Premenstrual dysphoric disorder is the severe, functionally impairing end of the premenstrual symptom spectrum, distinguished from premenstrual syndrome by its mood-symptom dominance and from major depressive disorder by its strict luteal-phase confinement. DSM-5-TR placed PMDD among the depressive disorders in 2013, reflecting evidence that affective symptoms — irritability, mood lability, depressed mood, anxiety — drive the disability rather than the somatic complaints that dominate PMS. Diagnosis is prospective: two consecutive cycles of daily symptom charting are required, because retrospective recall over-diagnoses PMDD by roughly two-fold. The pathophysiology is best understood as an abnormal central nervous system response to normal ovarian-steroid fluctuation, not a hormonal abnormality, with allopregnanolone and the serotonin system as the leading mechanistic candidates. SSRIs are first-line and uniquely effective within days when dosed in the luteal phase, in contrast to their delayed onset in MDD. The bottom line: chart prospectively, treat with serotonergic agents or ovulation suppression, and do not mistake premenstrual exacerbation of an underlying mood disorder for PMDD.

PMDD is common but frequently underdiagnosed, with most affected patients carrying symptoms for years before clinical recognition. The disorder clusters with other affective and anxiety conditions and carries substantial functional impact across work, relationships, and reproductive decision-making.

Prevalence and demographics

• Twelve-month prevalence of PMDD among menstruating individuals is estimated at 1.8 to 5.8 percent when strict prospective criteria are applied, with much higher rates (up to 20 percent) when retrospective self-report is used. ^1-2
• Premenstrual symptoms severe enough to meet criteria for premenstrual syndrome (Premenstrual syndrome) affect roughly 20 to 30 percent of menstruating individuals; PMDD represents the severe minority of this spectrum. ^1,3
• Onset is typically in the mid-to-late 20s, although symptoms often begin in adolescence; the disorder persists until menopause unless ovulation is suppressed. ^1,4
• Cross-cultural prevalence is broadly similar across high- and low-income countries, arguing against a purely cultural construct, although symptom expression and help-seeking vary. ²

Comorbidity

• Lifetime comorbidity with major depressive disorder is approximately 50 to 70 percent, and with any anxiety disorder roughly 40 to 60 percent. ^1,4
• Postpartum depression and perimenopausal depression are both more common in patients with a PMDD history, consistent with reproductive-hormone sensitivity as a shared trait. ⁴
• Suicidal ideation, suicide attempts, and completed suicide are elevated in PMDD; premenstrual worsening of suicidal ideation is well documented and clinically meaningful. ^1,5
• Bipolar disorder, eating disorders, and post-traumatic stress disorder show modestly elevated comorbidity rates. ^1,4

Risk factors

• Personal or family history of a mood or anxiety disorder is the strongest replicated risk factor. ^1,4
• Childhood trauma and adverse life events are associated with PMDD across multiple cohorts. ^4,6
• Cigarette smoking and high body mass index show modest associations in epidemiologic studies. ^2,4
• Twin studies estimate heritability of premenstrual symptoms at roughly 30 to 50 percent. ^4,7

PMDD is not driven by abnormal hormone levels; affected patients have ovulation, estradiol, and progesterone profiles indistinguishable from controls. The disorder is best framed as a heritable central sensitivity to normal cyclic ovarian-steroid changes, expressed through serotonergic and GABAergic systems.

