Female Sexual Dysfunction

Female sexual dysfunction (FSD) is a persistent or recurrent difficulty with sexual desire, arousal, orgasm, or pain that causes the patient personal distress — distress is the operative word, since normal variation in sexual interest or response without distress is not itself a disorder requiring treatment.^[1] The DSM-5-TR organizes FSD into 3 diagnoses that matter clinically because their treatment differs meaningfully: female sexual interest/arousal disorder (FSIAD), which merges what were previously the separate diagnoses of hypoactive sexual desire disorder (HSDD) and female arousal disorder; female orgasmic disorder (FOD); and genito-pelvic pain/penetration disorder (GPPPD), which merges the older separate diagnoses of dyspareunia and vaginismus.^[2] Sexual response is best understood as circular and context-dependent rather than a fixed linear drive: for many patients, especially in established relationships, willingness to begin a sexual encounter arises from a receptive state shaped by intimacy and context rather than spontaneous desire, and subjective arousal correlates poorly with genital blood flow. This chapter covers the biopsychosocial assessment framework; the medication-induced-FSD differential that pharmacists are well positioned to catch on medication review; flibanserin and bremelanotide for HSDD in premenopausal patients; vaginal DHEA (prasterone) and oral ospemifene for GSM-related arousal and pain (local vaginal estrogen dosing itself is covered in depth in this platform's Menopause chapter and is not re-derived here); and an honest account of the evidence — for most FSD presentations, pharmacotherapy alone is, at best, a modest adjunct to addressing the underlying biological, psychological, and relational contributors, not a substitute for doing so.^[3]

Provoked vestibulodynia (PVD)

PVD is the single most common cause of dyspareunia. Pain is typically triggered by touch to the vaginal opening, including attempted penetration, and is associated with allodynia (a pain response to a normally non-painful stimulus) around the outer edge of the hymen, with no abnormal physical findings other than variable redness. Other chronic pain syndromes are often also present, including severe dysmenorrhea beginning in adolescence.^[4]

Genitourinary syndrome of menopause (GSM) presenting as GPPPD

Dyspareunia from the pallor, loss of elasticity and skin turgor, and atrophy of the labia minora seen in GSM can closely resemble PVD: painful introitus, pain with penetration and movement, and post-coital burning. GSM and PVD can coexist in the same patient, and both need to be actively considered — this platform's Menopause chapter covers GSM diagnosis and local vaginal estrogen treatment in full.

• Depression, current or past — the factor most consistently correlated with sexual function in both well and chronically ill patients.^[3]
• Anxiety, sexual anxiety, distraction during sexual activity, low self-esteem or poor body image.
• A history of physical, sexual, or emotional abuse.
• Insufficient emotional intimacy, relationship conflict, or a partner's own sexual dysfunction.
• A past history of dyspareunia — pain that has resolved can still interfere with processing of sexual stimuli going forward.
• Severe dysmenorrhea beginning in adolescence — a recognized risk marker for later provoked vestibulodynia.
• Menopause and estrogen-deficient states, including chemotherapy- or radiation-induced menopause.
• Chronic pelvic pain conditions: endometriosis, interstitial cystitis, chronic pelvic inflammatory disease, inflammatory bowel disease.
• Neurologic conditions affecting genital sensation or vasocongestion: multiple sclerosis, spinal cord injury, diabetic neuropathy.
• Pelvic cancer surgery or radiation, scleroderma, lichen sclerosus.
• Irregular or absent menstrual cycles suggesting hyperprolactinemia; hypothyroidism or hyperthyroidism.
• Urinary incontinence, or fear of incontinence during sexual activity.
• Fatigue from chronic illness, a sleep disorder, shift work, or disturbed sleep.
• Obesity and other chronic medical conditions.
• A medication associated with FSD (see Assessment & Diagnosis for the full list).

Differentiating causes of genito-pelvic pain by timing

Because GSM, infection, lack of arousal, other pelvic pathology, and provoked vestibulodynia (PVD) can all present with genito-pelvic pain but need different treatment, use when the pain occurs to help narrow the cause.

