49 Zeiad A. El‐Gizawy1 and P.M. Shaughn O’Brien1,2 1 Royal Stoke University Hospital, University Hospitals of North Midlands NHS Trust, Stoke on Trent, UK 2 Keele University School of Medicine, Royal Stoke University Hospital, Stoke on Trent, UK Premenstrual symptoms occur in most women and there may have been evolutionary benefit to this. Social behaviour resulting in intercourse would have occurred more frequently at the time of ovulation and less frequently once ovulation had passed. As the female becomes less receptive and possibly aggressive to males during the non‐fertile premenstrual phase, the males would seek more receptive ovulating females leading to an increase in the population. This is pure conjecture of course – but that is the nature of evolutionary theory. As with all biological parameters there are extremes so that some women have minimal or no symptoms (5–9%) while a similar number have such severe symptoms that there is major impairment of their lives, that of their families, their interpersonal relationships and normal day‐to‐day functioning. This extreme is premenstrual syndrome (PMS). The terminology used for premenstrual disorders is complex. Premenstrual tension (PMT) was the term originally used, but it has now become the usual lay term; PMS is the medical term most often used in the UK. Premenstrual dysphoric disorder (PMDD) is the extreme, predominantly psychological end of the PMS spectrum, estimated to occur in 3–8% of women [1]. It is the term used increasingly by psychiatrists in the USA but, strictly speaking, originally only for research purposes. It should be noted that much recent research into aetiology and treatment has been undertaken on women who fulfil the criteria for PMDD, particularly for clinical trials on selective serotonin reuptake inhibitors (SSRIs). Women designated as having PMDD will also fulfil criteria for PMS but not necessarily vice versa. PMS is defined in the Tenth Revision of the International Classification of Disease (ICD‐10): a woman is considered to have PMS if she complains of recurrent psychological or somatic symptoms (or both) occurring specifically during the luteal phase of the menstrual cycle and which resolve in the follicular phase at least by the end of menstruation [2]. PMDD is more specific with regard to psychological symptoms and (reflecting the introduction of the term by psychiatrists) pays little attention to physical symptoms. Because the ICD‐10 definition makes no reference to impairment, it is probably too liberal to be of practical use clinically or for research purposes. The classification in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM‐V) is too restrictive for clinical use and may have the detrimental effect of under‐recognizing patients who are severely debilitated. The International Society for Premenstrual Disorders (ISPMD) has published four consensus statements since the previous edition of this textbook. The first, widely cited, is on classification and diagnosis [3]. Core premenstrual disorders (PMDs) are the most common type of PMS. Because most normal women have some degree of symptomatology in the days leading up to menstruation, it is considered that it is the impact of symptoms, namely that they significantly disrupt normal functioning, that distinguishes those women with PMS from those with no more than normal physiological symptoms. The symptoms of core PMDs are non‐specific and recur in ovulatory cycles. They must occur during the luteal phase and resolve as menstruation begins. There is no limit on the type or number of symptoms; however, some women will have predominantly psychological symptoms, some will have predominantly physical symptoms and some will have a mixture of both. There are also PMDs that are not typical core PMDs. These are called ‘variant’ PMDs and there are four categories. Psychological symptoms of PMS vary greatly, from depression, anxiety, irritability, loss of confidence and mood swings up to suicidal ideation (and, in extreme cases, suicide) [4]. Physical symptoms are typically in the form of mastalgia and bloatedness. There are no objective tests (physical, blood, biochemical, endocrine or imaging) to assist the diagnosis of PMS and so the use of prospectively completed symptom charts is essential (Fig. 49.1). Retrospective reporting of symptoms is inaccurate, but significant numbers of women who present to a PMS clinic have separate underlying problems such as perimenopause, thyroid disorder, migraine, chronic fatigue syndrome, irritable bowel syndrome, seizures, anaemia, endometriosis, drug or alcohol abuse and menstrual disorders as well as psychiatric disorders such as depression, bipolar illness, panic disorder, personality disorder and anxiety disorder. Fig. 49.1 Daily Record of Severity of Problems (DRSP) chart prospectively completed by a patient suffering from moderately severe premenstrual syndrome (PMS) demonstrating (a) the cyclicity of symptoms, (b) occurrence premenstrually, (c) absence of symptoms in the follicular phase and (d) impairment. The confirmation of luteal‐phase timing with the relief of symptoms by the end of menstruation is diagnostic, providing the symptoms are of such severity to impact on the patient’s normal functioning. It is also important to identify patients who have a premenstrual exacerbation of their underlying psychological, physical or medical disorder. For example, there are many documented cases of premenstrual suicide, asthma and epilepsy. Many validated assessment instruments