In a recent study we investigated whether pre- and postmenopausal women with sexual arousal disorder are less genitally responsive to visual sexual stimuli than pre- and postmenopausal women without sexual problems (42). Twenty-nine women with sexual arousal disorder (15 premenopausal and 14 postmenopausal), without any somatic or mental comorbidity, diagnosed using strict DSM-IV criteria, and 30 age-matched women without sexual problems (16 premenopausal and 14 postmenopausal) were shown sexual stimuli depicting cunnilingus and intercourse. Genital arousal was assessed as vaginal pulse amplitude (VPA) using vaginal photoplethysmography. We found no significant differences in mean and maximum genital response between the women with and without sexual arousal disorder, nor in latency of genital response. The women with sexual arousal disorder were no less genitally responsive to visual sexual stimuli than age- and menopausal status-matched women without such problems, even though they had been carefully diagnosed, using strict and unambiguous criteria of impaired genital responsiveness. These findings are in line with previous studies (43-45). The sexual problems these women report were clearly not related to their potential to become genitally aroused. In medically healthy women absent or impaired genital responsiveness is not a valid diagnostic criterion.
It is clear that the sexual stimuli used in this laboratory study (even though these stimuli were merely visual) were effective in evoking genital response. In an ecologically more valid environment (e.g., at home), sexual stimuli may not always be present or effective. Sexual stimulation must have been effective at one point in the participants' lives, because primary anorgasmia was an exclusion criterion. Even though a serious attempt was made to rule out lack of adequate sexual stimulation as a factor explaining the sexual arousal problems, data on sexual responsiveness collected in the anamnestic interview suggested that the women diagnosed with sexual arousal disorder are unable, in their present situation, to provide themselves with adequate sexual stimulation. The exclusion, halfway through the study, of a participant who no longer met the criteria for sexual arousal disorder after having met a new sexual partner, also illustrates that inadequate sexual stimulation may be one of the most important reasons for sexual arousal problems.
In this study, genital responses did not differ between the groups with and without sexual arousal disorder, but sexual feelings and affect did. The women with FSAD reported weaker feelings of sexual arousal, weaker genital sensations, weaker sensuous feelings and positive affect, and stronger negative affect in response to sexual stimulation than the women without sexual problems. Two explanations may account for this. Firstly, women with sexual arousal disorder may differ from women without sexual problems in their appreciation of sexual stimuli. These stimuli, even though they were effective in generating genital response, evoked feelings of anxiety, disgust, and worry. These negative feelings may have downplayed reports of sexual feelings, and were probably evoked by the sexual stimuli and not by the participants becoming aware of their genital response, because reports of genital response were unrelated to actual genital response. Negative appreciation of sexual stimuli may extend to, and perhaps even be amplified in, real-life sexual situations, because in such situations, any negative affect (i.e., towards the partner or the sexual interaction) may be more salient. Negative affect may, therefore, be partly responsible for the sexual arousal problems in the women diagnosed with sexual arousal disorder.
Secondly, women with sexual arousal disorder may be less aware of their own genital changes, with which they lack adequate proprioceptive feedback that may further increase their arousal. The general absence of meaningful correlations between VPA and sexual feelings in this and other studies (see next section) supports this notion. Perhaps women with sexual arousal disorder have less intense feedback from the genitals to the brain; there are no data, at present, to substantiate this idea. It is impossible to decide which of these explanations is more likely, because in real-life situations it can never be established with certainty that sexual stimulation is adequate, and awareness of genital response is dependent upon the intensity of the sexual stimulation. In addition, these explanations are not mutually exclusive. We can conclude, however, that the sexual problems of the women with sexual arousal disorder are not related to their potential to become genitally aroused. We propose that in healthy women with sexual arousal disorder, lack of adequate sexual stimulation, with or without concurrent negative affect, underlies the sexual arousal problems.
Organic etiology may underlie sexual disorders in women with a medical condition. There are only a handful of studies that have employed VPA measurements in women with a medical condition. The only psychophysiological study to date that found a significant effect of sildenafil on VPA in women with sexual arousal disorder was done in women with SCI (46), suggesting that in this group there was an impaired genital response that can be improved with sildena-fil. Another study compared genital response during visual sexual stimulation of women with diabetes mellitus and healthy women, showing that VPA was significantly lower in the first group (47). A very recent study measured VPA in medically healthy women, in women who had undergone a simple hysterectomy, and in women with a history of radical hysterectomy for cervical cancer (48). Only in the last group was VPA during visual sexual stimuli impaired, whereas the women with simple hysterectomies reported to experience more sexual problems than the other two groups. Not presence of sexual arousal problems but presence of a medical condition that influences sexual response may therefore be the most important determinant of impaired genital responsiveness (49).
Medical conditions that have been associated with sexual arousal disorder, other than SCI and diabetes, are pelvic and breast cancer, multiple sclerosis, brain injury, and cardiac disease (50). Mental disorders such as depression may also interfere with sexual function. It is important to consider the direct biological influence of disease on sexual pathways and function, but equally important is the impact of the experience of illness. Disease may change body presentation and body esteem; ideal sexual scenarios may be disturbed by constraints that accompany illness. In many patients, sexual arousal and desire may decrease in connection with grief about the loss of normal health and uncertainty about illness outcome (51). Damage to the autonomic pelvic nerves, which are not always easily identified in surgery to the rectum, uterus, or vagina, is associated with sexual dysfunction in women (52,53). Medications such as antihypertensives, selective serotonine reuptake inhibitors, and benzodiazepines, as well as chemotherapy, most likely due to chemotherapy-induced ovarian failure, impair sexual response (50). In addition, the incidence of women complaining of lack of sexual arousal increases in the years around the natural menopausal transition. According to Park et al. (54), postmenopausal women with sexual complaints, who are not on estrogen replacement therapy, are particularly vulnerable to what they call a vasculogenic sexual dysfunction. However, psychophysiological and preliminary functional magnetic resonance imaging studies of increases in genital congestion in response to erotic stimulation, fail to identify differences between pre- and postmenopausal women (55-57). This would suggest that although urogenital aging results in changes in anatomy and physiology of the genitals, postmenopausal women preserve their genital responsiveness when sufficiently sexually stimulated. The vaginal dryness and dyspareunia experienced by some postmenopausal women may result from longstanding lack of sexual arousal/protection from pain previously afforded by estrogen related relatively high blood flow in the unaroused state (58).
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