Sexual history — interview both the patient and any participating partner

Interview the patient and any interested partner together, and each separately — some symptoms (e.g., a total lack of desire) are easier for a patient to acknowledge alone.

Medical and psychosocial history

• Current and past depression — the factor most consistently correlated with sexual function; screen explicitly rather than assuming its absence.
• Biological factors impairing subjective arousal: fatigue, chronic pain, medical conditions, and the medications reviewed below.
• Psychological factors: distraction, sexual anxiety, ongoing stressors, relationship issues, a history of abuse.
• For patients in a partnered relationship: nonsexual intimacy, trust, respect, safety, birth control, fertility goals, and stressors.
• Whether required auditory, visual, or physical sexual stimuli are actually present and being used.

Medications associated with female sexual dysfunction

This list is not exhaustive. A trial off the suspected drug, where clinically safe to stop or switch, helps determine whether it is contributing to the problem.

Physical examination

Indicated when FSIAD/GPPPD occurs in the context of a medical disease that can limit genital vasocongestion (multiple sclerosis, pelvic cancer surgery/radiation, scleroderma) or when there is reported loss of genital sensitivity, which can result from lichen sclerosus or GSM.

• Abdominal exam for tenderness or a mass.
• Signs of GSM (pallor, loss of elasticity/turgor, atrophy of the labia minora).
• Interlabial fissures (associated with estrogen deficiency or candidiasis).
• Signs of a past tear of the posterior fourchette.
• Adhesions between the labia minora (preclude penetration and need surgical division) or a tight posterior fourchette (needs topical estrogen or perineoplasty).
• Abnormal discharge — suggests vaginal infection or, less commonly, more serious pelvic pathology.
• Erythema of the introital margin — consistent with, but not diagnostic of, PVD; allodynia of the introital margin on light touch (e.g., with a cotton swab) — diagnostic of PVD.
• Lichen sclerosus involving the introitus.
• Bimanual exam: pain on palpation of the uterus, cervix, or adnexae, or nodularity along the uterosacral ligaments or in the pouch of Douglas, all suggest possible pelvic pathology; pelvic floor muscle hypertonicity with trigger points in the deep levator ani muscles; abnormalities of the urethra, bladder, or rectum.

For a patient unable to tolerate examination: encourage a graduated, patient-controlled approach at home for 10 minutes daily — reclining and partially abducting the thighs, touching the vulva and eventually the introitus, and spreading the labia so the introitus can be seen. When the patient presents for exam, let her stay in control (separating the labia herself, with any touch, e.g. with a cotton swab for suspected PVD, performed by the patient). A full examination is preferably delayed to a subsequent visit if needed rather than forced at the first.

Investigations

• Vaginal pH and microscopy for bacterial vaginosis, candidiasis, and trichomoniasis when discharge or infection is suspected.
• KOH whiff test (a fishy odour intensified by adding a few drops of 10% potassium hydroxide to vaginal secretions) to detect bacterial vaginosis.
• Fasting glucose and HIV status if chronic or recurrent candidiasis is present.
• Biopsy of any vulvar area with an abnormal appearance.
• NAAT and/or culture for gonorrhea and chlamydia when clinically indicated.
• Laboratory investigation otherwise only as indicated by history and physical exam — do not order a broad panel by default.

• Improve the patient's (and, where relevant, the partner's) understanding of the sexual response cycle, and identify the specific point(s) at which it is breaking down.
• Identify and address every contributing biological factor — a medical condition, a contributing medication, or a hormonal deficiency — before or alongside any FSD-specific pharmacotherapy.
• Identify and address contributing psychological and relationship factors, with referral to CBT, sex therapy, or MBCT when indicated.
• For GPPPD: reduce or eliminate pain with attempted penetration, and reduce the fear/anxiety and involuntary pelvic floor tensing that accompany it.
• For FSIAD/HSDD: restore desire and arousal to a level the patient herself defines as satisfying — not a fixed frequency or intensity target set by the clinician.
• For FOD: restore the ability to reach orgasm, or reduce the distress associated with its absence, through a structured, patient-directed approach.
• Set realistic expectations from the outset: pharmacotherapy alone produces at most a modest benefit for most FSD presentations and works best combined with the nonpharmacologic measures above.

