The multifactorial model and additional research suggest that female sexual response is not uniformly linear, the distinction between desire and arousal phases is likely artificial, and desire and arousal are difficult to separate because normal desire can include a responsive component. These findings shaped the revision of female sexual dysfunction by the American Psychiatric Association in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) [4,15]. Low sexual desire, termed hypoactive sexual desire disorder (HSDD) in the DSM-IV-TR, was merged with female sexual arousal disorder to form the diagnostic entity of female sexual interest/arousal disorder (FSIAD) in the DSM-5 [4,17,18]. This remains the case in the text revision of the DSM-5 released in 2022 [4].

Furthermore, FSIAD may be described as primary, if the woman has never experienced sufficient arousal (even with sufficient desire and sexual stimulation), or secondary, if the woman has been sufficiently aroused in the past but currently experiences decreased arousal [4]. If the problem occurs in all sexual situations, it is generalized; if the problem occurs only in some sexual situations, it is considered situational.

Genitopelvic pain or penetration disorder is characterized by persistent or recurrent difficulties with one or more of the following [4]:

Genitourinary syndrome of menopause is the term now used in place of vaginal atrophy and vulvovaginal atrophy. Introduced in 2014 by the International Society for the Study of Women's Sexual Health and the North American Menopause Society, genitourinary syndrome of menopause is a medically more accurate, all-encompassing, and publicly acceptable term than its predecessor. It is defined as a constellation of symptoms and signs associated with age-related decreases in estrogen and other sex steroids, including changes to the labia majora/minora, clitoris, vestibule/introitus, vagina, urethra, and bladder. Symptoms of genitourinary syndrome of menopause must be bothersome and not be better explained by another diagnosis and include genital dryness, burning, and irritation; sexual symptoms of lack of lubrication, discomfort or pain, and impaired function; and urinary symptoms of urgency, dysuria, and recurrent urinary tract infections. Women may present with some or all of these signs and symptoms [24]. In a survey of 3,046 women with genitourinary syndrome of menopause, 85% of partnered women reported some loss of intimacy, 59% reported diminished enjoyment of sex, and 47% reported interference with their relationship [25]. In addition, 29% reported sleep disruption and 27% described a negative effect on their general quality of life. Only 7% stated their provider initiated a discussion about genitourinary syndrome of menopause.

The Female Sexual Function Index (FSFI) is the criterion standard instrument in assessing female sexual dysfunction and treatment response in clinical trials and can also be used in clinical practice. The FSFI consists of 19 questions with a severity scale, rated by the patient or subject. Sexual function is assessed across six domains: desire, arousal, lubrication, orgasm, satisfaction, and pain. The total FSFI score is the sum of all six domain scores. Higher scores indicate better sexual function, with a highest possible total score of 36. Scores of 26.55 or less are considered female sexual dysfunction in premenopausal and postmenopausal women [26,27].

The lifetime prevalence of any female sexual dysfunction is 40% [1,2]. In one study, roughly 40% to 45% of adult women had at least one manifest sexual dysfunction (somewhat often, often, nearly always, or always), although distress over the dysfunction was not measured [29]. At any time, around 10% of women experience low or absent sexual desire, making it the most common female sexual dysfunction, followed by orgasmic impairment [4].

Alcohol acts acutely to disinhibit behavior and may increase sexual receptivity or initiation [19]. However, chronic alcohol use may lead to loss of desire, decreased arousal, and anorgasmia. Inhibition of hypothalamic-pituitary-adrenal (HPA) axis function decreases estradiol levels, which may interfere with vaginal lubrication [19].

Among the prescribed drugs with known potential to impair sexual functioning, antidepressants are perhaps the most widely prescribed [46]. Among antidepressants, selective serotonin reuptake inhibitors (SSRIs) and serotonergic/noradrenergic reuptake inhibitors (SNRIs) show the highest rates of sexual dysfunction, including impaired sexual motivation, desire, arousal, and orgasm affecting men and women.

