There are 4 main components of male sexual function
Sexual dysfunction is a problem with one of these components that interferes with interest in or ability to engage in sexual intercourse. Many drugs and numerous physical and psychologic disorders affect sexual function.
Libido is the conscious component of sexual function. Decreased libido manifests as a lack of sexual interest or a decrease in the frequency and intensity of sexual thoughts, either spontaneous or in response to erotic stimuli. Libido is sensitive to testosterone levels as well as to general nutrition, health, and drugs. Conditions particularly likely to decrease libido include hypogonadism (see Male Reproductive Endocrinology and Related Disorders: Male Hypogonadism), chronic kidney disease, and depression; up to 25% of men with diabetes may meet the definition of hypogonadism. Drugs that potentially decrease libido include weak androgen receptor antagonists (eg, spironolactone, cimetidine), luteinizing hormone-releasing hormone (LHRH) agonists (eg, leuprolide, goserelin, buserelin) and antagonists (eg, degarelix) used to treat prostate cancer, antiandrogens used to treat prostate cancer (eg, flutamide, bicalutamide), 5α-reductase inhibitors (eg, finasteride, dutasteride) used to treat benign prostatic hyperplasia, some antihypertensives, and virtually all drugs that are active in the CNS (eg, SSRIs, tricyclic antidepressants, antipsychotics). Loss of libido due to SSRIs or tricyclic antidepressants sometimes is reversible with the addition of bupropion or trazodone.
Erection is a neurovascular response to certain psychologic and/or tactile stimuli. Higher cortical input and a sacrally mediated parasympathetic reflex arc mediate the erectile response. Neural output travels through the cavernous nerves, which traverse the posterolateral aspect of the prostate. Terminating in the penis, these nonadrenergic, noncholinergic nerves activate nitric oxide synthase, producing nitric oxide, which relaxes cavernous smooth muscle within the corpora cavernosa. Blood flow within the sinusoids increases markedly, distending them and compressing outflow from the venules, causing veno-occlusion. The increased inflow and veno-occlusion together produce penile rigidity. Many factors affect the ability to have an erection (see Male Sexual Dysfunction: Erectile Dysfunction).
Ejaculation and Orgasm
Ejaculation is controlled by the sympathetic nervous system. Neural stimulation of the α-adrenergic receptors in the male adnexa (eg, penis, testes, perineum) causes contractions of the epididymis, vas deferens, and prostate that transport semen to the posterior urethra. Then, rhythmic contractions of the pelvic floor muscles result in pulsatile ejaculation of the accumulated seminal fluid. With reciprocal action, the neck of the bladder closes, preventing retrograde ejaculation of semen into the bladder. SSRIs may delay or inhibit ejaculation by receptor inhibition at these sites.
Orgasm is the highly pleasurable sensation that occurs in the brain generally simultaneously with ejaculation. Anorgasmia may be a physical phenomenon due to decreased penile sensation (eg, from neuropathy) or a neuropsychologic phenomenon due to psychiatric disorders or psychoactive drugs.
Ejaculatory dysfunction is reduced or absent semen volume. It may result from retrograde ejaculation, which may occur in men with diabetes or as a complication of bladder neck surgery or transurethral resection of the prostate. It also may result from sympathetic interruption, either due to surgery (eg, retroperitoneal lymph node dissection) or to drugs (eg, guanethidine, phentolamine, phenoxybenzamine, thioridazine). Radical prostatectomy eliminates any ejaculation.
Premature ejaculation is defined as ejaculation occurring sooner than desired by the man or his partner and causing distress to the couple. It is usually caused by sexual inexperience, anxiety, and other psychologic factors instead of disease. It can be treated successfully with sex therapy and SSRIs.
Last full review/revision February 2013 by Irvin H. Hirsch, MD
Content last modified March 2013