Hormonal trigger, central response

• Suppression of ovulation with GnRH agonists abolishes PMDD symptoms, and add-back estradiol or progesterone reproduces them in PMDD patients but not in controls — the cleanest evidence that the trigger is normal ovarian-steroid fluctuation acting on a sensitized brain. ^8-9
• Circulating levels of estradiol, progesterone, and gonadotropins do not differ between PMDD patients and controls. ^4,8

Allopregnanolone and the GABA-A receptor

• Allopregnanolone, a neurosteroid metabolite of progesterone, is a potent positive allosteric modulator of GABA-A receptors and rises in the luteal phase. ^10-11
• PMDD patients show altered GABA-A receptor sensitivity to allopregnanolone, with paradoxical anxiogenic rather than anxiolytic responses in some experimental paradigms. ^10-11
• This mechanism underpins the therapeutic rationale for agents that block allopregnanolone synthesis or modulate GABA-A receptor subunit composition. ¹⁰

Serotonergic system

• Tryptophan depletion worsens premenstrual symptoms in PMDD patients, and serotonergic agents are uniquely and rapidly effective, supporting a serotonergic vulnerability model. ¹²
• The rapid onset of SSRI benefit in PMDD (within 1 to 2 days) is mechanistically distinct from the 2- to 6-week onset in MDD and may reflect direct effects on neurosteroid synthesis rather than monoamine reuptake inhibition. ¹³

Genetics and neuroimaging

• Variants in the estrogen receptor alpha gene (ESR1) have been associated with PMDD in candidate-gene studies. ^4,7
• Functional imaging shows altered amygdala reactivity and prefrontal regulation across the menstrual cycle in PMDD patients compared with controls. ^4,14

DSM-5-TR places PMDD in the depressive disorders chapter and requires symptoms in the final week before menses, improving within a few days of menses onset and minimal or absent in the week postmenses, confirmed prospectively across two consecutive symptomatic cycles. The criteria emphasize affective symptoms over somatic ones and require functional impairment.

DSM-5-TR criteria, summarized

• Criterion A: in most menstrual cycles during the past year, at least five symptoms are present in the final premenstrual week, improve within a few days of menses, and become minimal or absent in the week postmenses. ¹⁵
• Criterion B: at least one of the following must be present — marked affective lability, marked irritability or anger or increased interpersonal conflicts, marked depressed mood or hopelessness or self-deprecating thoughts, marked anxiety or tension or feeling on edge. ¹⁵
• Criterion C: at least one of the following must additionally be present, to reach a total of five symptoms with B and C combined — decreased interest in usual activities, subjective difficulty concentrating, lethargy or marked low energy, marked change in appetite or food cravings, hypersomnia or insomnia, sense of being overwhelmed or out of control, physical symptoms such as breast tenderness, joint or muscle pain, bloating, or weight gain. ¹⁵
• Criterion D: the symptoms cause clinically significant distress or interference with work, school, social activities, or relationships. ¹⁵
• Criterion E: the disturbance is not merely an exacerbation of another disorder such as MDD, panic disorder, persistent depressive disorder, or a personality disorder, although it may co-occur with these. ¹⁵
• Criterion F: criterion A should be confirmed by prospective daily ratings during at least two symptomatic cycles; provisional diagnosis is permitted before this confirmation. ¹⁵
• Criterion G: the symptoms are not attributable to a substance or another medical condition such as hyperthyroidism. ¹⁵

ICD-11 placement

• ICD-11 lists premenstrual dysphoric disorder under chapter 16, diseases of the genitourinary system (GA34.41), with a cross-listing in mental and behavioural disorders, reflecting its dual identity. ¹⁶
• ICD-11 criteria align broadly with DSM-5-TR but do not require five symptoms or two cycles of prospective charting in the same explicit way; the practical threshold is similar. ¹⁶

Specifiers and provisional diagnosis

• DSM-5-TR allows a provisional diagnosis when criteria are met retrospectively but the two-cycle prospective confirmation has not yet been completed. ¹⁵
• There are no severity specifiers, but symptom intensity is captured by validated daily-rating instruments. ¹⁵

The hallmark is a predictable, severe affective shift in the late luteal phase that resolves with menses, leaving the patient functionally well for the follicular two weeks. Patients often describe two versions of themselves and an exhausting cycle of damage repair after each episode.

