The success of treatment for sexual dysfunction depends on the underlying cause of the problem. The outlook is good for dysfunction that is related to a condition that can be treated or reversed. Mild dysfunction that is related to stress, fear, or anxiety often can be successfully treated with counseling, education, and improved communication between partners.
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.
Injections: Injections are a reliable way to restore testosterone levels, but this therapy requires periodic injections (usually every two weeks) to sustain an effective level. It also causes high hormone levels right after the injection and low hormone levels just before the next shot. This is thought to be slightly more risky than other methods that maintain a moderate hormone level throughout the treatment period.
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In the short term, alcohol relaxes muscles in the penis, letting blood to flow in (which is a good thing). However, alcohol also prevents other blood vessels from closing and trapping all the extra blood. Erections depend on trapping increased blood flow in the erectile tissue of the penis. If you don’t trap that extra blood, you don’t get an erection. In the long run, excessive alcohol consumption can cause liver scarring, high blood pressure, and can damage your blood vessels resulting in erectile dysfunction.
The next new treatments for erectile dysfunction will probably be improvements in some ED drugs already being used. "A dissolvable form of Levitra that you put under your tongue is coming that may work more quickly than the pills we have now," says Feloney. A new form of alprostadil may make it possible for you to rub it directly on the penis instead of inserting or injecting it. And newer phosphodiesterase inhibitors that last even longer and cause fewer side effects are being developed. Stay tuned!
Besides PDE5 inhibitors and among second-line therapies are VCDs which are clear plastic chambers placed over the penis, tightened against the lower abdomen with a mechanism to create a vacuum inside the chamber. This directs blood into the penis. If an adequate erection occurs inside the chamber, the patient slips a small constriction band off the end of the VCD and onto the base of the penis. An erection beyond 30 min is not recommended. These devices can be a bit cumbersome, but are very safe.40
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.
SD in MS can be classified into three categories. Primary SD is due directly due to MS-related neurological deficits, secondary SD is related to physical impairments and symptoms or drugs used for MS treatment, and tertiary SD is due to the psychological, social and cultural problems attributed to MS (38). These classifications are important, and underscore the importance of addressing all the issues leading to SD not just the neurologic impairment.

It is important to understand that ED is frequently, if not usually, directly related to endothelial dysfunction, and that the release of NO by the vasculature of the penile arteries is directly related to the function of intact, healthy endothelium. In the face of endothelial dysfunction, the process of erection fails to occur in a normal fashion.16
Injections: Injections are a reliable way to restore testosterone levels, but this therapy requires periodic injections (usually every two weeks) to sustain an effective level. It also causes high hormone levels right after the injection and low hormone levels just before the next shot. This is thought to be slightly more risky than other methods that maintain a moderate hormone level throughout the treatment period.
Sexual functioning involves a complex interaction among biologic, sociocultural, and psychological factors, and the complexity of this interaction makes it difficult to ascertain the clinical etiology of sexual dysfunction. Before any diagnosis of sexual dysfunction is made, problems that are explained by a nonsexual mental disorder or other stressors must first be addressed. Thus, in addition to the criteria for erectile disorder, the following must be considered:

Watts and coworkers, in their review article, make several points about this ED/CAD nexus. Endothelial dysfunction is present in both CVD and ED, and is linked through the NO mechanism. The authors note that PDE5 inhibitors improve endothelial function and have a salutary effect on both CVD and ED. Both ED and cardiac disease respond to modifications in lifestyle as well as pharmacologic manipulation. These authors also report that the presence of ED gives the clinician an opportunity to assess CVD and prevention as well.20


This is similar to magnetic resonance imaging. Magnetic resonance angiography uses magnetic fields and radio waves to provide detailed images of the blood vessels. Doctors may inject a "contrast agent" into the person's bloodstream that causes vascular tissues to stand out against other tissues. The contrast agent provides for enhanced information regarding blood supply and vascular anomalies.

Erectile dysfunction can occur as a side effect of medication taken for another health condition. Common culprits are high blood pressure meds, antidepressants, some diuretics, beta-blockers, heart medication, cholesterol meds, antipsychotic drugs, hormone drugs, corticosteroids, chemotherapy, and medication for male pattern baldness, among others.


