eMedicine Specialties > Urology > Erectile Dysfunction, Premature Ejaculation, and Sexual Disorders

Erectile Dysfunction

Author: Stanley A Brosman, MD, Clinical Professor, Department of Urology, University of California at Los Angeles Medical School
Contributor Information and Disclosures

Updated: Jul 22, 2009

Introduction

Background

Sexual health and function are important determinants of quality of life. Disorders such as erectile dysfunction (ED) and female sexual dysfunction are becoming increasingly more important as a result of the aging US population and newer therapies. Because this subject is discussed widely in the media, men and women of all ages are seeking guidance in an effort to improve their relationships and experience satisfying sexual lives.

This review article discusses the physiology of the normal erection and the pathophysiology, etiology, and treatment of ED. For additional resources, visit Erectile Dysfunction.

Successful treatment of sexual dysfunction has been demonstrated to improve sexual intimacy and satisfaction, improve sexual aspects of quality of life, improve overall quality of life, and relieve symptoms of depression.

Although this article focuses primarily on ED in males, one must remember that the sexual partner plays an integral role. If successful and effective management is to be achieved, the evaluation and discussion of any intervention should include both partners.

The Process of Care Model for the Evaluation and Treatment of Erectile Dysfunction has been developed to advance new guidelines for the diagnosis and management of ED in the primary care and multidisciplinary setting. The model was developed under the auspices of the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School. The chairman of the group of experts who prepared the guidelines was Raymond Rosen, MD.

The key components of this model are (1) a rational approach to diagnosis and treatment, (2) emphasis on clinical history taking and a focused examination, (3) specialized testing and referral in predefined situations, (4) a step-wise management approach with ranking of treatment options, and (5) incorporation of patient and partner needs and preferences in the decision-making process.

An alternative model is the patient goal-oriented approach as suggested by Tom Lue, MD, in which a minimum of testing is performed. The patient and his partner express a preference for reasonable and appropriate treatment options and work with the physician to implement this plan.

The availability of three phosphodiesterase-5 (PDE-5) inhibitors, ie, sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis), has permanently altered the medical management of ED. Many patients no longer expect or are willing to undergo a long evaluation and testing process to obtain a better understanding of their sexual problem, and they are less likely to involve their partner in a discussion of their sexual relationship with the physician.

Because of intense mass-media marketing efforts, the sexual expectations of men have risen to new highs and the attitude that something is wrong with a man if he does not achieve a perfect erection is prevalent. Men who have no difficulty obtaining erections are taking these PDE-5 inhibitor medications in the belief that their sexual performance will be enhanced and the opportunity for multiple orgasms will increase. Their medications are often obtained by a phone call to their doctor or even over the Internet with minimal or no physician contact at all. The misuse and overuse of these remarkable medications are likely to have a major impact on how sexual performance and sexual relationships are viewed.

Physiology of normal erections

Penile erections involve an integration of complex physiologic processes involving the CNS, peripheral nervous system, and hormonal and vascular systems. Any abnormality involving these systems, whether from medication or disease, has a significant impact on the ability to develop and sustain an erection, ejaculate, and experience orgasm. Tumescence, the vascular filling of the cavernous bodies, relies on neural and hormonal mechanisms operating at various levels of the neural axis. This is unique among visceral functions because it requires central neurological input.

Erectile dysfunction. These images depict penile ...

Erectile dysfunction. These images depict penile anatomy. Note the sinusoidal makeup of the corpora and thick fascia (ie, Buck fascia) that covers the corpora cavernosa. The major blood vessels to the corpora cavernosa enter through tributaries from the main vessels running along the dorsum of the penis.

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Erectile dysfunction. These images depict penile ...

Erectile dysfunction. These images depict penile anatomy. Note the sinusoidal makeup of the corpora and thick fascia (ie, Buck fascia) that covers the corpora cavernosa. The major blood vessels to the corpora cavernosa enter through tributaries from the main vessels running along the dorsum of the penis.

Andersson summarized some of the information related to the pathways involved in erectile function.1 The degree of contraction of corpus cavernosal smooth muscle determines the functional state of the penis. The balance between contraction and relaxation is controlled by central and peripheral factors that involve many transmitters and transmitter systems. At the cellular level, smooth muscle relaxation occurs following the release of acetylcholine from the parasympathetic nerves.

The nerves and endothelium of sinusoids and vessels in the penis produce and release transmitters and modulators that control the contractile state of corporal smooth muscles. Although the membrane receptors play an important role, downstream signaling pathways are also important. The RhoA–Rho kinase pathway is involved in the regulation of cavernosal smooth muscle contraction.

The nitric oxide (NO) pathway is of critical importance in the physiologic induction of erections. The drugs currently used to treat erectile dysfunction were developed as a result of experimental and clinical work that demonstrated that NO released from nerve endings relaxes the vascular and corporal smooth muscle cells of the penile arteries and trabeculae, resulting in an erection.

NO is produced by the enzyme nitric oxide synthase (NOS). Three forms have been identified: nNOS, eNOS, and iNOS, which are produced by the genes NOS1 (nNOS), NOS2 (iNOS), and NOS3 (eNOS). This nomenclature is derived from the source of the original isolates. nNOS was found in neuronal tissue, iNOS was found in immunoactivated macrophage cell lines, and eNOS was found in vascular endothelium. All forms of NOS produce NO, but various factors trigger and regulate this process. NOS plays many roles, ranging from homeostasis to immune system regulation. These subtypes are not limited to the tissues from which they were first isolated. Each NOS subtype may play a different biological role in various tissues.

nNOS and eNOS are considered constitutive forms because they share biochemical features. They are calcium-dependent, they require calmodulin and reduced nicotinamide adenine dinucleotide phosphate for catalytic activity, and they are competitively inhibited by arginine derivatives. These 2 subtypes use the biochemical pathway that targets cyclic guanosine monophosphate (cGMP). They are involved in the regulation of neurotransmission and blood flow, respectively.

iNOS is considered inducible because it is calcium-independent. iNOS is induced by the inflammatory process, in which it is involved in the production nitrogenous amines. This subtype has been shown to be involved in the carcinogenic process, leading to transitional cell carcinoma.

All 3 NOS subtypes produce NO by oxidation of L-arginine, which is one of the basic amino acids. It circulates in the blood and is found in cells synthesized from the urea cycle or from oral ingestion. The concentration of L-arginine within the cell far exceeds that in the circulation. Inside the cell, NOS catalyzes the oxidation of L-arginine to NO and L-citrulline. Endogenous blockers of this pathway have been identified.

The gaseous NO that is produced acts as a neurotransmitter or paracrine messenger. Its biologic half-life is only 5 seconds. NO may act within the cell or diffuse and interact with nearby target cells.

