1. Substance + claimed effects

Premenstrual dysphoric disorder (PMDD) is a severe, cyclical mood disorder in which the luteal phase of the menstrual cycle reliably triggers a constellation of affective, cognitive, and somatic symptoms that remit within a few days of menses. It was added to DSM-5 in 2013 as a discrete depressive disorder, distinguishing it from premenstrual syndrome (PMS) by symptom severity and the requirement of functional impairment Hantsoo & Epperson 2015. Diagnosis requires at least five DSM-5 symptoms (one of which must be a "core" affective symptom — affective lability, marked irritability, depressed mood, or anxiety/tension), and — critically — prospective daily symptom ratings across at least two cycles using a validated instrument such as the Daily Record of Severity of Problems Endicott et al. 2006. The entry covers what PMDD is and is not, its felt effects on mood, day-to-day function, cognition, energy, sleep, and relationships, the elevated suicide risk it carries, and the three tiers of treatment with the strongest evidence: SSRIs (continuous or luteal-phase), hormonal suppression of ovulation (drospirenone-containing combined oral contraceptives and GnRH agonists), and lifestyle / adjunctive therapies (aerobic exercise, CBT, calcium). Surgical management (bilateral oophorectomy) is mentioned but framed as the last-resort it is.

2. Evidence by addressing question

mechanism

The defining mechanistic finding for PMDD is that it is not a disorder of abnormal hormone levels. Circulating estradiol and progesterone in PMDD sufferers are indistinguishable from those of unaffected controls; what differs is the central nervous system's response to normal cyclical changes Yonkers et al. 2008. The seminal demonstration came from Schmidt and colleagues at NIMH: in a double-blind crossover trial, they used leuprolide to shut down ovarian steroid production in women with prospectively confirmed PMDD and controls. Suppression abolished symptoms. Reintroducing either estradiol or progesterone reproduced symptoms in PMDD women but not in controls Schmidt et al. 1998. A follow-up using continuous stable add-back of ovarian steroids showed symptoms only re-emerged when steroid levels were changed, not when they were held high or low — implicating the cyclical change itself, not the level, as trigger Schmidt et al. 2017.

The leading biological story for that differential sensitivity centres on allopregnanolone (ALLO), a neuroactive metabolite of progesterone that is a positive allosteric modulator of the GABA_A receptor. In unaffected women, rising luteal ALLO is anxiolytic and sedating, much like a low-dose benzodiazepine. In PMDD, the GABA_A receptor appears to respond paradoxically — ALLO produces dysphoria rather than calm — possibly because of altered receptor subunit composition or impaired ability of the receptor to adapt to fluctuating ALLO concentrations Hantsoo & Epperson 2015. The strongest direct validation of the ALLO model is the Bixo et al. trial of sepranolone (UC1010), an isoallopregnanolone that selectively blocks ALLO's action at the GABA_A receptor: blunting ALLO signalling in the luteal phase reduced symptom severity versus placebo Bixo et al. 2017.

A genetic / cellular substrate for the differential response has also been identified. Dubey and colleagues found that lymphoblastoid cells from women with PMDD show altered expression of the ESC/E(Z) complex (a chromatin-regulatory complex), with a different transcriptional response to estradiol and progesterone exposure compared with control cells. This was the first plausible cell-intrinsic marker of the disorder and supports the framing of PMDD as a heritable trait of hormonal sensitivity rather than a hormonal abnormality Dubey et al. 2017. Serotonergic dysregulation is also implicated — SSRIs work within hours-to-days in PMDD versus weeks in major depression, and tryptophan depletion can re-trigger symptoms — pointing to a fast, non-trophic serotonin mechanism distinct from how SSRIs treat depression Pearlstein & Steiner 2008.

evidence

PMDD is one of the better-validated mood disorders. The condition is DSM-5 classified, has FDA-approved treatments, has a Cochrane meta-analysis supporting the first-line pharmacological treatment, and is the subject of formal international consensus guidelines.