Core affective cluster

• Irritability and interpersonal conflict are the most commonly reported and most disabling symptoms, often exceeding depressed mood in clinical severity. ^1,4
• Affective lability — rapid shifts between tearfulness, anger, and anxiety within hours — is highly characteristic. ^1,15
• Anxiety, tension, and a sense of being overwhelmed are present in the majority and may be misdiagnosed as a primary anxiety disorder. ^1,4
• Depressed mood, hopelessness, and self-critical rumination are common; suicidal ideation is more frequent than in PMS and warrants explicit assessment. ^1,5

Cognitive and somatic features

• Difficulty concentrating, anhedonia (Anhedonia), and fatigue mimic an MDD episode but resolve within days of menses. ^1,15
• Hyperphagia with carbohydrate craving, hypersomnia or insomnia, and a sense of physical heaviness are typical. ^1,15
• Breast tenderness, bloating, headache, and joint or muscle pain are nearly universal but are not the primary disability driver. ^1,15

Course over the cycle

• Symptoms emerge in the late luteal phase, typically 5 to 10 days before menses, with peak severity in the final 2 to 3 days. ^1,15
• Resolution occurs within 2 to 3 days of menses onset; the follicular phase is symptom-free or near-symptom-free. ^1,15
• Symptom expression is stable across cycles within an individual but varies between individuals. ^1,4

Atypical and red-flag presentations

• Symptoms that worsen rather than resolve with menses, persist throughout the cycle, or fail to remit in the follicular week argue against PMDD and toward a primary mood, anxiety, or personality disorder with cyclical exacerbation. ^15,17
• Onset of new severe premenstrual symptoms in perimenopause may reflect emerging perimenopausal depression rather than PMDD. ^4,17
• Premenstrual exacerbation of suicidal ideation, self-harm, or psychotic symptoms requires urgent safety assessment. ^1,5

The single highest-yield distinction is PMDD versus premenstrual exacerbation of another psychiatric disorder; getting this wrong means treating the wrong illness. Prospective daily charting across two cycles is the diagnostic gold standard and resolves most ambiguity.

Premenstrual syndrome (PMS)

• PMS lacks the affective severity and functional impairment of PMDD; somatic symptoms (bloating, breast tenderness, fatigue) dominate. ^1,3
• PMS does not require five symptoms or one of the four core affective B-criterion symptoms. ^3,15

Major depressive disorder with premenstrual exacerbation

• A substantial minority of patients with MDD experience worsening in the luteal phase but remain symptomatic in the follicular phase, which excludes PMDD by criterion A. ^15,17
• Prospective charting reveals baseline depression with luteal worsening rather than the symptom-free follicular interval that defines PMDD. ^15,17

Bipolar disorder

• Rapid cycling and ultradian mood instability can be confused with PMDD; the absence of cycle-locked symptom resolution and the presence of hypomanic or manic episodes distinguish bipolar disorder. ^4,17
• PMDD and bipolar II disorder may co-occur and require parallel treatment of both. ⁴

Anxiety disorders

• Generalized anxiety disorder, panic disorder, and PTSD can show premenstrual exacerbation; the persistence of baseline symptoms in the follicular phase distinguishes them from PMDD. ^4,17

Borderline personality disorder

• Affective lability, interpersonal conflict, and self-harm in BPD are not cycle-locked, although premenstrual exacerbation of BPD symptoms is common. ^4,17
• Daily charting is essential when both diagnoses are entertained. ¹⁷

Medical mimics and substance-induced presentations

• Hypothyroidism, perimenopausal hormonal fluctuation, anemia, and chronic fatigue should be screened for when symptoms are atypical. ^1,4
• Hormonal contraceptives can both improve and worsen mood; a careful temporal history is needed. ⁴
• Alcohol and stimulant use disorders cause cyclical mood disturbance independent of menses and require separate assessment. ⁴

Assessment is anchored on prospective daily symptom charting; the rest of the workup serves to exclude mimics and characterize comorbidity. Validated rating scales standardize what the patient is already tracking.

