Is Premenstrual Dysphoric Disorder more than just your typical PMS?

Most of us are aware of premenstrual syndrome (PMS). PMS is an endocrine condition affecting women’s psychological, behavioural and physical wellbeing during the luteal phase of menstruation. This phase refers to the time from ovulation to the onset of menstruation. Around 90% of women experience an unpleasant collection of physical and psychological symptoms during PMS, such as bloating or stomach pain, mood swings, anxiousness or irritability, breast tenderness, changes in appetite, headaches, and acne. However, up to 8% experience more severe and distressing symptoms on the PMS continuum ─ premenstrual dysmorphic disorder (PMDD).

PMDD straddles the experiences of a hormonal disorder and a mental health disorder. It is comprised of disruptive physical and emotional manifestations, that, unlike PMS, result in severe functional impairment and a reduction in a woman’s quality of life. Emotionally, PMDD may present through a variety of symptoms, including severe mood swings, panic attacks, loss of interest in relationships and activities, irritability, binge eating, changes in sleep patterns and feelings of tension, anxiety, despair, and suicidal ideations. Physically, back and joint pain, cramps, headaches, breast swelling, joint or muscle pain, reduced libido, bloating and other gastrointestinal issues are commonly experienced. Whilst PMS is often manageable, PMDD is on the severe end of the PMS spectrum and necessitates the attention of a medical professional.

Whilst the aetiology and pathophysiology of PMDD remain largely unknown, various studies have highlighted the involvement of GABAergic and serotonergic systems. It is important to note that unlike PMDD and other mood disorders, PMS is unrelated to dysregulated neurotransmitter levels. Both PMS and PMDD are recognised to be caused by a hormonal event ─ the production of progesterone from the ovaries following ovulation. Progesterone and its metabolites are vital for the formation of new neurons, reduction of neuroinflammation and maintaining cholesterol levels within a normal range. However, in PMDD, increased progesterone metabolites are produced by the corpus luteum (the cellular mass formed in the ovaries following release of a mature ovum from an ovarian follicle) and in the brain following ovulation brain bind to the neurosteroid site on the GABA receptor. This binding changes the receptor configuration, resulting in a reduction of GABA-mediated inhibition. This inhibition is an “off switch” to the central nervous system and reduces regulation of mood and cognitive functioning, which can trigger the onset of negative mood symptoms in the luteal phase of the menstrual cycle. Other symptoms of PMDD are also likely attributed to this abnormal response to progesterone metabolites. The symptoms of PMDD resolve with menstruation when progesterone levels fall, solidifying that high progesterone levels following ovulation contribute to disease pathophysiology.

PMDD affects females of reproductive potential and is more common than what is currently assumed. Whilst approximately 3–8% of women have been estimated to suffer from PMDD globally, determined by strict diagnostic criteria, it is likely to be much higher. Up to 13–18% may not meet the official PMDD diagnostic criteria, but experience disabling PMDD-related symptoms ─ so much so that the reduction in their quality of life is similar to that of a major depressive disorder. Whilst the prevalence varies amongst ethnic groups and cultural locations, the epidemiology and incidence rates are difficult to predict due to the highly variable frequency reported across studies using different methodologies.