Defining Ejaculatory Disorders
Defining Ejaculatory Disorders
Ejaculatory response is the efferent (motor) component of a spinal reflex that typically begins with sensory stimulation to the glans penis (Kedia, 1983; McKenna, 1999). This reflex actually consists of two distinct efferent phases: an emission phase involving sympathetically controlled bladder neck closure and seminal emission from the prostate; and an expulsion phase involving somatically controlled (pudendal nerve) contractions of striate bulbo-cavernosal muscle and subsequent semen expulsion. Because this reflex is modulated by central processes, it is not surprising that most men report some degree of control over its timing (Rowland, Cooper, Houtsmuller, & Slob, 1997; Rowland, de Goveia Brazao, Strassberg, & Slob, 2000).
Men show substantial variation in ejaculatory thresholds and, therefore, along the latency-to-ejaculation continuum, with most men reporting latencies between about 2 and 10 minutes. However, some men ejaculate uncontrollably before or shortly after vaginal intromission and consequently may be classified as having premature ejaculation (PE). Others have difficulty reaching ejaculation and may be classified as having retarded or inhibited ejaculation (IE). These men either do not reach orgasm during intercourse or do so only after prolonged stimulation.
Although a number of measures have been suggested to define ejaculatory disorders, those that seem to have the most efficacy (and are most likely to show change following therapy) include latency to ejaculation and a sense of self-control over the timing of ejaculation (Rowland, Cooper, & Schneider, 2001; Rowland, 2003). Men who indicate no ejaculatory problems typically report fairly high control over the timing of ejaculation (e.g., 5 or higher on a 7 pt scale, where 1 = none at all). In contrast, men with PE report short latencies of less than one or two minutes, as well as a lack of control over ejaculatory timing (e.g., 4 or lower). Men with IE typically report very long latencies or an absence of ejaculation, although no specific criteria have yet been proposed for men with this understudied dysfunction.
The context in which the rapid or delayed ejaculation occurs is also relevant to a diagnostic classification. For example, some men classified as PE or IE report difficulty controlling the timing of their ejaculatory response only during coitus and not during masturbation, that is, the problem is most likely to surface during coital activity. Even then, mitigating factors such as the novelty of the partner or situation need to be considered when making an ejaculatory dysfunction diagnosis (DSM-IV, American Psychiatric Association, 2000). Other factors such as time since the last ejaculation (and, more generally, the frequency of orgasm: Grenier & Byers, 2001), use of medication, and the persistence of the problem are important to the diagnosis of an ejaculatory disorder. In all instances, the lack of efficacy regarding the problem is presumed to cause sufficient distress for the man and/or his partner to interfere with normal healthy sexual interaction. In some instances the couple may eventually avoid sexual activity altogether because of the problem.
Purported Causes of Ejaculatory Disorders in Men
Various somatic pathologies are known to disrupt normal ejaculatory function in men. For example, various medications and surgical procedures (radical prostatectomy) have been associated with PE. Spinal cord injury, multiple sclerosis, pelvic-region surgery, severe diabetes, SSRI antidepressants, and medications that inhibit -adrenergic innervation of the ejaculatory system have been associated with inhibited or retarded ejaculation in men (Master & Turek, 1999; Vale, 1999; Witt & Grantmyre, 1993). In the absence of obvious pathologies, however, no single etiology can clearly account for the majority of cases of PE or IE. Rather, as with most components of sexual response, ejaculation appears to be under the influence of both psychological-behavioral and biological processes. Therefore, it is not surprising that causes for ejaculatory disorders have been attributed to one or the other domains, or both (see Waldinger, 2003).
Premature ejaculation. Cognitive-behavioral explanations of PE have typically focused on centrally-mediated processes, and more specifically, on the interactions among levels of sexual arousal, awareness of arousal, and ejaculatory control. For example, such explanations posit that PE men may be less accurate in their ability to anticipate the moment of ejaculation, perhaps because they are less attuned to their level of arousal and therefore tend to underestimate it. Alternatively, these men may ejaculate rapidly because they reach high levels of sexual arousal very quickly, the result of a lack of control over their rapidly rising levels of sexual arousal (Kaplan, 1974; Masters & Johnson, 1970). Although recent studies are mixed regarding the idea that PE men may be less attuned to their arousal than functional counterparts, PE men may nevertheless ejaculate prior to their anticipated maximal arousal. That is, instead of ejaculating when they have reached maximum sexual excitement, they do so well before that moment, thus climaxing unexpectedly or prematurely. Due to the repeated experience of sexual failure, such cognitive inaccuracy and lack of control may be coupled with negative affect or anxiety, which itself may lower the sympathetically-mediated threshold to ejaculation.
