Treatment of Male Orgasmic Disorder

Because male orgasmic disorder is relatively rare, little systematic data are available regarding the outcome of psychotherapeutic treatment. The few studies that are available all suffer from small sample size, ranging from 1 to 10 patients. One review of the results of psychotherapy concluded that "the outcome is rather poor" (Dekker 1993). Given that the majority of male orgasmic disorder cases seen in practice probably involve some medical or pharmacological problem, the poor outcome may reflect inadequate medical screening or lack of a combined psychotherapeutic-physiological approach to treatment.

Psychotherapeutic Treatment

The standard psychotherapeutic treatment strategy for inhibited orgasm involves eliminating performance anxiety and ensuring adequate levels of physical stimulation. In this approach, the couple is instructed to caress the penis manually (and, if acceptable to the couple, orally) until erection is attained, but to cease stimulation whenever arousal is approaching the point of impending orgasm. This paradoxical instruction reduces goal-focused anxiety about performance and allows the man to enjoy the sexual pleasure provided by this caressing. Elements from the treatment program originally developed for inorgasmic women, including sexual activities that trigger orgasm and having the patient role-play an exaggerated orgasm, are also prescribed (Heiman and LoPiccolo 1988; LoPiccolo 1994). Once orgasm is occurring reliably with manual or oral stimulation, the same procedure is used during intravaginal intercourse.

Pharmacological Treatment

The most common cases of inhibited male orgasm now arise out of medication use, often to treat depression within this population of patients. Those most frequently experiencing this side effect are those taking SRI antidepressants that do not also block the 5-hydroxytryptamine type 2 (HT2) receptor (Ashton et al. 1997; Montejo-Gonzalez et al. 1997). There are five strategies to limit this side effect. Patients can wait for accommodation to this side effect to occur, although one study of 97 patients followed up to 38 months revealed that this was achieved in only 9.8% of patients (Ashton and Rosen 1998a). Another strategy would be to switch to an antidepressant with less likelihood of sexual dysfunction, although this may also put the patient at risk for relapse or alternative side effects. Drug holiday has been proposed and may be helpful for some well-informed patients but also may encourage noncompliance or lead to serotonin withdrawal syndrome (Rothschild 1995). A fourth strategy would be dosage reduction, but this, too, could lead to relapse if a prior unsuccessful dose is prescribed. Finally, an increasingly common strategy is to augment with a pharmacological antidote. Reports of successful use of these agents are accumulating without a clearly superior recommendation that can, as yet, be made. Strongest evidence for triumph in reversing SRI-induced sexual dysfunction appears to be for yohimbine at 5.4 mg three times a day (Ashton et al. 1997; Hollander and McCarley 1992; Jacobsen 1992). Other antidotes that appear promising include amantadine (Ashton et al. 1997; Balogh et al. 1992; Shrivastava et al. 1995), cyproheptadine (Ashton et al. 1997; Feder 1991; McCormick et al. 1990; Segraves 1993), stimulants (Bartlik et al. 1995), bupropion (Ashton and Rosen 1998b; Labbate and Pollack 1994), buspirone (Landen et al. 1999; Norden 1994), and sildenafil (Ashton 1999; Ashton and Bennett 1999; Nurnberg et al. 1999).