Potential ways to alter NO levels include the following:

  • Directly administering NO as a gas
  • Administering NO donors such as nitrates, nitrites, and inorganic nitroso compounds
  • Administering of NO agonists such as ACE, which enhances the production of NO within endothelial cells
  • Preserving cGMP: Inhibitors of phosphodiesterase, which primarily hydrolyze cGMP type 5, provided the basis for the development of sildenafil, vardenafil, and tadalafil.
  • Lowering endogenous inhibitors: Some analogs of L-arginine act as competitive and sometimes irreversible inhibitors of NOS. Some of these are present in the plasma and urine.
  • Administering exogenous NOS activators: One example is methylene blue.
  • Increasing the substrate for NO synthesis: Oral supplementation of NO has generated interest. Chen et al administered oral L-arginine and reported subjective improvement in 50 men with ED.2 These supplements are readily available commercially. Reported adverse effects include nausea, diarrhea, headache, flushing, numbness, and hypotension.

Increasing evidence indicates that NO acts centrally to modulate sexual behavior and to exert its effects on the penis. NO is thought to act in the medial preoptic area and the paraventricular nucleus. Injection of nitric acid synthase inhibitors prevents the erectile response in rats that have been given erectogenic agents.

Factors that mediate contraction in the penis include noradrenaline, endothelin-1, neuropeptide Y, prostanoids, angiotensin II, and other factors not yet identified. Factors that mediate relaxation include acetylcholine, NO, vasoactive intestinal polypeptide, pituitary adenylyl cyclase–activating peptide, calcitonin gene–related peptide, adrenomedullin, adenosine triphosphate, and adenosine prostanoids.

Sexual behavior involves the participation of autonomic and somatic nerves and the integration of numerous spinal and supraspinal sites in the CNS. The penile portion of the process that leads to erections represents only a single component. The ability to achieve and maintain a full erection also depends on the status of the peripheral nerves, integrity of the vascular supply, and biochemical events within the corpora.

Erections occur in response to tactile, olfactory, and visual stimuli. The hypothalamic and limbic pathways play an important role in the integration and control of reproductive and sexual functions. The medial preoptic center, paraventricular nucleus, and anterior hypothalamic regions modulate erections and coordinate autonomic events associated with sexual responses. Afferent information is assessed in the forebrain and relayed to the hypothalamus. The efferent pathways from the hypothalamus enter the medial forebrain bundle and project caudally near the lateral part of the substantia nigra into the midbrain tegmental region.

Several pathways have been described to explain how information travels from the hypothalamus to the sacral autonomic centers. One pathway travels from the dorsomedial hypothalamus through the dorsal and central gray matter, descends to the locus ceruleus, and projects ventrally in the mesencephalic reticular formation. Input from the brain is conveyed through the dorsal spinal columns to the thoracolumbar and sacral autonomic nuclei.

The primary nerve fibers to the penis are from the dorsal nerve of the penis, a branch of the pudendal nerve. The cavernosal nerves are a part of the autonomic nervous system and incorporate both sympathetic and parasympathetic fibers. They travel posterolaterally along the prostate and enter the corpora cavernosa and corpus spongiosum to regulate blood flow during erection and detumescence. The dorsal somatic nerves are also branches of the pudendal nerves. They are primarily responsible for penile sensation.

Sexual stimulation causes the release of neurotransmitters from the cavernosal nerve endings and relaxation factors from the endothelial cells that line the sinusoids. NOS produces NO from arginine. This, in turn, produces other muscle-relaxing chemicals such as cGMP and cyclic adenosine monophosphate, which work via calcium channel and protein kinase mechanisms. This results in the relaxation of smooth muscle in the arteries and arterioles that supply the erectile tissue, producing a dramatic increase in penile blood flow. Relaxation of the sinusoidal smooth muscle increases its compliance, facilitating rapid filling and expansion (40-52% of the corpora cavernosa tissue is composed of smooth muscle cells). The venules beneath the rigid tunica albuginea are compressed, resulting in near-total occlusion of venous outflow. These events produce an erection with an intracavernosal pressure of 100 mm Hg.

Additional sexual stimulation initiates the bulbocavernous reflex. The ischiocavernous muscles forcefully compress the base of the blood-filled corpora cavernosa, and the penis reaches full erection and hardness when intracavernous pressure reaches 200 mm Hg or more. At this pressure, both the inflow and outflow of blood temporarily cease.

Detumescence results from the cessation of neurotransmitter release, the breakdown of second messengers by phosphodiesterases, and sympathetic nerve excitation during ejaculation. Contraction of the trabecular smooth muscle reopens the venous channels, allowing the blood to be expelled, which results in flaccidity.

Pathophysiology of erectile dysfunction

ED is essentially a vascular disease. It is often associated with other vascular diseases and conditions such as diabetes, hypertension, and coronary artery disease. Other conditions associated with ED include neurologic disorders, endocrinopathies, benign prostatic hyperplasia, and depression. Conditions associated with reduced nerve and endothelium function, such as aging, hypertension, smoking, hypercholesterolemia, and diabetes, alter the balance between contraction and relaxation factors. These conditions cause circulatory and structural changes in penile tissues, resulting in arterial insufficiency and defective smooth muscle relaxation. In some patients, sexual dysfunction may be the presenting symptom of these disorders.

Additionally, ED is often an adverse effect of many commonly prescribed medications. Some psychotropic drugs and antihypertensive agents are associated with ED.

Trauma that affects the neurologic or vascular components can also lead to ED. Men with severe Peyronie disease, an inflammatory vasculitis, may have enough scar tissue in the corpora to impede blood flow. Men with sleep disorders commonly experience ED.

Another important consideration is the hormonal status of the patient. Hypogonadism that results in low testosterone levels adversely affects libido and erectile function. Hypothyroidism is a very rare cause of ED.

Most patients with ED have multiple etiological factors; thus, assessing how much each is contributing to the problem is difficult. Because most men with ED have an organic cause, a thorough evaluation is necessary to correctly identify the specific etiology in any given individual.

Frequency

United States

Sexual dysfunction is highly prevalent in men and women. In the Massachusetts Male Aging Study (MMAS), a community-based survey of men aged 40-70 years, 52% of the respondents reported some degree of erectile difficulty. Complete ED, defined as (1) the total inability to obtain or maintain an erection during sexual stimulation and (2) the absence of nocturnal erections, occurred in 10% of the respondents. Lesser degrees of mild and moderate ED occurred in 17% and 25% of responders, respectively.

In the National Health and Social Life Survey, a nationally representative probability sample of men and women aged 18-59 years, 10.4% of men reported being unable to achieve or maintain an erection during the past year. This has a striking correlation to the proportion of men in the MMAS who reported complete ED.

Both studies noted a strong correlation with age. Although the rate of mild ED in the MMAS remained constant (17%) in men aged 40-70 years, the number of men reporting moderate ED doubled (17-34%) and the number of men reporting complete ED tripled (5-15%). Extrapolating the MMAS data to the American population, an estimated 18-30 million men are affected by ED.

Other male sexual dysfunctions, such as premature ejaculation and hypoactive sexual desire, are also highly prevalent. The National Health and Social Life Survey found that 28.5% of men aged 18-59 years reported premature ejaculation and 15.8% lacked sexual interest during the past year. An additional 17% reported anxiety about sexual performance, and 8.1% had a lack of pleasure in sex.

Long-term predictions based on an aging population and an increase in risk factors (eg, hypertension, diabetes, vascular disease, pelvic and prostate surgery, benign prostatic hyperplasia, lower urinary tract symptoms) suggest a large increase in the number of men with ED. Also, the prevalence of ED is underestimated because physicians frequently do not question their patients about this disorder.

