Pharmacological Treatment

Although the behavioral techniques described above are generally successful in the treatment of premature ejaculation, there are some limitations associated with and concerns about this mode of treatment. While most patients who are able to comply with the full treatment course do well, about 25% of patients do not respond to behavioral treatments (Hawton et al. 1986). In addition, the treatment requires a cooperative partner for optimal outcome, which is not always feasible. There is also some evidence that the benefits from behavioral techniques are not always maintained in the long term. Hawton et al. (1986) found that in a 3-year follow-up, 75% of patients showed no lasting improvement over baseline. De Amicis et al. (1985) also found that immediate posttherapy improvement was not sustained by 3 years posttreatment. Some patients prefer pharmacotherapy because it is more easily hidden from a partner than scheduled psychotherapy sessions and requires less of a time and behavioral investment. The issue of payment for intensive behavioral therapy must be considered in the age of managed care. The cost-effectiveness argument is made less compelling by the availability of patient self-help books and films (e.g., Kaplan 1989), which can greatly reduce the need for frequent psychotherapy sessions.

Pharmacological options for the treatment of premature ejaculation have become more varied and better studied in recent years. Pharmacological agents that block sympathetic arousal, raise serotonin or prolactin levels, or have sedative effects may have the effect of delaying ejaculation (Buffum 1992; Segraves 1988, 1989, 1993). Multiple medications have been reported in individual case reports to be useful in the treatment of premature ejaculation. These include Korean red ginseng (Choi et al. 1995), prilocaine-lidocaine cream (Berkovitch et al. 1995), intracavernous injection of vasoactive drugs (Fein 1990), lorazepam (Segraves 1987), a-blockers (Beretta et al. 1986), and b-blockers (Cooper and Magnus 1984). While these options may have some efficacy, they are all associated with unwanted side effects that make them of limited value for most patients.

Interest in the role of antidepressants in the treatment of premature ejaculation arises from the many reports of delayed ejaculation as a side effect of these medications. Several reviews have described the potential utility of antidepressants in the management of premature ejaculation (Balon 1996; Rosen et al. 1999; St. Lawrence and Madakasira 1992). Multiple reports exist documenting the effect on ejaculation of various psychotropic agents, including the monoamine oxidase inhibitors (MAOIs) tranylcypromine (Simpson et al. 1965), phenelzine (Harrison et al. 1985; Rapp 1979), and isocarboxazid (Gross 1982); lithium (Blay et al. 1982); the tricyclic antidepressants imipramine (Glass 1981), clomipramine (Klug 1984; Quirk and Einarson 1983; Yassa 1982), and amitriptyline (Ninninger 1978); the atypicals trazodone, amoxapine, and maprotiline (Segraves 1992); and the serotonin reuptake-inhibiting antidepressants (SRIs) (Ashton et al. 1997; Forster and King 1994; McGilp 1993; Montejo-Gonzalez et al. 1997; Wise 1994). Delayed ejaculation is thus a potential side effect of nearly all antidepressants and appears to be dose-related and reversible with discontinuation of the medication. For the majority of patients taking antidepressants, this side effect is undesirable and can lead to noncompliance. However, for patients suffering from premature ejaculation, the side effect can be used to advantage.