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To the Editor:

This Journal's overlapping readership with the November 2002 “Male Infertility,” issue of the Urologic Clinic of North America prompted this submission. That periodical's Schuster and Ohl (2002) article provided an excellent review of ejaculatory anatomy, physiology, and processes, but requires 2 corrections. They wrote: “Three distinct physiologic phases of the ejaculatory process have been described: 1) bladder neck contraction, 2) emission, and 3) ejaculation.” This description failed to incorporate “ejaculatory process” into the entire sexual response cycle: desire, arousal, orgasm, and resolution (Kaplan, 1995). The ejaculatory process is part of the orgasm phase of the male sexual response. The male orgasmic response consists of 4 stages: bladder neck contraction, emission, ejaculation, and orgasm. Sexual arousal typically leads to this response. The fourth stage of orgasm is usually coincident with ejaculation, but represents a distinct, phenomenological central nervous system event experienced both cognitively and emotionally. Schuster and Ohl (2002) implied this, but did not articulate it directly. This 4-stage model recognizes both organic and psychogenic factors in our understanding of sexual function. Four stages provide a better heuristic model for understanding ejaculatory dysfunctions because disruptions of any stage in the orgasmic response result in the need for appropriate and specific treatments.

Schuster and Ohl's (2002) excellent review also did not recognize the clinically observed increasing incidence of inhibited ejaculation (IE). The incidence and prevalence of IE (retarded or delayed ejaculation) has increased in the last decade as the result of 2 iatrogenic factors: 1) wide-spread use of selective serotonin reuptake inhibitors with recognized antisexual adverse effects; and 2) IE is sometimes an unexpected sequela of treatments for erectile dysfunction (ED) (Perelman, 2001). Urologists hear some early complaints of IE secondary to penile prosthesis surgery and intercavernosal injection. However, sildenafil brought huge numbers of patients to physicians. Often, these patients experienced restored erections and orgasm. However, the effect of phosphodiesterase 5 inhibitors may be bimodal. Sildenafil successfully reversed some antidepressant sexual adverse effects (Nurnberg et al, 2003). Yet some sildenafil users became frustrated by the appearance of a new disconcerting symptom of IE. These men confused erection with sexual arousal, when for them it was merely a vasocongestive event. These men were not physically, emotionally, and sexually aroused enough to reach orgasm for many different reasons (Perelman, 2001). A pharmacological explanation offered by Master and Turek (2001), speculated that nitric oxide may negatively inhibit ejaculation. Contradictory evidence for the enhancing or inhibiting orgasmic value of sildenafil requires further exploration, but some of these men can become orgasmic with sex coaching. This author has used a cognitive-behavioral sex therapy integrated with medical/surgical ED treatments with over 100 cases in order to prevent and treat IE.

Respectfully, Michael A. Perelman, PhD NY Weill Cornell Medical Center

References

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  2. References
  • Kaplan HS. Disorders of Sexual Desire and Other New Concepts and Techniques in Sex Therapy. New York: Brunner/Mazel; 1995.
  • Master VA, Turek PJ. Erectile dysfunction, ejaculatory physiology, and dysfunction. Urol Clin North Am. 2001;28: 363375.
  • Nurnberg HG, Hensley PL, Gelenberg AJ, Fava M., Lauriello J., Paine S.. Treatment of antidepressant-associated sexual dysfunction with sildenafil: a randomized controlled trial. JAMA. 2003;289: 5664.
  • Perelman M.. Sildenafil, sex therapy, and retarded ejaculation. J Sex Educ Ther. 2001;26: 1321.
  • Schuster TG, Ohl DA. Diagnosis and treatment of ejaculatory dysfunction. Urol Clin North Am. 2002;29: 939948.