Physiologically-based explanations of PE emphasize the spinal reflexive processes involved in the ejaculatory process. A number of studies have examined the latency and strength of event-related potentials (ERP’s) measured along afferent or efferent pathways of the spinal reflex, or within specific areas of somatosensory cortex. Although the evidence does not uniformly support differences between PE men and others (Rowland, Haensel, Bloom, & Slob, 1993; Xin, Chung, Choi, Seong,, & Choi, 1996), several studies report that PE men show greater penile sensitivity and stronger cortical ERP’s to stimulation of the pudendal afferent nerves and shorter latencies in the efferent processes involved in bulbo-cavernosal contractions eliciting seminal expulsion (Colpi, Fanciullacci, Beretta, Negri, & Zanollo, 1986; Fanciullacci, Colpi, Beretta, & Zanollo, 1988). Furthermore, because many antidepressants that affect central monoaminergic functioning also inhibit ejaculation, a role for centrally acting serotonin and/or norepinephrine has been postulated. While animal studies strongly argue for a role for serotonergic (5-HT1a) receptors in ejaculatory latency (e.g., Ahlenius, Larsson, Svensson, Hjorth, & Carlsson, 1981; Haensel, Mos, Olivier, & Slob, 1991), no direct neurophysiological evidence yet exists to support a role for this system in the etiology of rapid ejaculation in men. Indeed, due to the efficacy of pharmacological and/or biomedical treatments in countering rapid ejaculation, the cause of PE may sometimes be misattributed to physiological factors. Since all psychological and/or psychosocial factors are ultimately mediated through biological systems, any ejaculatory problem, whether the cause is biological or psychological, may be ameliorated by alterations in the functioning of biological pathways. With the investigative tools currently available, it is difficult to distinguish psychological-arousal processes related to ejaculation from the neural pathways and systems that mediate these processes.
Until more evidence becomes available, a clear understanding of the etiology of PE is unlikely. However, two ideas are worth reiterating. (1) As with most sexual disorders, there is probably no single cause for PE; rather this behavioral endpoint may result from a number of different causes. And (2), in the absence of either an obvious somatic or psychological etiology, premature ejaculation probably represents a mix of psychogenic and organogenic factors, and therefore might best be viewed in terms of a psychophysiological model (Strassberg, Kelly, Carroll, & Kircher, 1987). Such a model postulates that the disorder represents a combination of physiological vulnerabilities (e.g., hyperresponsivity or low threshold within the spinal reflex) and psychological conditions that interact to establish and maintain the dysfunction.
Given the lack of consensus (and supporting data) regarding possible etiologies of PE, it is not surprising that identification of clear subtypes of PE based upon cause has not been successful. Nevertheless, classification of PE into various subtypes based upon developmental histories and response characteristics has sometimes proved useful. For example, most clinicians and researchers distinguish between lifelong and acquired PE, and between PE that is limited to specific situations or partners and that which is more global. Thus, knowing that the patient has had a lifelong history of PE not specific to one partner may argue toward a biological and/or cognitive etiology. As such, the need to address interpersonal and relationship issues may be less important in these men. In contrast, knowing that the PE developed recently in specific situations and in conjunction with erectile dysfunction may suggest the need to address relationship issues and attend less to a biological etiology.
Inhibited ejaculation. Many men with inhibited or retarded ejaculation have no clear somatic factors that account for the disorder. As the result of their inability to ejaculate, these men also do not experience orgasm. Such men have been characterized as lacking awareness of their bodies, being inhibited psychologically due to guilt or wanting to maintain control, having inadequate sexual arousal and performance anxiety, being overly focused on pleasing the partner, or exhibiting negative affect (e.g., resentment or hostility) toward their partner (Geboes, Steeno, & DeMoor, 1975; Frank, Anderson, & Kupfer, 1976; Kaplan, 1974; Masters & Johnson, 1970; Muntjack & Kanno, 1979; Perelman, 2001). Largely due to the dearth of men with this dysfunction, empirical evidence supporting such assumptions has been based primarily on a handful of individual case studies rather than a systematic investigation of populations of men with this disorder. In fact, so little is known about this group that until recently no normative data have currently existed on general aspects of these men’s sexual response, for example, whether they demonstrate normal erectile response or levels of arousal in response to psychosexual stimulation. It is, therefore, not surprising that, in the absence of any commonly-delineated biological, psychological or behavioral etiology, standardized treatment procedures for this disorder have not been fully developed (Perelman, 2001).
