Sexual desire disorders

Normal sexual drive can be thought of as a balance between an “erotic motor,” which incites a desire for sexual activity, and a “sexual brake,” which keeps urges in check. These excitatory and inhibitory signals appear to converge upon specific centers in the hypothalamus and limbic system to produce a continuum of sexual desire. It is probably only the polar ends of this range that are abnormal (Fig. 33.1). There is no specific test for abnormal sexual desire. Instead, the diagnosis of a sexual desire disorder is based on the subjective reporting of abnormal libido that results in individual distress or interpersonal difficulty.

The two formally recognized sexual desire disorders are hypoactive sexual desire disorder (HSDD) and sexual aversion disorder. HSDD is defined as persistently or recurrently deficient (or absent) sexual fantasies or desire for sexual activity. Sexual aversion disorder is the persistent or recurrent extreme aversion to, and avoidance of, all (or almost all) genital sexual contact with a sexual partner. Of patients seeking treatment for sexual desire disorders, 79% have HSDD, 20% have sexual aversion disorder and 1% have hyperactive sexual desires. The causes of sexual desire disorders may be either organic or psychosocial. Organic causes include testosterone deficiency, chronic illness, certain centrally acting medications and underlying psychiatric disturbances. Psychogenic causes involve psychologically repressive stimuli such as anxiety, anger, perception of a partner as repulsive, or previous negative sexual experiences.

Treatment of the sexual desire disorders is directed first toward evaluation and correction of any underlying organic problem. Psychotherapy may be useful in the treatment of sexual desire disorders of nonorganic etiologies. Patients with long-standing sexual dysfunction of organic etiology often develop concomitant psychosocial issues. Individual or group counseling may be extremely useful as adjunctive therapy in these patients.

Erectile dysfunction (impotence)

Erectile dysfunction (ED) is the recurrent inability of a man to get and keep an erection sufficient for intercourse. ED is mild if a man can usually get and keep an erection, moderate if he can only can get or keep an erection sometimes and complete if he never can. Risk factors for ED include aging, chronic illnesses, a variety of medications and cigarette smoking. It is a common problem among older men; estimates report that 50% of 40- to 70-year-old men have some degree of ED. Even more are affected after the age of 70.

ED can occur because of vasculogenic, neurogenic, hormonal or psychogenic problems. Eighty per cent of the diagnosable conditions leading to ED are organic. They include, in decreasing order of frequency, atherosclerosis, diabetes, hypertension, medication side effects, prostate surgery, hyperthyroidism and hypothyroidism, hyperprolactinemia and hypogonadism. While depression is present in 60% of men with ED, it is often unclear whether this mood disorder is the cause or the result of long-standing ED.

Successful penile erection involves the activity of autonomic nerves upon the vascular smooth muscle of the penis. Relaxation of penile vascular smooth muscle allows blood to flow into the penis. Here it remains trapped and erection occurs (Chapter 13). Most of the organic causes of ED involve neuropathies of the autonomic nervous system, vascular compromise or, occasionally, testosterone deficiency. Psychogenic ED involves abnormal central inhibition of the erectile mechanism in the absence of demonstrable physical abnormality. The presence of morning erections in a man with ED may suggest a psychogenic etiology. Drugs that produce ED are myriad and typically affect the neural reflex pathways necessary for integrating the erection. Examples of medications associated with ED include antidepressants, antipsychotics, sedatives, antianxiety medications, antihypertensives and anticonvulsants. Alcohol and street drugs, including amphetamines, cocaine, marijuana, methadone and heroin, can also cause ED.

Until recently, treatment options for ED were limited to medication changes, implantable erection devices, intracavernosal injections of prostaglandins and psychotherapy. The discovery that the drug sildenafil can facilitate and maintain erections in impotent men has changed the treatment of ED dramatically. Sildenafil was originally tried as an antiangina medication and found to be ineffective. The study subjects were reluctant to turn in their leftover pills and soon the drug’s unexpected side effect was uncovered. Since then sildenafil, and related drugs, have been shown to be effective in the treatment of ED and have become widely available for this use. These medications work by inhibiting phosphodiesterase type V (PDE5), a cyclic guanosine monophosphate (cGMP) metabolizing enzyme found predominantly in the penis. Nitric oxide (NO) activates guanylate cyclase in the penis, increasing cGMP, the major mediator of the vascular relaxation necessary for penile erection. The longer cGMP stays around, the longer the duration of erection. Blockade of cGMP metabolism promotes and maintains NO proerectile activity. PDE5 inhibitors will not cause erections in the absence of sexual stimuli.