The name says it all. Or does it? Are premenstrual tension (PMT), premenstrual syndrome (PMS) and premenstrual dysphoric disorder (PMDD) one and the same or variants of the same affliction, or are they separate entities? Are they afflictions at all, or just part of the human condition? We aim to disentangle any confusion that has arisen.
It has long been recognised that many women experience a predictable, cyclic pattern of moliminal symptoms, which begin in the late luteal phase of the menstrual cycle and end shortly after menstruation begins. The symptoms may cluster and include physical, emotional, psychological and behavioural components and constitute a syndrome or a disorder, depending on their impact. However, from the outset, it needs to be recognised that for many women, symptoms represent a premenstrual exacerbation of an underlying condition (PME), such as a major depressive disorder, bipolar disorder, anxiety disorder or eating disorder that may be undiagnosed and untreated, partially treated, or treatment non-responsive. It has been suggested that a significant percentage of women who seek treatment for premenstrual symptoms are in this category.1
PMT is said to involve the experience of one or more of the following symptoms: tender swollen breasts, headaches and/or migraines, abdominal cramping and bloating, backache, acne outbreaks, fluid retention, weight gain, constipation and/or diarrhoea, food cravings, emotional irritability, anxiety, nervous tension, lowered coping ability, impairment of concentration, reduced libido, aggression, mood swings, depression, clumsiness, lethargy, insomnia and tearfulness. PMS is the same thing. However, many argue that the latter label better describes the symptom cluster, with the term ‘syndrome’ de-emphasising the emotional and psychological symptoms implied in the term ‘tension’. Overall, diagnostically, it is a loose and informal label, as it only requires one or two symptoms to qualify and is reported to be experienced by up to 50 per cent of women globally.2
While PMS is generally manageable and minimally impairs psychosocial functioning, it has been recognised that three to eight per cent of women experience multiple symptoms that can significantly affect their quality of life and daily interpersonal and occupational functioning, to the point of transient impairment.3 The term premenstrual dysphoric disorder aims to capture this sub-group.
The clustering of more severe premenstrual symptoms was first described by Frank in 1931 and he coined the phrase PMT.4 His view was that ovarian functioning needed to be obliterated with oophorectomy or radiation therapy in order to restore order in the home and the workplace. The term PMS was later introduced in 1953 by Green and Dalton, who felt that the condition was responsible for decreased worker productivity, increased divorce rates and even murder.5 Later, Mortola was the first to recognise that depressive mood symptoms sometimes only occur during the luteal phase of the menstrual cycle.6
In 1987, the Diagnostic and Statistical Manual of Mental Disorders (DSM-III-R) introduced the diagnostic category of late luteal phase dysphoric disorder in the appendix as a proposed diagnostic category needing further study. Prior to the release of the DSM-IV in 1994, there was much debate as to whether the category should be elevated to a distinct diagnosis, kept in the appendix, or entirely eradicated. They decided to keep it in the appendix with an elaboration of diagnostic criteria to aid further study. In 1995, a large study, subsidised by Eli Lilly, suggested that the selective serotonin reuptake inhibitor (SSRI) fluoxetine assisted 60 per cent of women with symptom relief.7 In reaction, some argued that such symptoms were a culture-bound syndrome and represented ‘an unnecessary pathologising of cyclical changes in women’, with the diagnostic category potentially being harmful, as it could lead to women believing that they are mentally ill, leading others to mistrust them in situations as important as job promotions or child custody cases.8 Others argued that it represented a valid condition that was only poorly studied because it didn’t affect men.
The DSM-IV-TR, published in 2000, again decided to keep the condition in the appendix. This view was further supported in 2003 by the Committee for Proprietary Medicinal Products requirement for the manufacturer of Prozac (fluoxetine) to remove PMDD from the list of indications for fluoxetine sold in Europe. However, with the 2013 introduction of DSM-V, PMDD was introduced as a formal diagnostic category. Soon afterwards, in 2014, a published review addressed reservations regarding this introduction, finding that such a label does not harm women economically, politically, domestically or legally, that financial conflict of interest concerns did not render the diagnosis invalid or the research unusable, and that the condition had been identified worldwide.9 The International Classification of Diseases, 10th revision (ICD-10), first published in 2010, introduced the diagnostic category of premenstrual tension syndrome, with broad and easily endorsed criteria compared with the DSM-V’s narrow and specific criteria. This difference in diagnostic criteria has impaired research and therapeutic guideline development, as the former criteria captures 91.4 per cent of the female population and the latter only 3.7 per cent, when applied to a sample of college students.10 In Australia, the Therapeutic Goods Administration recognises the validity of the diagnosis of PMDD, however, the Pharmaceutical Benefits Scheme does not reimburse the cost of SSRIs used for its treatment.
In order to meet the DSM-V definition of PMDD, a patient must meet the following specific criteria.
