Most people—men and women—engage in sexual activity because of attraction or a desire for pleasure, affection, love, romance or intimacy. However, women are more likely to report emotional motivations. Many women initiate or agree to sexual activity because they want one or more of the following:
Especially in established relationships, women often have little or no initial sense of sexual desire but access sexual desire (responsive desire) once sexual stimulation triggers excitement and pleasure (subjective arousal) and genital congestion (physical genital arousal). Desire for sexual satisfaction, which may or may not include one or multiple orgasms, builds as sexual activity and intimacy continue, and a physically and emotionally rewarding experience fulfills and reinforces the woman's original motivations.
A woman's sexual response cycle is strongly influenced by her mental health and by the quality of her relationship with her partner. Initial desire typically lessens with age but increases with a new partner at any age.
Sexual response consists of the following:
Physiology of the female sexual response is incompletely understood but involves hormonal and CNS factors.
Estrogens and androgens both appear to influence arousal. Androgens probably act via androgen receptors and estrogen receptors (after intracellular conversion of testosterone to estradiol).
After menopause, ovarian estrogen production ceases, while ovarian androgen production varies. However, adrenal production of prohormones (eg, DHEAS) that are converted to both androgens and estrogens in peripheral cells decreases starting in a woman's 30s. Ovarian production of prohormones also declines after menopause. Whether this decrease plays any role in diminishing sexual desire, interest, or arousal is unclear.
The brain produces sex hormones (neurosteroids) from cholesterol, and production may increase after menopause. Whether this documented increase is universal, whether it facilitates arousal as peripheral production decreases, and whether it is affected by exogenous hormone administration are all unknown.
Brain areas involved in cognition, emotion, motivation, and organization of genital congestion are activated. Neurotransmitters acting on specific receptors are involved. Based on known actions of drugs and on animal studies, some neurotransmitters appear to be prosexual; they include dopamine, norepinephrine, and melanocortin. Serotonin is usually sexually inhibitory, as are prolactin and γ-aminobutyric acid (GABA).
This reflexive autonomic response occurs within seconds of an erotic stimulus and causes genital engorgement and lubrication. Smooth muscle cells around blood spaces in the vulva, clitoris, and vaginal arterioles dilate, increasing blood flow (engorgement) and transudation of interstitial fluid across the vaginal epithelium (lubrication). Women are not always aware of congestion, and it may occur without subjective arousal. As women age, basal genital blood flow decreases, but genital congestion in response to erotic stimuli (eg, erotic videos) may not.
Peak excitement occurs, characterized by contractions of pelvic muscles every 0.8 sec, and is followed by slow release of genital congestion. Thoracolumbar sympathetic outflow tracts appear to be involved, but orgasm is possible even after complete spinal cord transection (eg, when a vibrator is used to stimulate the cervix). Prolactin, ADH, and oxytocin are released at orgasm and may contribute to the sense of well-being, relaxation, or fatigue that follows. However, many women experience a sense of well-being and relaxation without experiencing orgasm.
Female sexual dysfunction may involve decreased or increased sexual responsiveness. Classification is determined by symptoms. There are 5 major categories of decreased responsiveness and one of increased responsiveness (persistent genital arousal disorder).
Sexual desire/interest disorder is absence of or a decrease in sexual interest, desire, sexual thoughts, and fantasies and an absence of responsive desire.
Sexual arousal disorder is lack of subjective or genital arousal or both.
Orgasmic disorder involves orgasm that is absent, markedly diminished in intensity, or markedly delayed in response to stimulation despite high levels of subjective arousal.
Vaginismus is reflexive tightening around the vagina when vaginal entry is attempted or completed despite women's expressed desire for penetration and when no structural or other physical abnormalities are present.
Dyspareunia is pain during attempted or completed vaginal penetration or intercourse. Provoked vestibulodynia (PVD, formerly called vulvar vestibulitis), the most common type of superficial (introital) dyspareunia, is a chronic pain syndrome associated with altered immune function and sensitization of the nervous system.
Persistent genital arousal disorder involves excessive genital arousal.
A disorder is diagnosed when symptoms cause distress. Some women may not be distressed or bothered by decreased or absent sexual desire, interest, arousal, or orgasm.
Almost all women with sexual dysfunction have features of more than one disorder. For example, the chronic dyspareunia of PVD often leads to sexual desire/interest and arousal disorders; impaired arousal may make sex less enjoyable or even painful, decreasing the likelihood of orgasm and subsequent sexual desire. However, dyspareunia due to impaired lubrication may occur as an isolated symptom in women with a high level of sexual desire, interest, and subjective arousal.
