Sexual dysfunction is a perturbation of normal sexual function that interferes with an individual's ability to engage in satisfactory sexual activity. Sexual dysfunctions are largely defined and described as disruptions of particular parts of the sexual response cycle.
The traditional view of a sexual response is an orderly progression through discrete phases in sequence (desire, arousal, orgasm, and resolution). This linear model, advocated by Masters and Johnson and later by Kaplan, has recently been challenged principally by Basson, who has advocated a circular model that emphasizes the interrelationships between the psychoemotional aspects of sexuality in women (Figure 40–12). In this model, innate sexual desire may play a variable role in an individual woman's sexual response, influencing a woman's sexual incentives, receptiveness, and response to stimuli. There is continuing controversy regarding the accuracy of these competing models, although data are emerging that the circular model of Basson may be more frequently endorsed by women with sexual dysfunction. This is parsimonious as women who have difficulties with, or reduced interest in, sex may be primarily motivated to engage in sex for emotional and psychosocial reasons.
Circular female sexual response cycle of Basson. (Adapted from Basson R et al: Summary of the recommendations on sexual dysfunction in women. J Sex Med 2004;1(1):24–34.)
Disorders of female sexual function are summarized in Table 40–1. Many existing definitions of female sexual dysfunction are based on scant empiric evidence, although distress regarding the situation is an important component of most modern definitions. Traditionally, sexual desire disorders have been diagnosed in the setting of infrequent sexual thoughts and fantasies. However, sexual thoughts are infrequent in many women without apparent sexual dissatisfaction and the frequency of sexual fantasies or sexual thoughts has shown little correlation with sexual satisfaction in women. Most contemporary definitions incorporate an absence of receptive desire, that is, interest in sex initiated by a partner's initiation of a sexual encounter. Arousal disorders may be subdivided into subjective arousal disorders, genital arousal disorders, and combined (mixed) arousal disorder. Of note, the Diagnostic and Statistical Manual of Mental Disorders Volume IV Text Revision (DSM-IV-TR) focuses specifically on lubrication in their definition of sexual arousal disorder, whereas the American Urological Association (AUA) definitions do make a distinction between subjective and genital arousal response. There are no defined cut-off scores (objective or subjective) to establish the diagnosis of arousal disorder and therefore the diagnosis is based purely on patient report for both subjective and genital arousal disorders. At the time of this writing, there is controversy over whether there will be a distinction between sexual desire and sexual arousal disorders in the upcoming DSM-V; currently, there is an impetus to combine these disorders into a unifying diagnosis that incorporates both disorders, consistent with the model of Basson.
Table 40–1. Definitions of Sexual Dysfunction. ||Download (.pdf)
Table 40–1. Definitions of Sexual Dysfunction.
Hypoactive sexual desire disorder
Sexual desire/interest disorder
Persistent or recurrent deficiency or absence of sexual fantasies and desire for sexual activity. Judgment of deficiency is made by the clinician, taking into account factors that affect sexual functioning
Absent or diminished feelings of sexual interest or desire, absent sexual thoughts or fantasies, and a lack of responsive desire. Motivations for attempting to become sexually aroused are scarce or absent. Lack of interest goes beyond a normal lessening with increasing age and relationship duration
Combined arousal disorder
Absent or markedly reduced feelings of sexual arousal (sexual excitement and sexual pleasure) from any type of stimulation, and absent or impaired genital sexual arousal (vulvar swelling and lubrication)
Subjective arousal disorder
Absent or markedly reduced feelings of sexual arousal (sexual excitement and sexual pleasure) from any type of stimulation. Vaginal lubrication and other signs of physical response still occur
Female sexual arousal disorder
Genital arousal disorder
Persistent or recurrent inability to attain, or to maintain until completion of sexual activity, adequate lubrication, and swelling response of sexual excitement
Absent or impaired genital sexual arousal (minimal vulvar swelling or vaginal lubrication from any type of sexual stimulation, and reduced sexual sensations when genitalia are caressed).
