Brain processing of visual sexual stimuli in men with hypoactive sexual desire disorder

Abstract

Although hypoactive sexual desire disorder (HSDD) is a common condition and has long been hypothesized to result from malfunctions of the cerebral control mechanisms that adjust the level of sexual motivation, very little is known about the pathophysiology of this disorder. The primary objective was to identify in patients with HSDD brain regions where functional perturbations disrupt the regulation of sexual motivation. We used positron emission tomography to compare seven male patients with HSDD with eight healthy men on their regional cerebral blood flow responses to visual sexual stimuli (VSS) of graded intensity. Statistical Parametric Mapping was used to locate brain regions that demonstrated a differential activation (or deactivation) across the groups. Whereas in control subjects the medial orbitofrontal cortex showed a deactivation in response to VSS, in HSDD patients there was an abnormally maintained activity of this region, which has been implicated in the inhibitory control of motivated behavior. By contrast, the reverse pattern—activation in control subjects, deactivation or unchanged activity in patients—was found in the secondary somatosensory cortex and inferior parietal lobules, regions mediating emotional and motor imagery processes, as well as in those areas of the anterior cingulate gyrus and of the frontal lobes that are involved in premotor processes.

Introduction

The diagnostic category of ‘Inhibited Sexual Desire,’ introduced with the publication of DSM-III (American Psychiatric Association, 1980), was replaced in DSM-III-R by ‘Hypoactive Sexual Desire Disorder’ (HSDD), which does not imply any etiological assumption (American Psychiatric Association, 1987). High prevalence rates ranging from 1 to 15% of adult men (Nathan, 1986) have been reported in epidemiological studies. Regarding clinical studies, HSDD was reported to be the most frequent cause for consultation among sexual disorders (LoPiccolo and Friedman, 1988). In a trial of pharmacological therapy for sexual dysfunctions, 65% of the patients qualified for a primary diagnosis of HSDD (Segraves and Segraves, 1991). Little is known, however, about the etiology of HSDD, and it has been considered as the most difficult to treat among psychosexual disorders (Lief, 1977, LoPiccolo, 1980).

Regarding comorbidity, male patients with a DSM-III diagnosis of inhibited sexual desire with no associated current axis I disorder had elevated lifetime prevalence rates of affective disorder compared with controls free of sexual disorders (Schreiner-Engel and Schiavi, 1986). Similarly, elevations of scores on the depression scale of the Symptom Checklist-90-R have been reported in HSDD patients (Donahey and Carroll, 1993). HSDD is commonly concomitant with erectile dysfunction. In a sample of 113 males with HSDD, 53 (47%) had erectile impairment (Segraves and Segraves, 1991). Although erectile dysfunction is likely to be a consequence of HSDD, it has also been proposed that lack of sexual pleasure and performance anxiety due to erectile dysfunction may decrease sexual desire.

Relationship problems have been considered by some authors (Schwartz and Masters, 1988, Trudel et al., 1993) as contributing to HSDD, whereas the level of marital adjustment was found by others to lie within normative limits (Schiavi et al., 1992). Kaplan (1977) and psychoanalytic theorists (Apfelbaum, 1988, Scharff, 1988) have stressed the role of anxiety associated with sexual relationships. Kaplan (1995) later added a cognitive component, emphasizing that these patients unconsciously down-regulate their sexual desires by selectively focusing on features that they judge negative in their partners.

Few studies have been conducted on the role of biological factors. Compared with findings in healthy controls, lower levels of plasma testosterone (T) and a negative correlation between plasma T level and a global severity index of HSDD were observed in the patients during sleep (Schiavi et al., 1988). Even less is known about the neurophysiological aspects of HSDD. According to Kaplan (1995), HSDD results from malfunctions of the central nervous system control mechanism that normally adjusts the level of sexual motivation. In Kaplan's view, unless the brain structures that control sexual motivation are activated, it is impossible to experience sexual desire and HSDD results from a pathological overcontrol of these structures.

Interestingly, HSDD is generally attributed to an inhibition of an inherently normal sexual motivation. Given the change from inhibited sexual desire to HSDD, the possibility that these patients’ sexual motivation may be intrinsically low has rarely been considered. Because they can show which brain regions are activated or deactivated in response to sexual stimuli (Stoléru et al., 1999), brain functional imaging techniques are likely to be helpful in determining whether the essential pathophysiological mechanism of HSDD is an abnormal functioning of brain regions controlling sexual motivation and, more specifically, whether HSDD results from an intrinsically low level or from an inhibition of sexual motivation or from both mechanisms. The objective of this study was to identify the brain regions where functional perturbations disrupt the regulation of sexual motivation and are associated with HSDD. The brain responses of HSDD patients to visual sexual stimuli were compared with those of healthy subjects. This study is the first to apply a functional brain-imaging technique, namely positron emission tomography (PET), to investigate the cerebral correlates of HSDD. As these correlates may vary with gender, we began by studying male patients, because of our knowledge base in normal men (Stoléru et al., 1999) and the additional methodological difficulties entailed by cyclical hormonal changes in women.

On the basis of our previous study in normal men (Stoléru et al., 1999), we hypothesized that, compared with healthy controls, HSDD patients would respond to visual sexual stimuli (VSS) with a lesser activation of the left anterior cingulate gyrus, the right inferior frontal gyrus, the head of the right caudate nucleus and the right inferior temporal gyrus. Moreover, on the basis of the literature (Meisel and Sachs, 1994), we hypothesized that the hypothalamus would be more activated in controls than in HSDD patients. Finally, on the basis of the phenomenological experience of sexual desire as an urge to perform actions of a sexual nature, we hypothesized that premotor areas would be more activated in healthy men than in patients. We conceived of these various areas as participating in mediating the subjective perception of sexual desire. They could thus represent the ‘final common pathway’ (Kaplan, 1995) through which biological and psychosocial factors might interact in the perception of sexual desire.