Female sexual disorders may be secondarily categorized as lifelong or acquired; situation-specific or generalized; and mild, moderate, or severe based on the degree of distress it causes the woman.
Although research is limited, these disorders probably apply equally to women in heterosexual and homosexual relationships.
The traditional separation of psychologic and physical etiologies is artificial; psychologic distress causes changes in hormonal and neurologic physiology, and physical changes may generate psychologic reactions that compound the dysfunction. There are often several causes of symptoms within and between categories of dysfunction, and the cause is often unclear.
Primarily psychologic factors:
Mood disorders are closely correlated with low desire and arousal. In up to 80% of women with major depression and sexual dysfunction, sexual dysfunction becomes less severe when antidepressants effectively treat the depression. However, sexual dysfunction persists or worsens when antidepressants are ineffective. Women with an anxiety disorder are also more likely to have sexual dysfunction involving desire, arousal, and orgasm. Various fears—of letting go, of being vulnerable, of being rejected, or of losing control—and low self-esteem can contribute.
Previous experiences can affect a woman's psychosexual development, as in the following:
Concerns about a negative outcome (eg, unwanted pregnancy, sexually transmitted diseases [STDs], inability to have an orgasm, sexual dysfunction in a partner) can also impair sexual response.
Contextual causes (those specific to a woman's current circumstances) include the following:
Distractions (eg, from family, work, or finances) can interfere with arousal.
Primarily physical factors:
Various genital lesions, systemic and hormonal factors, and drugs may lead or contribute to dysfunction (see Table 1: Sexual Dysfunction in Women: Some Physical Factors Contributing to Female Sexual Dysfunction).
|Some Physical Factors Contributing to Female Sexual Dysfunction
Genital herpes simplex
Postsurgical introital narrowing
Recurrent tearing of the posterior fourchette
Vaginal infections or vaginitis
Other physical factors
Bilateral oophorectomy in premenopausal women
Hypothyroidism, hypoadrenal states, hypopituitary states
Nerve damage (eg, due to diabetes, multiple sclerosis, or spinal cord dysfunction)
Antiandrogens (eg, spironolactone, gonadotropin-releasing hormone agonists)
Certain antidepressants, particularly SSRIs
Hormones (eg, oral estrogen therapy, hormonal contraceptives)
SSRIs are a particularly common drug cause. Systemic estrogen therapy (postmenopausal or in hormonal contraceptives) has mixed effects. It can improve mood and help maintain skin and genital sexual sensitivity and vaginal lubrication. However, it also increases sex hormone–binding globulin (SHBG), decreasing the amount of free androgens available for tissue receptor binding. Decreasing free androgens can counteract the other sexual benefits of systemic estrogens, contributing to sexual dysfunction. Alcohol dependence can cause sexual dysfunction.
Diagnosis of sexual dysfunction and its causes is based on history and physical examination. Ideally, history is taken from both partners, interviewed separately and together; it begins by asking the woman to describe the problem in her own words and should include specific elements (see Table 2: Sexual Dysfunction in Women: Components of the Sexual History for Assessment of Female Sexual Dysfunction). Problematic areas (eg, past negative sexual experiences, negative sexual self-image) identified at the first visit can be investigated more fully at a follow-up visit.
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Physical examination is most important for determining causes of dyspareunia; the technique may differ slightly from that used in a routine gynecologic examination. Explaining what will occur during the examination helps the woman relax and should be continued throughout the examination. The woman should be asked whether she wants to sit up and view her genitals in a mirror during the examination; doing so may impart a sense of control.
Wet-preparation examination of vaginal discharge and Gram stain with culture or DNA probe to detect Neisseria gonorrhoeae and chlamydiae are indicated when history or examination suggests vulvitis, vaginitis, or pelvic inflammatory disease.
Although low estrogen and testosterone activity may contribute to sexual dysfunction, measuring levels is rarely indicated. Low estrogen and testosterone are detected clinically. If hyperprolactinemia is clinically suspected, the prolactin level is measured. If hypothyroidism is clinically suspected, the TSH level is measured and sometimes other thyroid function tests are done
Treatment varies by disorder and cause; often, more than one treatment is required because disorders overlap. Sympathetic understanding of the patient and careful evaluation may themselves be therapeutic. Mood disorders are treated. Explaining what is involved in the female sexual response may also help.
Because SSRIs may contribute to several categories of sexual dysfunction, switching to an antidepressant that has fewer sexual adverse effects (eg, bupropion, moclobemide, mirtazapine, venlafaxine) may be considered. Alternatively, some evidence suggests that adding bupropion to an SSRI may help.
Last full review/revision January 2009 by Rosemary Basson, MD, FRCP(UK)
Content last modified February 2012