International

Studies conducted around the world report similar risk factors and similar prevalence rates for ED.

Age

All studies demonstrate a strong association with age, even when data are adjusted for the confounding effects of other risk factors. The independent association with aging suggests that vascular changes in the arteries and sinusoids of the corpora cavernosae, similar to those found elsewhere in the body, are contributing factors. Other risk factors associated with aging include depression, sleep apnea, and low levels of high-density lipoproteins.

Clinical

History

Taking the patient's history is informative to the physician and is an opportunity to educate the patient. Adequate time must be set aside for a full interview and to conduct a physical examination. Even clinicians who are not comfortable dealing with ED should inquire into this important aspect of the patient's health. A simple way to do this is simply ask, "How's your sex life? Everything working all right?" This type of inquiry should elicit a clear, quick, direct "Everything's fine" from the patient. Any other response or even just a delay in answering should suggest potential ED in that patient.

  • The first step in the management of erectile dysfunction (ED) is taking a thorough sexual, medical, and psychosocial history. This is a sensitive topic, and the clinician must be sensitive to the patient's comfort level. Taking the history provides an opportunity for the physician to initiate patient and partner education about ED and its treatments and to facilitate communication. It also allows the physician to establish a rapport with the couple, which assists in treatment.
  • A clear description of the problem entails determining if the patient has difficulty obtaining an erection, if the erection is suitable for penetration, if the erection can be maintained until the partner has achieved orgasm, if ejaculation occurs, and if both partners have sexual satisfaction.
  • Rapid (premature) ejaculation generally occurs in men younger than 40 years. This situation can cause a great deal of stress on the couple's relationship. A history of premature ejaculation can be obtained from many men who present in later years with erectile difficulty. Effective treatments, including SSRI medications and sex therapy, are available to remedy this condition. (See Premature Ejaculation.)
  • Obtain information about current medications, prior surgeries, and other disorders, and begin forming an objective opinion regarding the interpersonal relationship between the partners. In addition to general medical information, any history of pelvic surgery, trauma, prior prostate surgery, or radiation to the prostate should be elicited.
  • A detailed list of all medications taken during the past year, including all vitamins and other dietary supplements, should be obtained. Patients often neglect to list dietary supplements they may have tried to improve their sexual function.
    • One of the commonly used medications in the treatment of men with benign prostatic hyperplasia is one of the 5-alpha reductase inhibitors, finasteride (Proscar) or dutasteride (Avodart).
    • The Proscar Long-Term Efficacy and Safety Study was a 4-year randomized, placebo-controlled trial in 3040 male subjects aged 45-78 years. At screening, 46% of the subjects reported some history of sexual dysfunction. During the first year of the study, 15% of subjects treated with finasteride and 7% of control subjects had evidence of sexual dysfunction that was thought to be related to the drug.
    • During the second-through-fourth years of the trial, no difference was reported between these 2 groups. No difference was noted between subjects who reported prior sexual problems and those who had not.
    • Sexual dysfunction occurred in 12% of subjects taking finasteride and in 19% of control subjects. In the 4% of the subjects who discontinued the study because of this adverse effect, 50% experienced resolution of the problem. Only 2% of control subjects discontinued the study because of the adverse effect, and 41% of these men had resolution of the problem.
  • Tobacco use, alcohol intake, caffeine intake, and illicit drug use should be documented.
  • Explore stress factors and tension at work and at home. Assess the patient's psychological state; in particular, look for indications of depression, loss of libido, problems and tension in the sexual relationship, insomnia, lethargy, moodiness, and stress from work or other sources.
  • The patient needs to explain his interpretation of the problem. Elicit information by asking the following types of questions:
    • How long has a problem existed? Did a specific event such as a major surgery or a divorce occur at the same time? Have you experienced the death of a spouse or family member?
    • Do you have diminished sexual desire? How long have you noticed this? Is your diminished sexual desire a primary symptom or a reaction to poor performance? Do you have any feelings of performance anxiety?
    • Is adequate foreplay occurring? Are you ever able to obtain an erection suitable for penetration, even momentarily? Is maintaining the erection a problem? Is your sexual partner satisfied with the sexual experience?
    • Are you able to achieve orgasm and ejaculation?
    • Do you experience nocturnal or morning erections? Does pain or discomfort occur with ejaculation? Do you have rapid (premature) ejaculation?
    • Is penile curvature (Peyronie disease) a problem?
    • What is your preferred frequency of intercourse, assuming your erections were functional? Do you and your sexual partner agree on this issue?
    • Have you already tried any treatments? If so, what were they? Are you interested in trying a particular treatment first? Are you opposed to trying a particular type of therapy?
    • To what degree do you wish to proceed in determining the cause of his ED? How important is this to you?
  • Questionnaires have been developed to gather objective data regarding impotence and to assist clinicians in the evaluation of their patients.
    • The International Index of Erectile Function (IIEF) is a sensitive, specific, and standardized tool that has been validated in several languages. This 15-question method evaluates 5 domains. These include erectile and orgasmic function, sexual desire, intercourse satisfaction, and global satisfaction. The IIEF is used to evaluate pharmacologic and other therapies for the treatment of ED.
    • A 5-question tool has been developed as a sexual health inventory for men, termed the IIEF-5. This is helpful for the clinician to screen patients for ED because many men are hesitant to discuss the problem. The IIEF-5 scores the answers on a scale of 0-5. A score of 25 is typical for a healthy man, while scores of 11 or less indicate moderate-to-severe ED. The patient is asked the following 5 questions relating to the past 6 months:
      • How do you rate your confidence that you could achieve and maintain an erection?
      • When you had erections with sexual stimulation, how often were your erections hard enough for penetration?
      • During sexual intercourse, how often were you able to maintain your erection after you had penetrated your partner?
      • During sexual intercourse, how difficult was it to maintain your erection to the completion of intercourse?
      • When you attempted sexual intercourse, how often was it satisfactory for you?
    • Following completion of the IIEF or the IIEF-5 and a discussion with the patient, the physician should have a good understanding of the nature and scope of the patient's problem.

Physical

  • A physical examination is necessary for every patient, with particular emphasis on the genitourinary, vascular, and neurologic systems.
    • The physical examination may corroborate history findings and reveal unsuspected physical findings, such as penile plaques, small testes, evidence of possible prostate cancer, prostate infections, or hypertension.
    • Several studies have demonstrated a strong correlation between hypertension and ED. This is not surprising since both are manifestations of a vascular disorder. In a large hypertension clinic, men who also demonstrated ED had a much higher prevalence of complications related to high blood pressure. Another investigator has suggested that hypertensive patients with ED and poor cavernosal artery blood flow as measured during duplex ultrasonography studies should proceed to a full cardiac evaluation because of the high prevalence of associated problems.
    • A number of recent studies have shown a correlation between benign prostatic hyperplasia and ED. The causality for this relationship is not yet clear.
    • A focused physical examination entails an evaluation of the patient's blood pressure, peripheral pulses, sensation, status of the genitalia and prostate, size and texture of the testes, the presence of the epididymis and vas deferens, and abnormalities of the penis such as hypospadias and Peyronie plaques.

