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2002 Selected Articles

Female Sexual Dysfunction

Diana L. Dell, MD, FACOG

Sexuality is a core human function. However, personal sexual function or dysfunction remains a difficult topic to discuss for both patients and physicians. Medical students have difficulty including a sexual history in their interviews, viewing sex as a "private matter" or fearing that the discussion may cause distress and embarrassment on both sides.¹ Nurses and nurse practitioners likewise shy away from taking sexual histories in a broad range of patient encounters.² Experienced physicians also see the exploration of sexual dysfunction as fraught with psychological and social difficulties not found in other clinical situations.³

Nonetheless, many women seek the advice of their primary care physician or a nurse practitioner for issues related to sexuality. Regardless of how difficult it is to discuss, primary sexual dysfunction is common, and sexual dysfunction secondary to chronic illness or its treatment has become almost universal.¹

The physiology of the female sexual response cycle was defined by Masters and Johnson⁴ based on their extensive research in the 1960s (Figure 1). They noted that the initial excitement phase is induced by any source of somatogenic or psychogenic stimulation. The stimulus is paramount in establishing sufficient sexual tension to extend the cycle.⁴

FIGURE 1.

From: Masters WH, Johnson VE. Human Sexual Response. Boston: Little, Brown & Co.; 1966;5.

Two important issues have emerged over the ensuing years. First, Masters and Johnson used a male model based on the supposition that male and female sexual responses were highly analogous, with women having a longer plateau phase than men and a shorter refractory period for repeat orgasm. Secondly, they concluded that excitement was first stage without adequately addressing libidinal issues. Subsequent work in this area clearly indicates that sexual desire or a cognitive decision to engage in sexual activity to meet nonsexual needs precedes the excitement phase in women.^4,5

FIGURE 2.

From: Basson R. Human sex-response cycles. J Sex & Marital Ther. 2001;27:34.

Basson⁶ has produced an intimacy-based model for the female sexual response cycle (Figure 2). She has expanded the model to integrate intimacy-based and sex-drive-based cycles (Figure 3).⁷

FIGURE 3.

From: Basson R. Female sexual response: the role of drugs in the management of sexual dysfunction. Obstet Gynecol. 2001;351.

Female sexual dysfunction appears to have many causes and many dimensions, including biologic, psychological, and interpersonal determinants. It is also age-related, worsening over time, and highly prevalent, affecting 20% to 50% of women by conservative estimates.⁵ Neither the classification systems in the World Health Organization International Classifications of Diseases-10 (ICD-10) nor the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, ed. 4 (DSM-4) has adequately addressed the complexities of female sexual dysfunction. To help remedy these inadequacies in classification, the Sexual Function Health Council of the American Foundation for Urologic Disease convened a consensus conference to revise definitions and classification in 1999. Using the Rand method, leading experts from multiple disciplines proposed the classification of female sexual dysfunction shown in Table 1.⁵

HYPOACTIVE SEXUAL DESIRE DISORDER

Hypoactive sexual desire disorder is defined as the persistent or recurrent deficiency (or absence) of sexual fantasies/ thoughts and/or desire for or receptivity to sexual activity that causes personal distress. It can be lifelong or acquired, generalized or situational, and have single or multiple etiologies.⁵ It is important to note that the condition must cause personal distress, which means that the partner’s distress alone is not sufficient to warrant diagnosis.

More than 30% of women aged 18 to 60 years lack interest in sexual activity, compared with approximately 15% of men.⁸ It is not uncommon for women with hypoactive sexual desire to have concomitant difficulties with sexual arousal and/or orgasm, but this is not universally true. The physiologies of desire, arousal, and orgasm are different entities, and therefore not interdependent. Women with decreased desire may have adequate sexual functioning; they just do not initiate sexual contact.⁹

Organic causes of hypoactive sexual desire have always included possible endocrine abnormalities, especially in women with lifelong difficulties and acquired postmenopausal dysfunction. Full endocrine evaluation should include at least follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels, thyroid function testing, prolactin values, and free testosterone levels. Numerous small studies continue to indicate that amount of circulating free testosterone may correlate with the experience of sexual thoughts, need for sex, and average coital frequency.¹⁰ Testosterone evaluation and supplementation in women are still relatively primitive clinically, with large-scale prospective studies clearly indicated.

Psychogenic etiologies for hypoactive sexual desire are numerous. The most common are depression, anxiety, stress, substance abuse, and fatigue. In addition, it is difficult to disentangle psychological causes from the many social roles women assume in our culture. Early in a relationship, women may have limited roles, being only a student/worker and daughter. As she evolves, her roles may broaden to include professional/worker, housewife, mother, daughter, friend, and lover. For many women, it appears that the importance of the lover role diminishes as the responsibilities in her other roles increase.⁹

Lifelong, generalized hypoactive sexual desire is more difficult to diagnose and treat, so the assistance of a sex therapist can be extremely helpful. Acquired and/or situational loss of desire requires thorough exploration of biopsychosocial changes that are temporally associated with the changes in sexual desire.

