However, in contrast, a recent systematic review of published studies, the authors concluded that overall, the addition of testosterone to PDE-5 inhibitors might benefit patients with ED associated with testosterone levels of less than 300 ng/dL (10.4 nmol/L) who failed monotherapy. [20] A limitation of existing studies are their heterogeneous nature and methodological drawbacks.
Measurement of the penile vibration perception threshold provides an inexpensive, reproducible, and painless screening test with acceptable sensitivity for detecting neuropathy. Abnormalities at the level of the sacral cord can be documented by sacral latency testing, while upper motor neuron impotence can be demonstrated with genital-cerebral evoked response testing. These latter procedures are not indicated in unselected patients with impotence.
Impotence: A common problem among men characterized by the consistent inability to sustain an erection sufficient for sexual intercourse or the inability to achieve ejaculation, or both. Impotence can vary. It can involve a total inability to achieve an erection or ejaculation, an inconsistent ability to do so, or a tendency to sustain only very brief erections.

Risks associated with injection therapy including bleeding, pain with injection, penile pain, priapism, and corporal fibrosis (scarring inside of the corpora cavernosa). There is also concern that repetitive injections in the same area could cause scar tissue to build up in the tunica albuginea that could create penile curvature. Thus, doctors recommended that one alternate sides with injection and perform injections no more frequent than every other day.
Dr. Liou says that some men come to him after getting a prescription from their primary care doctors, claiming that the drug doesn't work. Sometimes it's because they used it incorrectly. "The biggest misconception is that these drugs are an on/off switch for erections," Dr. Liou says. But the drugs don't work well without sexual stimulation. "During that time, you need to be with your partner and have foreplay," Dr. Liou says. "Don't take it, do the taxes or the dishes, and then meet at the bedroom thinking you'll be ready to go. It's not like that."
It is important that physicians and other health care providers treating patients for chronic conditions periodically inquire into the sexual functioning of their patients and be prepared to offer counsel for those who experience erectile difficulties. Lack of sexual knowledge and anxiety about sexual performance are common contributing factors to erectile dysfunction. Education and reassurance may be helpful in preventing the cascade into serious erectile failure in individuals who experience minor erectile difficulty due to medications or common changes in erectile functioning associated with chronic illnesses or with aging.

To a significant degree, the public, particularly older men, is conditioned to accept erectile dysfunction as a condition of progressive aging for which little can be done. In addition, there is considerable inaccurate public information regarding sexual function and dysfunction. Often, this is in the form of advertisements in which enticing promises are made, and patients then become even more demoralized when promised benefits fail to materialize. Accurate information on sexual function and the management of dysfunction must be provided to affected men and their partners. They also must be encouraged to seek professional help, and providers must be aware of the embarrassment and/or discouragement that may often be reasons why men with erectile dysfunction avoid seeking appropriate treatment.


There are hundreds of medications that have the side effect of ED and/or decreased libido. Examples of drugs implicated as a cause of ED include hydrochlorothiazides and beta-blocking agents. Medications used to treat depression, particularly the SSRIs such as citalopram (Celexa), escitalopram (Lexapro), fluoxetine (Prozac, Prozac Weekly, Sarafem), fluvoxamine (Luvox, Luvox CR), paroxetine (Paxil, Paxil CR, Pexeva) and sertraline (Zoloft), may also contribute to ED.9 Bupropion (Wellbutrin) which has a predominant effect on blocking the reuptake of dopamine is an antidepressant with lower incidence of ED.10 The side effects of 5ARIs occurring in fewer than 5% of patients can include gynaecomastia, ED, loss of libido and ejaculatory dysfunction.11
Associated morbidity may include various other male sexual dysfunctions, such as premature (early) ejaculation and male hypoactive sexual desire disorder. The NHSLS 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. [51]
ED is often the result of atherosclerosis, and as a result, men with ED frequently have cardiovascular disease. Sexual activity is associated with increased physical exertion, which in some men may increase the risk of having a heart attack (myocardial infarction or MI). The major risk factors associated with cardiovascular disease are age, hypertension, diabetes mellitus, obesity, smoking, abnormal lipid/cholesterol levels in the blood, and lack of exercise. Individuals with three or more of these risk factors are at increased risk for a heart attack during sexual activity. The Princeton Consensus Panel developed guidelines for treating ED in men with cardiovascular disease. Thus, if you have ED and cardiovascular disease (for example, angina or prior heart attack), you should discuss whether or not treatment of ED and sexual activity are appropriate for you.

