Of the drugs used for depression, tricyclic antidepressants may be associated with erectile problems and other drugs may be substituted to prevent this complication. Currently available substitutes include bupropion, nefazodone, and trazodone. The selective serotonin reuptake inhibitors (eg, fluoxetine, sertraline, paroxetine, citalopram) can also cause difficulties with ED, but they might also have other significant sexual side effects, including decreased libido and anorgasmia.
One study examined the role of testosterone supplementation in hypogonadal men with ED. These men were considered nonresponders to sildenafil, and their erections were monitored by assessing nocturnal penile tumescence (NPT). After these men were given testosterone transdermally for 6 months, the number of NPTs increased, as did the maximum rigidity with sildenafil. [18] This study suggests that a certain level of testosterone may be necessary for PDE5 inhibitors to function properly.

Once a complete sexual and medical history has been completed, appropriate laboratory studies should be conducted. In the initial evaluation of ED, sophisticated laboratory testing is rarely necessary. For example, serum testosterone (and sometimes prolactin) is typically only useful when the patient demonstrates hypogonadal features or testicular atrophy, or when clinical history is suggestive. Additional hormonal evaluation may include thyroid stimulating hormone in those with a clinical suspicion of hypothyroidism or appropriate diabetes screening in those presenting with a concern for impaired glucose metabolism. If the patient has not been evaluated with a lipid panel and hyperlipidemia is suspected, measurement and appropriate referral to internal medicine or cardiology is recommended. In most cases, a tentative diagnosis can be established with a complete sexual and medical history, physical examination, and limited or no laboratory testing.
Erectile dysfunction may be an unpleasant condition that no one really wants to talk about, failing to acknowledge it won’t make the problem go away. Your best defense against health problems like this is to learn everything you can about it so you can tackle the problem at the root. If you’re ready to stop living in embarrassment about your sexual function, become an advocate for yourself and your own health and talk to your doctor.
Move a muscle, but we're not talking about your biceps. A strong pelvic floor enhances rigidity during erections and helps keep blood from leaving the penis by pressing on a key vein. In a British trial, three months of twice-daily sets of Kegel exercises (which strengthen these muscles), combined with biofeedback and advice on lifestyle changes — quitting smoking, losing weight, limiting alcohol — worked far better than just advice on lifestyle changes.
Apomorphine is a non-selective D1/D2 receptor agonist with moderate efficacy and good tolerability in the treatment of mild ED (80). Apomorphine can be administered via subcutaneous injection or sublingually. However, studies have shows a lower efficacy for apomorphine compared to oral sildenafil (81,82). Apomorphine has a set role in the management of PD for non-motor symptoms, and has been reported to cause spontaneous erections and possible hypersexuality in PD men (83,84). Its role in the management of ED has been postulated for men with PD but should be considered as an alternative to sildenafil.