General measures — FSIAD

• Screen for and treat mood disorders, especially depression, with CBT or MBCT.
• Counsel or refer when insufficient emotional intimacy is failing to motivate the patient sexually, or is impairing subjective arousal/pleasure.
• Address a lack of stimuli — a range is often needed: nonphysical (erotic conversation or music), nongenital (caressing or kissing the neck, breasts, thighs), and genital but nonpenetrative (manual, oral, or vibrator stimulation of the mons pubis and vulva).
• Address psychological factors inhibiting the effectiveness of stimulation: distraction and nonsexual stressors; dysphoric arousal (may indicate previous abuse); constant sexual self-monitoring; low self-esteem or poor body image; a past experience of pain that interferes with processing sexual stimuli even once the pain has resolved; a negative outcome such as a partner's own sexual dysfunction or dyspareunia leading to avoidance (address the primary problem directly); negative emotions accompanying arousal; suppressed anger and, with it, suppressed sexual emotion; a learned pattern of minimal emotional expression.
• Address biological factors limiting the effectiveness of stimulation, other than depression: conditions impairing genital vasocongestion (e.g., estrogen deficiency); a contributing medication (see Assessment & Diagnosis); fatigue from illness, a sleep disorder, shift work, or chronic pain; irregular or absent cycles suggesting hyperprolactinemia; hypo- or hyperthyroidism; urinary incontinence or fear of leakage during sexual activity.

Specific to female orgasmic disorder (FOD)

• Guided self-stimulation: education and information followed by body-awareness exercises to enhance the patient's awareness of her own genitals and challenge negative or distorted thoughts. Explain that letting go of control is part of orgasm, which is genuinely difficult for many people — learning to orgasm alone may be the necessary first step.
• Coital alignment technique: a behavioural technique that increases pubis-to-pubis contact during intercourse to stimulate the deep clitoral bulbar tissue within the perineal muscles.
• Vibrostimulation: use of a vibrator, especially useful when genital nerve damage is present (e.g., multiple sclerosis, diabetes).
• Refer to a mental health professional when a lack of trust, fear of closeness, or fear of losing control is identified as the primary barrier.

Specific to genito-pelvic pain/penetration disorder (GPPPD)

• Assess pelvic floor hypertonicity and address it with pelvic floor physiotherapy and biofeedback — teach "reverse Kegel" exercises together with graduated vaginal dilators of increasing diameter.
• Explain the role of stress in chronic pain, and counsel on stress management.
• Advise focusing on sexual activity that does not include any vaginal penetration, in order to break the pain-avoidance cycle.
• Address any concomitant lack of arousal or desire that differs from the patient's own normal baseline.
• Refer for definitive treatment if pelvic pathology is suspected, and refer if conservative therapy for recurrent tearing of the posterior fourchette fails.

Vaginal moisturizers and lubricants

Regular (not as-needed) use of a non-hormonal vaginal moisturizer gives longer-lasting relief of dryness than an as-needed lubricant, and a lubricant used at the time of intercourse reduces dyspareunia. Either can be used alone for mild symptoms, or alongside local vaginal estrogen for more significant symptoms — this platform's Menopause chapter covers specific moisturizer and lubricant products in more detail.

Pregnancy

Flibanserin, bremelanotide, testosterone, and ospemifene are not studied in, and should not be used during, pregnancy — bremelanotide and ospemifene are specifically contraindicated. Local vaginal estrogen is not typically needed in pregnancy given physiologic hyperestrogenism. Postpartum dyspareunia is common, from perineal trauma, lactational hypoestrogenism, and breastfeeding-associated vaginal dryness — manage with a water- or silicone-based lubricant, pelvic floor physiotherapy, and time, and refer if pain persists beyond the expected healing period.

Breastfeeding

Flibanserin, bremelanotide, testosterone, and ospemifene lack breastfeeding safety data — avoid. Local vaginal estrogen has minimal systemic absorption and is not typically restricted, but lactational hypoestrogenism itself is a common, self-limited cause of dyspareunia during breastfeeding that improves with weaning or reduced breastfeeding frequency; a lubricant is the usual first step.