The Cochrane review of SSRIs for PMS/PMDD (31 RCTs, n > 4,000) found SSRIs significantly more effective than placebo at reducing both overall premenstrual symptoms and specific symptom clusters, with an odds ratio for symptom improvement of roughly 0.28 (favouring SSRI). Effects were present for both continuous and luteal-phase-only dosing schedules; the two were broadly comparable in efficacy, though continuous dosing edged ahead on some endpoints Marjoribanks et al. 2013. The first major RCT, Steiner et al.'s fluoxetine trial, established the effect: 65% response on 20 mg fluoxetine vs 28% on placebo over six cycles Steiner et al. 1995.

For hormonal management, the Cochrane review of drospirenone-containing combined oral contraceptives (specifically drospirenone 3 mg + ethinylestradiol 20 µg in a 24/4 regimen — marketed as Yaz / Yasminelle) found modest but real improvement in PMDD symptoms versus placebo; the 24/4 regimen reduced symptom-free intervals and so is preferred over older 21/7 cycles Lopez et al. 2012. The FDA approved drospirenone/EE for PMDD in 2006 on the strength of two RCTs. The drospirenone progestin is unusual in being anti-androgenic and anti-mineralocorticoid, mimicking spironolactone — other progestins have generally not shown the same benefit and can worsen mood.

For GnRH agonists (leuprolide, goserelin), Wyatt et al.'s meta-analysis confirmed efficacy for severe PMS / PMDD, with response rates of around 60–75%; add-back hormone therapy modestly reduces benefit but is necessary to mitigate the iatrogenic menopause that long-term GnRH use creates (hot flushes, accelerated bone loss) Wyatt et al. 2004. The ISPMD consensus places GnRH at the fourth treatment tier after SSRIs and combined OCPs Nevatte et al. 2013.

For lifestyle: aerobic exercise has consistent if modest effect-size evidence across multiple small RCTs and one systematic review; the proposed mechanism is endogenous opioid and serotonergic modulation Daley 2009. CBT delivered specifically for PMDD shows medium effect sizes in a systematic review, with benefits persisting after treatment ends (unlike SSRIs, which wane with discontinuation) Lustyk et al. 2009. Calcium carbonate 1,200 mg/day across two cycles reduced premenstrual symptoms by ~48% vs ~30% placebo response in a 466-woman trial Thys-Jacobs et al. 1998; this remains one of the few well-conducted nutrient trials in PMS. Vitex agnus-castus (chasteberry) outperformed placebo in a 170-woman RCT, with 52% vs 24% global improvement Schellenberg 2001. Vitamin B₆ and magnesium evidence is sparser and more contested.

protocol

Standard sequence per ISPMD consensus and ACOG practice Nevatte et al. 2013:

1. Confirm diagnosis prospectively. Two cycles of DRSP tracking, scored against the C-PASS criteria — daily ratings, with symptom intensity confined to luteal phase and remitting by day 4 of menses Endicott et al. 2006 Eisenlohr-Moul et al. 2017. Retrospective recall is unreliable — about 40% of women seeking treatment for "PMDD" don't meet criteria on prospective tracking, and many have an alternative or comorbid condition (MDD, GAD, bipolar II, premenstrual exacerbation of an underlying mood disorder) that masquerades as PMDD.
2. First-line: SSRI. Sertraline 50–150 mg, fluoxetine 20 mg, escitalopram 10–20 mg, paroxetine 12.5–25 mg are all approved or evidence-supported. Either continuous daily dosing or luteal-phase-only dosing (typically from ovulation, around cycle day 14, until menses). Onset of effect is fast — within days, often within the first treated luteal phase — which is why luteal-only dosing is viable. Response rate ~60–70%.
3. Second-line: hormonal suppression. Continuous (skip-the-pill-free-interval) drospirenone/EE combined OCP, or other COCs taken continuously to abolish luteal cycling. Use as monotherapy if SSRI fails, or in combination with an SSRI when partial response.
4. Third-line: GnRH agonist with add-back. Monthly leuprolide injection + low-dose continuous estradiol + progestin add-back to manage iatrogenic menopause. Reserved for severe SSRI-and-OCP-refractory PMDD.
5. Fourth-line (definitive): bilateral oophorectomy ± hysterectomy. Considered only after GnRH has demonstrated benefit (as a "test" of whether ovarian suppression resolves symptoms). Permanent and life-altering — surgical menopause requires HRT in younger patients to preserve bone and cardiovascular health.
6. Adjuncts. Aerobic exercise ~150 min/week, CBT (especially if interpersonal patterns repeat), calcium 1,200 mg/day, sleep hygiene through the luteal phase, alcohol restriction (alcohol's anxiolytic effect via the same GABA_A pathway makes withdrawal worse in PMDD).

