CHAPTER 52—DISORDERS OF SEXUAL FUNCTION
Our understanding of sexual function and dysfunction in older men has increased significantly in recent years. However, there is less scientific information on the sexuality of older women, possibly because of the difficulty of measuring the female sexual response and the exclusion of older adults from research. For example, the National Health and Social Life Survey, a study of adult sexual behavior, sampled adults only up to age 59.
Many factors play an important role in the sexual response of older women, including changes that occur with menopause, cultural expectations, relationship problems, previous sexual experiences, chronic illnesses, and depression. American women live about 29 years after menopause and outlive their spouses an average of 8 years. Although the frequency of intercourse decreases with aging, sexuality remains important for older women. One study found that among Swedish women aged 61 years, 59% were sexually active, but 43% experienced vaginal dryness and 10%, vaginal burning. In a study of British women aged 55 to 85, only 24% were found to be sexually active; 62% did not have a sexual partner. Lack of sexual activity among women with partners was found to be due to lack of the woman’s interest in intercourse (43%), lack of the man’s interest (24%), or the man’s illness or erectile dysfunction (29%).
The female sexual response cycle changes with aging. During the excitement phase, the clitoris may require longer direct stimulation, and genital engorgement is decreased. Vaginal lubrication is reduced, although with increased foreplay and gentle stimulation lubrication is usually adequate for intercourse. During the plateau phase, there is less expansion and vasocongestion of the vagina. During orgasm, fewer and weaker contractions occur, although older women can still achieve multiple orgasms. Occasionally during orgasm, the older woman experiences spastic and painful contractions of the uterine musculature. During the resolution phase, vasocongestion is lost more rapidly. Most of these changes are thought to be due to a decline in serum estrogen concentration after menopause, but a vasculogenic component may contribute to postmenopausal sexual dysfunction.
For the most part, menopause is accompanied by decreased sexual function, with decreased sexual interest, responsiveness, and coital frequency. In addition, there is an increase in urogenital symptoms, often not discussed with the physician. For example, a study of older British women found that 16% reported urinary urgency, dysuria, or frequency, 9% urinary incontinence, 11% vaginal itching, 8% vaginal dryness, and 2% painful intercourse. Among the women affected by vaginal dryness or painful intercourse, 33% did not seek professional advice and 36% resorted to over-the-counter medication (ie, lubricating jelly).
Dyspareunia, defined as pain with intercourse, can be due to organic or psychologic factors, or a combination of the two. For example, a woman may experience an episode of dyspareunia because of postmenopausal vaginal atrophy. With each subsequent sexual encounter she anticipates pain, causing inadequate arousal with decreased lubrication. Because of this cycle, the woman continues to experience dyspareunia, even after the vaginal atrophy has been treated. The most common organic cause of dyspareunia is atrophic vaginitis due to estrogen deficiency. Other causes include localized vaginal infections, cystitis, Bartholin cyst, retroverted uterus, pelvic tumors, excessive penile thrusting, or improper angle of penile entry.
Estrogen replacement can improve vaginal lubrication and sense of well-being, but it has little effect on libido. Libido is thought to be dependent on testosterone (even in women), rather than estrogen. The ovaries and adrenals are the main sources of androgens in women. Many investigators believe that there is a “female androgen deficiency syndrome,” with impaired sexual function, loss of energy, depression, and serum total testosterone concentrations in the lower end of normal for women (< 15 ng/dL), but there is no clear-cut definition. The effects of female androgen deficiency were originally identified in women treated for advanced breast cancer with oophorectomy and adrenalectomy. When deprived of androgens, these women reported loss of libido. In a double blind, randomized controlled trial, surgically menopausal women on estrogen replacement were randomized to placebo or testosterone patches that deliver 150 or 300 μg of testosterone daily. After 12 weeks, only the women randomized to the higher dose reported improvements in frequency of sexual activity, pleasure, orgasm, sexual fantasies, masturbation, and positive well-being. This dose increased mean serum free testosterone into the upper normal range for healthy younger women. In naturally postmenopausal women, some, but not all, studies have shown that the addition of testosteroneOL to estrogen replacement therapy improves sexual function. (Testosterone has not been approved by the U.S. Food and Drug Administration [FDA] for the treatment of sexual dysfunction in women.)