Interview approach

• Establish symptom timing relative to menses across at least three recent cycles in the history. ^1,15
• Probe for symptom-free intervals in the follicular phase; their absence is a stronger negative indicator than any positive symptom is a positive one. ^15,17
• Assess functional impact at work, in primary relationships, and on parenting; patients commonly minimize disability they have normalized. ^1,17
• Screen for suicidal ideation in the luteal phase specifically, not as a generic past-month item. ^1,5

Prospective charting instruments

• The Daily Record of Severity of Problems (DRSP) is the most widely used and validated daily-rating instrument and operationalizes DSM-5-TR criteria across two cycles. ¹⁸
• The Calendar of Premenstrual Experiences (COPE) and the Premenstrual Symptoms Screening Tool (PSST) are alternatives, with the PSST useful as a screening rather than diagnostic instrument. ^19-20

History elements not to omit

• Reproductive history including parity, contraception, recent pregnancy or postpartum status, and breastfeeding. ^1,4
• Past mood, anxiety, postpartum, and perimenopausal episodes. ^1,4
• Trauma history, including intimate-partner violence, which both contributes to and is worsened by premenstrual symptom flares. ^4,6
• Substance use, including alcohol patterns that may be cycle-linked. ⁴

Physical examination and laboratory workup

• Targeted physical exam to screen for thyroid disease and anemia is reasonable in atypical presentations. ^1,4
• TSH should be checked when fatigue or depressed mood dominates or when symptoms are atypical. ^1,4
• Routine hormonal assays (estradiol, progesterone, FSH, LH) are not indicated for PMDD diagnosis and do not differ from controls. ^4,8

Treatment selection is shaped by symptom severity, fertility plans, contraceptive needs, and comorbidities. SSRIs and ovulation suppression are the two evidence-supported first-line options, with cognitive behavioral therapy as an adjunct or alternative for patients who decline pharmacotherapy.

Pharmacotherapy

• SSRIs are first-line and supported by strong evidence across multiple RCTs and meta-analyses; sertraline, fluoxetine, paroxetine, citalopram, and escitalopram have all shown efficacy. ²¹
• Three SSRI dosing strategies are evidence-supported, with comparable efficacy in head-to-head and meta-analytic comparisons. ²¹
  • Continuous daily dosing across the cycle, which suits patients with comorbid MDD or anxiety. ²¹
  • Luteal-phase dosing from ovulation (approximately cycle day 14) until menses onset, which reduces cumulative exposure and adverse effects. ²¹
  • Symptom-onset dosing initiated at the first premenstrual symptom and continued until menses, which suits patients with predictable, stereotyped onset. ²¹
• Typical effective doses: sertraline 50 to 150 mg/day, fluoxetine 20 mg/day, paroxetine 10 to 25 mg/day or paroxetine CR 12.5 to 25 mg/day, citalopram 20 to 40 mg/day, escitalopram 10 to 20 mg/day. ²¹
• Onset of benefit in PMDD is rapid (within 1 to 2 days of dosing), in contrast to the 2- to 6-week onset in MDD, allowing intermittent dosing strategies. ¹³
• SNRIs (venlafaxine) have RCT support and are a reasonable second-line serotonergic option. ²²
• Tricyclic antidepressants and bupropion lack evidence and are not recommended. ²¹

Ovulation suppression

• Combined oral contraceptives containing drospirenone with a 24/4 regimen (drospirenone 3 mg / ethinyl estradiol 20 mcg, 24 active days followed by 4 hormone-free days) are FDA-approved for PMDD and reduce symptoms in the majority of patients. ²³
• Other combined oral contraceptives have inconsistent or negative trial evidence and are not first-line for PMDD specifically. ²³
• GnRH agonists (leuprolide, goserelin) achieve symptom remission by inducing medical menopause; their use is limited by hot flashes, bone loss, and cost, and they require add-back estrogen and progesterone for use beyond 6 months. ^8-9
• Bilateral salpingo-oophorectomy is a definitive option reserved for severe, treatment-resistant PMDD after a confirmed therapeutic response to GnRH-induced ovarian suppression. ²⁴