are available, but they are all paper‐based self‐assessment scales and are not objective. Most researchers and clinicians opt for the Daily Record of Severity of Problems (DRSP) (Fig. 49.1), which is recommended in the 2016 (downloadable) Green‐top Guideline No. 48 from the Royal College of Obstetricians and Gynaecologists (RCOG) [5]. Such charts are invaluable. They enable the clinician to characterize instantly the pattern of premenstrual symptoms, their absence during the follicular phase and the degree of impairment caused. Despite the earlier (2007) guideline’s recommendation that the DRSP charts be administered for 2 months prospectively in order to establish the diagnosis before initiating treatment, less than 10% of clinical directors report that this strategy had been adopted in their gynaecology/PMS clinics (O’Brien and Samad, unpublished national survey data) (Fig. 49.2). More recently developed smartphone apps such as Prementrics (for smartphones) may be valuable. Fig. 49.2 National Survey of Clinical Directors. Implementation of RCOG Guidance on Diagnosis. DRSP, Daily Record of Severity of Problems; PSST, Premenstrual Symptom Screening Tool. The use of the so‐called gonadotrophin‐releasing hormone (GnRH) analogue test may be of benefit in clarifying the diagnosis where there is a mixed or uncertain picture. Although there are several studies to demonstrate that this group of drugs successfully eradicates symptoms in well‐defined patients, it has never been proven scientifically as a clinical test nor indeed even assessed as such. It is used extensively by gynaecologists (off‐licence and with due discussion with the patient) for the purposes of removing the ovarian cycle to determine which of an individual patient’s symptoms are clearly related to the menstrual cycle and which (i.e. those that persist despite suppression of the cycle) are not. It is also a valuable way of demonstrating whether symptoms or medical problems such as premenstrual migraine, asthma and epilepsy are truly related to the cycle or are independent. This can be illustrated by the following commonly encountered clinical problem. If a woman is to be considered for hysterectomy for a gynaecological indication such as heavy menstrual bleeding due to fibroids, symptom information gathered during GnRH therapy may help the patient make the decision about whether to conserve or remove her ovaries. If her PMS (or other significant premenstrual symptom) is severe and is eradicated by GnRH, it is likely (though not guaranteed) that she would also benefit from removal of ovaries when the hysterectomy is being undertaken. This information would be invaluable in the final preoperative counselling. PMS is not due to a single factor but its basis is multifactorial, with genetic, environmental and underlying psychological influences being important. This is of course true for all mood disorders but in PMS the ovarian cycle comes into play, with ovulation being almost certainly the key factor. The principal cause of PMS is uncertain. There is evidence to suggest that the cyclical endogenous progesterone produced in the luteal phase of the cycle after ovulation is the key provoking factor. Women with PMS appear to be unusually ‘sensitive’ to normal levels of progesterone [6]; differences in progesterone levels have not been demonstrated between women with and without PMS [7]. It has been hypothesized that the mechanism of this increased sensitivity is related to a neurochemical factor, and most evidence points to a dysregulation of serotonin metabolism [6]. Throughout reproductive life, progesterone production seems to be linked to women’s psychological health. Progesterone and metabolites, such as allopregnanolone, are produced by the ovary and the adrenals, and also de novo in the brain. These hormones are effectively neurosteroids that readily cross the blood–brain barrier. Progesterone has known mood‐altering and sedative effects when administered. It is well known that women have no PMS symptoms before puberty, during pregnancy or after the menopause; these are times where ovarian hormone cycling has not begun or ceases temporarily or permanently. Not surprisingly, if the assumptions made above are true, PMS‐like symptoms can also be reintroduced by the administration of oestrogen/progestogen hormone replacement therapy (HRT) and this is frequently seen in clinical practice. Suppression of the ovarian endocrine cycle with danazol, by administration of analogues of GnRH or following bilateral oophorectomy results in the elimination of PMS symptoms. Therefore, the hypothesis that ovarian steroids, particularly ovulatory progesterones, have a role in the pathophysiology of the syndrome is intuitively obvious. Research, none of which is recent, into PMS has generated data which could support theories of progesterone deficiency, oestrogen/progesterone imbalance or progesterone excess. However, the consensus is that ovarian steroid concentrations in blood do not differ in these women. Interactions of fluctuating levels of ovarian steroids or their metabolites with neurotransmitter systems or receptor imbalances in the brain are directly relevant to the pathogenesis of PMS [8]. This is believed to render women more sensitive to physiological levels of progesterone.
Premenstrual Syndrome
Definitions
Symptoms and classification of PMS
Diagnosis
Gonadotrophin‐releasing hormone agonists in diagnosis
Aetiology
Ovulation and progesterone
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