Subjective sexual excitement still occurs from nongenital sexual stimuli (eg, erotica, breast stimulation, kissing)
Female orgasmic disorder
Persistent or recurrent delay or absence of orgasm after a normal sexual excitement phase
Lack of orgasm, markedly diminished intensity of orgasmic sensations, or marked delay of orgasm from any kind of stimulation, despite self-reported high sexual arousal or excitement
Recurrent or persistent genital pain associated with intercourse
Persistent or recurrent pain with attempted or complete vaginal entry and/or vaginal intercourse
Recurrent or persistent involuntary spasm of the musculature of the outer third of the vagina that interferes with sexual intercourse
Persistent difficulties to allow vaginal entry of a penis, a finger, and/or any object, despite the woman's expressed wish to do so. Structural or other physical abnormalities must be ruled out/addressed
Sexual aversion disorder
Extreme anxiety and/or disgust at the anticipation of/or attempt to have any sexual activity
Persistent genital arousal disorder
Spontaneous, intrusive, and unwanted genital arousal (eg, tingling, throbbing, pulsating) in the absence of sexual interest and desire. Any awareness of subjective arousal is typically but not invariably unpleasant.
The diagnosis of an orgasmic disorder per both American Psychiatric Association (APA) and AUA guidelines necessitates that an acceptable and preferred form of sexual stimulation has occurred and orgasm has not resulted. A substantial proportion of the female population does not climax from coital intercourse and absence of climax from coitus should not be diagnosed as a sexual dysfunction unless it represents a distressing change from a woman's prior state of affairs.
The basis of desire and perceived arousal in women is poorly understood, but it involves complex interactions among the central nervous system, sex hormones, and psychoemotional factors. The sexual response cycle incorporates numerous changes throughout the body as well; for the purpose of brevity in this chapter, we will focus on genital responses.
The genital arousal response in women is mediated in large part by activity of the parasympathetic and sympathetic nervous system as well as the vascular endothelium. These systems release nitric oxide and vasointestinal polypeptide. These messengers promote vasodilatation, which in turn leads to genital vasocongestion. In the clitoris, this causes engorgement of the corporal bodies and clitoral erection. In the vagina, increased oncotic pressure leads to production of a transudate fluid that is expressed through the vaginal epithelium, producing lubrication. It is important to note that there is no evidence for a glandular component to vaginal lubrication; vaginal wetness is derived entirely from this transudate.
Genital vasocongestive responses occur in women within seconds after erotic stimulation. Interestingly, the genital arousal response appears to be an automated response to sexual stimulation; indeed, it has been shown in many studies that women may exhibit an arousal response to stimuli that are not of subjective interest. For instance, it has been shown that women often exhibit a genital arousal response (increased blood flow) in response to viewing of erotic videos, irrespective of the subject matter, sexual orientation, and personal interest in the sexual activities depicted. Genital arousal response may also occur in response to depictions of nonpreferred activities, such as threat. The reason for this automatic “priming” of genital response is unclear but may be an evolutionarily protective mechanism to ensure adequate genital lubrication for possible sexual activity.
The effect of estrogen levels on sexual function is complex. Although low estrogen levels and vaginal atrophy are associated with reduced measures of vaginal congestion when the woman is not receiving sexual stimulation, the percent increase in congestion in response to erotic stimuli is similar in the presence of low and high estrogen levels (ie, pre- and postmenopausal women). Similarly, changes in the volume of the vaginal wall and clitoris and the relative volume of regional blood in response to sexual stimulation are similar before and after menopause. Estrogen deficiency does not necessarily preclude adequate lubrication, provided that stimulation is sufficient. It is important to note that a woman who is postmenopausal will generally have less baseline lubrication and therefore the necessity of adequate stimulation to prevent painful intercourse is often more apparent in women who are postmenopausal.
Indirect evidence suggests that testosterone and dopamine play a role in modulating sexual response, since testosterone supplementation or treatment with a dopaminergic agonist can augment sexual response. However, large population studies have failed to find the expected positive correlations between sexual function and baseline serum testosterone levels. One possible explanation is that serum levels do not reflect the intracellular production of testosterone from adrenal and ovarian precursors.