Aging can affect all aspects of female sexual function, and the greatest prevalence of low desire/arousal and distress occurs in women 45 to 64 years of age. Intensity of sexual desire may decline due to neuroendocrine changes, such as declining testosterone, changes in neurochemistry, and indirect changes from loss of estrogen. Genital sensation may change, with arousal and orgasm requiring stronger and longer stimulation. Low estrogen levels can lead to vulvovaginal atrophy and dyspareunia associated with decreased desire. These factors, and the unique psychosocial factors present during this life phase, influence sexual function during the menopausal transition [8,49,50]. The Nurses' Health Study II included 68,131 women 48 to 68 years of age. Sexual activity and dysfunction symptoms were assessed using the FSFI index. Of the participants, 73% were sexually active; 50% of these women reported symptoms of sexual dysfunction. Symptoms were less common among unpartnered (42%) than partnered women (51%). A positive association between menopause and sexual dysfunction was greater among unpartnered than partnered women [51].

Individual vulnerability factors that increase the risk for sexual dysfunction in women include a history of sexual or emotional abuse, current psychiatric conditions (e.g., depression), and life stressors (e.g., job loss).

Vaginismus may be precipitated by painful intercourse, painful pelvic examination, sexual assault, pelvic inflammatory disease, gynecologic surgery, urogenital atrophy, vulvar dermatologic conditions, or childbirth. Generalized anxiety levels are usually elevated in patients with vaginismus, suggesting that vaginismus and anxiety disorders share common predisposing factors [83]. Maintaining factors should be considered, and continuation of intercourse despite pain can promote anticipatory muscle spasm [19].

Vaginismus is difficult to delineate from provoked vestibulodynia, and they often co-occur. Pelvic examination may be very difficult but, if tolerated, enables vaginismus diagnosis as follows [19,83,89]:

Psychotherapy should be initiated before medication in patients with severe depression, substance abuse disorders, or in abusive/chaotic relationships, as medication has little benefit in these contexts. Medical therapy alone is appropriate in couples in which the sexual dysfunction has a clear medical precipitant, couples in a high-quality relationship, or patients with few psychologic concerns [11].

First-line therapy for mild-to-moderate genitourinary syndrome of menopause and dyspareunia involves nonhormonal vaginal lubricants used with intercourse/vaginal sexual activity, long-acting vaginal moisturizers, and regular sexual activity [84]. If improvement is not noted with these approaches, hormone or other pharmacotherapy may be initiated.

Management of provoked vestibulodynia includes lidocaine or xylocaine 2% gel or 5% ointment applied to the vestibule 15 to 30 minutes before sexual activity to reduce intercourse-provoked pain. In one trial, lidocaine 5% ointment applied on the vestibule at bedtime for seven weeks resulted in ≥50% pain reduction [128]. Corticosteroid creams are frequently prescribed but are rarely effective [19].

Exercises for systematic desensitization to vaginal penetration are the mainstay of vaginismus treatment, with the goal of control over and relaxation of levator ani muscles. Therapy starts with reverse Kegel exercises, progresses to gentle stretching of the vagina using lubricated vaginal dilators of graduated sizes to help restore and maintain vaginal function, followed by introduction a partner's fingers, with intercourse the final step [19].

As noted, in 2015 flibanserin became the first medication approved for the treatment of female sexual dysfunction (specifically HSDD) and the first medication approved to treat sexual desire disorders in either sex [104]. This medication is a mixed 5-HT1A agonist/5-HT2A antagonist—the first in its class. Its mechanism of action is presumed to be primarily the result of postsynaptic action on 5-HT1A receptors, but the actual action is not clear [133].

A guideline for testosterone therapy in FSIAD was jointly updated in 2014 by the Endocrine Society and other professional organizations [21]. The guideline recommends initiating a three- to six-month trial in postmenopausal women requesting testosterone therapy for verified FSIAD (when not contraindicated). Mid-normal premenopausal testosterone values should be used as the reference standard to avoid testosterone over-administration. Testosterone levels should be measured at baseline, monitored at three- to six-week and six-month follow-up, and then every six months for signs of excessive use and androgen excess. Therapy should be halted in patients lacking response by six months.

Plant-derived and herbal remedies are a popular alternative to medical treatments for patients with sexual dysfunction. While some preparations seem effective, no safety data are available with long-term use.

Ginkgo biloba extract efficacy in female sexual dysfunction was evaluated in a study with highly rigorous design, which found gingko biloba extract offered no benefit beyond placebo [144]. A study published in 2014 examined the effect of ginkgo biloba extract on sexual desire in 80 postmenopausal women [145]. Half of the healthy female volunteers received ginkgo biloba extract (120–240 mg) and the other half received placebo for 30 days. Sexual desire was significantly improved in the ginkgo biloba extract group compared with the placebo group.