Several treatments were promoted in the pre-PGE1, pre-prostaglandin era, including yohimbine, trazodone, testosterone, and various herbal remedies. None of these is currently recommended under the updated American Urological Association Guidelines for the Treatment of Erectile Dysfunction.15 Testosterone supplementation is only recommended for men with low testosterone levels.
In 1983, Brindley injected the corpora of several SCI men with phentolamine (85). Two out of the three men had a sufficient erection produced. Since then multiple reports on the efficacy of intracavernosal therapy have been published using, phentolamine, papaverine, prostaglandin, vasoactive intestinal peptide (VIP), and these medications in combination (86-90). These medications have been found to be extremely effective for neurogenic ED due to their ability act locally and essentially bypassing neuronal pathways. Local therapies are usually considered second-line after PDE5i fail to elicit a desired response which can occur in about 25–30% of men with ED, in general (91). Furthermore, the locally delivered medications can be quite dangerous if not used appropriately as priapism and significant pain with injections can occur. These specific occurrences have been suggested as a reason for high discontinuation rates with intracavernosal therapy (92).
Conditions that may be associated with ED include diabetes, [25, 26, 27] hypertension, [28] , and CAD, as well as neurologic disorders, endocrinopathies, benign prostatic hyperplasia, [29] , sleep apnea [30] , COPD, [31] and depression (see Table 1 below). [32, 33, 34, 35] In fact, 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 psychological mood and behavior.
The vacuum constriction device consists of a vacuum cylinder, various sizes of tension rings, and a vacuum pump, either hand-operated or electric. The penis is placed in a cylinder to which a tension ring is attached. Air is evacuated from the cylinder by means of the pump, creating a vacuum, which produces the erection. The cylinder is removed, leaving the tension ring at the base of the penis to maintain the erection.
Inflatable prostheses are complex mechanical devices that imitate the natural process of erection. Parts are inserted surgically into the penis and scrotum, and activated by squeezing. When erection is no longer desired, a valve on the pump is pressed, and the penis becomes flaccid. Self-contained single-unit prostheses are similar to the inflatable types, but more compact. The entire device is implanted into the penis. When erection is desired, the unit is activated by either squeezing or bending, depending on which of the two types of self-contained prostheses is used.

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 Society of Clinical Oncology, American Urological Association, Association of Women Surgeons, New York Academy of Sciences, Society of Government Service Urologists, Society of University Urologists, Society of Urology Chairpersons and Program Directors, and Society of Women in Urology
It appears that testosterone has NOS-independent pathways as well. In one study, castrated rats were implanted with testosterone pellets and then divided into a group that received an NOS inhibitor (L-nitro-L-arginine methyl ester [L-NAME]) and a control group that received no enzyme. [24] The castrated rats that were given testosterone pellets and L-NAME still had partial erections, a result suggesting the presence of a pathway independent of NOS activity.
Both ED and low testosterone (hypogonadism) increase with age. The incidence of the latter is 40% in men aged 45 years and older. [15] Testosterone is known to be important in mood, cognition, vitality, bone health, and muscle and fat composition. It also plays a key role in sexual dysfunction (eg, low libido, poor erection quality, ejaculatory or orgasmic dysfunction, reduced spontaneous erections, or reduced sexual activity). [16]

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


I started meditating about three years ago. I jumped in at the deep end. After a month of goofing around with apps, I signed up for a Vipassana—a ten-day silent retreat, where you sit cross-legged and meditate for about ten hours a day and spend the remaining 14 questioning everything you've ever done. After the retreat all sorts of changes took place: My anxiety disappeared, and my decision-making improved; but one of the most pronounced changes was my sex life. For the first time, I could have sex while thinking about sex rather than how broke I was or how quickly my career was imploding. And I'm not alone; meditation forums are full of people who have had similar experiences.
When a man becomes sexually excited, muscles in their penis relax. This relaxation allows for increased blood flow through the penile arteries. This blood fills two chambers inside the penis called the corpora cavernosa. As the chambers fill with blood, the penis grows rigid. Erection ends when the muscles contract and the accumulated blood can flow out through the penile veins.
Obesity and metabolic syndrome can cause changes in blood pressure, body composition, and cholesterol which may lead to ED. Other conditions that may contribute to erectile dysfunction include Parkinson’s, multiple sclerosis, Peyronie’s disease, sleep disorders, alcoholism, and drug abuse. Taking certain medications can also increase your risk for ED.
Oral ED medication is considered highly effective and studies show it works on the majority of men. But no medication works for everyone and ED medication is no exception. Everyone’s reaction to a medication is unique and anything potent enough to help is strong enough to have side effects. If the medication isn’t working, it is important to tell your doctor. Sometimes it is a matter of needing a higher dose. Also, it has been shown that it takes 6 to 8 tries using the medication to experience the best result.
Does diabetes cause erectile dysfunction? Diabetes can lead to lower levels of testosterone, and this can result in erectile dysfunction. Controlling blood sugar levels, maintaining a healthy weight, getting exercise, and reducing stress are all ways of reducing this problem. Hormone therapy, Viagra, and counseling are some ways that medicine can help. Read now