Psychophysiological Exploration of Ejaculatory Disorders
One of the advantages of the psychophysiological approach is that it enables the exploration of interacting psychological and physiological factors in the study of sexual response in the context of a controlled laboratory environment. Not only can fairly precise control over stimulus conditions be achieved, but both outcome and predictor variables can be assessed with substantial precision and reliability. Psychophysiological analysis, then, allows investigation of genital response measures such as erection and ejaculation as a function of variables of presumed salience to these outcomes, such as the kinds of stimuli that are most likely to elicit the dysfunctional response, the patient’s self-reported levels of sexual arousal, the mitigating effects of anxiety and negative affect, dyadic relationship factors, and so on. Although the generalizability of laboratory findings to men’s response during sexual activity with their partner has been raised as a concern, psychophysiological studies for the most part seem to generate findings consistent with sexual response under more natural conditions, for example, with one’s partner (see Rowland, 1999; Rowland et al., 2000).
Psychophysiology of Premature Ejaculation
Stimulus relevance. Early psychophysiological research on men with PE was unable to differentiate their response from that of sexually-functional counterparts. For example, contrary to the expectation of hyperarousal in PE men (defined by shorter latencies to maximum arousal), several researchers (Kockett, Feil, Ferstl, Aldenhoff, & Besinger, 1980; Speiss, Geer, & O’Donohue, 1984) reported no differences between PE men and controls on erectile response to erotic visual stimuli. More recent research, however, suggests that in order to simulate conditions most likely to evoke the dysfunctional response of rapid ejaculation in PE men, the inclusion of direct penile stimulation (e.g., vibrotactile) is critical (Rowland et al., 1997).
Interestingly, self-selected intensity of penile vibrotactile stimulation (based on the criterion of “most pleasant”) does not seem to differ between controls and PE men. Nevertheless, when vibrotactile stimulation (VIB) is applied to the penis in conjunction with visual sexual stimulation (VSS), PE men’s responses clearly diverge from those of functional counterparts in several ways. First, regarding maximum penile response, penile stimulation has greater impact on men with PE than functional controls. Specifically, comparing across stimulus conditions (VSS vs. VSS + VIB), functional controls respond with equivalent maximum penile response, whether or not penile stimulation is included. In contrast, PE men’s maximum erectile responses increase by 20% when penile stimulation is included. Second, comparing across PE and functional groups, under VSS alone, PE men show lower maximum erectile response than functional counterparts, but equivalent erectile response under the stronger stimulus condition of both VSS + VIB. In other words, compared with controls, PE men do not show stronger maximum penile response to VSS + VIB, but rather weaker maximum penile response to just VSS.
Actual ejaculation as well as self-assessed measures of impending ejaculation also differ across PE and control groups. In the presence of VSS only, ejaculatory rates between PE men and controls are about the same. However, with the inclusion of penile stimulation, about 50-60% of PE men ejaculate compared with only about 0-8% of controls. In addition, those PE men who do not ejaculate during the session consistently report greater proximity to the ejaculatory threshold than functional counterparts. Furthermore, when subjects are asked about the control they felt over their ejaculation, functional subjects indicate no change between VSS alone vs. VSS + VIB, whereas PE men report a significant decrease in control during the combined visual and penile stimulation. Exactly what factors contribute to this sense of decreasing control in men with PE continues to be the subject of ongoing investigation and is discussed later in this review. Interestingly, when men with just PE group are compared with those with coexisting ED, the latter group reports greater loss of control over ejaculation than men with just PE. This finding calls into question the assumption that men with coexisting PE and ED may ejaculate rapidly primarily because they fear losing their erection (e.g., Kaplan, 1974; Buvat, Buvat-Herbaut, Lemaire, Marcolin, & Quittelier, 1990).