Psychotherapy

• Cognitive behavioral therapy adapted for PMDD shows moderate evidence of benefit on mood symptoms and functional impairment, with effects smaller than SSRIs but durable. ²⁵
• CBT is a reasonable first-line option for patients who decline pharmacotherapy or who have mild-to-moderate symptoms. ²⁵
• Mindfulness-based interventions have low-quality but suggestive evidence. ²⁵

Neuromodulation

• Neuromodulation is not standard of care for PMDD; preliminary work on transcranial magnetic stimulation exists but does not support routine use. ²¹

Adjunctive and complementary

• Calcium 1200 mg/day shows modest benefit in some trials and is reasonable as a low-risk adjunct. ²⁶
• Vitamin B6 at doses up to 100 mg/day has weak supportive evidence; higher doses risk peripheral neuropathy. ²⁶
• Chasteberry (Vitex agnus-castus) has limited but positive RCT data of moderate quality. ²⁷
• Aerobic exercise, sleep regularization, and reduction of caffeine and alcohol have low-quality but consistent supportive evidence and minimal harm. ²⁶
• Spironolactone reduces somatic symptoms (bloating, breast tenderness) but does not reliably address the affective core. ²⁸

Treatment-resistant PMDD

• Confirm the diagnosis by reviewing prospective charts and excluding premenstrual exacerbation of MDD or another disorder. ¹⁷
• Trial a different SSRI dosing strategy or a different SSRI before declaring resistance. ²¹
• Combine an SSRI with a drospirenone-containing combined oral contraceptive in patients who tolerate both. ^21,23
• GnRH agonist with add-back hormone therapy is the next step in confirmed treatment-resistant disease. ^8-9

Most patients tolerate SSRIs and ovulation-suppression strategies well, but the evidence base has limitations the prescriber should be candid about. Treatment effects are real but partial; complete remission is the exception, not the rule.

Adverse-effect profile of first-line agents

• SSRI adverse effects in PMDD include nausea, headache, insomnia, fatigue, and sexual dysfunction; rates broadly mirror those in MDD trials. ²¹
• Sexual dysfunction is common and may be especially burdensome given the cyclic dosing context. ²¹
• Discontinuation syndrome with paroxetine and venlafaxine can complicate intermittent dosing; sertraline and fluoxetine are easier to start and stop. ²⁹
• Drospirenone-containing combined oral contraceptives carry a small but real increased venous thromboembolism risk relative to levonorgestrel-containing pills, and a hyperkalemia risk in patients on potassium-sparing medications or with renal impairment. ^23-24

Serious or rare harms

• Suicidal ideation can emerge or worsen with antidepressant initiation, particularly in patients younger than 25; the FDA black-box warning applies to PMDD prescribing. ²⁹
• GnRH agonists cause hot flashes, mood changes, vaginal dryness, and bone mineral density loss; these limit duration of use and mandate add-back hormone therapy beyond 6 months. ^8-9
• Surgical menopause from oophorectomy is irreversible and requires lifelong consideration of hormone replacement and cardiovascular and bone-health monitoring. ²⁴

Monitoring and discontinuation

• Patients on intermittent SSRI dosing should be counseled about onset and offset patterns and the possibility of mild discontinuation symptoms with shorter-half-life agents. ²¹
• Patients on drospirenone-containing pills should be screened for VTE risk factors and counseled on warning signs. ^23-24
• Annual reassessment of treatment necessity is reasonable, as remission rates fall and side-effect burden rises with prolonged use. ²¹

Limitations of the evidence base

• Most PMDD trials are short (2 to 6 cycles), industry-funded, and enriched with patients meeting the strictest research criteria, limiting generalizability. ²¹
• Long-term efficacy data beyond 12 months are sparse for all interventions. ²¹
• Trials underrepresent adolescents, perimenopausal patients, racial and ethnic minorities, and patients with significant psychiatric comorbidity. ²¹
• Head-to-head trials between SSRIs and ovulation suppression are few; choice is often guided by reproductive plans rather than comparative efficacy data. ^21,23

Reproductive context — adolescence, pregnancy, lactation, perimenopause — shapes both the differential and the treatment plan. The disorder begins and ends with the reproductive years.