Adolescents

FSD as defined here applies to sexually active adults. In an adolescent with an unconsummated relationship or vaginismus-type presentation, evaluate for a congenital anomaly (e.g., vaginal septum) and psychosexual factors rather than assuming primary FSD. Severe dysmenorrhea in adolescence is a recognized risk marker for later provoked vestibulodynia and warrants its own assessment.

Renal and hepatic impairment

Flibanserin is contraindicated in any degree of hepatic impairment and with moderate/strong CYP3A4 inhibitors; it is not specifically restricted by renal function, though clinical experience in significant renal impairment is limited. Bremelanotide has not been studied in severe hepatic or severe renal impairment — avoid. Ospemifene has not been specifically studied in severe hepatic impairment — use with caution. Compounded topical/transdermal testosterone avoids the hepatotoxicity historically associated with oral 17-alkylated androgens, which are not used for this indication.

Breast cancer history

This platform's Menopause chapter covers the nuanced use of local vaginal estrogen in a patient with a breast cancer history, including tamoxifen and aromatase inhibitor use — not reproduced here. Ospemifene is contraindicated with known or suspected estrogen-dependent neoplasia. Flibanserin, bremelanotide, and testosterone have no specific breast-cancer-related restriction beyond standard caution, but the psychosocial impact of cancer treatment on sexual function is significant and often under-addressed — proactively offer CBT or sex therapy referral.

Neurologic conditions

Vibrostimulation is particularly useful for orgasmic or arousal difficulty related to genital nerve damage (multiple sclerosis, spinal cord injury, diabetic neuropathy). Sildenafil's one positive small trial was specific to antidepressant-induced arousal difficulty and does not extend to arousal impairment from neurologic injury, where trial evidence has been negative.

Flibanserin: reassess desire and associated distress at 8 weeks and discontinue if there is no improvement; reinforce the alcohol-avoidance counselling at every refill, not just at initiation; monitor for dizziness, somnolence, and hypotension, especially early in treatment. Bremelanotide: reassess at 8 weeks and discontinue if there is no benefit; check blood pressure at baseline and periodically given the transient hemodynamic effect of each dose; examine the skin and gingiva periodically for hyperpigmentation with frequent use; confirm the patient is respecting the dose-frequency limits (no more than 1 dose per 24 hours, no more than 8 per month). GSM-related therapy: follow this platform's Menopause chapter for the standard local-estrogen follow-up cadence. Testosterone (if used off-label): monitor for androgenic effects (acne, hirsutism, voice change, alopecia) at every visit; given the lack of long-term safety data beyond 2 years, limit duration and reassess ongoing need regularly, and discontinue if there is no benefit after a defined trial or if androgenic effects emerge. GPPPD/PVD: track a pain scale and penetration tolerance over successive visits, reassess pelvic floor physiotherapy progress, and confirm partner communication is improving alongside physical measures. Medication-induced FSD: reassess sexual function 4-6 weeks after any medication switch or dose reduction, and track mood status alongside sexual function, since achieving full remission of an underlying depression improves sexual function beyond simply switching the antidepressant.^[6] At every follow-up, reassess whether the nonpharmacologic and psychological measures have genuinely been engaged with — pharmacotherapy alone is often insufficient regardless of which agent is used.