Older women commonly have multiple medical ailments, some of which affect sexuality. However, there are limited scientific studies of the effect of chronic diseases and medications on the sexuality of older women. Women with diabetes mellitus report decreased libido and lubrication, and longer time to reach orgasm. Rheumatic diseases affect sexuality via functional disability. After mastectomy for breast cancer, 20% to 40% of women experience sexual dysfunction, possibly because of disruption of body image, marital and family problems, spousal reaction, adjuvant therapy, or the psychologic impact of a breast cancer diagnosis. Several drugs can adversely affect sexual function, including antihistamines, antihypertensives, antidepressants, antipsychotics, antiestrogens, central nervous system stimulants, narcotics, alcohol, and anticholinergic drugs.
Psychosocial factors have an important role in sexual dysfunction. Women commonly marry men older than themselves and live longer than men. Consequently, heterosexual older women are likely to spend the last years of their lives alone. Even when a partner is available, he might have erectile dysfunction. Finally, lack of privacy may be a problem when the older couple lives with their children or in a nursing home.
The history is the most important part of the evaluation of sexual function, and careful questioning can detect problems that the woman might not otherwise volunteer. First, it is important to attempt to provide a comfortable atmosphere. Clinicians should ask about dyspareunia, lack of vaginal lubrication, and previous negative experiences, like rape, child abuse, or domestic violence. Medications should be carefully reviewed. A woman with dyspareunia should undergo a pelvic examination to exclude organic causes.
Dyspareunia due to atrophic vaginitis and decreased lubrication responds well to topical or systemic estrogen therapy. However, it is important to explain to the patient that complete restoration of vaginal tissue function may take up to 2 years. A vaginal estradiol ring delivers low-dose estrogen locally with lower systemic absorption and risks of systemic side effect than do vaginal estrogen creams. The ring is inserted into the upper third of the vaginal vault and replaced every 3 months. If the patient is not a candidate for or does not want to use estrogen, water-soluble vaginal lubricants (eg, Replens, Astroglide, K-Y jelly) are beneficial. Importantly, local stimulation through regular intercourse helps maintain a healthy vaginal mucosa. Longer foreplay allows more time for vaginal lubrication, just as older men often need longer and more direct stimulation to achieve an adequate erection.
Decreased libido may respond to testosterone, but no androgen preparation is approved by the FDA for female sexual desire disorders. Testosterone for women is available only in combination with estrogens and is FDA approved for moderate to severe vasomotor symptoms that are not improved with estrogens alone. Therapy is usually initiated with oral esterified estrogen 0.625 mg and methyltestosterone 1.25 mg. If symptoms do not improve, the dose can be doubled to esterified estrogen 1.25 mg and methyltestosterone 2.5 mg. Pharmacokinetic studies identifying appropriate replacement doses are lacking. The masculinizing side effects of testosterone, such as increased facial hair, are infrequent, dose dependent, and, for the most part, reversible upon discontinuation. Hepatic toxicity has been noted only in female-to-male transsexuals receiving very high doses of oral methyltestosterone. Oral methyltestosterone should not be used in women with liver disease and uncontrolled hyperlipidemia, as it may decrease high-density lipoproteins. In a 9-week study of postmenopausal women, esterified estrogens (1.25 mg a day) were found to decrease low-density lipoproteins and increase high-density lipoproteins, while the same dose of estrogens plus oral methyltestosterone (2.5 mg a day) decreased high-density lipoproteins. Lipid profile and liver function should be checked at baseline and every 6 months during therapy. Further studies of the best dosage, delivery system, long-term efficacy, and safety of testosterone are needed.
Randomized trials of sildenafil for female sexual dysfunction yielded conflicting results. The manufacturer has therefore decided not to apply for a license to use sildenafil in women.
Finally, the older woman should receive education about male sexual aging in addition to female sexual aging. Otherwise, she might mistakenly attribute her partner’s diminished erection and need for more genital stimulation to her own inability to arouse her partner. Other psychologic issues, including depression, history of sexual abuse, and relationship problems, should be addressed and treated with antidepressants, psychotherapy, and marital therapy, as necessary. Table 52.1 summarizes treatments for female sexual dysfunction.
