 80% of women report at least one physical or psychiatric symptom during the luteal phase of their menstrual cycle; however, most do not report significant impairment in their daily life. There does not seem to be any association between PMS and age, education and employability.
40% of women experience symptoms of PMS and of these 5–8% suffer from severe PMS. 24% of women aged 20–34 years have symptoms of moderate-to-severe PMS. The incidence is 23% in perimenopausal women. PMDD, which is at the most severe end of the spectrum, affects about 3–8% of women in the reproductive age group. Prevalence in Asian countries is reportedly lower than Western countries. This geographical difference in the prevalence of PMS may be attributed to socio-economic factors such as lifestyle and diet with a background of cultural practices around menstruation.
Classification
Premenstrual disorders vary over a wide spectrum range. In 2012, the International Society for Premenstrual Disorders (ISPMD) produced a classification of PMD, categorizing it into either ‘Core PMD’ or ‘Variants of PMD’. A year later, the Diagnostic and Statistical Manual of Mental Disorders-5 (DSM-5) of the American Psychiatric Association (2013) defined the diagnostic criteria for PMDD, at the most severe end of the spectrum.
Core premenstrual disorders (PMDs)
This is the most encountered type of PMD. This is associated with ovulatory cycles. This type typically fits into the definition of PMS where the physical and psychological symptoms start in the luteal phase and subside as menstruation begins or soon after, which is then followed by a symptom-free period. The symptoms experienced are severe enough to affect daily functioning or interfere with the woman’s work, school, performance, or interpersonal relationships.
Premenstrual dysphoric disorder (PMDD) is a severe form of PMS defined in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) as occurring when a woman suffers from at least five out of the eleven distinct psychological menstrual symptoms, one of which must include mood ( Box 1 ).
A) Five (or more) of the following symptoms occurred during the week before menses and remitted a few days after the onset of menses.
At least one of the symptoms being either 1, 2, 3 or 4:
1. Marked lability (e.g., mood swings, suddenly feeling sad or tearful, or increased sensitivity to rejection)
2. Marked irritability or anger
3. Markedly depressed mood
4. Marked anxiety and tension
5. Decreased interest in usual activities
6. Difficulty in concentration
7. Lethargy and marked lack of energy
8. Marked change in appetite (e.g., overeating or specific food cravings)
9. Hypersomnia or insomnia
10. Feeling overwhelmed or out of control
11. Physical symptoms (e.g., breast tenderness or swelling, joint or muscle pain, a sensation of ‘bloating’ and weight gain)
B) The symptoms interfere with work, school, usual social activities or relationships with others
C) The symptoms are not an exacerbation of the symptoms of another disorder (e.g., major depressive disorder, panic disorder, dysthymic disorder or a personality disorder)
D) Criteria A, B and C should be confirmed by prospective daily ratings during at least two consecutive cycles
E) The symptoms are not due to the direct physiologic effects of drugs of abuse, medications or an underlying medical disorder
Variant PMDs
These are the premenstrual disorders which do not meet criteria for core PMDs. There are four subtypes, as follows.
- 1.
Premenstrual exacerbation of an underlying disorder – symptoms of an underlying disorder (such as diabetes, depression, epilepsy, asthma, and migraine) significantly worsen premenstrual.
- 2.
Non-ovulatory PMDs – symptoms result from ovarian activity other than during ovulation. This is hypothesised to be due to the ovarian activity during the follicular phase of menstrual cycle.
- 3.
Progestogen-induced PMD – symptoms result from exogenous progesterone administration, for example hormone replacement therapy (HRT) or the combined oral contraceptive (COC) pill. This is especially seen with older generation of progestogens like Levonorgestrel.
- 4.
PMDs with absent menstruation – symptoms arise from continued ovarian activity even if the woman is not menstruating, for example after a hysterectomy or endometrial ablation, or in women using the levonorgestrel-releasing intrauterine system (LNG-IUS).
Aetiopathogenesis
Although the aetiology remains uncertain, it revolves around the luteal phase of menstrual cycle. The strongest risk factor of PMS is presence of ovulatory menstrual cycles. The other risk factors are family history of PMS, mood disorders especially depression, cigarette smoking, alcohol intake, physical and emotional abuse, weight gain and stress.
Researchers are yet to find conclusive evidence regarding why some women are more sensitive to ovarian hormone fluctuation during the different phases of menstrual cycle. Some theories explaining PMS include:
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Abnormal sensitivity of the central nervous system to female hormones.
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Estrogen-serotonin dysregulation.
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Genetic factors.
Women with PMS have an increased sensitivity to hormonal fluctuations during a normal menstrual cycle, especially to progesterone and its GABAergic metabolite allopregnanolone, which is secreted following ovulation.
Serotonin is a key etiological factor in the pathogenesis of PMS. Mood changes are attributed to changes in the estrogen levels in the luteal phase of menstrual cycle. Trials have indicated that serotonin precursors significantly increase between days 7–11 and 17 to 19 of the menstrual cycle. This suggests an association of mood disorders with estrogen-serotonin regulation.
Decrease in estrogen at ovulation causes the hypothalamus to release norepinephrine, which triggers a decline in acetylcholine, dopamine, and serotonin that may lead to insomnia, fatigue, depression, which are common symptoms of PMS and PMDD.
The aetiology of PMDD may have a genetic basis. Single nucleotide polymorphism in the ESR1 (Estrogen Receptor Alpha) gene encoding sex steroid hormone receptors may result in differential sensitivity to hormones in women who suffer from PMDD.
Dietary causes like excessive consumption of fast food, drinks containing sugar, deep-fried foods, and lifestyle factors such as less habitual exercise and poor sleep quality are closely related to PMS.
The pathophysiology of premenstrual syndrome is complex, imprecise, and not fully understood. PMS seems to reflect the action of progesterone metabolite, allopregnanolone on neurotransmitters like gamma-aminobutyric acid (GABA), opioids, serotonin, and catecholamine. Women with PMS have lower levels of allopregnanolone.
Diagnosis
Meticulous history taking is important. The key points should include the timing of the symptoms in relation to the menstrual cycle, the severity, medication history especially use of hormonal contraception, medical history and presence of comorbidities, history of mood disorders, surgeries like endometrial ablation or hysterectomy.
Diagnostic criteria for PMS:
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Strong relationship between physical, psychological and behavioural symptoms to the luteal phase of the cycle.
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Symptoms subside with the onset of menstruation.
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Presence of symptom free period prior to ovulation.
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Symptoms severely impacting quality of life including personal, professional and social aspects.
Diagnostic criteria for PMDD are elaborated in Box 1 .
When clinically reviewing women for PMS, symptoms should be recorded prospectively, over two cycles using a symptom diary (like the Daily Record of Severity of the Problem (DRSP) chart), as retrospective recall of symptoms is unreliable.
If symptom diary is inconclusive – GnRH analogues, can be useful in separating those with and those without PMS by inhibiting cyclical ovarian function. These can be used for 3 months to establish a definitive diagnosis.
Investigations
Symptom recording is the most important aspect while investigating PMS to arrive at a conclusive diagnosis. There are various prospective and retrospective tools available to help women record the symptoms. The DRSP is the most widely used and is simple for patients to use. The DRSP has also been consistently shown to provide a reliable result ( Box 2 ).