For most menstrual cycles during the past year, at least five of the following 11 symptoms (including at least one of the first four) must be present in the final week before the onset of menses, start to improve within a few days after the onset of menses, and become minimal or absent in the week post-menses:
- Marked lability (for example, mood swings)
- Marked irritability or anger
- Markedly depressed mood
- Marked anxiety and tension
- Decreased interest in usual activities
- Difficulty in concentration
- Lethargy and marked lack of energy
- Marked change in appetite (for example, overeating or specific food cravings)
- Hypersomnia or insomnia
- Feeling overwhelmed or out of control
- Physical symptoms (for example, breast tenderness or swelling, joint or muscle pain, a sensation of ‘bloating’ and weight gain).
One (or more) of the following symptoms must be present:
- Marked affective lability (for example, mood swings, feeling suddenly sad or tearful, or increased sensitivity to rejection)
- Marked irritability, anger or increased interpersonal conflicts
- Marked depressed mood, feelings of hopelessness or self-deprecating thoughts
- Marked anxiety, tension and/or feelings of being ‘keyed up’ or on edge.
One (or more) of the following symptoms must be present, additionally, to reach a total of five symptoms when combined with symptoms from Criterion B above:
- Decreased interest in usual activities (for example, work, school, friends, hobbies)
- Subjective difficulty in concentration
- Lethargy, easy fatigability or marked lack of energy
- Marked change in appetite, overeating or specific food cravings
- Hypersomnia or insomnia
- A sense of being overwhelmed or out of control
- Physical symptoms, such as breast tenderness or swelling, joint or muscle pain, a sensation of ‘bloating’ or weight gain.
The aetiology of PMS and PMDD remains an active area of research. While the timing of symptom occurrence and disappearance suggests that sex hormone flux is relevant, there are no demonstrable differences in reproductive hormone levels in women who do or don’t experience symptoms.11 Thus, hormone levels and flux alone appear to be irrelevant, however, the relevant neurobiological and physiological changes may represent an underlying sensitivity to such changes. There is evidence that oestrogen acts as a neuro-modulator, with diverse effects on the central nervous system through its influence on the serotonergic, dopaminergic and GABA neurotransmitter systems, as well as exerting influence on the expression and responsiveness of androgens, progesterone, prolactin and gonadotropin-releasing hormone, all of which have been shown to have effects on immunomodulation.1 Some women may thus have an abnormal central nervous system response to normal hormone levels and variation. Symptoms are no longer considered to be simply cultural or psychological phenomenon, but biologically based occurrences, with hormonal, neurobiological, genetic and epigenetic aetiological components.
In a recent publication, Jablensky suggests that ‘there is little evidence that the majority of recognised mental disorders are separated by natural boundaries and that diagnostic categories defined by their clinical syndromes should be regarded as ‘valid’ only if they have been shown to be truly discrete entities’.12 The disorders PMT, PMS and PMDD, to date, have not met such a standard. However, they may possess ‘utility’ by virtue of the information they convey about presenting symptoms, outcome and treatment response. A greater understanding of aetiology is essential before we commit to these diagnostic categories unconditionally. Hopefully, research into genetics, epigenetics, neurobiology and population epidemiology will allow a conceptual reconciliation between the emerging continuum and dimensional view of the variation in symptomatology, and the categorical approach embodied in current classifications such as ICD-10 and DSM-5.
- Pinkerton J, Guico-Pabia C, Taylor H. Menstrual cycle-related exacerbation of disease. Am J Obstet Gynecol. 2010 Mar;
- Direkvand-Moghadam A, Sayehmiri K, Delpisheh A, Kaikhavandi S. Epidemiology of premenstrual syndrome (PMS) – a systematic review and meta-analysis. J Clin Diagn Res. 2014 Feb;
- Yonkers K, O’Brien P, Eriksson E. Premenstrual syndrome. Lancet 2008 Apr 5;371(9619): 1200-1210.
- Frank R. The hormonal causes of premenstrual tension. Arch Neurolog Psychiatry 1931;26:1053.
- Greene R, Dalton K. The premenstrual syndrome. BMJ 1953; (4818):1007-14.
- Mortola J, Girton L, Yen S. Depressive episodes in premenstrual syndrome. Am J Obstet Gynecol 1989;161(6,Pt1):1682-1687.
- Steiner M, Steinberg S, Stewart D, et al. Fluoxetine in the treatment of premenstrual dysphoria. New England Journal of Medicine 1995;332(23):1529-34.
- Severino S. Premenstrual Dysphoric Disorder: Controversies surrounding the diagnosis. Harv Rev Psychiatry 1996 Jan-Feb; 3(5):293-295.
- Hartlage S, Breaux C, Yonkers K. Addressing concerns about the inclusion of premenstrual dysphoric disorder in DSM-5. J Clin Psychiatry 2014 Jan;75(1):70-76.
- Raval C, Panchal B, Tiwari D, et al. Prevalence of premenstrual syndrome and premenstrual dysphoric disorder among college students of Bhavnagar, Gujarat. Indian J Psychiatry 2016
- Hantsoo L, Epperson C. Premenstrual Dysphoric Disorder: Epidemiology and Treatment. Current Psychiatry Reports. 2015 Nov;17(11):87.
- Jablensky A. Psychiatric classifications: validity and utility. World Psychiatry 2016 Feb;15(1):26-31.