Numerous psychosocial factors have been associated with reduced subjective arousal. These include distractions from other life stressors, expectations of a negative experience (eg, as a result of dyspareunia, the partner's sexual dysfunction, or negative experiences in the past), sexual anxiety, fatigue, and depression. Medications including selective serotonin-reuptake inhibitors and oral contraceptives have also been implicated in decreased sexual arousal. Oral contraceptives increase levels of sex hormone–binding globulin, which in turn reduces free testosterone levels; it is hypothesized that some women are particularly sensitive to these effects and may exhibit symptoms, whereas others would not.
On the basis of survey data, several factors have been closely linked to women's sexual satisfaction and desire. These include stable past and current mental health, positive emotional well-being and self-image, rewarding past sexual experiences, positive feelings for the partner, and positive expectations for the relationship. Certain diseases such as multiple sclerosis, renal failure, and premature menopause induced by chemotherapy are also associated with a high incidence of sexual dysfunction. In women, unlike men, vascular diseases associated with age (diabetes, metabolic syndrome, atherosclerosis) have not been clearly correlated with sexual dissatisfaction and problems in women.
A detailed history is the main tool in the assessment and diagnosis of sexual dysfunction and is best obtained from both partners. Important aspects of the history include the quality of the couple's relationship, the woman's mental and emotional health, the quality of past sexual experiences, specific concerns related to sexual activity (such as insufficient nongenital and nonpenetrative genital stimulation), and the woman's thoughts and emotions during sexual activity. A description of a recent sexual encounter may be instructive as it may reveal details that are not immediately disclosed in the history.
A physical examination, including a pelvic examination, is part of routine care. It is of primary usefulness in cases of dyspareunia to rule out superficial conditions (such as candidiasis, vestibulitis) and pelvic conditions (uterine leiomyomas, ovarian pathology) that may be associated with pain during sexual activity. Table 40–2 details features that are potentially relevant to sexual dysfunction that need to be assessed during an examination.
Table 40–2. Physical Examination Findings Potentially Relevant to Sexual Dysfunction. ||Download (.pdf)
Table 40–2. Physical Examination Findings Potentially Relevant to Sexual Dysfunction.
Sparsity of pubic hair, suggestive of low adrenal androgen levels
Vulvar skin disorders (eg, lichen sclerosus)
Cracks or fissures in interlabial folds suggestive of candidiasis
Labial abnormalities that may cause embarrassment
Splitting of posterior fourchette
Abnormalities of the hymen
Swelling of vestibular glands
Pelvic organ prolapse
Abnormal vaginal discharge
Hypertonicity of pelvic muscles
Presence of tender “trigger points” on palpation of levator ani muscles
Fixed retroversion of uterus, tenderness of vaginal fornix on bimanual exam causing deep dyspareunia
The possibility that laboratory testing will identify causes of sexual dysfunction is low. Estrogen deficiency, for example, can typically be detected by history and physical examination alone. In addition, serum testosterone has not been shown to clearly correlate with sexual function. Measurement of these hormones is of course warranted if supplementation of some kind is contemplated. Measurement of prolactin or thyrotropin is warranted if other symptoms or signs suggest the presence of abnormal levels.
The management of sexual dysfunction in women is guided by the history. Data from randomized trials that support the use of any particular intervention are limited.
Cognitive behavioral therapy focuses on identifying and modifying factors that contribute to sexual dysfunction, such as maladaptive thoughts, unreasonable expectations, behaviors that reduce the partner's interest or trust, insufficient erotic stimuli, and insufficient nongenital physical stimulation. Strategies are suggested to improve the couple's emotional closeness and communication and to enhance erotic stimulation. Sex therapy for couples is focused on similar issues but also includes sensate focus techniques, consisting initially of nonsexual physical touch, with gradual progression toward sexual touch; partners are encouraged to alternately touch each other and to provide feedback about what touches are pleasurable. These techniques may help to reduce performance pressure in situations where a “goal-oriented” approach toward sexual activity detracts from sexual enjoyment. Attention should also be directed to life stressors and relationship stress, as these factors are likely to exert an influence on a woman's sexual enjoyment.
