Erections are more complicated than you think. Your brain, nerves, heart, blood vessels, and a whole lot of hormones have to work together perfectly or nothing happens. It’s a lot to ask, and sometimes things break down. And while ED happens to most guys at some point in their lives, erectile dysfunction isn’t something you can just ignore and hope it goes away.
ED occurs in up to 70% of men with MS, and MS is one of the most prevalent neurological disorders that affect the younger adult population worldwide (33-35). The mean time for SD and ED to develop is about 9 years and is rarely a presenting symptom of MS (36). Men with MS and ED may continue to have nocturnal erections, and psychogenic erections; however, this does not mean they have psychogenic ED but could be an indicator that MS involves the spinal cord (37).
Your doctor will ask you questions about your symptoms and health history. They may do tests to determine if your symptoms are caused by an underlying condition. You should expect a physical exam where your doctor will listen to your heart and lungs, check your blood pressure, and examine your testicles and penis. They may also recommend a rectal exam to check your prostate. Additionally, you may need blood or urine tests to rule out other conditions.
Zerman et al. performed penile implant surgery in 245 men with neurolgic impairment caused by spinal cord injury, CNS neoplasm, CNS infection, MS and SB (110). Mean follow-up time of 7.2 years was achieved in 195 patients, 50 patients were excluded for lost to follow-up or death from nonurological causes. Interestingly, 135 patients underwent penile implantation to assist with management of urinary incontinence and improve ability for condom/intermittent catheterization. Ninety-two patients patient underwent implantation for ED. Eighty two percent of patients were satisfied with implantation for ED, and 67% of partners were satisfied. Complications included infection (5%), perforation (0–18%), and technical dysfunction (7–33%). Perforation rates were high with the malleable device when it was placed through a subcoronal incision. After adopting an infrapubic approach the perforation rates dropped substantially.
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Other factors leading to erectile dysfunction are diabetes mellitus, which is a well-known cause of neuropathy). ED is also related to generally poor physical health, poor dietary habits, obesity, and most specifically cardiovascular disease, such as coronary artery disease and peripheral vascular disease. Screening for cardiovascular risk factors, such as smoking, dyslipidemia, hypertension, and alcoholism is helpful.
MalaCards based summary : Impotence, also known as erectile dysfunction, is related to vasculogenic impotence and hyperprolactinemia, and has symptoms including angina pectoris, pelvic pain and tremor. An important gene associated with Impotence is NOS1 (Nitric Oxide Synthase 1), and among its related pathways/superpathways are Response to elevated platelet cytosolic Ca2+ and Platelet homeostasis. The drugs Methyltestosterone and Testosterone have been mentioned in the context of this disorder. Affiliated tissues include prostate, spinal cord and endothelial, and related phenotypes are normal and reproductive system
Recently, several advances in the uses of stem cells have bet met with great anticipation. Stem cells have the ability to differentiate into different cell lines based on the cellular signaling they receive. Bone marrow mononuclear cells in particular have been used for the treatment of ED in animal models. Yiou et al. recently delivered bone marrow-mononuclear cells (BM-MNC) into the intracavernous smooth muscle of post radical prostatectomy men (123). The open label, dose escalation phase I/II trial showed improvements in IIEF-15 assessment as well as increased vascularization of the corpora based on penile Doppler arterial velocity measurements. Although promising, further investigation in humans is required to substantiate BM-MNCs impact on erections, and erectile function recovery going forward.
The first line and by far the most common treatment today is with the prescription drug sildenafil citrate, sold under the brand name Viagra. An estimated 20 million prescriptions for the pill have been filled since it was approved by the FDA in March 1998. It is also the most effective treatment with a success rate of more than 60%. The drug boosts levels of a substance called cyclic GMP, which is responsible for widening the blood vessels of the penis. In clinical studies, Viagra produced headaches in 16% of men who took it, and other side effects included flushing, indigestion, and stuffy nose.
In a prospective, multicenter, single-armed study of ED patients who exhibited a suboptimal response to PDE5 inhibitors, the investigators found that percutaneous implantation of zotarolimus-eluting stents in focal atherosclerotic lesions was both safe and feasible and was associated with clinically meaningful improvement on subjective and objective measures of erectile function. 
There are many different treatment options for erectile dysfunction but your individual diagnosis will determine which treatment option is right for you. It is important to realize that not all treatment options will work for everyone. A doctor who has specialized in men’s sexual health (typically a urologist) will be the most qualified to discuss all of your treatment options with you. Many specialists will often encourage you to schedule additional follow up appointments to review how your treatment is working for you or if a different option may be more beneficial.
There are many different body parts that play an important role for a man to get and maintain an erection during sexual intercourse. Beyond the physical causes that can lead to ED, it has been reported that 20% of ED is related to psychological causes.2 With so many possibilities leading to erectile dysfunction, it becomes particularly important to find a specialist who can correctly diagnosis the direct cause of your ED and find a treatment option that is right for you.
