The Sexual Psychophysiology Laboratory - Resources - FSD

Female Sexual Arousal Disorder
Cindy Meston, Ph.D., Alessandra Rellini, Ph.D., & Christopher Harte, B.A.

The DSM-IV-TR defines Female Sexual Arousal Disorder (FSAD) exclusively in physiological terms as a persistent or recurrent inability to attain or maintain an adequate lubrication swelling response until completion of sexual activity. It has been suggested by a committee of experts in the field of women’s sexuality that three subtypes of FSAD would more accurately reflect women’s experiences with sexual arousal problems (Basson et al., 2003). These are: Subjective Sexual Arousal Disorder, which refers to the absence of feelings of sexual arousal, (sexual excitement and sexual pleasure), but vaginal lubrication or other signs of physical response still occur; Genital Sexual Arousal Disorder, which refers to absent or impaired genital sexual arousal (e.g., minimal vaginal lubrication from any type of sexual stimulation and reduced sexual sensations from caressing genitalia) but psychological sexual excitement still occurs; and Combined Genital and Subjective Arousal Disorder. Most women who complain of arousal problems would meet criteria for the combined category. While no prevalence data is available on the FSAD subtypes, the estimated lifetime prevalence of problems with general FSAD is 20% (Laumann et al., 1999).

Estrogen is critical for the maintenance of vaginal tissue function and structure and estrogen deficiency has been linked with various vaginal problems, including reduced or delayed lubrication, reduced vaginal blood flow, and increased likelihood of pain during sex. The majority of research on the effects of estrogen on sexual function has been conducted in postmenopausal women and women who have undergone surgery to remove their ovaries (oophorectomy). In post-menopausal women, the reduction in estrogen levels that occurs when the menstrual cycle ends is associated with increased pH levels in the vagina, a reduction or delayed onset of lubrication in response to sexual stimulation, and structural changes to the vagina and vulva such as thinning and reduction of elasticity of the vaginal wall, changes to the vaginal epithelium, and loss of collagen in the vulva (Bachmann, Ebert, & Burd, 1999). All of these changes can lead to arousal difficulties due to a reduction in tissue sensitivity and vaginal lubrication.

As noted earlier, in pre-menopausal women, androgens secreted from the adrenal glands and the ovaries and have been linked to desire mechanisms in women. Some speculate that androgens are also involved in female sexual arousal. One study found a positive correlation between testosterone and genital arousal in healthy, premenopausal women when levels of testosterone and arousal were compared across the menstrual cycle (Schreiner-Engel, Schiavi, Smith, & White,1981). A more recent study found that administering testosterone to premenopausal women increased their genital arousal (Tuiten, et al., 2002). Nitric oxide, the neurotransmitter involved in male erection, is produced in clitoral tissue and may also be important for women’s sexual arousal.

Sympathetic and parasympathetic nervous system arousal (SNS and PNS) both play a role in genital arousal in women, but the relationship between the two systems is not well understood. Norepinephrine (NE) is the primary neurotransmitter involved in SNS communication, and when measured after exposure to a sexually arousing film, blood levels of NE are higher than pre-film levels (Exton et al., 2000). Women with spinal cord injuries between areas T10 and T12 in the spinal cord show a lack of lubrication during psychological sexual arousal (Berard, 1989). This is the area of the spinal cord where sympathetic nerves project to the genital region. A number of laboratory studies have also provided evidence for the role of SNS involvement in women’s sexual arousal. Anxiety-evoking films, thought to increase SNS activity, have been shown to increase vaginal blood volume (a measure of genital engorgement) during subsequent erotic films in functional and dysfunctional women (e.g., Palace & Gorzalka, 1990). Recent research has shown a curvilinear relationship between acute anxiety and vaginal engorgement, with the optimal arousal response occurring at moderate levels of anxiety (Bradford & Meston, in press). Meston and colleagues have done several studies on the effects of exercise (e.g., Meston & Gorzalka, 1996) and ephedrine (Meston & Heiman, 1998) on sexual arousal, two manipulation techniques designed to increase SNS activity. These studies also support the notion that there is an optimal level of SNS arousal that is necessary for adequate genital arousal in women. Mechanisms that interfere with normal SNS activity, such as stress, can negatively impact a woman’s ability to become aroused.

Given the high coexistence of sexual desire and arousal problems in women, it is not surprising that myriad factors affecting women’s sexual desire noted earlier also affect women’s sexual arousal. According to the Dual-Control Model proposed by Bancroft and colleagues (Bancroft & Janssen, 2000), sexual arousal is the combination of both excitatory and inhibitory forces. Five main themes have been described as potential inhibitors or enhancers of sexual arousal for women ages 18 to 84 years: feelings about one’s body, negative consequences of sexual activity (e.g., bad reputation, pregnancy), feeling desired and accepted by a sexual partner, feeling ‘used’ by a sexual partner, and negative mood (Graham, Sanders, Milhausen, & McBride, 2004).

The assessment of FSAD is similar to that of HSDD in women and should include a comprehensive sexual, medical, and psychosocial history. Levels of physiological sexual arousal can be assessed indirectly using a vaginal photoplethysmograph to assess vaginal blood engorgement, sonograms (pictures of internal organs derived by sound waves bouncing off organs and other tissues) and fMRI (imaging techniques that track changes in blood concentration in inner organs) to assess blood engorgement in the genitals. These techniques are more commonly used for research purposes than as diagnostic tools.

Many of the psychological treatments described earlier to treat HSDD are used to treat psychological feelings of impaired sexual arousal. Physiological aspects of FSAD are most commonly treated with topical lubricants that help mask impairments in vaginal lubrication. They do not, however, enhance genital/clitoral blood flow or genital sensations that are often decreased with FSAD, and they do not directly impact psychological sexual arousal.

Currently, there are no Food and Drug Administration (FDA) approved pharmacological treatments for FSAD. However, since the enormous success of using PDE 5 inhibitors (e.g., sildenafil, levitra, cialis) for treating male arousal disorder (ED), a number of pharmaceutical companies have examined whether these and similar vasodilator drugs may also be effective for treating FSAD. Evidence from limited placebo-controlled studies indicate Viagra increases genital engorgement in healthy, premenopausal women (Laan, et al., 2002), and in postmenopausal women with severe levels of genital arousal concerns (Basson and Brotto, 2003). Despite reports of increased physiological sexual arousal, studies in general have not found these drugs positively impact a woman’s psychological experience of sexual arousal. This suggests that, for women, psychological factors such as relationship satisfaction, mood state, and sexual scenarios may play a more important role in assessing feelings of sexual desire and arousal than do physiological genital cues. The EROS clitoral therapy device (Urometrics, St. Paul , MN , USA ) is an FDA-approved treatment for women’s sexual concerns. This small hand held device increases vasocongestion in the clitoral and labial region via a suction mechanism and has been reported to increase vaginal lubrication and sensation (Billups, et al., 2001).