Diabetes is an example of an endocrine disease that can cause a person to experience impotence. Diabetes affects the body’s ability to utilize the hormone insulin. One of the side effects associated with chronic diabetes is nerve damage. This affects penis sensations. Other complications associated with diabetes are impaired blood flow and hormone levels. Both of these factors can contribute to impotence.
Chancellor et al. (109) compared VEDs with papaverine injections in 18 males with SCI. The injections and pumps were equally effective in inducing erections and no adverse effects from the treatments were reported. Treatment arms were crossed over, subsequently seven men chose the VED and seven men chose the papavarine highlighting equal efficacy in this population. In another treatment arm topical minoxidil was applied without any effective erections achieved by the study subjects.
Exercise and lifestyle modifications may improve erectile function. Weight loss may help by decreasing inflammation, increasing testosterone, and improving self-esteem. Patients should be educated to increase activity, reduce weight, and stop smoking, as these efforts can improve or restore erectile function in men without comorbidities. Precise glycemic control in diabetic patients and pharmacologic treatment of hypertension may be important in preventing or reducing sexual dysfunction. [49]
A physical cause can be identified in about 80% of cases.[2] These include cardiovascular disease, diabetes mellitus, neurological problems such as following prostatectomy, hypogonadism, and drug side effects. Psychological impotence is where erection or penetration fails due to thoughts or feelings; this is somewhat less frequent, in the order of about 10% of cases.[2] In psychological impotence, there is a strong response to placebo treatment.
Erectile dysfunction may be the result of arterial and non-arteritic causes. Hardening of the arteries that bring blood into the penis, atherosclerosis, is a common cause of erectile dysfunction, particularly in men with cardiovascular disease. However, problems with the nerves that supply the penis as well as the veins that drain blood out of the penis can also cause troubles with erection. Erectile dysfunction may also have a psychological cause.
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Erections are initiated and maintained via integration of afferent inputs in the supra sacral regions of the central nervous system. Regions of the brain cited to have key roles in the integration of signals include the medial amygdala, MPOA, periaqueductal gray matter, paraventricular nucleus (PVN), and ventral tegmentum among others (16). Studies in animal models, particularly in rats, have been paramount in identifying these key areas of signal integration and control. Electrostimulation of the MPOA, PVN and hippocampus lead to erection and lesions in these areas may prevent erection (17). Marson et al. injected labeled pseudorabies virus into rat corpora cavernosa and traced them to neurons in the spinal cord, brain stem and hypothalamus (18). Stimulation of the rat dorsal nerve led to increased firing in the MPOA not found elsewhere (19). Axonal tracing in animals have shows direct projections from the hypothalamus to the lumbosacral autonomic erection centers. Oxytocin and vasopressin have been identified as central neurotransmitters within the hypothalamic nuclei and may have a role in penile erection (17). These signaling studies identifying key areas of erectile response integration may explain how ED is associated with cerebrovascular accident (CVA), Parkinson’s, epilepsy and MS.
Treatments include psychotherapy, adopting a healthy lifestyle, oral phosphodiesterase type V (PDE5) inhibitors (Viagra, Levitra, Cialis, Stendra, and Staxyn), intraurethral prostaglandin E1 (MUSE), intracavernosal injections (prostaglandin E1 [Caverject, Edex], Bimix and Trimix), vacuum devices, penile prosthesis and vascular surgery, and (in some cases) changes in medications when appropriate.

3. An intact, anatomically correct penis; 25% of impotence may be psychologic or 'partner-specific', 25% has an organic component and 50% of impotence is organic in nature; in organic impotence, nocturnal penile tumescence is absent Management-surgical Microvascular surgery to bypass occluded vessels–most effective in younger ♂, penile prosthesis Management-medical Combined therapy with phentolamine and papaverine–self-injected by the Pt, wielding an erection of 1 hr's duration is useful for arterial, neurologic, psychogenic impotence; other therapies–zinc, bromocriptine–Parlodel, isoxsuprine-Vasodilan, Voxsuprine, nitroglycerine, yohimbine–Yocon, Yohimex Etiology Smoking, CAD, HTN, DM, medications–hypoglycemic agents, vasodilators, cardiac drugs, antihypertensives, anger and depression; it is inversely correlated to dehydroepiandrosterone, HDL-C, and an index of dominant personality Primary impotence Complete absence of successful sexual coupling Secondary impotence Priapism, penile plaques, Peyronie's disease; drugs linked to impotence: antihypertensives–eg, methyldopa, guanethidine, reserpine, clonidine, due to ↓ BP, antidepressants–eg, phenelzine, isocarboxazide, amitriptyline–causing altered moods and decreased libido, tranquilizers–eg, chlordiazepoxide and lorazepam, and the muscle-relaxing diazepam, cimetidine, which ↑ prolactin, and is associated with impotence and loss of libido. Cf Infertility, Orgasmic dysfunction.
Erectile dysfunction - (ED) or impotence is sexual dysfunction characterized by the inability to develop or maintain an erection of the penis during sexual activity. A penile erection is the hydraulic effect of blood entering and being retained in sponge-like bodies within the penis. The process is most often initiated as a result of sexual arousal, when signals are transmitted from the brain to nerves in the penis.
Surgical intervention for a number of conditions may remove anatomical structures necessary to erection, damage nerves, or impair blood supply.[8] Erectile dysfunction is a common complication of treatments for prostate cancer, including prostatectomy and destruction of the prostate by external beam radiation, although the prostate gland itself is not necessary to achieve an erection. As far as inguinal hernia surgery is concerned, in most cases, and in the absence of postoperative complications, the operative repair can lead to a recovery of the sexual life of people with preoperative sexual dysfunction, while, in most cases, it does not affect people with a preoperative normal sexual life.[13]
In one study, 9.6% reported ‘occasional’ erectile dysfunction, 8.9% reported erectile dysfunction occurring ‘often’, and 18.6% reported erectile dysfunction occurring ‘all the time’. Of these, only 11.6% had received treatment.In another study, only 14.1% of men reported that they had received treatment, despite experiencing erectile dysfunction for longer than 12 months.
Causes of impotence are many and include heart disease, high cholesterol, high blood pressure, obesity, metabolic syndrome, Parkinson's disease, Peyronie's disease, substance abuse, sleep disorders, BPH treatments, relationship problems, blood vessel diseases (such as peripheral vascular disease and others), systemic disease, hormonal imbalance, and medications (such as blood pressure and heart medications).