Some injectable formulations need to be refrigerated — yet another reason many men steer away from the needle option. Among ED treatments, injections are also the most common cause of extended erections — rigidity lasting more than four hours, also called priapism — which afflict about 3 to 7 percent of users, Kohler says. That condition, while easily treated with an adrenaline shot, requires urgent attention at a clinic or hospital. The cost of this ED treatment is $2 to $5 per injection.
Monitoring erections that occur during sleep (nocturnal penile tumescence) can help you and your doctor to understand if the erectile dysfunction is due to psychological or physical causes. The nocturnal penile tumescence test is a study to evaluate erections at night. Normally men have three to five erections per eight hours of sleep. The test can be performed at home or in a sleep lab. The most accurate way to perform the test involves a special device that is connected to two rings. The rings are placed around the penis, one at the tip of the penis and the other at the bottom (base) of the penis. The device records how many erections occur, how long they last, and how rigid they are. The test is limited in that it does not assess the ability to penetrate.
Trauma to the pelvic blood vessels or nerves can also lead result in ED. Bicycle riding for long periods has been implicated as an etiologic factor; direct compression of the perineum by the bicycle seat may cause vascular and nerve injury.  On the other hand, bicycling for less than 3 hours per week may be somewhat protective against ED.  Some of the newer bicycle seats have been designed to diminish pressure on the perineum. [37, 38]
Physicians on the Ro platform use telemedicine technologies to diagnose ED in the same way they diagnose patients in-person. Doctors ask questions to evaluate your symptoms and make sure it’s safe and appropriate to prescribe ED medication. The physicians on the Ro platform use your answers to diagnose your condition and create a treatment plan. That’s why it’s vital you answer each question to the best of your knowledge and ensure that every communication with your physician is truthful, accurate, and thorough.
Modern drug therapy for ED made a significant advance in 1983, when British physiologist Giles Brindley dropped his trousers and demonstrated to a shocked Urodynamics Society audience his papaverine-induced erection. The drug Brindley injected into his penis was a non-specific vasodilator, an alpha-blocking agent, and the mechanism of action was clearly corporal smooth muscle relaxation. The effect that Brindley discovered established the fundamentals for the later development of specific, safe, and orally effective drug therapies.[better source needed][better source needed]
Replacement testosterone is available as oral pills, intramuscular injections, skin patches, and a gel that is rubbed into the skin. Men with low sexual desire and ED may have low testosterone (male hormone) levels. Hormone replacement may occasionally be of some benefit, especially when used in combination with other therapies. Testosterone supplementation alone is not particularly effective in treating erectile dysfunction. Sexual desire and an overall sense of well-being are likely to improve when serum testosterone levels (the levels in the blood) are restored. This can take several months after starting testosterone replacement.
Her remark was entirely destructive of poetry, since it was to the effect that poetry had nothing whatever to do with her; all her friends spent their lives in making up phrases, she said; all his feeling was an illusion, and next moment, as if to taunt him with his impotence, she had sunk into one of those dreamy states which took no account whatever of his existence.
Penile prostheses are very effective, and most patients who have a prosthesis placed are satisfied with the prosthesis. However, placement of a prosthesis causes scarring of the tissue within the corpora cavernosa, and if the prosthesis requires removal, other forms of therapy, except for the vacuum device, are often not effective. Thus, most physicians reserve placement of a prosthesis for men who have tried and failed or have contraindications to other therapies.
The American Urological Association Guideline on the Management of ED states oral PDE5i are considered first line therapy for the treatment of ED, unless contraindicated (57). Sildenafil, the first oral PDE5i, was introduced in 1998 and has revolutionized ED therapy due to its broad applicability, effectiveness and safety profile. PDE5i work by preventing hydrolysis of cGMP by the PDE5 enzyme in the smooth muscle of the corpora cavernosa. cGMP degradation typically leads to smooth muscle contraction and detumescence prevented by PDE5i administration. Two other PDE5i, vardenafil and tadalafil are other PDE5i with different pharmacokinetics, PDE receptor selectivity and side effect profiles.