While these findings suggest that maximal erotic pleasure is derived from about the same penile stimulation intensity for both groups, they also verify the long-standing supposition regarding the particular relevance of penile stimulation to overall genital arousal and dysfunctional sexual response in PE men. Furthermore, this pattern appears consistent with the findings of Fanciullacci et al. (1988) who report that sensory stimulation of the penis has greater cortical representation (electrophysiologically), and thus perhaps subjective significance, in PE men than controls.
Self-reported sexual arousal. Conceptualizations of PE have often included the idea that men with this dysfunction become hyperaroused during sexual activity. For example, Kaplan (1974) has suggested that perhaps due to their anxiety, PE men are less cognizant of their sexual arousal, and in underestimating their state of high arousal, they ejaculate prior to expectation. Furthermore, the finding of a positive correlation between ejaculatory latency and frequency of sexual activity (Spiess et al., 1984; Grenier & Byers, 2001) has also implicated level of sexual arousal as a factor in PE. This correlation has been interpreted in two ways. The first is based on the fact that sexual arousal habituates to repeated stimulation (O’Donohue & Geer, 1985; Over & Koukounas, 1995). Specifically, habituation of arousal to sexual stimulation and/or ejaculatory inhibition due to the impact of refractory periods is less likely to occur in PE men because of their lower overall frequency of activity (LoPiccolo & Stock, 1986). The second is that because of their lower sexual activity along with their short ejaculatory latency, PE men may have had fewer opportunities to learn adequate control over their level of arousal and therefore the ejaculatory process (Kaplan, 1974). To date, however, such relationships are merely correlational.
The issue of arousal is actually twofold. First, whether PE men report higher levels of sexual arousal to psychosexual stimulation than functional controls. And second, whether PE men are less aware of their level of sexual arousal than others. Regarding the former, overall levels of self-reported sexual arousal to erotic visual stimulation appear to be no greater in PE men than controls (Kockott et al., 1980; Speiss et al., 1984). More recent analysis of self-reported sexual arousal to sexual stimuli that include penile stimulation seems to confirm this pattern. PE men report neither higher levels of arousal nor greater ease of becoming aroused to psychosexual stimulation than controls (Rowland et al., 2000).
Regarding the second issue—whether PE men are less cognizant of their high levels of arousal—again there is no clear distinction between PE men and controls. Strassberg et al. (1987), for example, have demonstrated that self-assessments of level of sexual arousal were not less accurate for PE men than controls. Furthermore, Rowland et al. (2000) reported no differences in the correlation between erectile response and self-reported arousal, or between erectile response and estimated erectile response, for PE men vs. controls. Such findings tend to negate the idea that PE men are less attuned to their level of sexual excitation.
However, one puzzling finding has emerged. Given their closer (self-reported) proximity to ejaculation than controls under conditions of penile stimulation, the fact that PE men do not report higher levels of arousal (Rowland et al., 2000) is surprising. Perhaps simple correlations between genital and subjective arousal do not capture all the relevant parameters regarding such psychophysiological relationships. For example, it is plausible that PE men show strong correlations between genital and subjective response, while at the same time consistently underestimating their genital response.
Anxiety and affective response of PE men. Relevant to the understanding of PE is whether affective states play a critical role in the etiology of the disorder. The affective component of sexual response—particularly anxiety—has long been theorized to play an underlying role in causing or sustaining sexual dysfunctions in men (Barlow, 1986; Kaplan, 1974; Masters & Johnson, 1970; Strassberg, Mahoney, Schaugaard, & Hale, 1990). However, even when specific affective states have been related to dysfunctional sexual response, it often remains unclear whether these states are part of the original etiology of the dysfunction, or whether they represent a reaction to failed genital response that then serves to exacerbate the problem (Bancroft, 1989).
Psychophysiological laboratory studies have provided some insight into the role of affect in dysfunctional response in men. Compared with sexually functional groups, men with PE exhibit higher negative and lower positive affect in response to erotic stimulation (Rowland, Cooper, & Heiman, 1995; Rowland, Cooper, & Slob, 1996), although this pattern has not always been demonstrated consistently (Strassberg et al., 1990).