Studies to further define vasculogenic disorders include pharmacologic duplex grey scale/color ultrasonography, pharmacologic dynamic infusion cavernosometry/ cavernosography, and pharmacologic pelvic/penile angiography. Cavernosometry, duplex ultrasonography, and angiography performed either alone or in conjunction with intracavernous pharmacologic injection of vasodilator agents rely on complete arterial and cavernosal smooth muscle relaxation to evaluate arterial and veno-occlusive function. The clinical effectiveness of these invasive studies is severely limited by several factors, including the lack of normative data, operator dependence, variable interpretation of results, and poor predictability of therapeutic outcomes of arterial and venous surgery. At the present time these studies might best be done in referral centers with specific expertise and interest in investigation of the vascular aspects of erectile dysfunction. Further clinical research is necessary to standardize methodology and interpretation, to obtain control data on normals (as stratified according to age), and to define what constitutes normality in order to assess the value of these tests in their diagnostic accuracy and in their ability to predict treatment outcome in men with erectile dysfunction.
Erectile dysfunction (previously called impotence) is the inability to get or maintain an erection that is sufficient to ensure satisfactory sex for both partners. This problem can cause significant distress for couples. Fortunately more and more men of all ages are seeking help, and treatment for ED has advanced rapidly. The enormous demand for “anti-impotence” drugs suggests that erection problems may be more common than was previously thought. Find out more about the causes and treatment of erectile dysfunction here.

The Latin term impotentia coeundi describes simple inability to insert the penis into the vagina; it is now mostly replaced by more precise terms, such as erectile dysfunction (ED). The study of erectile dysfunction within medicine is covered by andrology, a sub-field within urology. Research indicates that erectile dysfunction is common, and it is suggested that approximately 40% of males with erectile dysfunction or impotence, at least occasionally.[35] The condition is also on occasion called phallic impotence.[36] Its antonym or opposite condition is priapism.[37][38]
Erections are neurovascular events, meaning that nerves and blood vessels (arteries and veins) are involved in the process of an erection and all must work properly to develop a hard erection that lasts long enough. Erection begins with sexual stimulation. Sexual stimulation can be tactile (for example, by a partner touching the penis or by masturbation) or mental (for example, by having sexual fantasies, viewing porn). Sexual stimulation or sexual arousal causes the nerves going to the penis to release a chemical, nitric oxide. Nitric oxide increases the production of another chemical, cyclic GMP (cGMP), in the muscle of the corpora cavernosa. The cGMP causes the muscles of the corpora cavernosa to relax, and this allows more blood to flow into the penis. The incoming blood fills the corpora cavernosa, making the penis expand.
Under normal circumstances, when a man is sexually stimulated, his brain sends a message down the spinal cord and into the nerves of the penis. The nerve endings in the penis release chemical messengers, called neurotransmitters, that signal the corpora cavernosa (the two spongy rods of tissue that span the length of the penis) to relax and fill with blood. As they expand, the corpora cavernosa close off other veins that would normally drain blood from the penis. As the penis becomes engorged with blood, it enlarges and stiffens, causing an erection. Problems with blood vessels, nerves, or tissues of the penis can interfere with an erection.

Sildenafil (Viagra) was the first oral phosphodiesterase type 5 (PDE5) inhibitor approved by the FDA in the United States for the treatment of erectile dysfunction (it is not approved for women). Sildenafil inhibits PDE5, which is an enzyme that destroys cGMP. By inhibiting the destruction of cGMP by PDE5, sildenafil allows cGMP to accumulate. The cGMP in turn prolongs relaxation of the smooth muscle of the corpora cavernosa. Relaxation of the corpora cavernosa smooth muscle allows blood to flow into the penis resulting in increased engorgement of the penis. In short, sildenafil increases blood flow into the penis and decreases blood flow out of the penis.

Normal erectile function depends on the release of NO and endothelial-dependent vasodilation of the penile arteries. The ‘artery size’ hypothesis, first described by Dr Montorsi, offers an explanation why men are more likely to develop ED before a myocardial infacrtion. It is believed that atherosclerosis affects all vascular beds equally but smaller arteries are more likely to become occluded than larger arteries.31 32 The penile arteries are 1–2 mm while the coronary arteries are 3–4 mm. Thus, the same degree of endothelial dysfunction and atherosclerosis is more likely to occlude blood flow in the penile arteries compared with the coronary arteries. The penile arteries therefore serve as a sensitive indicator for subsequent CVD. This theory is supported by the fact that ED occurs approximately 3 years prior to cardiac symptoms in virtually all patients with chronic coronary syndrome whereas patients with acute coronary syndrome have a much lower prevalence of sexual dysfunction.32
Not to give your already stressed-out dude one more thing to worry about, but stress is the cause of 20 percent of all erectile problems, from one-off boner blunders to a lingering inability to get and maintain an erection. Of course, sex difficulties are just the tip of the stress-induced health problem iceberg — sustained stress can also lead to insomnia, stomach troubles, chest pains, anxiety, and more severe health issues in the long term.

ED usually has something physical behind it, particularly in older men. But psychological factors can be a factor in many cases of ED. Experts say stress, depression, poor self-esteem, and performance anxiety can short-circuit the process that leads to an erection. These factors can also make the problem worse in men whose ED stems from something physical.
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