Other than estrogen therapy for dyspareunia related to genitourinary atrophy, no medications are currently approved by the US Food and Drug Administration (FDA) for the treatment of sexual dysfunction in women. However, a testosterone patch for management of hypoactive sexual desire disorder has been approved for use in several European countries. In the United States, off-label use of several drugs has been reported, although data about effectiveness are sparse.
The involvement of nitric oxide in neurogenic vasodilatation suggests that phosphodiesterase type 5 inhibitors (PDE5I, used most commonly for erectile dysfunction in men) may ameliorate genital arousal disorder. In a small, laboratory-based, randomized trial, a single 50-mg dose of sildenafil (Viagra, Pfizer) increased subjective arousal, genital sensations, and ease of orgasm in some women with genital arousal disorder. The benefit was observed only among women who had a marked reduction in the normal vasocongestive response to subjectively arousing visual erotic stimulation. Sildenafil has also been shown to enhance orgasmic response in women with sexual dysfunction related to selective serotonin reuptake inhibitors (SSRIs). However, most large-scale studies of women with sexual dysfunction have not demonstrated meaningful improvements in sexual satisfaction amongst women treated with PDE5I. It is logical to speculate that PDE5I may be useful in women with a physical condition that tends to retard genital response with no or limited subjective component to the arousal disturbance; however, evidence to support this hypothesis is generally scant. Future studies are warranted to determine the potential role of PDE5I in this subset of women.
The prevalence of sexual disorders that are associated with the use of antidepressants in women is estimated at 22–58%, with higher rates reported for selective SSRIs and lower rates reported for bupropion. A recent meta-analysis of strategies to ameliorate dysfunction associated with antidepressants did not recommend any particular drug, although the potential advantages of adding bupropion were noted.
Flibanserin is a centrally acting agent with complex actions (both agonist and antagonist) on serotonergic and dopaminergic receptors. Flibanserin has reported efficacy in the treatment of hypoactive sexual desires disorder in women based on a series of phase III clinical trials in women. Approval for flibanserin was not granted by the FDA and its current status as a potential treatment for sexual problems in women is unclear.
Supraphysiologic androgen therapy has been prescribed for sexual dysfunction since the 1930s. More recently, testosterone at lower doses has been studied in randomized trials. The results of four recent randomized trials of testosterone in women have generally shown increases in sexually satisfying events, sexual desire, and response. Important limitations of these studies include their brevity (which is of particular importance, given the expected long-term use of the drug) and that their results are generalizable only to women in whom menopause was surgically induced and who also receive estrogen therapy. In some women who have undergone natural menopause, the ovaries continue to be an important source of androgens, and thus, the effects of androgen supplementation may differ from those whose ovaries have been surgically removed.
There are ongoing health concerns about the long-term supplementation of either androgens or estrogens. There are scant safety or efficacy data of testosterone supplementation for estrogen-deficient women. A chief concern with long-term androgen use is a potential increase in insulin resistance, which could predispose a woman to the metabolic syndrome or exacerbate the syndrome if it is already present. This is in addition to concerns regarding cosmetic side effects including hirsutism and acne.
The role of systemic estrogen in increasing desire and subjective arousal remains unclear. In the Women's Health Initiative trial, no significant differences were found between the estrogen and placebo groups in reported satisfaction after sexual activity. However, sexual dysfunction was not a primary focus of the trial, and the assessment tool was inadequate.
Recommendations and Conclusions
Recommendation guidelines for the evaluation and management of sexual dysfunction in women advocate attention to mental and physical health. Careful attention must also be directed toward both interpersonal and personal psychological issues. Local estrogen therapy is recommended for dyspareunia that is associated with vulvar atrophy that results in reduced sexual motivation. Testosterone therapy and PDE5I should be viewed as investigational and should be prescribed only by clinicians who are knowledgeable about sexual dysfunction in women.
A better understanding is needed of the endogenous and environmental factors that mediate sexual desire and arousal. Randomized clinical trials are also needed to assess the effects of psychological and pharmacologic therapies alone and in combination. The risks and benefits of long-term testosterone therapy require further study. The search for a nonhormonal medical treatment for female sexual dysfunction continues, although recent setbacks may lessen interest in this line of inquiry.