contraindications

SSRIs are broadly safe but specific risks need clinical management: bleeding risk when combined with NSAIDs or anticoagulants, hyponatraemia in older patients, sexual dysfunction (a meaningful issue for many PMDD patients given relationship effects already in play), and SSRI discontinuation syndrome with paroxetine particularly. In pregnancy, the risk-benefit calculation shifts — and PMDD typically remits during pregnancy because the cycle stops. Combined OCPs are contraindicated in smokers over 35, those with a history of venous thromboembolism, migraine with aura, and active breast cancer. Drospirenone's mild diuretic action mandates caution in women on potassium-sparing diuretics or with kidney disease. GnRH agonists, especially long-term, accelerate bone loss; current practice requires add-back hormone therapy to mitigate and limits courses without add-back to ~6 months Wyatt et al. 2004.

misconceptions

The single largest misconception is that PMDD is PMS with worse marketing. Up to 80% of menstruating women report some premenstrual symptoms; ~20% meet criteria for PMS; only 3–8% meet prospective criteria for PMDD Halbreich et al. 2003 Hantsoo & Epperson 2015. PMS is defined primarily by somatic discomfort with mild mood changes; PMDD requires functional impairment from severe affective symptoms and is categorised among the depressive disorders, not the gynaecological complaints.

A second is that PMDD is "just hormones" or "a chemical imbalance" — both of which mis-frame the mechanism. PMDD is a heritable trait-level CNS sensitivity to normal cyclic steroid changes. Hormone levels are normal. Treatments work either by re-tuning the CNS response (SSRIs, very fast) or by removing the trigger (ovulation suppression).

A third, with real clinical consequences: PMDD is often confused with bipolar II or borderline personality disorder because of the affective cycling. The differentiator is the menstrual cycle synchrony — PMDD episodes are restricted to the luteal phase and remit within days of menses; bipolar episodes don't track the cycle, and borderline patterns aren't cyclical. Prospective DRSP tracking discriminates reliably Eisenlohr-Moul et al. 2017. Mis-diagnosis matters: mood stabilisers and antipsychotics, prescribed for the wrong diagnosis, can mask but not resolve PMDD and add their own side-effect burden.

Fourth: "natural" remedies for PMS (B₆, evening primrose oil, magnesium) are routinely promoted for PMDD with no clear evidence base for the severe form of the disorder. Calcium has the best supplement evidence; chasteberry has one well-conducted trial; the rest are largely PMS-level interventions with minimal effect on the affective core of PMDD.

audience

PMDD by definition affects only people who menstruate, so the entry's primary audience is premenopausal women. Adolescents are affected but under-diagnosed; the disorder typically becomes recognisable in the early twenties and worsens through the thirties. Perimenopause is the highest-risk life stage — the irregular, large hormone fluctuations of perimenopause can amplify pre-existing PMDD or unmask it in women who were borderline before. After menopause, PMDD resolves (no cycle = no trigger). Partners and family members are a meaningful secondary audience — the relational damage from undiagnosed PMDD is often what brings the disorder to clinical attention.