As men age, their sexuality changes. The frequency of sexual intercourse and the prevalence of engaging in any sexual activity decrease. Young men report having intercourse three to four times per week, whereas only 7% of men aged 60 to 69 years and 2% of those aged 70 years and older report the same frequency. Fifty percent to 80% of men 60 to 70 years old engage in any sexual activity, a prevalence rate that declines to 15% to 25% among those aged 80 years and older. However, sexual interest often persists despite decreased activity. The man’s level of sexual activity, interest, and enjoyment in younger years often determines his sexual behavior with aging. Factors contributing to a man’s decreased sexual activity include poor health, social issues, partner availability, decreased libido, and erectile dysfunction.
Aging is associated not only with changes in sexual behavior but also with changes in the stages of sexual response. During the excitement phase, there is a delay in erection, decreased tensing of the scrotal sac, and loss of testicular elevation. The duration of the plateau stage is prolonged, and pre-ejaculatory secretion is decreased. Orgasm is diminished in duration and intensity, with decreased quantity and force of seminal emission. During the resolution phase, there is rapid detumescence and testicular descent. The refractory period between erections is also prolonged. However, erectile dysfunction is not a part of healthy aging.
Erectile dysfunction is the inability to achieve or maintain an erection adequate for sexual intercourse. The prevalence of erectile dysfunction increases with age; by age 70 years, 67% of men have erectile dysfunction. This high prevalence is important; in a study comparing affected and unaffected men, men with sexual dysfunction reported impaired quality of life. The causes of sexual dysfunction in men are summarized in Table 52.2.
The most common cause of erectile dysfunction in older men is vascular disease. Risk for vascular erectile dysfunction increases with traditional vascular risk factors such as diabetes mellitus, hypertension, hyperlipidemia, and smoking. In fact, erectile dysfunction is a predictor of future major atherosclerotic vascular disease (ie, myocardial infarction and stroke).
Obstruction from atherosclerotic arterial occlusive disease likely impedes the intracavernosal blood flow and pressure needed to achieve a rigid erection. In addition, atherosclerotic disease may cause ischemia of trabecular smooth muscle and result in fibrotic changes leading to failure of venous closure mechanisms. Venous leakage leading to vascular erectile dysfunction may also result from Peyronie’s disease, arteriovenous fistula, or trauma-induced communication between the glans and the corpora. In anxious men who have excessive adrenergic-constrictor tone and in men with injured parasympathetic dilator nerves, erectile dysfunction can occur from insufficient relaxation of trabecular smooth muscle.
The second most common cause of erectile dysfunction in older men is neurologic disease. Disorders that affect the parasympathetic sacral spinal cord or the peripheral efferent autonomic fibers to the penis impair penile smooth muscle relaxation and prevent the vasodilation necessary for erection. In patients with spinal cord injury, the extent of erectile dysfunction largely depends on the completeness and the level of the spinal injury; those who have complete lesions or injury to the sacral spinal cord are more likely to have loss of erectile function. Common health problems such as diabetes mellitus, stroke, and Parkinson’s disease can cause autonomic dysfunction that results in erectile failure. Finally, surgical procedures such as radical prostatectomy, cystoprostatectomy, and proctocolectomy commonly disrupt the autonomic nerve supply to the penis, resulting in postoperative erectile dysfunction.
Numerous commonly used medications have been associated with erectile dysfunction for which the mechanism, for the most part, is unknown. Those medications with anticholinergic effects, such as antidepressants, antipsychotics, and antihistamines, may cause erectile dysfunction by blocking parasympathetic-mediated penile artery vasodilatation and trabecular smooth muscle relaxation. Almost all antihypertensive agents have been associated with erectile dysfunction; of these, β-blockers, clonidine, and thiazide diuretics have higher incidence rates. One mechanism may be the lowering of blood pressure below the critical threshold needed to maintain sufficient blood flow for penile erection, especially in those men who already have penile arterial disease. Over-the-counter medications such as cimetidine and ranitidine may also cause erectile dysfunction. Cimetidine, an H2-receptor antagonist, acts as an antiandrogen and increases prolactin secretion and thus has been associated with loss of libido and erectile failure. Ranitidine can also increase prolactin secretion, although less commonly than does cimetidine.
The prevalence of psychogenic erectile dysfunction correlates inversely with age. Psychogenic erectile dysfunction may occur via increased sympathetic stimuli to the sacral cord, inhibiting the parasympathetic dilator nerves and thus inhibiting erection. Common causes of psychogenic erectile dysfunction include relationship conflicts, performance anxiety, childhood sexual abuse, and fear of sexually transmitted diseases. Older men may have “widower’s syndrome,” in which the man involved in a new relationship feels guilt as a defense against subconscious unfaithfulness to his deceased spouse.