Recently we (Rowland, Tai, & Slob, 2003) attempted to identify ways in which men with premature ejaculation differ from functional counterparts on specific positive and negative emotional dimensions, as well as to identify patterns of emotional responding that undergo change as the result of pharmacotherapy. Consistent with previous findings, PE men reported higher levels of negative emotions such as embarrassment/guilt, tense/worry, and anger/annoyed during baseline—prior to any psychosexual stimulation—than controls. Although specific negative affects diminished somewhat in PE men who responded positively to the ejaculatory-retarding effects of clomipramine, levels of both guilt/embarrassed and anger/annoyed were still elevated in comparison with controls.
Positive affect was also different between PE men and controls. Both at baseline and throughout the treatment phases, global positive affect was lower in PE men who did not experience beneficial effects from clomipramine than in either PE men who did or controls. Specific positive affects showed different patterns of variation. For example, arousal/sensual increased during erotic stimulation (relative to baseline) but decreased under clomipramine (relative to placebo). In contrast, pleasant/enjoyable decreased for PE “non-responders” during erotic stimulation (relative to baseline) under clomipramine, whereas under these same conditions, it increased for PE “responders.” The decrease in arousal/sensual during erotic stimulation under clomipramine in these presumably “strongly aroused” PE men may help explain why pleasant/enjoyable increased in PE-responders during treatment—attenuated arousal due to clomipramine might have been one of several factors that counteracted the dysfunctional response of rapid ejaculation. However, PE men who did not respond positively to clomipramine also showed a decrease in arousal/sensual during pharmacotherapy, indicating that the ejaculatory-inhibiting effects of clomipramine involve more than merely a blunting of sexual arousal.
The fact that successful pharmacotherapeutic treatment of rapid ejaculation imparts beneficial effects with respect to the overall enjoyment of sex suggests that the initial lower positive affect in PE men emanates from their dysfunctional response. Because positive affect increased spontaneously with successful treatment—perhaps due to a greater sense of efficacy and control over ejaculation—such emotions appear to be tied directly to the man’s level of functionality. The greater the level of sexual functioning, the greater the positive affect. In contrast, the finding that two of three negative emotions continued at higher levels in PE men relative to functional counterparts, even among PE men who were benefiting from the pharmacotherapy, suggests that elevated negative affect may play a role in the etiology of dysfunctional response in PE men. Further study is needed to determine whether specific negative affects associated with sexual dysfunction might generally be resistant to the beneficial effects of drugs that delay ejaculation in PE men. It may be, for example, that particular negative affects are more dispositional than response-related in PE men, an idea consistent with various psychometric analyses of men with this disorder (Cooper, Cernovsky, & Colussi, 1993; Tondo, Cantone, Carta, Laddomada, Mosticoni, & Rudas, 1991). Alternatively, had alleviation of the dysfunctional response been sustained through clomipramine treatment over a longer period of time, specific negative affects may have eventually decreased to levels comparable to controls. In either case, the implications of these findings are clear. PE men undergoing treatment with ejaculatory-retarding agents might well benefit from psychological intervention emphasizing open communication and relaxation with the partner to ease embarrassment and tension and to assist in overcoming negative dispositions associated with sexual contexts.
Detailed analysis of penile and heart rate responses in PE men. Assuming that rapidly-induced high levels of arousal in PE men lead to their short ejaculatory latencies, then we might also expect PE men to show strong erectile responses and short latencies to maximum tumescence. Yet existing evidence does not support this expectation—the two psychophysiological studies investigating this possibility have found no differences between PE and control groups on various erectile parameters, including latency to maximum erection (Kockott et al., 1980; Strassberg et al., 1987). Perhaps the stimulus parameters in these studies were not adequate to reveal such differences, as they were limited to visual sexual stimulation only (VSS) or manual self-stimulation. Neither included controlled penile vibrotactile stimulation (VIB) which enables simulation of conditions leading to rapid ejaculation in PE men (Rowland et al., 1997; Rowland et al., 2000) yet minimizes variation in erectile and ejaculatory response due to individual differences in penile stroke pressure, duration, and rate, as might occur with self-stimulation.
