Premenstrual syndrome
"premenstrual syndrome"[MeSH Terms] AND treatment
premenstrual syndrome menstrual cycle hormones diagram

This pathophysiology diagram illustrates hallmarks of major depressive disorder (MDD) across various stages of the female reproductive lifespan, including reproductive age, pregnancy, and peri- and postmenopause. A line graph labeled 'Physiological Hormonal Fluctuations' depicts the 28-day menstrual cycle, showing estrogen peaks prior to ovulation (Day 14) and progesterone dominance during the luteal phase. A signaling pathway shows how progesterone fluctuations lead to GABA and serotonin receptor modulation, contributing to premenstrual syndrome (PMS) and premenstrual dysphoric disorder (PMDD). In the pregnancy/postpartum pathway, reduced allopregnanolone levels and GABA alterations are linked to postpartum depression (PPD). The peri- and postmenopausal section illustrates declining estradiol (E2) and progesterone, linked to the intensification of depressive symptoms. The diagram also highlights secondary factors, including impaired estrobolome function (gut-microbiome-estrogen axis) involving bacteria like Prevotella and Ruminococcus, and an immune component characterized by attenuated microglia and inflammatory responses compared to men. This visualization integrates endocrinology, neurobiology, and immunology to explain sex-specific vulnerabilities in mood disorders.

This visual content is a clinical qualitative tool known as a 'body map,' used in psychology and women's health to illustrate the embodied experience of Premenstrual Syndrome (PMS). The diagram features a life-sized human silhouette divided into two sides, representing the contrast between the premenstrual phase and the rest of the cycle. The left side (premenstrual) is densely populated with negative annotations and symbols, including terms like 'failure,' 'STRESSED,' 'Weight Loss,' 'Pain,' and 'Dirty,' accompanied by red crosses and images of a thin female figure to represent body dissatisfaction. The head region contains swirling lines and question marks labeled 'who I am,' signifying cognitive clouding or identity disruption. In contrast, the right side features positive descriptors like 'Confident,' 'ZEN,' 'Strong,' 'Painless,' and 'Enjoyment' with green checkmarks. Central themes include the 'Female Expectation' of thinness, the use of 'Oral Contraceptives,' and the impact on daily activities like 'Exercise' and 'Work.' This illustration serves as an educational tool for healthcare providers to understand the psychosocial and physical dimensions of premenstrual distress through the patient's subjective narrative.

A pathophysiology diagram illustrating the multifactorial etiology of Premenstrual Syndrome (PMS). The central focus features two human figures depicting somatic and psychological symptoms, labeled 'Premenstrual Syndrome'. Surrounding this center are five key influencing factors: 1) Hormone fluctuations, shown via a graph of estradiol and progesterone levels throughout the follicular and luteal phases; 2) Genetics, represented by a DNA double helix; 3) Increased levels of inflammatory parameters, specifically high-sensitivity C-reactive protein (hsCRP) molecular structures; 4) Neurosteroid fluctuations, illustrated by the chemical structure of allopregnanolone; and 5) Neurotransmitter disturbances, depicted by the molecular structures of Serotonin and GABA. This educational graphic synthesizes hormonal, biochemical, and genetic contributors to the clinical manifestation of PMS, emphasizing the complex interplay between systemic inflammation, steroidal metabolites, and neurotransmission in reproductive health.
| Factor | Role |
|---|---|
| Hormone fluctuations | Normal cyclical changes in estradiol and progesterone trigger symptoms in vulnerable women - not abnormal hormone levels per se |
| Neurosteroid changes | Progesterone metabolite allopregnanolone is a positive allosteric modulator of GABA-A receptors; its fluctuations during the luteal phase alter GABAergic tone |
| Serotonin dysregulation | Estrogen and progesterone modulate serotonergic pathways; decreased serotonin activity in the luteal phase contributes to mood symptoms |
| Genetics | Women who are constitutionally sensitive to normal hormonal changes are at highest risk |
| Inflammation | Elevated hsCRP and other inflammatory markers have been found in women with PMS |

| Agent | Use | Notes |
|---|---|---|
| SSRIs (e.g., fluoxetine 10-20 mg, sertraline) | First-line for PMDD; emotional symptoms | Can be given continuously or intermittently (luteal phase only). Luteal-phase dosing works by directly promoting progesterone-to-allopregnanolone conversion, enhancing GABAergic tone |
| NSAIDs | Pain, headaches | Symptomatic relief |
| Spironolactone (up to 100 mg/morning) | Cyclic edema | Mild diuretic, antiandrogenic |
| Anxiolytics/mild sedatives | Insomnia, anxiety | Short-term, as needed |
| Bromocriptine (2.5 mg twice daily, off-label) | Mastalgia | Evidence limited |
| Danazol (100-400 mg/day, off-label) | Mastalgia | Evidence limited |
| Agent | Notes |
|---|---|
| Combined oral contraceptive pill (COCP) | First-line hormonal option. Can be prescribed cyclically or continuously (e.g., 3 months back-to-back). Drospirenone/EE (3 mg/20 μg) on a 24/4 schedule is widely used. Improves overall symptoms but not specifically premenstrual depressive symptoms |
| Transdermal/percutaneous estradiol (bioidentical, continuous) | Second-line if COCP fails; requires progestogen cover if uterus is present |
| GnRH agonists ± addback therapy | Induce reversible medical menopause. Used as a diagnostic test for PMDD or before surgical decision. Requires estradiol ± progestogen addback to prevent menopausal side effects |