alternatives

Within the evidence-based menu: the choice between continuous and luteal-phase SSRI dosing, between SSRI and hormonal as first-line, and between OCP and GnRH are the real decision points. There is no rigorous evidence base for naturopathic protocols, "hormone balancing" supplements, or progesterone replacement (often promoted, generally counter-productive because it loads the trigger). Investigational alternatives include sepranolone (ALLO antagonist) and ulipristal-style selective progesterone receptor modulators; neither is yet approved for PMDD.

failure-modes

~30–40% of PMDD patients are partial or non-responders to first-line SSRI Marjoribanks et al. 2013. Common reasons: under-dosing, wrong SSRI for that patient (cross-trial of different SSRIs is reasonable), comorbid MDD or GAD requiring continuous rather than luteal-only dosing, premenstrual exacerbation of an underlying disorder rather than true PMDD (the cyclical worsening is real but won't fully remit between cycles), and missed diagnosis on prospective tracking. Hormonal management fails most commonly when a non-drospirenone progestin is used or when 21/7 cycling preserves luteal-equivalent intervals. GnRH failure is rare when leuprolide has fully suppressed ovarian function and symptoms persist — that pattern points away from a hormonal mechanism and toward a comorbid mood disorder.

practicalities

Diagnosis is the chokepoint. Most primary-care clinicians lack training in PMDD-specific assessment; gynecologists and reproductive psychiatrists are better equipped. Self-tracking with a free DRSP app or paper chart for two cycles is the practical first step — it confirms or refutes the cyclical pattern before any specialist appointment. SSRIs are generic and inexpensive (under $10/month with insurance); drospirenone OCPs run $20–50/month; GnRH agonists run thousands per year. Cost is rarely the barrier; clinician access and diagnostic delay are.

history

Premenstrual symptoms have been described since Hippocrates; modern medicalisation began with Frank's 1931 paper on "premenstrual tension." The DSM-IV included "premenstrual dysphoric disorder" only in an appendix as a "criteria set provided for further study" (1994), and DSM-5 moved it into the depressive disorders chapter in 2013 — a contested decision opposed by some advocacy groups concerned about pathologising normal women's experience and by some researchers concerned about the medicalisation of female biology. Counter-arguments emphasised the severity of the disorder, the elevated suicide risk, and the existence of effective treatments unavailable to patients without a billable diagnosis.

stakes

Untreated PMDD compounds across years. The lifetime suicidality data is striking: a meta-analysis covering 13 studies and roughly 9,500 women found PMDD was associated with substantially elevated odds of suicidal ideation (OR ~4.0), suicide planning (OR ~4.1), and suicide attempts (OR ~4.0) Yan et al. 2021. A large global sample of 599 prospectively confirmed PMDD patients reported lifetime self-injurious thoughts in 72% and lifetime attempts in 34% — multiples of the general-population rate Eisenlohr-Moul et al. 2022. Crucially, this risk is concentrated in the luteal phase: the symptomatic week is when the danger is real.

Beyond suicidality, untreated PMDD imposes a substantial functional and economic burden. Work absenteeism, presenteeism, and impaired social and family functioning during luteal weeks translate into a quality-of-life decrement comparable to major depressive disorder; aggregated across cycles a patient with untreated PMDD spends roughly a quarter of her reproductive years in significant symptomatic distress Halbreich et al. 2003 Hantsoo & Epperson 2015. Relationships — partners, children, close colleagues — bear the social cost; relationship dissolution is over-represented in PMDD samples versus controls.

payoff

Treatment changes the trajectory fast. Within the first treated luteal phase on an effective SSRI dose, the majority of responders see meaningful symptom reduction Marjoribanks et al. 2013 — onset of action is days, not the 4–6 weeks of SSRI treatment for depression. Hormonal suppression takes longer (the first few cycles of OCP can be wash-out months) but stabilises within 3–6 cycles. CBT effects are slower to onset (weeks) but persist after treatment ends Lustyk et al. 2009. The combined picture: a diagnosed and adequately treated PMDD patient typically reports she has half her month back within a few menstrual cycles.