On the other hand, and somewhat counterintuitive, even though PE men ejaculate rapidly, there is reason to believe that they might actually exhibit weaker erectile responses compared with functional counterparts. As mentioned previously, men with PE report higher negative affect—a condition generally considered anti-erectile—in response to erotic stimuli than functional counterparts (Rowland, et al., 1996; Rowland et al., 2003). In addition, in response to psychosexual stimulation, PE men report greater difficulty getting an erection and weaker overall erections than functional counterparts, despite greater self-reported proximity to ejaculation (Rowland et al., 2000). Such affective states and self-perceptions of erectile response might suggest disruption of the typical autonomic processes involved in erection and ejaculation in these men. Specifically, parasympathetic dominance early in the sexual response cycle is normally necessary to initiate and sustain erection, with later sympathetic dominance responsible in part for mediating ejaculation. In men with PE, this typical progression from parasympathetic to sympathetic control may be disrupted, such that sympathetic activation dominates earlier in the sexual response cycle (e.g., from anxiety or negative affect), which in turn could interfere with parasympathetically-controlled erectile tumescence. At the same time, this sympathetic dominance may trigger ejaculation prematurely, perhaps even before the man reaches maximum sexual arousal. That is, even though PE men ejaculate rapidly following intromission and/or once coital or manual stimulation has begun, they might have greater difficulty and take longer to achieve an erection sufficient for intromission than functional counterparts. Although direct evidence supporting this hypothesis has yet to be garnered, circumstantial evidence is provided in a study by Ertekin, Colakoglu, & Altay (1995), who reported that during papaverine induced erections, PE men showed less suppression of sympathetically-mediated skin potentials than controls. Such findings suggest greater sympathetic activation than usual in PE men during the earlier phases of sexual response.
To determine whether the physiological response of PE men differs from that of sexually-functional counterparts, we undertook a detailed minute-by-minute analysis of penile response and heart rate in groups of PE and functional men during visual sexual stimulation and penile vibrotactile stimulation. Interestingly, 4 of 25 PE men (16%) did not show any erectile response (< 5 mm increase) during one or more of these sessions (VSS or VSS + VIB), whereas only 1 of 13 (8%) of controls showed no response. Under VSS, PE men showed lower average penile response than controls (Fig 1). Under VSS + VIB (Fig 2), PE men who did not ejaculate during the session continued to show lower average penile response than controls. PE men ejaculating after 3 min into the session did not differ from controls, and PE men ejaculating prior to 3 min showed greater average penile response (although due to the small sample, this was not significant).
Patterns of heart rate appear to distinguish PE men more clearly from functional counterparts (Fig 3 and 4). PE men exhibited higher heart rate throughout most of the VSS and VSS + VIB sessions. During VSS by itself, functional men showed a pattern of slightly decreasing heart rate as sexual arousal increased, whereas PE men showed an initial decrease followed by significant elevation (relative to controls) toward the end of the session. Differences between the groups were more pronounced when penile stimulation—the stimulus condition more likely to evoke the dysfunctional response—was introduced. Under VSS + VIB, functional men continued to exhibit a pattern of decreasing heart rate, just as they did under VSS alone. However, three PE men who ejaculated within the first 3 min of VSS + VIB showed immediate acceleration of heart rate. Nine PE men who ejaculated sometime after 3 min during the session showed an initial deceleration followed by an increase. And 12 PE men who did not ejaculate showed gradually increasing heart rates. Indeed, rapidly rising heart rate appears to be a reliable precursor to ejaculation in PE men. Maximum heart rates, maximum heart rate change from baseline (positive or negative), and heart rates at the end of each man’s recordings (this was variable, due to differing ejaculation times for these men), were all higher in PE men than controls.
Such patterns suggest that the physiological responses of PE men and controls may serve as distinguishing characteristics. Assuming both penile tumescence and heart rate adequately reflect sympathetic vs. parasympathetic control, these patterns suggest that sympathetic dominance may appear earlier in the session in PE men than controls. And because ejaculation is a sympathetically-mediated reflex, such early sympathetic dominance may partially explain the rapid ejaculation typical of PE men. These findings do not, however, clarify why sympathetic dominance might dominate earlier during psychosexual stimulation in PE men than controls. For example, might higher negative affect or some other psychobiological process shift control from the parasympathetic system, normally dominant during the erectile phase, to the sympathetic system, normally dominant during the ejaculatory phase? Or is the rapid sympathetic activation merely the manifestation of close proximity to ejaculation because of low ejaculatory thresholds?