Recognized risk factors for ED include cardiovascular disease (CVD) (hypertension, atherosclerosis, and hyperlipidemia), diabetes, depression, alcohol use, smoking, pelvic/perineal surgery or trauma, neurologic disease, obesity, pelvic radiation, and Peyronie’s disease. One study suggested that the relationship between arterial disease and ED is very strong, with 49% (147 of 300) of patients with coronary artery disease noted on cardiac catheterization reporting significant erectile dysfunction.6 Endothelial dysfunction has been indicated as the pathophysiologic mechanism responsible for both CVD and ED.7 The Boston Area Community Health survey demonstrated a dose-response between smoking and incidence of erectile dysfunction.8 Animal studies have demonstrated both smooth-muscle disruption and decreased production of neural nitric oxide synthase in cigarette-exposed animals.9

When stimulated by the nerves, the spongy tissue arranges itself in such a way that more blood can be stored in the penis. The veins running through the outer sheath of the penis then compress which stops the blood from leaving the penis. As the blood is stopped from flowing out, the penis fills with blood and stretches within the outer casing, giving an erection.
Another study compared the response of surgically and medically castrated rabbits to vardenafil with that of control rabbits. [22] Castrated rabbits did not respond to vardenafil, whereas noncastrated rabbits did respond appropriately. This result suggests that a minimum amount of testosterone is necessary for PDE5 inhibitors to produce an erection.
The laboratory results should be discussed with the patient and, if possible, with his sexual partner. This educational process allows a review of the basic aspects of the anatomy and physiology of the sexual response and an explanation of the possible etiology and associated risk factors (eg, smoking and the use of various medications). Treatment options and their benefits and risks should be discussed. This type of dialogue allows the patient and physician to cooperate in developing an optimal management strategy.
ED is a common occurrence after SCI, occurring in up to 80% of men, and results from disruption of the nerve pathways essential for erection (24,25). Different degrees of ED may occur depending on the spinal cord level of injury (LOI), extent of lesion and timing from injury. Reflexogenic erections can occur with lesions above L3 or L4 when the erectile spinal reflex arc remains intact. Psychogenic erections can occur with low lesions in the sacral and lumbar spinal cord but may not occur in complete lesions above T9 that can damage sympathetic outflow. Additionally, reflexogenic erections are not likely to occur in the spinal shock period that occurs after the initial cord trauma. Conversely, their occurrence may signal that the period of shock is over (26). Typically SCI affects younger men in their “sexual prime” and ED is associated with decreased quality of life (27).

There are, as you listen to all of the advertisements, if your erection lasts for more than four hours, there are very, very unusual cases where that can happen. There are very rare cases of visual problems. There are even rarer cases of hearing problems. But with every medication, there always a potential downside. But the absolute contraindication is an unstable medical condition, an unstable cardiovascular condition, being on nitrates.
The Prostate Cancer Prevention Trial was a landmark study by Thompson et al that prospectively assessed the time to developing CVD after the diagnosis of ED. There were 4247 men with no ED at study entry; 2420 developed incident ED (defined as the first report of ED of any grade) over 5 years. Those men that developed ED had a 1.45-fold higher probability of experiencing a CV event compared with men who did not develop ED.27
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.

These are not currently approved by the FDA for ED management, but they may be offered through research studies (clinical trials). Patients who are interested should discuss the risks and benefits (informed consent) of each, as well as costs before starting any clinical trials. Most therapies not approved by the FDA are not covered by government or private insurance benefits.
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