out-of-scope

Premenstrual exacerbation of an underlying mood disorder (PME) — distinct from PMDD, more common, with different treatment. Perimenopausal depression — overlapping mechanism (steroid-fluctuation sensitivity) but a different life-stage syndrome. Postpartum depression — same hormonal-sensitivity framing but its own trigger (parturition) and its own treatment paradigm (brexanolone, zuranolone). Menstrual migraine — same trigger (oestrogen withdrawal), different organ. PMS without the affective severity — addressed in mainstream gynecology rather than reproductive psychiatry.

3. The credibility range

The optimist case

PMDD is one of the cleanest cases in psychiatry. The Schmidt NIMH experiments effectively replicated Koch's postulates for hormonal triggering: remove the trigger, symptoms vanish; restore the trigger, symptoms return; do so in controls and nothing happens Schmidt et al. 1998 Schmidt et al. 2017. A specific neurosteroid mechanism (ALLO at GABA_A) has experimental support including the sepranolone trial that selectively blocked ALLO and reduced symptoms Bixo et al. 2017. A cellular substrate (ESC/E(Z) complex differential expression) provides a heritability anchor Dubey et al. 2017. The first-line treatment has Cochrane-level evidence over 30+ RCTs Marjoribanks et al. 2013. The second-line treatment is FDA-approved Lopez et al. 2012. The disorder has formal diagnostic criteria with a validated prospective assessment instrument Eisenlohr-Moul et al. 2017. International consensus guidelines exist Nevatte et al. 2013. The optimist position is: this is a real, severe, treatable, biologically-understood disorder, and the public-health task is closing the diagnostic-delay gap, not litigating the diagnosis.

The skeptic case

Three skeptic threads worth taking seriously. First, the prevalence is contested. Retrospective recall and self-reported PMDD inflate prevalence to ~20%; prospective DRSP confirmation collapses it to 3–8% Hantsoo & Epperson 2015. A large fraction of women diagnosed in routine practice — without prospective tracking — don't meet C-PASS criteria. Some skeptics argue this means the diagnosis is over-applied, treatments are over-prescribed, and what's actually being treated is heterogeneous (PMS, PME, MDD with cyclical fluctuation, normal variation). Second, the DSM-5 inclusion was politically contested and remains so among some scholars who frame medicalisation of cyclical female mood as a category error. Third, the mechanism story, while strong, is incomplete: only ~60–70% respond to first-line SSRI and the residual ~30% point at heterogeneity the ALLO-GABA_A story doesn't fully explain. Sepranolone reduced symptoms but didn't abolish them Bixo et al. 2017. Genetic markers are early-stage Dubey et al. 2017.

The author's call

PMDD as a diagnostic entity is real, well-evidenced, and severely under-treated relative to its burden. Prospective DRSP confirmation matters — both for the patient (separating PMDD from PME and MDD changes treatment) and for the diagnostic stability of the literature — and is the appropriate response to the prevalence-inflation concern, not abandoning the diagnosis. Treatment evidence is robust enough to recommend the standard sequence (SSRI → drospirenone COC → GnRH) with confidence. Mechanism is sufficiently understood to explain clinical patterns and treatment response, even if the picture has unfilled corners. The entry lands firmly toward the optimist pole — recognition + adequate treatment + correct diagnosis — while keeping the diagnostic-rigour requirement front and centre.