Causes

The etiology of ED is usually multifactorial. Organic, physiologic, endocrine, and psychogenic factors are involved in the ability to obtain and maintain erections. In general, ED is divided into organic and psychogenic impotence, but most men with organic etiologies usually have an associated psychogenic component. Almost any disease may affect erectile function by altering the nervous, vascular, or hormonal systems. Various diseases may produce changes in the smooth muscle tissue of the corpora cavernosa or influence the patient's psychologic mood and behavior. Pure psychogenic ED is an uncommon disorder, although most ED was once attributed to psychological factors.

Diabetes is a well-recognized risk factor, with approximately 50% of diabetic men experiencing ED. The etiology of ED in diabetic men probably involves both vascular and neurogenic mechanisms. Evidence indicates that establishing good glycemic control can minimize this risk.

Vascular disease often associated with diabetes m...

Vascular disease often associated with diabetes mellitus is found in the majority of men with erectile dysfunction. In these patients, the medications they take for hypertension often exacerbate their erectile dysfunction.

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Vascular disease often associated with diabetes m...

Vascular disease often associated with diabetes mellitus is found in the majority of men with erectile dysfunction. In these patients, the medications they take for hypertension often exacerbate their erectile dysfunction.

Cigarette smoking has been shown to be an independent risk factor. In studies evaluating more than 6000 men, the risk of developing ED increased by a factor of 1.5

Mental health disorders, particularly depression, are likely to affect sexual performance. The MMAS data indicate an odds ratio of 1.82. Other associated factors, both cognitive and behavioral, may contribute. Also, ED alone can induce depression. The new oral agents have been shown to be effective for men who develop depression following prostatectomy.

Cosgrove et al have reported a higher rate of sexual dysfunction in veterans with posttraumatic stress syndrome than in those veterans who did not develop this problem.3 The domains on the IIEF questionnaire that demonstrated the most change included overall sexual satisfaction and erectile function. This study suggests that regardless of etiology, men with posttraumatic stress syndrome should be evaluated and treated if they have sexual dysfunction.

A sedentary lifestyle is a contributing factor to ED. Exercise has a beneficial effect on the cardiovascular system, and some data from the MMAS indicate that men who exercise regularly have a lower risk of ED. However, Goldstein et al reported an increased risk of ED in men who rode a bicycle for long periods.4 Therefore, the type of exercise may be important.

The MMAS study also showed an inverse correlation between ED risk and high-density lipoprotein cholesterol levels but no effect from elevated total cholesterol levels. Another study involving male subjects aged 45-54 years found a correlation with abnormal high-density lipoprotein cholesterol levels but also found a correlation with elevated total cholesterol levels. The MMAS study had a preponderance of older men.

Vascular diseases account for nearly half of all cases of ED in men older than 50 years. Vascular diseases include atherosclerosis, peripheral vascular disease, myocardial infarction, and arterial hypertension.

Vascular damage may accompany radiation therapy to the pelvis and prostate in the treatment of prostatic cancer. In this situation, both the blood vessels and the nerves to the penis may be affected. Radiation damage to the crura of the penis, which are quite susceptible to radiation damage, can induce ED. The radiation oncologist must take precautions to avoid treating this area. Data indicate that 50% of men undergoing radiation therapy lose erectile function within 5 years after completing therapy. Fortunately, some of these men tend to respond to one of the PDE-5 inhibitors.

Prostatic surgery for benign prostatic hyperplasia has been documented to be associated with ED in 10-20% of men. This is thought to be related to nerve damage from cautery. Newer procedures such as microwave, laser, or radiofrequency ablation have rarely been associated with ED.

Radical prostatectomy for the treatment of prostate cancer poses a significant risk of ED. A number of factors are associated with the chance of preserving erectile function. If both nerves that course on the lateral edges of the prostate can be saved, the chance of maintaining erectile function is reasonable. This depends on the age of the patient. Men younger than 60 years have a 75-80% chance of preserving potency, but men older than 70 years have only a 10-15% chance. Sural nerve grafts are used by some surgeons. Following surgery, one of the PDE-5 inhibitors, such as sildenafil, vardenafil, or tadalafil, is frequently used to assist in the recovery of erectile function.

Trauma to the pelvic blood vessels and nerves is another potential etiologic factor in the development of ED. Bicycle riding for long periods has been implicated as an etiologic factor by causing vascular and nerve injury. Some of the newer bicycle seats have been designed to diminish pressure on the perineum.

Diseases associated with ED are summarized as follows:

  • Vascular diseases associated with erectile dysfunction
    • Atherosclerosis
    • Peripheral vascular disease
    • Myocardial infarction
    • Arterial hypertension
    • That resulting from radiation therapy
    • That related to prostate cancer treatment
    • Blood vessel and nerve trauma (eg, due to long-distance bicycle riding)
    • Medications related to treatment of vascular disease
  • Systemic diseases associated with erectile dysfunction
    • Diabetes mellitus
    • Scleroderma
    • Renal failure
    • Liver cirrhosis
    • Idiopathic hemochromatosis
    • Cancer and cancer treatment
    • Dyslipidemia
    • Hypertension
  • Neurogenic diseases associated with erectile dysfunction
    • Epilepsy
    • Stroke
    • Multiple sclerosis
    • Guillain-Barré syndrome
    • Alzheimer disease
    • Trauma
  • Respiratory disease associated with erectile dysfunction
    • Chronic obstructive pulmonary disease
    • Sleep apnea
  • Endocrine conditions associated with erectile dysfunction
    • Hyperthyroidism
    • Hypothyroidism
    • Hypogonadism
    • Diabetes
  • Penile conditions associated with erectile dysfunction
    • Peyronie disease
    • Epispadias
    • Priapism
  • Psychiatric conditions associated with erectile dysfunction
    • Depression
    • Widower syndrome
    • Performance anxiety
    • Posttraumatic stress disorder
  • Nutritional states associated with erectile dysfunction
    • Malnutrition
    • Zinc deficiency
  • Hematologic diseases associated with erectile dysfunction
    • Sickle cell anemia
    • Leukemias
  • Surgical procedures associated with erectile dysfunction
    • Procedures on the brain and spinal cord
    • Retroperitoneal or pelvic lymph node dissection
    • Aortoiliac or aortofemoral bypass
    • Abdominal perineal resection
    • Surgical removal of the prostate for cancer
    • Surgical treatment of the prostate for benign disease
    • Proctocolectomy
    • Radical prostatectomy
    • Transurethral resection of the prostate
    • Cryosurgery of the prostate
    • Cystectomy
  • Medications associated with erectile dysfunction
    • Antidepressants
    • Antipsychotics
    • Antihypertensives
    • Antiulcer agents, such as cimetidine and finasteride
    • 5-Alpha reductase inhibitors
    • Cholesterol-lowering agents

More on Erectile Dysfunction

Overview: Erectile Dysfunction
Differential Diagnoses & Workup: Erectile Dysfunction
Treatment & Medication: Erectile Dysfunction
Follow-up: Erectile Dysfunction
Multimedia: Erectile Dysfunction
References
Further Reading
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References

  1. Andersson KE. Erectile physiological and pathophysiological pathways involved in erectile dysfunction. J Urol. Aug 2003;170(2 Pt 2):S6-13; discussion S13-4. [Medline].