Induction of erection occurs after stimulation of the cavernous and pelvic nerve plexus. Conversely, stimulation of the sympathetic trunk leads to detumescence. The reflex erectile response requires that the sacral reflex arc remain intact. Tactile and sensory signals are received by the somatic sensory pathways and integrate with parasympathetic nuclei within the sacral spinal cord (S2-4) leading to induction of erection via cholinergic signaling. These reflexogenic erections remain intact with upper motor neuron injuries. Psychogenic erections do not require that the sacral reflex arc remain intact. In a cat models, spinal cord removal below L4/L5 led to absence of a reflexogenic erection but stimulation of the medial preoptic area (MPOA) or placement near a female cat in heat led to erection (5,6). Psychogenic erections occur via induction of central pathways traveling from the brain through the sympathetic chain. Non-penile sensory pathways induced by sight, sound, touch and smell travel through the MPOA to the erection centers within the cord T11-L2, and S2-S4 to induce erections (7). When a sacral lower motor neuron injury is present in men, below T12 these types of erections are more likely to occur (8). Spinal cord lesions above T9 are not associated with psychogenic erections (9). Rigidity of erections is less with psychogenic erections because the thoracolumbar sympathetic outflow may contain a decreased concentration of neurons compared to the parasympathetic outflow from the sacral spinal cord.
Similar to heart-disease-related to atherosclerosis (plaque formation within the blood vessels), the concept of bypassing or angiographically dilating and stenting penile arteries has been entertained recently with improvements in microvascular surgery and interventional radiology. However, the main drawback with most erectile dysfunction is the failure of vascular relaxation within the corpora cavernosa rather than the one feeding penile artery. Stenting or surgical grafting to bypass a blockage would be ideal for a single obstruction site along a penile artery. Because most erectile dysfunction pathology resides within the sponge-like vascular plexus of the penis, the ability of diffusely dilating and expanding the many vascular chambers of the penis is difficult to impossible. As such, unless the situation is that the penile artery was injured during a pelvic trauma, and the potential to bypass another vessel into the single penile artery, the concept of vascular reconstruction or angio-radiology stenting has very low yield.
Injection therapy: The modern age of such drug therapies began in 1993 when the injection of papaverine (Pavabid), an alpha-blocker that produces vasodilatation (widening of the blood vessels), was shown to produce erections when injected directly into the penis. Soon afterward, other vasodilators, such as prostaglandin E1 (PGE 1) monotherapy (Caverject, Edex), PGE1 and phentolamine (Regitine), and Trimix (papaverine, phentolamine and prostaglandin E1), were demonstrated to be effective. The benefit of combination therapy is the decreased dosing of each with less side effects. Most important is the reduction of the prostaglandin PGE1 dosing, which is associated to the localized pain.
When sexually stimulated there is a release of a chemical, nitric oxide (NO) in the blood vessels of the corpus cavernosum. The NO stimulates the production of a compound called cGMP, which causes relaxation of the smooth muscle in the blood vessels supplying the corpus cavernosum. PDE 5 is an enzyme that breaks down cGMP. By inhibiting the breakdown of cGMP by PDE5, these medications allow cGMP to build up in the penis. cGMP causes muscles in the corpora cavernosa of the penis to relax. When the muscle is relaxed, more blood can flow into the penis and fill the spaces in the penis. As the penis fills with blood, the veins in the penis are compressed, and this results a hard erection. When the effect on PDE5 decreases, the cGMP levels go down and the muscle in the penis contracts, causing less blood to flow into the penis and allowing the veins to open up and drain blood out of the penis.
Diabetes mellitus: Erectile dysfunction tends to develop 10 to 15 years earlier in diabetic men than among nondiabetic men. The increased risk of erectile dysfunction among men with diabetes mellitus may be due to the earlier onset and greater severity of atherosclerosis (hardening of the arteries) that narrows the arteries and thereby reduces the delivery of blood to the penis. Atherosclerosis can affect the arteries in the penis, as well as the arteries in the pelvis that supply the penile arteries. Diabetes mellitus also causes erectile dysfunction by damaging nerves that go to the penis, much like the effect of diabetes on nerves in other areas of the body (diabetic neuropathy). Diabetes can also affect the muscles in the penis, leading to troubles with erections. Smoking cigarettes, obesity, poor control of blood glucose levels, and having diabetes mellitus for a long time further increase the risk of erectile dysfunction in people with diabetes.
PDE5i medications are absolutely not to be taken by men with heart conditions who are taking nitrates such as nitroglycerine or isosorbide (Isordil, Ismo, Imdur). Those with serious heart disease, exertional angina (chest pain), and those taking multiple drugs for high blood pressure are advised to seek the advice of a heart specialist before beginning therapy with sildenafil.
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In patients with low testosterone, testosterone treatment can improve libido and erectile dysfunction, but many men still may need additional oral medications such as sildenafil, vardenafil, or tadalafil. Some studies suggest that men with ED and low testosterone may respond better to PDE5 inhibitors when given testosterone therapy; however, this is controversial.
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).
Having erection trouble from time to time isn't necessarily a cause for concern. If erectile dysfunction is an ongoing issue, however, it can cause stress, affect your self-confidence and contribute to relationship problems. Problems getting or keeping an erection can also be a sign of an underlying health condition that needs treatment and a risk factor for heart disease.