ICD-11GA34.41	PREMENSTRUAL DYSPHORIC DISORDER (PMDD) Premenstrual dysphoric disorder
ICD-10N94.3	Premenstrual tension syndrome
DSM-5-TRN94.3	Premenstrual Dysphoric Disorder

1. Definition and nosology

Premenstrual Dysphoric Disorder (ICD-11: GA34.41; DSM-5-TR: N94.3) — a recurrent disorder with significant emotional and behavioral symptoms in the last week before the menstrual cycle (luteal phase), fully remitting within a few days after menses onset. Distinguished from Premenstrual Syndrome (PMS) by clinical severity and significant functional impairment.

2. History

• Frank R.T. (1931) — “Premenstrual tension” term.
• DSM-IV (1994) — “Premenstrual Dysphoric Disorder” is included in Section III as a research category.
• DSM-5 (2013) — officially accepted as a diagnosis in the category of depressive disorders.
• ICD-11 (2019) — as separate category within mood disorders.

3. Epidemiology

• Prevalence in reproductive-age women: 3–8% (Yonkers K.A. et al. Lancet 2008 review).
• PMS — milder form — in 30–80% of women.
• Comorbidity: major depressive disorder, anxiety, bipolar disorder — increases risk.
• Suicidal thoughts significantly increase in the luteal phase.

4. Aetiology and pathogenesis

• Genetic: heritability ~30–50% (Treloar S.A. et al. Psychol Med 2002 twin studies).
• Hormonal sensitivity: In PMDD patients, ovarian hormones (estrogen, progesterone) are at normal levels; however sensitivity Increased — allopregnanolone (progesterone metabolite) exerts abnormal effect on GABA-A receptors (Schmidt P.J. et al. NEJM 1998 ovarian suppression and hormone supplementation study).
• Serotonergic dysregulation: The rapid effect of SSRIs (1–2 days, unlike classical depression) supports this mechanism.

5. Clinical features

5.1 Affective and behavioral symptoms (in the luteal phase)

• Affective lability (rapidly changing mood, tearfulness, rejection sensitivity).
• Irritability and angry outbursts (interpersonal conflict).
• Low mood, hopelessness, self-criticism.
• Anxiety, tension.

5.2 Behavioral and somatic symptoms

• Decreased interest in usual activities.
• Difficulty concentrating.
• Lethargy and fatigue.
• Appetite changes (especially carbohydrate craving), excess.
• Sleep disturbance (insomnia or hypersomnia).
• Sense of loss of control.
• Somatic — swelling of body, back pain, headache, breast tenderness.

5.3 Duration and rhythm

Symptoms begin in luteal phase (1 week pre-menses), completely resolve within a few days post-menses onset; complete remission in follicular phase (post-menses).

6. Diagnosis

6.1 Unified diagnostic criteria (DSM-5-TR · ICD-11)

A. In most menstrual cycles, 5+ symptoms in the last week of luteal phase; diminish within a few days after onset of menses; complete remission in postmenstrual phase.

B. At least 1 of the following:

1. Affective lability;
2. Irritability or anger;
3. Low mood or self-criticism;
4. Anxiety and tension.

C. Additional symptoms from the following (B + C total 5+):

5. Decreased interest;
6. Difficulty concentrating;
7. Lethargy, fatigue;
8. Appetite changes, excess;
9. Sleep disturbance;
10. Sense of loss of control;
11. Somatic (swelling, pain, etc.)

D. Significant distress or functional impairment.

E. Prospective mood diary for ≥ 2 cycles — mandatory for confirmation of diagnosis.

F. The symptoms are not merely an exacerbation of the symptoms of another psychiatric disorder (MDD, panic, dysthymic) (PMDD is a separate diagnosis; however, it can also occur against this background—“premenstrual exacerbation”).

6.2 Diagnostic algorithm

1. Clinical interview — rhythm of cycle-related symptoms.
2. Prospective mood diary for 2 cycles — DRSP (Daily Record of Severity of Problems, Endicott J.) or PRISM (Premenstrual Record of Impact and Severity of Menstruation) — diagnosis cannot be confirmed by retrospective anamnesis.
3. Comorbidity screening (depression, anxiety, bipolar).
4. Medical (thyroid, anemia, polycystic ovary).

6.3 Differential diagnosis

7. Examination and assessment

• DRSP or PRISM mood diary.
• PHQ-9, GAD-7 — comorbidity.
• Pelvic examination (gynecologist) and TSH — somatic causes excluded.

8. Treatment

8.1 General principles (ACOG · ISPMD · APA 2010)

1. SSRI first-line: Fluoxetine, sertraline, paroxetine (FDA approved for PMDD), escitalopram. Two modes possible:
   • Persistent (daily): Throughout the entire cycle.
   • Luteal-phase intermittent: From ovulation to start of menses (14 days) — equally effective (Steiner M. et al. NEJM 1995 RCT).
2. Hormonal suppression — combined oral contraceptives (especially those containing drospirenone — Yaz, Beyaz; FDA-approved); GnRH agonists (leuprolide) in refractory cases.
3. Oophorectomy — last choice, in refractory severe cases; with estrogen replacement therapy.
4. CBT — adjunctive; Lustyk M.K. et al. reviews have shown modest effect.
5. Lifestyle: Physical activity, caffeine and alcohol reduction — adjunct.
6. Calcium supplementation (1200 mg/day) — Thys-Jacobs S. et al. Am J Obstet Gynecol 1998 RCT — moderate effect; adjunct role.