Adolescents

• PMDD can begin shortly after menarche; diagnosis requires the same prospective charting standard as in adults. ^4,15
• SSRIs in adolescents carry the FDA black-box warning for suicidality; fluoxetine and escitalopram have the strongest pediatric evidence base, though not specifically in PMDD. ²⁹
• Combined oral contraceptives are appropriate after menarche when contraceptive needs and bone-health considerations are addressed. ²³

Pregnancy and the postpartum period

• PMDD symptoms remit during pregnancy because ovulation is suppressed; this is diagnostically informative. ⁴
• Patients with PMDD are at elevated risk for postpartum depression and require enhanced perinatal screening. ⁴
• Lactation does not reliably suppress symptoms once menses returns; breastfeeding-compatible SSRIs (sertraline) are preferred when treatment is needed. ²²

Perimenopause

• Symptoms often worsen in the perimenopause as ovarian-steroid fluctuation becomes more erratic, then resolve at menopause. ^4,17
• New-onset severe premenstrual symptoms in a patient older than 40 should prompt consideration of perimenopausal depression rather than late-onset PMDD. ^4,17

Comorbid medical illness

• Patients with a history of VTE, migraine with aura, or smoking after age 35 should not receive estrogen-containing contraceptives; SSRIs and progestin-only options should be considered. ^23-24
• Patients with renal impairment or on potassium-sparing medications require caution with drospirenone-containing pills. ^23-24

Cultural considerations

• Symptom expression and help-seeking vary across cultures; somatic presentations may dominate in some settings, and the concept of cyclical mood disorder is unfamiliar in many primary care contexts. ^2,4
• Stigma around menstruation can delay presentation; explicit normalization of cyclical symptom inquiry is useful. ²

PMDD is a chronic condition of the reproductive years, but treatment outcomes are good when the diagnosis is correct and the regimen is matched to the patient's reproductive plans. The natural history is full resolution at menopause.

Natural history

• Untreated PMDD is generally chronic and persistent across the reproductive years, with cycle-to-cycle stability but symptom severity that may worsen over decades. ^4,15
• Spontaneous remission outside of pregnancy or menopause is uncommon. ⁴
• Symptoms cease at menopause; persistence of symptoms beyond menopause should prompt diagnostic reconsideration. ^4,17

Response and remission

• SSRI response rates are approximately 60 to 70 percent in pooled trial data; remission rates are lower, in the range of 30 to 50 percent. ²¹
• Drospirenone/ethinyl estradiol 24/4 produces clinically meaningful improvement in approximately half of patients in placebo-controlled trials. ²³
• GnRH agonist response approaches 80 percent in patients who tolerate the medical menopause it produces. ^8-9

Functional outcome and mortality

• PMDD is associated with elevated suicidal ideation, suicide attempts, and completed suicide, particularly during the luteal phase. ^1,5
• Functional impairment is comparable to that of major depressive disorder when measured across the cycle. ¹
• Occupational and relational consequences (job loss, divorce) are documented in long-term observational data. ⁴

The dangerous moment in PMDD is the late luteal phase. Safety planning should be cycle-anchored, not generic.

Suicide risk

• Premenstrual worsening of suicidal ideation and attempts is well documented; women with PMDD are over-represented in luteal-phase suicide attempts compared with the follicular phase. ^1,5
• A cycle-specific safety plan — identifying the high-risk window, removing means, arranging support — is more useful than a generic plan. ⁵

Hospitalization

• Inpatient admission is rarely necessary for PMDD itself but may be required for comorbid major depressive episodes, severe substance-use exacerbation, or imminent suicide risk during the luteal phase. ^1,5

Acute symptom management

• For patients with predictable severe luteal-phase episodes, an as-needed luteal SSRI initiated at symptom onset can shorten the high-risk window. ²¹
• Short-course benzodiazepines (alprazolam) have evidence for premenstrual anxiety but carry dependence risk and should not be a first-line strategy. ³⁰

PMDD has been a contested diagnostic category since its introduction. The clinical reality of severe cyclic affective dysregulation is well documented; the framing of that reality remains debated.