Pharmacologic treatments are generally directed toward the underlying cause (eg, major depression, menopausal vaginal changes). The primary endocrine treatment has been the use of oral or parenteral testosterone, although guidelines for appropriate treatment are still evolving.¹¹ Nonendocrine agents that have been used to treat hypoactive sexual desire include dopamine agonists (eg, sublingual apomorphine), [GK alpha]-blockers (eg, oral phentolamine, yohimbine), sildenafil (Viagra), and sustained-release bupropion (Wellbutrin-SR).^12-16 Limited sample size, limited efficacy, and intolerable side effects continue to hamper pharmacotherapy at present.

SEXUAL AVERSION DISORDER

Sexual aversion disorder is the persistent or recurrent phobic aversion to and avoidance of sexual contact that causes personal distress. It can be lifelong or acquired, generalized or situational, and have single or multiple etiologies.⁵

Women with low sexual desire may have neutral affect (eg, "take it or leave it" attitude) or negative affect (eg, sadness, frustration, embarrassment) about their condition. Women with sexual aversion disorder are generally fearful about sexual activity, and wish to avoid it.¹⁷

From a medical perspective, these women are more likely to have congenital abnormalities or chronic medical conditions. Psychologically, they are often victims of sexual trauma. Others received negative sex messages as children from their families or from school. Smaller numbers of women with sexual aversion disorder have extremely low self-esteem or confusion about sexual orientation. Trauma therapy or other forms of psychotherapy are generally most helpful for women in this group.^18,19

SEXUAL AROUSAL DISORDER

Sexual arousal disorder is the persistent or recurrent inability to attain or maintain sufficient sexual excitement, causing personal distress. It may be expressed as a lack of subjective excitement, genital response (lubrication/ swelling), or other somatic responses. It can be lifelong or acquired, generalized or situational, and have single or multiple etiologies.⁵

Physiologically, women with sexual arousal disorder do not produce adequate vaginal lubrication and engorgement. Organic causes include menopause and other medical illnesses. Psychologically, these women may have performance anxiety, conflict with their partners, or environmental interference (eg, children nearby). Some women in this category also received negative sex messages from childhood, have a history of sexual trauma, or experience confusion about sexual orientation.²⁰

Treatment for endocrine abnormalities, whether lifelong or acquired, will often improve vaginal response. Oral, topical, or other estrogen applications (eg, estrogen vaginal ring) have been used successfully. Topical lubricants are also helpful to women who cannot or will not use estrogen products. Psychotherapy, couples therapy, and sex therapy are useful for those women with primarily psychogenic causes for impaired sexual arousal.

ORGASMIC DISORDER

Orgasmic disorder is the persistent or recurrent difficulty, delay in, or absence of attaining orgasm following sufficient sexual stimulation and arousal, causing personal distress. It can be lifelong or acquired, generalized or situational, and have single or multiple etiologies.⁵Orgasmic dysfunction in women can have a multitude of organic and psychosocial causes (Figure 4). Treatment is origin-specific, with variable levels of success.²¹Women using selective serotonin reuptake inhibitors (SSRIs) commonly complain of absent or delayed orgasm. The effects of SSRIs on sexual functioning appear strongly dose-related, and may vary according to serotonin and dopamine reuptake mechanisms, induction of prolactin release, anticholinergic effect, inhibition of nitric oxide synthetase, and propensity for accumulation over time. The most common strategies used to treat this side effect include waiting for tolerance to develop (about 4 months), dosage reduction, drug "holidays," changing medications, and various augmentation strategies (Table 2).²²

FIGURE 4.

From: Maurice WL. Sexual Medicine in Primary Care. St Louis: Mosby; 1999;262.

SEXUAL PAIN DISORDERS

Dyspareunia is recurrent or persistent genital pain associated with sexual intercourse. Vaginismus is recurrent or persistent involuntary spasm of the musculature of the outer third of the vagina that interferes with vaginal penetration, again causing personal distress. Noncoital sexual pain disorder is recurrent or persistent genital pain induced by noncoital sexual stimulation. All of these sexual pain disorders may be lifelong or acquired, generalized or situational, and have single or multiple etiologies.⁵Dyspareunia is caused by both medical and psychological conditions that lead to the common clinical complaint of pain during intercourse. Among younger women, 10% to 15% complain of varying degrees of dyspareunia; among menopausal women, rates as high as 33% have been reported. Physical examination is extremely critical in this population to diagnose and treat organic causes. Mixed, psychogenic, or unknown causes are also common, so medical treatment that parallels psychosocial treatment is optimal.²³Vulvodynia is an especially challenging form of dyspareunia. During the 1990s, vulvodynia was the subject of a large volume of basic and clinical research. While there is little or no data to support the assumption of a psychological etiology, women are forced to cope with the psychological stress and relationship issues that result. There is usually a cascade of responses to chronic genital pain: initial pain experience, anticipation of subsequent pain, sexual avoidance, negative effects on the relationship, distressed emotional responses to both pain and relationship problems (eg, anxiety, fear, guilt, frustration, anger, depression), and development of additional sexual dysfunction. Cognitive-behavioral therapy and couples therapy have proved as helpful as vestibulectomy for this chronic pain condition.^24,25Vaginismus is a conditioned response resulting from associating sexual activity with pain and fear. The fear of vaginal penetration is accompanied by involuntary spasm of the pubococcygeal and associated muscles surrounding the lower third of the vagina. Attempted penetration not only causes pain, but exacerbates fear and feelings of inadequacy. Whether the condition is primary (lifelong, generalized) or secondary (acquired or situational), treatment is directed toward gaining control of the vaginal spasm. Anatomic education, cognitive therapy, and vaginal "trainers" of increasing diameters will help to desensitize the vagina and control the spasm.²⁶