4. Stakeholder + incentive map

• Pushing for recognition: reproductive psychiatry as a subspecialty, the International Society for Premenstrual Disorders (ISPMD), the International Association for Premenstrual Disorders (IAPMD, the patient-advocacy organisation), patient communities (notably the r/PMDD subreddit, ~100k members, often the first site of self-recognition).
• Pushing back: feminist-critique scholarship concerned with medicalisation of female biology, some primary-care clinicians who frame PMDD as a fashionable PMS-rebrand and resist the diagnosis, payer pressure to use cheaper first-line generic treatments without prospective workup.
• Commercial: Bayer holds drospirenone/EE; the brand-name OCP market is significant but generics now dominate. SSRI generics are commodity. Asarina Pharma (sepranolone) is the major investigational stakeholder in novel mechanism-targeted therapy.
• Cultural / community: the wellness / "hormone balancing" / functional-medicine community frames PMDD as treatable with cycle-syncing nutrition and progesterone replacement; the mainstream-medicine community treats with SSRIs and ovulation suppression. These camps disagree visibly online.

5. Population variability

• Age: onset typically late teens through twenties, worsening through thirties, severe peak in late thirties / perimenopause, full remission after menopause.
• Hormonal life stage: pregnancy and lactational amenorrhea typically remit PMDD (no cycle). Perimenopause is the worst-risk phase due to large, irregular hormone fluctuations. Continuous combined OCP, GnRH agonist, or — definitively — surgical menopause abolish the cycle and the disorder.
• Comorbidity: substantial overlap with MDD, GAD, PTSD, and ADHD. Lifetime MDD rates in PMDD populations are 50–78% Hantsoo & Epperson 2015. ADHD comorbidity is increasingly recognised — premenstrual oestrogen drop worsens executive function broadly and may interact with ADHD symptoms.
• Genetics: heritability estimates from twin studies are ~40–50% for premenstrual mood symptoms; the ESC/E(Z) finding hints at a chromatin-level substrate Dubey et al. 2017.
• Trauma history: childhood adversity is over-represented in PMDD samples; whether causal or correlated with detection / comorbidity is unsettled.
• Race / ethnicity: the literature is largely Western and white-dominated; cross-cultural prevalence comparisons are unreliable due to differing recognition and reporting norms.

6. Knowledge gaps

Mechanism: the ALLO-GABA_A story is the dominant frame but accounts for perhaps 60–70% of the variance in response; the rest implicates serotonergic, HPA-axis, and inflammatory pathways with weaker evidence. Why some women develop ALLO-paradoxical responses while others don't is not understood at the level of which GABA_A subunits or which receptor-trafficking machinery is involved.

Diagnostic refinement: the C-PASS criteria are validated but cumbersome; better, briefer prospective instruments would reduce the diagnostic gap. Differential diagnosis from PME (premenstrual exacerbation of an underlying mood disorder) is unsolved at the population level — clinical practice still often conflates them.

Treatment for non-responders: ~30% of patients fail or partial-respond to first-line; this group is under-studied. Novel mechanism-targeted agents (sepranolone and other ALLO antagonists, selective progesterone receptor modulators) are in early development. Whether luteal-phase SSRIs cause subclinical discontinuation symptoms each cycle is debated.

Adolescent PMDD: the disorder presents in adolescence and the diagnostic instruments are validated in adults; under-recognition in this group is likely substantial. SSRI use in adolescents carries the standard black-box considerations.

What would change the author's call: a well-powered RCT of prospective-DRSP-confirmed PMDD versus self-reported PMDD on standard treatment showing markedly different response rates would tighten the prevalence and treatment-rate estimates. A negative replication of the Schmidt hormone-add-back work would force a mechanism rethink (unlikely given the design).

Scope coverage vs. brief. The brief named mood, functioning, relationships, suicidality, SSRIs, hormonal management, and lifestyle. All covered end-to-end: mood & functioning anchor the mechanism / stakes / payoff arc; suicidality is the lead in stakes (with Yan 2021 meta-analysis and Eisenlohr-Moul 2022 confirmed-sample data); relationships are surfaced in stakes and payoff via the social-mirror voice; SSRIs are first-line in evidence + protocol + alternatives; hormonal management gets the drospirenone treatment and the GnRH escalation; lifestyle (exercise, CBT, calcium, alcohol, chasteberry) lives in protocol with the action callout. No silent narrowing.