  2. Chen J, Wollman Y, Chernichovsky T, et al. Effect of oral administration of high-dose nitric oxide donor L-arginine in men with organic erectile dysfunction: results of a double-blind, randomized, placebo-controlled study. BJU Int. Feb 1999;83(3):269-73. [Medline].

  3. Cosgrove DJ, Gordon Z, Bernie JE, et al. Sexual dysfunction in combat veterans with post-traumatic stress disorder. Urology. Nov 2002;60(5):881-4. [Medline].

  4. Goldstein I, Lurie AL, Lubisich JP. Bicycle riding, perineal trauma, and erectile dysfunction: data and solutions. Curr Urol Rep. Nov 2007;8(6):491-7. [Medline].

  5. Gutierrez P, Hernandez P, Mas M. Combining programmed intracavernous PGE1 injections and sildenafil on demand to salvage sildenafil nonresponders. Int J Impot Res. Jul-Aug 2005;17(4):354-8. [Medline].

  6. Rosano GM, Aversa A, Vitale C, Fabbri A, Fini M, Spera G. Chronic treatment with tadalafil improves endothelial function in men with increased cardiovascular risk. Eur Urol. Feb 2005;47(2):214-20; discussion 220-2. [Medline].

  7. Burchardt M, Burchardt T, Anastasiadis AG, Buttyan R, de la Taille A, Shabsigh A. Application of angiogenic factors for therapy of erectile dysfunction: protein and DNA transfer of VEGF 165 into the rat penis. Urology. Sep 2005;66(3):665-70. [Medline].

  8. [Best Evidence] Rosenberg MT, Adams PL, McBride TA, Roberts JN, McCallum SW. Improvement in duration of erection following phosphodiesterase type 5 inhibitor therapy with vardenafil in men with erectile dysfunction: the ENDURANCE study. Int J Clin Pract. Jan 2009;63(1):27-34. [Medline].

  9. Akash R, Hrishikesh D, Amith P, Sabah S. Case report: association of combined nonarteritic anterior ischemic optic neuropathy (NAION) and obstruction of cilioretinal artery with overdose of Viagra. J Ocul Pharmacol Ther. Aug 2005;21(4):315-7. [Medline].

  10. Althof SE, Corty EW, Levine SB, et al. EDITS: development of questionnaires for evaluating satisfaction with treatments for erectile dysfunction. Urology. Apr 1999;53(4):793-9. [Medline].

  11. Althof SE, Seftel AD. The evaluation and management of erectile dysfunction. Psychiatr Clin North Am. Mar 1995;18(1):171-92. [Medline].

  12. Andersson KE. Pharmacology of penile erection. Pharmacol Rev. Sep 2001;53(3):417-50. [Medline].

  13. Andersson KE, Wagner G. Physiology of penile erection. Physiol Rev. Jan 1995;75(1):191-236. [Medline].

  14. Araujo AB, Durante R, Feldman HA, et al. The relationship between depressive symptoms and male erectile dysfunction: cross-sectional results from the Massachusetts Male Aging Study. Psychosom Med. Jul-Aug 1998;60(4):458-65. [Medline].

  15. Aversa A, Isidori AM, De Martino MU, et al. Androgens and penile erection: evidence for a direct relationship between free testosterone and cavernous vasodilation in men with erectile dysfunction. Clin Endocrinol (Oxf). Oct 2000;53(4):517-22. [Medline].

  16. Aversa A, Isidori AM, Spera G, et al. Androgens improve cavernous vasodilation and response to sildenafil in patients with erectile dysfunction. Clin Endocrinol (Oxf). May 2003;58(5):632-8. [Medline].

  17. Baldwin K, Ginsberg P, Harkaway RC. Under-reporting of erectile dysfunction among men with unrelated urologic conditions. Int J Impot Res. Apr 2003;15(2):87-9. [Medline].

  18. Becker AJ, Stief CG, Machtens S, et al. Oral phentolamine as treatment for erectile dysfunction. J Urol. Apr 1998;159(4):1214-6. [Medline].

  19. Benet AE, Melman A. The epidemiology of erectile dysfunction. Urol Clin North Am. Nov 1995;22(4):699-709. [Medline].

  20. Boshier A, Pambakian N, Shakir SA. A case of nonarteritic ischemic optic neuropathy (NAION) in a male patient taking sildenafil. Int J Clin Pharmacol Ther. Sep 2002;40(9):422-3. [Medline].

  21. Braun M, Wassmer G, Klotz T, et al. Epidemiology of erectile dysfunction: results of the "Cologne Male Survey". Int J Impot Res. Dec 2000;12(6):305-11. [Medline].

  22. Brock G, Nehra A, Lipshultz LI, et al. Safety and efficacy of vardenafil for the treatment of men with erectile dysfunction after radical retropubic prostatectomy. J Urol. Oct 2003;170(4 Pt 1):1278-83. [Medline].

  23. Brock GB, McMahon CG, Chen KK, et al. Efficacy and safety of tadalafil for the treatment of erectile dysfunction: results of integrated analyses. J Urol. Oct 2002;168(4 Pt 1):1332-6. [Medline].

  24. Burchardt M, Burchardt T, Baer L, et al. Hypertension is associated with severe erectile dysfunction. J Urol. Oct 2000;164(4):1188-91. [Medline].

  25. Burnett AL. Erectile dysfunction: a practical approach for primary care. Geriatrics. Feb 1998;53(2):34-5, 39-40, 46-8. [Medline].

  26. Cheitlin MD, Hutter AM, Brindis RG, et al. ACC/AHA expert consensus document. Use of sildenafil (Viagra) in patients with cardiovascular disease. American College of Cardiology/American Heart Association. J Am Coll Cardiol. Jan 1999;33(1):273-82. [Medline].

  27. Chitaley K, Webb RC, Mills TM. RhoA/Rho-kinase: a novel player in the regulation of penile erection. Int J Impot Res. Apr 2001;13(2):67-72. [Medline].

  28. Chiu YJ, Reid IA. Effect of sildenafil on renin secretion in human subjects. Exp Biol Med (Maywood). Sep 2002;227(8):620-5. [Medline].

  29. Christ GJ. The penis as a vascular organ. The importance of corporal smooth muscle tone in the control of erection. Urol Clin North Am. Nov 1995;22(4):727-45. [Medline].

  30. Chuang AT, Steers WD. Neurophysiology of penile erection. In: Carson CC, Kirby RS, Goldstein I, eds. Textbook of Male Erectile Dysfunction. Oxford, England: Isis Medical Media; 1999:59-72.

  31. Costabile RA. Optimizing treatment for diabetes mellitus induced erectile dysfunction. J Urol. Aug 2003;170(2 Pt 2):S35-8; discussion S39. [Medline].

  32. Cunningham AV, Smith KH. Anterior ischemic optic neuropathy associated with viagra. J Neuroophthalmol. Mar 2001;21(1):22-5. [Medline].

  33. De Berardis G, Pellegrini F, Franciosi M, et al. Identifying patients with type 2 diabetes with a higher likelihood of erectile dysfunction: the role of the interaction between clinical and psychological factors. J Urol. Apr 2003;169(4):1422-8. [Medline].