Psychophysiology of Inhibited Ejaculation
To our knowledge, the sexual response of men with inhibited ejaculation has not been studied in the psychophysiological laboratory until recently. In a retrospective study using data from psychophysiological testing, we (Rowland, Keeney, & Slob, 2003) recently reported on the sexual response of men having retarded or inhibited ejaculation and orgasm with no overt somatic etiology. We were interested in whether IE men show inhibited erectile response or self-reported sexual arousal to psychosexual stimulation compared with sexually-functional men and other sexually-dysfunctional groups studied in our psychophysiological laboratory. We also attempted to identify dyadic relationship variables that might explain variation in erectile response and self-reported sexual arousal in men with this dysfunction. The exploration of this latter group of variables (dyadic relationship factors) was predicated upon prior theorizing that such factors may play a key role in this dysfunction.
Perhaps the most notable finding of this study was the relevance of self-reported maximum sexual arousal during psychosexual stimulation in the lab in differentiating IE men from the other groups. Specifically, IE men showed low self-reported sexual arousal relative to other groups of sexually-dysfunctional and functional men. This factor, more than actual erectile response, appeared to characterize men with this particular dysfunction. In fact, IE men had fairly robust erectile responses, comparable to PE men, suggesting that although their erectile response may have been adequate for achieving vaginal intromission, their level of subjective sexual arousal may not have been sufficient for the onset of the ejaculatory reflex. A similar pattern of adequate genital response in the absence of comparable subjective arousal has been described in women (Morokoff & Heiman, 1980).
Several dyadic relationship variables were correlated with self-reported arousal in IE men. Higher arousal value of the partner was significantly related to higher self-reported sexual arousal during psychosexual stimulation, whereas lower self-reported fear of sexual failure was related to higher sexual arousal. The fact that the few dyadic relationship variables investigated in this study could help explain variation in arousal among IE men reinforces the need to address potential dyadic interactions as part of an effective treatment strategy for this disorder. Procedures that reduce sexual anxiety and fear of failure through conflict resolution and trust-building, that reduce inhibition of arousal resulting from the need to control the sexual encounter, or that increase arousal through increased partner communication and stimulation strategies may serve to effectively increase subjective levels of sexual arousal in IE men.
Summary and Conclusions
The psychophysiological exploration of ejaculatory disorders both confirms and questions long-standing hypothetical assumptions about the causes and mechanisms of PE and IE. Through such analyses, a number of patterns have been uncovered:
• Rapid ejaculation in PE men occurs mainly in response to genital stimulation, not to erotic stimulation in general.
• The intensity of penile vibrotactile stimulation preferred by PE men is not different from that of sexually functional counterparts, as might have been anticipated.
• Self-reported sexual arousal is not greater in PE men than in sexually functional counterparts, suggesting that such men are not “hyperaroused.”
• PE men exhibit equally strong correlations between subjective arousal and penile response as controls, indicating either that they are adequately tuned to their levels of arousal or that this measure is not an adequate assessment of such attunement. The latter interpretation is made more likely by the fact that PE men, even though reporting closer proximity to ejaculation, do not report higher levels of sexual arousal than controls.
• PE men show lower positive affect to psychosexual stimulation than controls, although effective treatment of the disorder eliminates this difference, suggesting that low positive affect is primarily an outcome to the dysfunctional response rather than part of its cause.
• PE men are characterized by higher negative affect than controls, much of which does not diminish even with effective treatment. Negative affect may be more resistant to the beneficial effects of pharmacotherapy, supporting the idea that it may be more dispositional than situational in PE men.
• Penile response parameters in PE men may be weaker than in non-PE men. In addition, heart rate tends to accelerate in PE men but decelerate in sexually-functional controls during sexual stimulation. These differences suggest variation in autonomic control across groups during sexual arousal.
• Inhibited or retarded ejaculation my result from low arousal, as IE men show erectile responses comparable to PE men and, in some instances, controls. Relationship factors may play a mitigating role in levels of arousal in these men.
In conclusion, the psychophysiological model continues to afford heuristic value to the understanding of disorders of ejaculatory function in men. Despite the increasing availability of effective pharmacological agents for altering ejaculatory latencies, the causes of these disorders are yet largely unknown. Further delineation of the interaction between psychological and physiological covariates of ejaculatory dysfunction is likely to improve the application of integrated treatment approaches that take into consideration the psychological and dyadic relationship concerns that mediate and/or mitigate physiological response in men with PE or IE.