The role of androgens in erection is unclear. Hypogonadal men show smaller and slower developing erections in response to fantasy, which is improved with androgen replacement. However, even men with castrate levels of testosterone can attain erections in response to direct penile stimulation. It may be that erection to certain types of sexual stimuli (ie, direct penile stimulation) are androgen independent, whereas response to fantasy may be androgen sensitive. Overall, testosterone appears to play a minor role in erectile function and a larger role in libido. In addition, hypogonadal patients respond better to phosphodiesterase inhibitors after testosterone replacement therapy.
Hyperthyroidism, hypothyroidism, and hyperprolactinemia have been associated with erectile dysfunction. However, less than 5% of erectile dysfunction is caused by endocrine abnormalities. Thus, endocrine evaluation of men with erectile dysfunction but intact libido is of limited value.
The initial step in evaluation is to obtain a sexual, medical, and psychosocial history. Sexual history should clarify whether the problem consists of inadequate erections, decrease in libido, or orgasmic failure. The onset and duration of erectile dysfunction, the presence or absence of sleep-associated erections, and associated decline in libido may lead the clinician to the likely cause.
Sudden onset suggests psychogenic or drug-induced erectile dysfunction. A psychogenic cause is likely if there is sudden onset but sleep-associated erections or if erections with masturbation or another partner are intact. However, if the sudden onset is accompanied by lack of sleep-associated erections and lack of erection with masturbation, temporal association with new medication should be sought. A gradual onset of erectile dysfunction associated with loss of libido suggests hypogonadism.
Medical history is directed at discerning those factors likely to be contributing to erectile dysfunction. Vascular risk factors include diabetes mellitus, hypertension, coronary artery disease, peripheral arterial disease, hyperlipidemia, and smoking. Neurogenic risk factors include diabetes mellitus, history of pelvic injury or surgery, spinal injury or surgery, Parkinson’s disease, multiple sclerosis, and alcoholism. An extensive medication review, including over-the-counter medications, is also essential. Finally, the psychosocial history should assess the patient’s relationship with the sexual partner, the partner’s health and attitude toward sex, economic or social stresses, living situation, alcohol use, and affective disorders.
On physical examination, signs of vascular or neurologic diseases must be sought. Peripheral pulses should be palpated. Signs of autonomic neuropathy and loss of the bulbocavernosus reflex suggest neurologic dysfunction. The genital examination includes palpating the penis for Peyronie’s plaques and assessing for testicular atrophy. A femoral bruit and diminished (or absent) pedal pulses suggests arterial insufficiency. An absent bulbocavernosus reflex in a patient with diabetes mellitus suggests penile neuropathy. A loss of secondary sexual characteristics, small testes, and gynecomastia suggest hypogonadism.
Appropriate laboratory evaluation are those that target relevant comorbid conditions such as diabetes mellitus and vascular disease or that evaluate neurologic disorders if suggested by the physical examination. Consider the measurement of total testosterone in the setting of other symptoms of androgen deficiency. (See Endocrine and Metabolic Disorders.)
An office-based diagnostic tool that can help direct the treatment of erectile dysfunction is intracavernous injection of a vasoactive drug, such as papaverine or alprostadil (formerly prostaglandin E1, or PGE1). An initial test dose of 15 to 30 mg of papaverine is used if the history and examination suggest a neurogenic cause. A 30-gauge needle and 1-cc syringe are typically used for the injection. Hold the glans of the penis with one hand and clean the injection site with an alcohol swab. Then, holding the needle parallel to the floor, insert the needle into the side of the penis to avoid the urethra. Inject the vasoactive agent over 30 to 60 seconds. After withdrawing the needle, apply pressure to the injection site for 1 minute to prevent bruising. An erectile response will occur within 15 minutes and may last up to 40 minutes. A poor response suggests arteriogenic or venogenic erectile dysfunction, inadequate dose of vasoactive agent, or anxiety with excessive adrenergic tone. A second trial injection at the next office visit with a higher dose (30 to 60 mg papaverine) or alprostadil (5 to 20 μg) may be used.