  34. Derby CA, Araujo AB, Johannes CB, et al. Measurement of erectile dysfunction in population-based studies: the use of a single question self-assessment in the Massachusetts Male Aging Study. Int J Impot Res. Aug 2000;12(4):197-204. [Medline].

  35. Derby CA, Mohr BA, Goldstein I, et al. Modifiable risk factors and erectile dysfunction: can lifestyle changes modify risk?. Urology. Aug 1 2000;56(2):302-6. [Medline].

  36. Ernst E, Pittler MH. Yohimbine for erectile dysfunction: a systematic review and meta-analysis of randomized clinical trials. J Urol. Feb 1998;159(2):433-6. [Medline].

  37. Feldman HA, Goldstein I, Hatzichristou DG, et al. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol. Jan 1994;151(1):54-61. [Medline].

  38. Giuliano FA, Rampin O, Benoit G, Jardin A. Neural control of penile erection. Urol Clin North Am. Nov 1995;22(4):747-66. [Medline].

  39. Goldstein I. Oral phentolamine: an alpha-1, alpha-2 adrenergic antagonist for the treatment of erectile dysfunction. Int J Impot Res. Mar 2000;12 Suppl 1:S75-80. [Medline].

  40. Goldstein I. The mutually reinforcing triad of depressive symptoms, cardiovascular disease, and erectile dysfunction. Am J Cardiol. Jul 20 2000;86(2A):41F-45F. [Medline].

  41. Goldstein I, Lue TF, Padma-Nathan H, et al. Oral sildenafil in the treatment of erectile dysfunction. Sildenafil Study Group. N Engl J Med. May 14 1998;338(20):1397-404. [Medline].

  42. Goldstein I, Payton TR, Schechter PJ. A double-blind, placebo-controlled, efficacy and safety study of topical gel formulation of 1% alprostadil (Topiglan) for the in-office treatment of erectile dysfunction. Urology. Feb 2001;57(2):301-5. [Medline].

  43. Goldstein I, Young JM, Fischer J, et al. Vardenafil, a new phosphodiesterase type 5 inhibitor, in the treatment of erectile dysfunction in men with diabetes: a multicenter double-blind placebo-controlled fixed-dose study. Diabetes Care. Mar 2003;26(3):777-83. [Medline].

  44. Greiner KA, Weigel JW. Erectile dysfunction. Am Fam Physician. Oct 1996;54(5):1675-82. [Medline].

  45. Gresser U, Gleiter CH. Erectile dysfunction: comparison of efficacy and side effects of the PDE-5 inhibitors sildenafil, vardenafil and tadalafil--review of the literature. Eur J Med Res. Oct 29 2002;7(10):435-46. [Medline].

  46. Guay AT, Bansal S, Heatley GJ. Effect of raising endogenous testosterone levels in impotent men with secondary hypogonadism: double blind placebo-controlled trial with clomiphene citrate. J Clin Endocrinol Metab. Dec 1995;80(12):3546-52. [Medline].

  47. Hawton K. Integration of treatments for male erectile dysfunction. Lancet. Jan 3 1998;351(9095):7-8. [Medline].

  48. Heaton JP. Neural and pharmacological determinants of erection. Int J Impot Res. May 1998;10 Suppl 2:S34-9; discussion S49-51. [Medline].

  49. Heaton JP, Morales A, Adams MA, et al. Recovery of erectile function by the oral administration of apomorphine. Urology. Feb 1995;45(2):200-6. [Medline].

  50. Hedlund H, Hedlund P. Pharmacotherapy in erectile dysfunction agents for self-injection programs and alternative application models. Scand J Urol Nephrol Suppl. 1996;179:129-38. [Medline].

  51. Hellstrom WJ, Gittelman M, Karlin G, et al. Vardenafil for treatment of men with erectile dysfunction: efficacy and safety in a randomized, double-blind, placebo-controlled trial. J Androl. Nov-Dec 2002;23(6):763-71. [Medline].

  52. Holmes S. Tadalafil: a new treatment for erectile dysfunction. BJU Int. Apr 2003;91(6):466-8. [Medline].

  53. Incrocci L, Hop WC, Slob AK. Efficacy of sildenafil in an open-label study as a continuation of a double-blind study in the treatment of erectile dysfunction after radiotherapy for prostate cancer. Urology. Jul 2003;62(1):116-20. [Medline].

  54. Jain P, Rademaker AW, McVary KT. Testosterone supplementation for erectile dysfunction: results of a meta-analysis. J Urol. Aug 2000;164(2):371-5. [Medline].

  55. Kanno S, Wu YJ, Lee PC, et al. Angiotensin-converting enzyme inhibitor preserves p21 and endothelial nitric oxide synthase expression in monocrotaline-induced pulmonary arterial hypertension in rats. Circulation. Aug 21 2001;104(8):945-50. [Medline].

  56. Kawanishi Y, Lee KS, Kimura K, et al. Screening of ischemic heart disease with cavernous artery blood flow in erectile dysfunctional patients. Int J Impot Res. Apr 2001;13(2):100-3. [Medline].

  57. Kloner RA, Mullin SH, Shook T, et al. Erectile dysfunction in the cardiac patient: how common and should we treat?. J Urol. Aug 2003;170(2 Pt 2):S46-50; discussion S50. [Medline].

  58. Klotz T, Sachse R, Heidrich A, et al. Vardenafil increases penile rigidity and tumescence in erectile dysfunction patients: a RigiScan and pharmacokinetic study. World J Urol. Feb 2001;19(1):32-9. [Medline].

  59. Kuthe A. Phosphodiesterase 5 inhibitors in male sexual dysfunction. Curr Opin Urol. Sep 2003;13(5):405-10. [Medline].

  60. Larson TR. Current treatment options for benign prostatic hyperplasia and their impact on sexual function. Urology. Apr 2003;61(4):692-8. [Medline].

  61. Latini DM, Penson DF, Lubeck DP, et al. Longitudinal differences in disease specific quality of life in men with erectile dysfunction: results from the Exploratory Comprehensive Evaluation of Erectile Dysfunction study. J Urol. Apr 2003;169(4):1437-42. [Medline].

  62. Laumann EO, Paik A, Rosen RC. Sexual dysfunction in the United States: prevalence and predictors. JAMA. Feb 10 1999;281(6):537-44. [Medline].

  63. Leslie S. Impotence: current diagnosis and treatment. Monograph. 1997;1-36.

  64. Lewis RW. Long-term results of penile prosthetic implants. Urol Clin North Am. Nov 1995;22(4):847-56. [Medline].

  65. Lewis RW, Witherington R. External vacuum therapy for erectile dysfunction: use and results. World J Urol. 1997;15(1):78-82. [Medline].

  66. Lin CS, Ho HC, Chen KC, et al. Intracavernosal injection of vascular endothelial growth factor induces nitric oxide synthase isoforms. BJU Int. Jun 2002;89(9):955-60. [Medline].