8.2 Source-specific clarifications

• ACOG (American College of Obstetricians and Gynecologists) Practice Bulletin: SSRI first-line; oral contraceptive second.
• ISPMD (International Society for Premenstrual Disorders) consensus: continuous or luteal SSRIs equal efficacy; GnRH refractory.

Treatment methods

1. Daily Record of Severity of Problems (DRSP) — Endicott (Endicott J.) — 21 symptoms, daily rating of 1–6 points; prospective 2 cycles required for PMDD diagnosis.
2. SSRI — Luteal Phase Regimen — From ovulation (day 14) until menses onset; as effective as continuous use. Steiner M. et al. NEJM 1995.
3. Drospirenone-containing Oral Contraceptive — Yaz, Beyaz — FDA approval for PMDD; hormonal stabilization.
4. GnRH Agonist (Leuprolide) — Ovarian suppression in refractory cases; risk of osteoporosis with long-term use.

9. Prognosis

• SSRI or hormonal treatment leads to significant improvement in most patients.
• Persists during reproductive period; remission after menopause.
• Monitoring — cycle symptoms, compliance, side effects, comorbidity.

10. Myths and misconceptions

Myth 1: “PMDD is ‘female willpower weakness’, not a medical disorder”

Evidence: Schmidt P.J. NEJM 1998 — ovarian hormone suppression eliminates symptoms, hormone restart returns symptoms; neurobiologically based disorder. DSM-5 and ICD-11 official diagnosis.

Myth 2: “PMDD is also PMS, no difference”

Evidence: PMS mild form in 30–80% of women; PMDD characterized by clinical severity and functional impairment — 3–8% of women.

Myth 3: “SSRIs show no significant effect in PMDD, should be treated like depression”

Evidence: SSRI shows rapid effect (within 1–2 days) in PMDD — different pharmacokinetic mechanism from major depression; direct effect on serotonergic system.

Myth 4: “Only hormonal treatment (pregnancy, hormone replacement) is effective”

Evidence: SSRI and hormonal treatment both effective; SSRI first-line (for most patients); hormonal — with gynecological comorbidity or patient choice.

Myth 5: “Herbal preparations (chasteberry, evening primrose oil, St John's Wort) cure PMDD”

Evidence: Chasteberry (Vitex agnus-castus) has mild effect for PMS in some studies; evidence base for PMDD limited. Evening primrose oil — Cochrane negative results. St John's Wort — risk of interaction with SSRIs.

Myth 6: “Craniosacral therapy, homeopathy, acupuncture cure PMDD”

Evidence: Efficacy of these complementary interventions for PMDD has not been proven.

Myth 7: PMDD diagnosis can be made from retrospective history

Evidence: retrospective records are unreliable; Prospective 2-cycle diary is mandatory for diagnosis — this is the most frequent cause of underdetection.

11. Sources

1. WHO. ICD-11. GA34.41 Premenstrual dysphoric disorder. 2024.
2. APA. DSM-5-TR. 2022.
3. Yonkers K.A., O'Brien P.M., Eriksson E. Premenstrual syndrome. Lancet 2008;371(9619):1200–1210.
4. Schmidt P.J., Nieman L.K., Danaceau M.A., Adams L.F., Rubinow D.R. Differential behavioral effects of gonadal steroids in women with and in those without premenstrual syndrome. NEJM 1998;338(4):209–216.
5. Steiner M., Steinberg S., Stewart D. et al. Fluoxetine in the treatment of premenstrual dysphoria. NEJM 1995;332(23):1529–1534.
6. Thys-Jacobs S., Starkey P., Bernstein D., Tian J. Calcium carbonate and the premenstrual syndrome. Am J Obstet Gynecol 1998;179(2):444–452.
7. ACOG Practice Bulletin No. 15. Premenstrual syndrome. 2000 (reviewed).
8. Nevatte T., O’Brien P.M.S., Bäckström T. et al. ISPMD consensus on the management of premenstrual disorders. Arch Womens Ment Health 2013;16(4):279–291.
9. Ismaili E., Walsh S., O’Brien P.M.S. et al. Fourth consensus of the International Society for Premenstrual Disorders (ISPMD): auditable standards for diagnosis and management of premenstrual disorder. Arch Womens Ment Health 2016;19(6):953–958.
10. Treloar S.A., Heath A.C., Martin N.G. Genetic and environmental influences on premenstrual symptoms. Psychol Med 2002;32(1):25–38.
11. Marjoribanks J., Brown J., O’Brien P.M.S., Wyatt K. Selective serotonin reuptake inhibitors for premenstrual syndrome. Cochrane Database Syst Rev 2013;(6):CD001396.
12. Endicott J., Nee J., Harrison W. Daily Record of Severity of Problems (DRSP): reliability and validity. Arch Womens Ment Health 2006;9(1):41–49.
13. Lustyk M.K.B., Gerrish W.G., Shaver S., Keys S.L. Cognitive-behavioral therapy for premenstrual syndrome and premenstrual dysphoric disorder: a systematic review. Arch Womens Ment Health 2009;12(2):85–96.