An at-home therapeutic trial of a phosphodiesterase inhibitor (sildenafil or vardenafil) is easier than the in-office diagnostic penile injection of a vasodilator. The initial dose should be low (sildenafil 25 to 50 mg or vardenafil 5 to 10 mg) in men suspected of having neurogenic erectile dysfunction. A poor response suggests vasculogenic erectile dysfunction. Further therapeutic trial with sildenafil 100 mg or vardenafil 20 mg may prove to be effective. An at-home therapeutic trial using tadalafil (5 to 10 mg) can be considered, but the long half-life complicates matters if an adverse reaction occurs with the first dose.
More extensive diagnostic tools are available but not commonly used. Nocturnal penile tumescence testing is of little value, except to confirm a psychogenic cause. The penile brachial pressure index may be helpful in assessing arteriogenic erectile dysfunction. This index measures the loss of systolic pressure between the arm and the penis. When measured before and after exercise, it can be used to assess for a pelvic steal syndrome, which is the loss of erection associated with initiation of active pelvic thrusting, presumably due to the transfer of blood flow from the penis to the pelvic musculature. More invasive and expensive tests such as Doppler ultrasound to assess penile arterial function, dynamic infusion cavernosometry to assess venous leakage syndrome, and penile arteriography are generally reserved for research or penile vascular surgery candidates.
Multiple effective therapeutic options are now available for the treatment of erectile dysfunction. Treatment should be individualized and based on cause, personal preference, partner issues, cost, and practicality of the therapeutic modality (Table 52.3).
Oral therapy for erectile dysfunction consists of sildenafil, vardenafil, or tadalafil. Sildenafil is a type-5 phosphodiesterase inhibitor that potentiates the penile response to sexual stimulation. It is effective in improving the rigidity and duration of erection. It is taken 1 hour before sexual activity and has no effect until sexual stimulation occurs. Because absorption is attenuated when sildenafil is ingested with a fatty meal, patients need to be educated about this issue. Vardenafil is a more potent and specific phosphodiesterase inhibitor. A lower effective dose and better side-effect profile (no effect on color vision) make vardenafil a reasonable option. Tadalafil is a longer acting phosphodiesterase inhibitor with a similar side-effect profile. All three of these agents are contraindicated for concomitant use with nitrate drugs, since the combination can produce profound and fatal hypotension. Choosing between the three currently available phosphodiesterase inhibitors should likely be based on price. There are also labeling differences with the α-blockers that need to be taken into consideration.
Vacuum tumescence devices are an effective and accepted treatment. The apparatus consists of a plastic cylinder with an open end into which the penis is inserted. A vacuum device attached to the cylinder creates negative pressure within the cylinder, and blood flows into the penis to produce penile rigidity. A penile constriction ring placed at the base of the penis then traps the blood in the corpora cavernosa to maintain an erection for about 30 minutes. The vacuum device is effective for psychogenic, neurogenic, and venogenic erectile dysfunction, but it requires manual dexterity. Local pain, swelling, bruising, coolness of penile tip, and painful ejaculation are potential side effects. It is important to remove the constriction ring after 30 minutes.
Intracavernous injection of vasoactive drugs such as papaverine, phentolamine, and alprostadil are effective in producing erections adequate for sexual activity. Alprostadil, which is the only agent approved by the FDA for intracavernous injection, produces erections that last 40 to 60 minutes. PhentolamineOL is mainly used in combination therapy with papaverineOL or alprostadil, or both. Potential side effects are bruising, ecchymoses or hematoma, local pain, fibrosis from repeated injections, and priapism. Alprostadil appears to cause less scarring and priapism than papaverine. If an erection lasts longer than 4 hours, detumescence is necessary by aspiration of blood from the corpora cavernosa or injection of phenylephrine, since there is the potential for intracavernous hypoxia and fibrosis of trabecular smooth muscle, which may prevent future erections. In general, intracavernosal therapy should probably be reserved for patients who fail oral therapy with a phosphodiesterase inhibitor. Alprostadil can also be administered intraurethrally using MUSE (medicated urethral system for erection). This system contains a small pellet of alprostadil that is placed within the urethra and is rapidly absorbed through the urethral mucosa to produce an erection within 10 to 15 minutes. Possible side effects are penile pain, urethral burning, and a throbbing sensation in the perineum.
Testosterone supplementation increases libido and may improve erectile dysfunction in men with true hypogonadism. It is available as an intramuscular injection (testosterone enanthate or cypionate) or topical transdermal patch and gel. Possible side effects associated with testosterone include polycythemia, increase in prostate size, gynecomastia, and fluid retention. It is important to perform a digital rectal examination to assess the prostate and obtain a baseline prostate-specific antigen level prior to initiation of therapy. If there is a rise in prostate-specific antigen or hematocrit with testosterone therapy, it usually occurs within 6 months. Therefore, it is advisable to check these levels at 3-month intervals during the first year of therapy, then every 12 months thereafter.