  67. Lin CS, Xin ZC, Lin G, Lue TF. Phosphodiesterases as therapeutic targets. Urology. Apr 2003;61(4):685-91. [Medline].

  68. Linet OI, Ogrinc FG. Efficacy and safety of intracavernosal alprostadil in men with erectile dysfunction. The Alprostadil Study Group. N Engl J Med. Apr 4 1996;334(14):873-7. [Medline].

  69. Liu X, Lin CS, Graziottin T, et al. Vascular endothelial growth factor promotes proliferation and migration of cavernous smooth muscle cells. J Urol. Jul 2001;166(1):354-60. [Medline].

  70. Lue TF. Erectile dysfunction. N Engl J Med. Jun 15 2000;342(24):1802-13. [Medline].

  71. Lue TF, Giuliano F, Montorsi F, Rosen RC, Andersson KE, Althof S. Summary of the recommendations on sexual dysfunctions in men. J Sex Med. Jul 2004;1(1):6-23. [Medline].

  72. Marceau L, Kleinman K, Goldstein I, McKinlay J. Does bicycling contribute to the risk of erectile dysfunction? Results from the Massachusetts Male Aging Study (MMAS). Int J Impot Res. Oct 2001;13(5):298-302. [Medline].

  73. McGwin G Jr, Vaphiades MS, Hall TA, Owsley C. Non-arteritic anterior ischaemic optic neuropathy and the treatment of erectile dysfunction. Br J Ophthalmol. Feb 2006;90(2):154-7. [Medline].

  74. McKenna KE. Central control of penile erection. Int J Impot Res. May 1998;10 Suppl 1:S25-34. [Medline].

  75. Meuleman EJ, Diemont WL. Investigation of erectile dysfunction. Diagnostic testing for vascular factors in erectile dysfunction. Urol Clin North Am. Nov 1995;22(4):803-19. [Medline].

  76. Michel T, Feron O. Nitric oxide synthases: which, where, how, and why?. J Clin Invest. Nov 1 1997;100(9):2146-52. [Medline].

  77. Montorsi F, Salonia A, Deho' F, Cestari A, Guazzoni G, Rigatti P. Pharmacological management of erectile dysfunction. BJU Int. Mar 2003;91(5):446-54. [Medline].

  78. Morales A, Gingell C, Collins M, et al. Clinical safety of oral sildenafil citrate (VIAGRA) in the treatment of erectile dysfunction. Int J Impot Res. Jun 1998;10(2):69-73; discussion 73-4. [Medline].

  79. Morales A, Johnston B, Heaton JW, Clark A. Oral androgens in the treatment of hypogonadal impotent men. J Urol. Oct 1994;152(4):1115-8. [Medline].

  80. Mulhall JP, Ahmed A, Branch J, Parker M. Serial assessment of efficacy and satisfaction profiles following penile prosthesis surgery. J Urol. Apr 2003;169(4):1429-33. [Medline].

  81. Nehra A, Blute ML, Barrett DM, Moreland RB. Rationale for combination therapy of intraurethral prostaglandin E(1) and sildenafil in the salvage of erectile dysfunction patients desiring noninvasive therapy. Int J Impot Res. Feb 2002;14 Suppl 1:S38-42. [Medline].

  82. Niederberger C, Lonsdale J. Erectile dysfunction - patient characteristics and attitudes based on a large-scale male health study conducted in US, Europe, Mexico and Brazil. [abstract 594]. J Urol. 2002;167.

  83. NIH Consensus Conference. Impotence. NIH Consensus Development Panel on Impotence. JAMA. Jul 7 1993;270(1):83-90. [Medline].

  84. O'Leary MP, Fowler FJ, Lenderking WR, et al. A brief male sexual function inventory for urology. Urology. Nov 1995;46(5):697-706. [Medline].

  85. Padma-nathan H, Eardley I, Kloner RA, et al. A 4-year update on the safety of sildenafil citrate (Viagra). Urology. Sep 2002;60(2 Suppl 2):67-90. [Medline].

  86. Pomeranz HD, Bhavsar AR. Nonarteritic ischemic optic neuropathy developing soon after use of sildenafil (viagra): a report of seven new cases. J Neuroophthalmol. Mar 2005;25(1):9-13. [Medline].

  87. Pomeranz HD, Smith KH, Hart WM Jr, Egan RA. Sildenafil-associated nonarteritic anterior ischemic optic neuropathy. Ophthalmology. Mar 2002;109(3):584-7. [Medline].

  88. Porst H. IC351 (tadalafil, Cialis): update on clinical experience. Int J Impot Res. Feb 2002;14 Suppl 1:S57-64. [Medline].

  89. Porst H, Padma-Nathan H, Giuliano F, Anglin G, Varanese L, Rosen R. Efficacy of tadalafil for the treatment of erectile dysfunction at 24 and 36 hours after dosing: a randomized controlled trial. Urology. Jul 2003;62(1):121-5; discussion 125-6. [Medline].

  90. Porst H, Steidle C, Hollister A. Vardenafil demonstrated similar efficacy and tolerability among older and younger patients with marginal differences in PK characteristics between age groups. Int J Impot Res. 2001;13:S63.

  91. [Guideline] Process of Care Consensus Panel. The process of care model for evaluation and treatment of erectile dysfunction. The Process of Care Consensus Panel. Int J Impot Res. Apr 1999;11(2):59-70; discussion 70-4. [Medline].

  92. Raina R, Lakin MM, Agarwal A, et al. Long-term effect of sildenafil citrate on erectile dysfunction after radical prostatectomy: 3-year follow-up. Urology. Jul 2003;62(1):110-5. [Medline].

  93. Rajpurkar A, Dhabuwala CB. Comparison of satisfaction rates and erectile function in patients treated with sildenafil, intracavernous prostaglandin E1 and penile implant surgery for erectile dysfunction in urology practice. J Urol. Jul 2003;170(1):159-63. [Medline].

  94. Rogers RS, Graziottin TM, Lin CS, Kan YW, Lue TF. Intracavernosal vascular endothelial growth factor (VEGF) injection and adeno-associated virus-mediated VEGF gene therapy prevent and reverse venogenic erectile dysfunction in rats. Int J Impot Res. Feb 2003;15(1):26-37. [Medline].

  95. Romeo JH, Seftel AD, Madhun ZT, Aron DC. Sexual function in men with diabetes type 2: association with glycemic control. J Urol. Mar 2000;163(3):788-91. [Medline].

  96. Rosen RC, Cappelleri JC, Smith MD, et al. Development and evaluation of an abridged, 5-item version of the International Index of Erectile Function (IIEF-5) as a diagnostic tool for erectile dysfunction. Int J Impot Res. Dec 1999;11(6):319-26. [Medline].

  97. Rosen RC, Leiblum SR. Treatment of sexual disorders in the 1990s: an integrated approach. J Consult Clin Psychol. Dec 1995;63(6):877-90. [Medline].

  98. Rosen RC, Riley A, Wagner G, et al. The international index of erectile function (IIEF): a multidimensional scale for assessment of erectile dysfunction. Urology. Jun 1997;49(6):822-30. [Medline].

  99. Rotella DP. Phosphodiesterase 5 inhibitors: current status and potential applications. Nat Rev Drug Discov. Sep 2002;1(9):674-82. [Medline].