CONCLUSION

Successful therapy for sexual disorders begins with the clinician’s sensitivity to indirect "clues" from the patient and willingness to ask basic questions about sexual function. An open, candid, and practical approach helps to reassure the woman that such problems are both common and treatable. Even if the patient is referred to a specialist, follow-up is essential to assess the effectiveness of treatment, discuss alternatives, and demonstrate the clinician’s ongoing concern for the patient’s well-being.

Diane L. Dell, MD, FACOG, is an assistant professor, Department of Psychiatry and Behavioral Sciences, and an assistant professor, Department of Obstetrics and Gynecology, Duke University Medical Center, Durham, NC.

REFERENCES

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4. Masters WH, Johnson VE. Human Sexual Response. Boston, Mass: Little, Brown & Co.; 1966:5.
5. Basson R, Berman J, Burnett A, et al. Report of the International Consensus Development Conference on Female Sexual Dysfunction: definitions and classifications. J Urol. 2000;163: 888-893.
6. Basson R. Human sex-response cycles. J Sex Marital Ther. 2001;27:33-43.
7. Basson R. Female sexual response: the role of drugs in the management of sexual dysfunction. Obstet Gynecol. 2001;98:350-353.
8. Laumann EO, Paik A, Rosen RC. Sexual dysfunction in the United States: prevalence and predictors. JAMA. 1999;281:537-544.
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11. Guay AT. Advances in the management of androgen deficiency in women. Med Asp Hum Sexuality. 2001;1(4):32-38.
12. Rosen RC. Sexual pharmacology in the 21st century. J Gen-Spec Med. 2000;3:45-52.
13. Rosen RC, Phillips NA, Gendrano NC III, et al. Oral phentolamine and female sexual arousal disorder: a pilot study. J Sex Marital Ther. 1999;25:137-144.
14. Caruso S, Intelisano G, Lupo L, et al. Premenopausal women affected by sexual arousal disorder treated with sildenafil: a double-blind, cross-over, placebo-controlled study. Brit J Obstet Gynaecol. 2001;108:623-628.
15. Piletz JE, Segraves KB, Feng YZ, et al. Plasma MHPG response to yohimbine treatment in women with hypoactive sexual desire. J Sex Marital Ther. 1998;24:43-54.
16. Segraves RT, Croft H, Kavoussi R, et al. Bupropion sustained release (SR) for the treatment of hypoactive sexual desire disorder (HSDD) in nondepressed women. J Sex Marital Ther. 2001;27:303-316.
17. Wincze JP, Carey MP. Sexual Dysfunction, 2nd ed. New York, NY : Gilford Press; 2001:14-16.
18. Wincze JP, Carey MP. Sexual Dysfunction, 2nd ed. New York, NY: Gilford Press; 2001:140-141.
19. Schwartz LB. Family systems discourse: conversations with clients concerning the impact of family legacies upon sexual desire. J Sex Marital Ther. 2001;27:603-606.
20. Wincze JP, Carey MP. Sexual Dysfunction, 2nd ed. New York, NY: Gilford Press; 2001:146.
21. Maurice WL. Sexual Medicine in Primary Care. St Louis, Mo: Mosby; 1999:260-276.
22. Rosen RC, Lane RM, Menza M. Effects of SSRIs on sexual function: a critical review. J Clin Psychopharmacol. 1999;19:67-85.
23. Graziottin A. Clinical approach to dyspareunia. J Sex Marital Ther. 2001;27:489-501.
24. Slowinski J. Multimodal sex therapy for the treatment of vulvodynia: a clinician’s view. J Sex Marital Ther. 2001;27:607-613.
25. Bergeron S, Binik YM, Khalife S, et al. A randomized comparison of group cognitive-behavioral therapy, surface electromyographic biofeedback, and vestibulectomy in the treatment of dyspareunia resulting from vulvar vestibulitis. Pain. 2001;91:297-306.
26. Butcher J. ABC of sexual problems II: sexual pain and sexual fears. Br Med J. 1999;318:110-112.

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