Diagnostic legitimacy

• Critics have argued that PMDD pathologizes normal premenstrual experience and may reinforce gendered stereotypes; proponents counter that prospective charting identifies a distinct severe subset with measurable disability and biologic correlates. ³¹
• DSM-5-TR placement among depressive disorders (rather than in an appendix as in DSM-IV) reflects the maturation of the evidence base but remains contested in some feminist and sociologic literature. ³¹

Allopregnanolone-targeted therapeutics

• Sepranolone, a selective allopregnanolone modulator, has shown promising phase II data for PMDD but is not yet approved; ulipristal acetate, a selective progesterone-receptor modulator, has shown signal in small trials. ³²
• Brexanolone and zuranolone, approved for postpartum depression, have not been studied adequately in PMDD. ¹¹

Optimal SSRI dosing strategy

• Continuous, luteal-phase, and symptom-onset dosing all show efficacy, but head-to-head data on long-term tolerability and patient preference are limited. ²¹
• Whether intermittent dosing reduces sexual side effects to a clinically meaningful degree is unsettled. ²¹

Role of cognitive behavioral therapy

• The effect size of CBT for PMDD is smaller than for SSRIs, but the durability after treatment ends may be greater; how to position CBT relative to pharmacotherapy in stepped care is not standardized. ²⁵

Premenstrual exacerbation versus PMDD

• The boundary between PMDD and premenstrual exacerbation of MDD or anxiety remains a clinical judgment call when prospective charts show partial follicular remission rather than full resolution. ^15,17

• DSM-5-TR places PMDD in the depressive disorders chapter, not the anxiety disorders chapter. ¹⁵
• Diagnosis requires prospective daily ratings across at least two symptomatic cycles; provisional diagnosis is permitted before this confirmation. ¹⁵
• At least five symptoms are required, with at least one from the four core affective B-criterion symptoms (lability, irritability, depressed mood, anxiety). ¹⁵
• Symptoms must improve within a few days of menses onset and become minimal or absent in the follicular week. ¹⁵
• Twelve-month prevalence with strict prospective criteria is 1.8 to 5.8 percent; retrospective self-report over-estimates by approximately two-fold. ^1-2
• The pathophysiology is a normal hormonal trigger acting on a sensitized central nervous system, with allopregnanolone and serotonergic mechanisms most strongly implicated. ^8,10
• Estradiol, progesterone, and gonadotropin levels do not differ between PMDD patients and controls. ^4,8
• SSRIs are first-line and have rapid onset of benefit (within 1 to 2 days), distinguishing them from their use in MDD. ^13,21
• Three SSRI dosing strategies are evidence-supported: continuous, luteal-phase, and symptom-onset. ²¹
• Drospirenone 3 mg / ethinyl estradiol 20 mcg in a 24/4 regimen is the only combined oral contraceptive FDA-approved for PMDD. ²³
• GnRH agonists with estrogen and progesterone add-back are reserved for severe or treatment-resistant disease. ^8-9
• Suicidal ideation is concentrated in the luteal phase and warrants cycle-anchored safety planning. ^1,5
• PMDD remits during pregnancy and at menopause; persistence of symptoms outside ovulatory cycles argues against the diagnosis. ⁴
• Patients with PMDD are at elevated risk for postpartum depression and perimenopausal depression. ⁴
• The Daily Record of Severity of Problems (DRSP) is the most widely used and validated prospective charting instrument. ¹⁸

No external funding. No conflicts of interest declared. Peer-review status: pending.