  100. Saenz de Tejada I, Anglin G, Knight JR, Emmick JT. Effects of tadalafil on erectile dysfunction in men with diabetes. Diabetes Care. Dec 2002;25(12):2159-64. [Medline].

  101. Seftel AD, Strohl KP, Loye TL, et al. Erectile dysfunction and symptoms of sleep disorders. Sleep. Sep 15 2002;25(6):643-7. [Medline].

  102. Segraves RT, Bari M, Segraves K, Spirnak P. Effect of apomorphine on penile tumescence in men with psychogenic impotence. J Urol. Jun 1991;145(6):1174-5. [Medline].

  103. Shabsigh R, Kaufman JM, Steidle C. Testosterone replacement therapy with testosterone-gel 1% converts sildenafil nonresponders to responders in men with hypogonadism and erectile dysfunction who failed prior sildenafil therapy. [abstract 954]. J Urol. 2003;S169S.

  104. Shabsigh R, Padma-Nathan H, Gittleman M, et al. Intracavernous alprostadil alfadex (EDEX/VIRIDAL) is effective and safe in patients with erectile dysfunction after failing sildenafil (Viagra). Urology. Apr 2000;55(4):477-80. [Medline].

  105. Shochina M, Fellig Y, Sughayer M, et al. Nitric oxide synthase immunoreactivity in human bladder carcinoma. Mol Pathol. Aug 2001;54(4):248-52. [Medline].

  106. Siroky MB, Azadzoi KM. Vasculogenic erectile dysfunction: newer therapeutic strategies. J Urol. Aug 2003;170(2 Pt 2):S24-9; discussion S29-30. [Medline].

  107. Sommer F. [Continuous once a day treatment with sildenafil: daily sex prevents the "aging penis"]. MMW Fortschr Med. May 8 2003;145(19):59. [Medline].

  108. Steers WD. Viability and safety of combination drug therapies for erectile dysfunction. J Urol. Aug 2003;170(2 Pt 2):S20-3; discussion S23. [Medline].

  109. Thadani U, Smith W, Nash S, et al. The effect of vardenafil, a potent and highly selective phosphodiesterase-5 inhibitor for the treatment of erectile dysfunction, on the cardiovascular response to exercise in patients with coronary artery disease. J Am Coll Cardiol. Dec 4 2002;40(11):2006-12. [Medline].

  110. The European Alprostadil Study Group. The long-term safety of alprostadil (prostaglandin-E1) in patients with erectile dysfunction. Br J Urol. Oct 1998;82(4):538-43. [Medline].

  111. Valicenti RK, Bissonette EA, Chen C, Theodorescu D. Longitudinal comparison of sexual function after 3-dimensional conformal radiation therapy or prostate brachytherapy. J Urol. Dec 2002;168(6):2499-504; discussion 2504. [Medline].

  112. Vardi Y, Klein L, Nassar S, et al. Effects of sildenafil citrate (viagra) on blood pressure in normotensive and hypertensive men. Urology. May 2002;59(5):747-52. [Medline].

  113. Wessells H, Roy J, Bannow J, et al. Incidence and severity of sexual adverse experiences in finasteride and placebo-treated men with benign prostatic hyperplasia. Urology. Mar 2003;61(3):579-84. [Medline].

  114. Williams G, Abbou CC, Amar ET, et al. Efficacy and safety of transurethral alprostadil therapy in men with erectile dysfunction. MUSE Study Group. Br J Urol. Jun 1998;81(6):889-94. [Medline].

  115. Yucel S, Baskin LS. Identification of communicating branches among the dorsal, perineal and cavernous nerves of the penis. J Urol. Jul 2003;170(1):153-8. [Medline].

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Further Reading

For more information, visit Medscape's Erectile Dysfunction Resource Center.

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Keywords

erectile dysfunction, impotence, sexual dysfunction, male sexual dysfunction, ED, premature ejaculation, ejaculatory dysfunction, hypoactive sexual desire, erection, ejaculation, penis disorder, sexual disorder, penile curvature, Peyronie disease, Peyronie's disease, organic impotence, psychogenic impotence, sildenafil, Viagra, vardenafil, Levitra, tadalafil, Cialis, tadenafil, psychosocial sexual disorder, sexual health, flaccidity, flaccid penis, erectile difficulty, diminished libido

diabetes, hypertension, coronary artery disease, neurologic disorders, depression, pelvic surgery, prostate surgery, benign prostatic hyperplasia, sleep apnea, low levels of high-density lipoproteins, insomnia, lethargy

posttraumatic stress syndrome, posttraumatic stress disorder, cigarette smoking, atherosclerosis, peripheral vascular disease, myocardial infarction, radiation therapy to the pelvis, radiation therapy to the prostate, radical prostatectomy, scleroderma, dyslipidemia, idiopathichemachromatosis, liver cirrhosis, renal failure, epilepsy, Alzheimer disease, Guillain-Barré syndrome, multiple sclerosis

stroke, chronic obstructivepulmonary disease, hyperthyroidism, hypothyroidism, hypogonadism, epispadias, priapism, widower syndrome, performance anxiety, malnutrition, zinc deficiency, sickle cell anemia, leukemias, aortoiliac bypass, aortofemoral bypass, proctocolectomy, transurethral resection of the prostate, cryosurgery of the prostate, cystectomy, antiulcer agents, cholesterol-lowering agents, 5-alpha reductase inhibitors, antihypertensives, antipsychotics, antidepressants

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Contributor Information and Disclosures

Author

Stanley A Brosman, MD, Clinical Professor, Department of Urology, University of California at Los Angeles Medical School
Stanley A Brosman, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Association for Cancer Research, American Association for the Advancement of Science, American College of Surgeons, American Medical Association, American Society of Clinical Oncology, American Urological Association, Association of Clinical Research Professionals, International Society of Urological Pathology, Société Internationale d'Urologie (International Society of Urology), Society for Basic Urologic Research, Society of Surgical Oncology, Society of Urologic Oncology, and Western Section American Urological Association
Disclosure: Nothing to disclose.

Medical Editor

Martha K Terris, MD, FACS, Professor, Department of Surgery, Medical College of Georgia
Martha K Terris, MD, FACS is a member of the following medical societies: American Cancer Society, American College of Surgeons, American Institute of Ultrasound in Medicine, American Urological Association, New York Academy of Sciences, and Society of University Urologists
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Mark Jeffrey Noble, MD, Consulting Staff, Urologic Institute, Cleveland Clinic Foundation
Mark Jeffrey Noble, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Urological Association, Kansas Medical Society, Sigma Xi, Society of University Urologists, and Southwest Oncology Group
Disclosure: Nothing to disclose.

CME Editor

J Stuart Wolf Jr, MD, FACS, David A Bloom Professor of Urology, Director of Division of Minimally Invasive Urology, Department of Urology, University of Michigan
J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology
Disclosure: Terumo Corporation Consulting fee Consulting; Gyrus-ACMI Honoraria Speaking and teaching

Chief Editor

Edward David Kim, MD, FACS, Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center
Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, and Tennessee Medical Association
Disclosure: Lilly Consulting fee Consulting; Astellas Consulting fee Speaking and teaching; Indevus Consulting fee Speaking and teaching

 
 
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