1. Confirm the correct subtype was actually targeted — a patient treated for desire-predominant HSDD who in fact has undiagnosed GPPPD-related pain suppressing her desire will not respond to flibanserin or bremelanotide; re-examine for a pain component.
2. Confirm the biopsychosocial contributors were genuinely addressed (mood disorder treated to remission, a contributing medication actually changed, a relationship or psychological referral actually completed) rather than assuming pharmacotherapy alone would be sufficient.
3. Confirm an adequate trial occurred: flibanserin and bremelanotide both need a full 8-week trial before concluding failure; local vaginal estrogen may need several weeks for tissue-level improvement (see the Menopause chapter).
4. If flibanserin fails after an adequate trial, or is not tolerated or contraindicated, move to bremelanotide (acknowledging the Canadian access limitation via the Special Access Programme) or focus fully on psychological/sex-therapy approaches.
5. If GSM-directed local estrogen is inadequate despite an adequate trial and correct technique, add vaginal DHEA (prasterone) or trial oral ospemifene, and reconsider whether a coexisting PVD component is present — the two can coexist and need separate treatment.
6. If GPPPD/PVD pain persists despite pelvic floor physiotherapy and topical measures, refer to a pelvic pain specialist or gynecologist; do not add a topical corticosteroid or botulinum toxin injection, since current consensus specifically recommends against both for PVD.^[4]
7. If orgasmic difficulty persists despite guided self-stimulation and vibrostimulation, refer for structured sex therapy — no pharmacotherapy has an established role for FOD.
8. For refractory cases across any subtype, refer to a psychiatrist or psychologist when deep-seated childhood or developmental themes or a history of abuse are identified, or to a sex therapist when the primary barriers are a lack of sexual context, stimuli, or information.

• Prescribing flibanserin without explicit, quantified alcohol-timing counselling — this is not a general "drink less" caution.
• Missing a newly started interacting drug (a moderate/strong CYP3A4 inhibitor, e.g., fluconazole) in a patient already taking flibanserin.
• Assuming any complaint of low desire is HSDD requiring drug therapy without first completing the biopsychosocial assessment.
• Overlooking a contributing medication during a routine medication review — SSRIs, combined hormonal contraceptives, and antihypertensives are common, frequently missed contributors.
• Switching an antidepressant purely for its sexual side effects without confirming the underlying depression is actually in remission — unresolved depression itself suppresses sexual function independent of the drug.^[6]
• Using sildenafil as a general treatment for female arousal difficulty — trial evidence does not support this outside a narrow antidepressant-induced-dysfunction context.
• Recommending topical corticosteroids or botulinum toxin injection for provoked vestibulodynia — current consensus specifically recommends against both.
• Ordering serum testosterone or androgen levels to diagnose or guide treatment of low desire — no correlation with sexual function has been established.
• Conflating GSM-related dyspareunia with provoked vestibulodynia in a postmenopausal patient with introital pain — the two can coexist, and both need to be actively considered rather than assuming one explains the presentation.
• Advising intercourse as "practice" for GPPPD before pain is meaningfully reduced — this reinforces the pain-avoidance cycle rather than resolving it.
• Interviewing only the patient when a partner is present and willing to participate in the assessment.

How to use this table: Doses are adult doses and require patient-specific confirmation, including hepatic/renal adjustment where relevant. Select any drug name to open its complete Pharmasist Drug Database page.

Hypoactive sexual desire disorder (HSDD), premenopausal patients

Genitourinary syndrome of menopause (GSM) — arousal and pain

See this platform's Menopause chapter for the complete range of local vaginal estrogen formulations (ring, tablet, cream) and their full dosing — summarized here only for the estradiol vaginal formulations most relevant to FSD.

Testosterone — off-label, HSDD in postmenopausal patients only

No Health-Canada-approved product exists for this indication. The platform's existing testosterone-cypionate (100 mg/mL) and testosterone-enanthate (200 mg/mL) monographs are male-dose injectable esters and must not be used or linked for this indication — that formulation and dose would be a genuine, clinically significant mismatch.

Antidepressants relevant to sexual function

SSRIs, SNRIs, TCAs, and MAOIs are common causes of medication-induced FSD (see Assessment & Diagnosis). The agents below are lower-sexual-dysfunction-risk alternatives, useful either as a primary antidepressant switch or, for bupropion specifically, as an augmentation strategy for SSRI-induced sexual dysfunction.

Provoked vestibulodynia (PVD) — topical adjuncts

Evidence-based dosing guidelines for the pharmacologic treatment of PVD are genuinely lacking; both agents below are consensus-level, specialist-directed adjuncts to pelvic floor physiotherapy and CBT/MBCT, not stand-alone treatment.

Provoked vestibulodynia — other office-based options

Vaginal moisturizers and lubricants

Non-hormonal first step for GSM-related dryness/dyspareunia; can be used alone for mild symptoms or alongside any hormonal option for more significant symptoms. See this platform's Menopause chapter for further detail.