Rating difficulties.

• evidence: 4 vs 5. Cochrane meta-analysis, FDA-approved hormonal treatment, DSM-5 classification, ISPMD consensus, and NIMH mechanism crossover trials would justify 5. Held at 4 because ~30% non-response to first-line SSRI is real, the mechanism story (ALLO/GABA paradoxical response) has unfilled corners, and the prevalence question (retrospective vs prospective) is still litigated.
• longevity: 2. Hard call. PMDD-elevated suicidality is large at the individual level (Yan 2021 OR ~4 for attempts; Eisenlohr-Moul 2022 lifetime attempt 34%) but the population-level mortality impact is modest. Treatment lowers an elevated baseline. Landed on 2 — small additive — rather than 3, because the dominant treatment payoff is functional, not mortality-bending.
• energy / focus: both 3. Both are explicit DSM-5 symptoms; treatment restores function across ~half the cycle for the lifespan of the reproductive years. Not 4 because the deficit is cyclical, not chronic, so the daily-vitality-difference framing of 4 doesn't quite fit.
• sleep: 2. Hypersomnia / insomnia is a DSM-5 symptom but is downstream of mood; treatment resolves it but it's not the dominant axis.

Hard scoping calls.

• Kept the sepranolone reference brief — investigational, not approved, but mechanism-validating and worth signposting in the alternatives section.
• Did not fold premenstrual exacerbation (PME) into the entry — it is a distinct condition with different treatment and warrants its own entry (flagged below). Mentioned in misconceptions and failure-modes only where the differential diagnosis matters for treatment selection.
• Did not separately cover surgical management (bilateral oophorectomy ± hysterectomy) past one mention in the evidence section — it is the genuine last-resort and a deep treatment of it would unbalance the article.
• Did not enumerate the full DSM-5 criteria with numerical thresholds verbatim — the symptom list is in the mechanism section with the "five-of-eleven, one-of-four-core, functional impairment" gloss. Full criteria are clinician material, not reader material.

Future-link candidates. When these exist they should cross-link:

• ssris or antidepressants-overview — for the general medication-class explainer.
• hormonal-contraception or combined-oral-contraceptives — for the drospirenone discussion.
• perimenopause — strong cross-link because perimenopausal PMDD is a different management problem.
• postpartum-depression — same neurosteroid biology; brexanolone / zuranolone treatments target the ALLO pathway.
• cbt — for the CBT-for-PMDD reference.
• menstrual-cycle — basic cycle physiology, prerequisite background.

Separate-entry candidates.

• Premenstrual exacerbation (PME) — distinct enough condition, common confusion with PMDD, deserves its own entry.
• Perimenopausal depression — overlapping mechanism (steroid-fluctuation sensitivity), different life-stage syndrome, different treatment paradigm including HRT.
• Bilateral oophorectomy for severe PMDD — surgical last-resort, probably belongs as a sub-entry under a broader surgical-menopause topic rather than expanded here.
• DRSP / cycle-tracking for diagnosis — the prospective-tracking step is a discrete skill / tool, may warrant a how-to entry of its own.

Other notes. Action is decide rather than do because prescription treatment and diagnostic confirmation require clinician input — the reader's task is choosing a path with their clinician, not adopting a habit. Cadence is daily because both standard treatment patterns (continuous SSRI, drospirenone OCP) are daily; luteal-only SSRI exists but is the minority pattern. Contraindications field left empty: the entry as a whole is not unsafe in any of the closed-vocabulary states. Treatment-specific contraindications (pregnancy / breastfeeding for SSRIs, smokers over 35 for COCs, etc.) are handled in the article's contraindications section with a warning callout, which is the right place for them.