Malleable implants usually consist of paired rods, inserted surgically into each of the corpora cavernosa. The rods are stiff, and to have an erection, one bends them up and then when finished with intercourse one bends them down. They do not change in length or width. The malleable implants are the least mechanical and thus have the lowest risk of malfunction. However, also have the least "normal appearance."
Of the drugs used for depression, tricyclic antidepressants may be associated with erectile problems and other drugs may be substituted to prevent this complication. Currently available substitutes include bupropion, nefazodone, and trazodone. The selective serotonin reuptake inhibitors (eg, fluoxetine, sertraline, paroxetine, citalopram) can also cause difficulties with ED, but they might also have other significant sexual side effects, including decreased libido and anorgasmia.

In some cases, however, these drugs may be unsuitable for patients with heart disease. If you are considering one of these drugs and you have heart disease, as many diabetics do, be sure to tell your doctor. In rare cases, the pills may create “priapism,” a prolonged and painful erection lasting six hours or more (although reversible with prompt medical attention).
Erectile dysfunction is defined as the persistent inability to achieve or maintain penile erection sufficient for satisfactory sexual performance. The Massachusetts Male Aging Study surveyed 1,709 men aged 40–70 years between 1987 and 1989 and found there was a total prevalence of erectile dysfunction of 52 percent. It was estimated that, in 1995, over 152 million men worldwide experienced ED. For 2025, the prevalence of ED is predicted to be approximately 322 million worldwide.
Is your erectile dysfunction due to psychological (stress, relationship problems, etc.) or physical factors? Your doctor may ask if you note erections at night or in the early morning. Men have involuntary erections in the early morning and during REM sleep (a stage in the sleep cycle with rapid eye movements). Men with psychogenic erectile dysfunction (erectile dysfunction due to psychological factors such as stress and anxiety rather than physical factors) usually maintain these involuntary erections. Men with physical causes of erectile dysfunction (for example, atherosclerosis, smoking, and diabetes) usually do not have these involuntary erections. Men with psychogenic erectile dysfunction may relate the onset of problems to a "stressor," such as failed relationship. Your doctor may suggest a test to determine if you have erections during sleep, which may suggest that there may be a psychological cause of the erectile dysfunction.
Choosing the treatment that is best for you comes down to preference and efficacy. Montague cites a study that surveyed three groups of men, all of whom were successfully using an ED treatment. One group was on oral medications, one was using injections and a third had surgically implanted pumps. The most satisfied users were those with the implanted prostheses.
MSA is a neurodegenerative disease of undetermined etiology, where ED is an early prominent sign occurring in 40% of men at the time of diagnosis (46,47). ED occurs in the majority of patients and the exact cause of it is unknown (48). Like PD, MSA likely affects the dopaminergic pathways within the brain essential for arousal (49). Orthostatic hypotension (OH) as a causal factor has been refuted by evidence that sildenafil can overcome reduced filling pressures, and the ED usually precedes the development of OH (46,49,50). Similar to other neurologic disorders that lead to ED, other disease related factors such as psychosocial stress, the burden of chronic illness, changed appearance, fatigue, decreased fine motor movement of fingers, immobility and diminished self-esteem due to loss of independence may contribute as well (51).
All NOS subtypes produce NO, but each may play a different biologic 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. nNOS is involved in the regulation of neurotransmission, and eNOS is involved in the regulation of blood flow.
For many men, stopping smoking is an erectile dysfunction remedy, particularly when ED is the result of vascular disease, which occurs when blood supply to the penis becomes restricted because of blockage or narrowing of the arteries. Smoking and even smokeless tobacco can also cause the narrowing of important blood vessels and have the same negative impact. 
Research has even found possible links to frequent ejaculation and a lower risk of prostate cancer. In one study of 32,000 men published in 2016 in the journal European Urology, for example, men who ejaculated at least 21 times per month while in their 20s were less likely to be diagnosed with prostate cancer than those who ejaculated four to seven times per month. And men who ejaculated more often in their 40s were 22 percent less likely to get a prostate cancer diagnosis.