Surgical implantation of a penile prosthesis is another therapeutic option. Mechanical failure, infection, device erosion, and fibrosis are possible complications. However, since the availability of alprostadil and, more recently, phosphodiesterase inhibitors, surgical implantation of a penile prosthesis is rarely used (ie, men with severe arterial occlusive disease). Penile revascularization surgery has limited success.
Psychogenic erectile dysfunction should be referred for further evaluation and treatment.
■ Bodie J, Lewis J, Schow D, et al. Laboratory evaluations of erectile dysfunction: an evidence based approach. J Urol. 2003;169(6):2262–2264.
There is considerable conflict regarding the most cost-effective approach to the evaluation of erectile dysfunction. For example, in the absence of low libido, some would advocate no assessment other than a trial of sildenafil. On the other hand, some clinicians obtain numerous laboratory tests, most of which have normal results. This evidence-based review suggests that most patients should be evaluated with a complete blood cell count, electrolytes, and hemoglobin A1c, cholesterol, and testosterone levels.
■ Matthias RE, Lubben JE, Atchison KA, et al. Sexual activity and satisfaction among very old adults: results from a community-dwelling Medicare population survey. Gerontologist. 1997;37(1):6–14.
This survey investigated the relationship of sexual activity, sexual satisfaction, and psychosocial factors among 1216 well-educated, relatively affluent people with a mean age of 77. About one third reported sexual activity in the past month, and current level of sexual activity was satisfactory in 67%. The men were more likely to be sexually active, with younger age and higher educational level predicting greater activity. For the women, being married was the strongest predictor of sexual activity. Regardless of gender, the main predictors for sexual satisfaction were being sexually active and having positive mental health scores.
■ Mulligan T, Reddy S, Gulur PV, et al. Disorders of male sexual function. Clin Geriatr Med. 2003;19(3):473–481.
Sexuality remains an important issue in the older population. Sexual desire in men continues in spite of a decreased ability to achieve an erection. Many studies suggest that erectile dysfunction in the older man is caused primarily by age-associated chronic disease rather than by normal healthy aging. Therefore, preventive measures that are aimed at the underlying diseases should be sought. Nevertheless, effective treatment options are now available to successfully regain sexual function and thereby improve quality of life.
■ Padero MC, Bhasin S, Friedman TC. Androgen supplementation in older women: too much hype, not enough data. J Am Geriatr Soc. 2002; 50(6):1131–1140.
This review critically examines the literature on androgen supplementation in older women. Androgen supplementation may improve some aspects of cognitive function, sexual function, muscle mass, strength, and sense of well-being in older women. Measurement of free testosterone in women is not widely used because of methodologic difficulty; therefore, androgen deficiency in women is hard to define. More studies are needed to determine whether physiologic testosterone replacement in older women can improve important outcomes like physical function, muscle mass and performance, fracture risk, and cognitive and sexual function.
■ Rajpurkar A, Dhabuwala CB. Comparison of satisfaction rate and erectile function in patients treated with sildenafil, intracavernous prostaglandin E1, and penile implant surgery for erectile dysfunction in urology practice. J Urol. 2003;170(1):159–163.
This study investigated patient satisfaction after 1.5 years of treatment for erectile dysfunction using any of the three commonly used approaches. Surprisingly, patients who had undergone penile implant surgery were more satisfied than patients who were using either sildenafil or intracavernous prostaglandin E1. Prior to treatment, almost all patients opt for oral rather than surgical therapy. Nevertheless, this study suggests that we should not neglect implant surgery as a viable option.
■ Seftel AD. Erectile dysfunction in the elderly: epidemiology, etiology and approaches to treatment. J Urol. 2003; 169(6):1999–2007.
Erectile dysfunction is very common in older men. This paper reviews the normal age-associated physiologic changes, as well as the prevalence, pathophysiology, and treatment of erectile dysfunction in older men. It provides a good review of recently released treatments (ie, phosphodiesterase inhibitors), as well as a discussion of potential future approaches (ie, gene therapy).
Angela Gentili, MD
Thomas Mulligan, MD