However, a review of a United Kingdom medical record database found no evidence that the use of 5-alpha reductase inhibitors independently increase the risk for ED. In 71,849 men with benign prostatic hyperplasia (BPH), the risk of ED was not increased with the use of finasteride or dutasteride only (odds ratio [OR] 0.94), or a 5-alpha reductase inhibitor plus an alpha blocker (OR 0.92) compared with an alpha blocker only. In addition, the risk of ED was not increase in 12 346 men prescribed finasteride 1 mg for alopecia, compared with unexposed men with alopecia (OR 0.95). The risk of ED did increase with longer duration of BPH, regardless of drug exposure. [48]


Tadalafil (Cialis) is the third oral medicine approved by the U.S. FDA for the treatment of erectile dysfunction. Like sildenafil (Viagra) and vardenafil (Levitra), tadalafil inhibits PDE5 (as described earlier). Unlike the other PDE 5 inhibitors, patients should take tadalafil once daily and is approved for the treatment of BPH (benign enlargement of the prostate).
Due to the risk of hypotension, caution should be used in patients using alpha blockers for prostate hyperplasia and patients using other antihypertensive medications and alpha blockers, which should not be co-administered with PDE5 inhibitors. In patients who take 50 mg of sildenafil or more and use alpha blockers, sildenafil dosing should be avoided for at least 4 hours after the dose of the alpha blocker. In patients who take 25 mg of sildenafil, use of any alpha blockers is considered safe.
Ejaculatory incompetence, erectile difficulty, erectile dysfunction, erectile failure, frigidity–female Medtalk The inability to achieve or maintain a penile erection adequate for the successful completion of intercourse, terminating in ejaculation; penile erection is mediated by nitric oxide Epidemiology Prevalence of minimal, moderate, and complete impotence in the Massachusetts Male Aging Study was 52%; age is the most important factor; complete impotence ↑ from 5%–age 40 to 15%–age 70; for an erection to achieve a successful outcome, it requires
Although vardenafil does not seem to produce significant clinical QT prolongation, it has been suggested that it be avoided in patients who have congenital QT prolongation abnormalities and in patients using class I antiarrhythmic drugs, such as quinidine and procainamide. It is also best to avoid the use of vardenafil with class III antiarrhythmic drugs, such as amiodarone or sotalol.
• Blood Vessels: Diabetes damages blood vessels, especially the smallest blood vessels such as those in the penis. Diabetes can also cause heart disease and other circulatory problems. Proper blood flow is absolutely crucial to achieving erection. “Erection is a hydraulic phenomenon that occurs involuntarily,” says Arturo Rolla, MD, of Harvard University School of Medicine. “Nobody can will an erection!” Anything that limits or impairs blood flow can interfere with the ability to achieve an erection, no matter how strong one’s sexual desire.
MSA is a neurodegenerative disease of undetermined etiology, where ED is an early prominent sign occurring in 40% of men at the time of diagnosis (46,47). ED occurs in the majority of patients and the exact cause of it is unknown (48). Like PD, MSA likely affects the dopaminergic pathways within the brain essential for arousal (49). Orthostatic hypotension (OH) as a causal factor has been refuted by evidence that sildenafil can overcome reduced filling pressures, and the ED usually precedes the development of OH (46,49,50). Similar to other neurologic disorders that lead to ED, other disease related factors such as psychosocial stress, the burden of chronic illness, changed appearance, fatigue, decreased fine motor movement of fingers, immobility and diminished self-esteem due to loss of independence may contribute as well (51).
Vacuum devices for ED, also called pumps, offer an alternative to medication. The penis is placed inside a cylinder. A pump draws air out of the cylinder, creating a partial vacuum around the penis. This causes it to fill with blood, leading to an erection. An elastic band worn around the base of the penis maintains the erection during intercourse.
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