Diabetes is a well-recognized risk factor for ED. A systematic review and meta-analysis found that the prevalence of ED was 37.5% in type 1 diabetes, 66.3% in type 2 diabetes, and 52.5% in diabetes overall—a rate approximately 3.5 times higher than that in controls. [39]  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.
Meditation is known to lower the heart rate and regulate blood flow around the body, which bodes well for ED sufferers, as what's an erection if not a big gathering of blood? Meditation has also been shown to reduce anxiety and change negative thought associations. Sara Lazar, a neuroscientist at Harvard, was one of the first people to scan meditators' brains and discovered that the amygdala, the part of the brain where anxiety calls home, was smaller for meditators than the control group.
If a trial of oral therapy and withdrawal of offending medications do not restore erectile function or if a patient has medical or financial contraindications to pharmacologic therapy, most primary care practitioners should consider referring the patient to a specialist for additional evaluation and discussion of alternative treatment options. However, some primary care practitioners may recommend vacuum constriction devices.
Ultimately, PDE5i have had a significant impact on the treatment of ED in men with SCI. The ease of use and tolerability of the medication has also led to improved satisfaction and quality of life that had been previously affected by SD. Head to head trials evaluating specific PDE5i within the SCI population are required to further elucidate drug preference. PDE5i should be considered first line therapy, however men with high thoracic and cervical lesions should be warned about an increased chance of dizziness with sildenafil and possibly other PDE5i use.
Traditionally, erectile impotence (the classical definition of impotence) is the failure to achieve penile erection during intercourse. It may have either physical or psychological causes. Alcoholism, endocrine disease, and neurological disorders are typical physical causes. Psychological causes include anxiety over performance, hostility or other negative feelings toward the sexual partner, and stress, anxiety, depression, or other emotional conflicts outside of the relationship. Erectile impotence occasionally occurs with age and, although attributed by the individual to the aging process itself, it is usually secondary to disorders of aging, such as faulty blood circulation or prostate disease. In cases of impotence caused by blood vessel dysfunction, an insufficient supply of blood flows into the penis, or the blood diffuses out into adjacent tissues.
Nearly every primary care physician, internist and geriatrician now understand that many older men retain an interest in sexual activity as they age. Some primary care physicians think that sexual potency in older men is the norm, and that if it is lacking, it is ‘all in the head.’ This viewpoint has not been supported by current literature. The Massachusetts Male Aging Study (MMAS) found that 52% of men between 40 and 70 years old reported having some form of erectile dysfunction (ED).1 The reality is that ED is a natural part of ageing and that the prevalence increases with age. In the MMAS, they found that roughly 50% of men at 50 years old, 60% of men at 60 years old and 70% of men at 70 years old had ED. Thus, nearly all men who live long enough should develop ED. The myths that surround the problems of impotence or ED confound the attempts of patients to receive treatment and the attempts of physicians to help them.1
3. Testosterone replacement. Before oral medications like Viagra, testosterone was routinely used to treat erectile dysfunction as it is central in the male sexual response, including the desire for sex and the process of getting an erection. Testosterone can be administered in a number of ways, for example orally, by means of an injection, skin patch, or subcutaneous (under the skin) pellet. 
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.
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:

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.
Finally, there are NO-releasing polymers that are capable of delivering NO in a pharmacologically useful way. Such compounds include compounds that release NO upon being metabolised and compounds that release NO spontaneously in aqueous solution. Initial animal studies suggest that cavernosal injections of NO polymers can significantly improve erectile function.48
These medications don’t work for everyone but they are easy to use and work for around 60% of people who try them. They work by making it easier to get an erection by reducing the effect of (inhibiting) the chemical PDE-5. This chemical is used in the body to make sure there isn’t too much blood in the penis during an erection, but if you have erectile dysfunction then this chemical ends up over-compensating.
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.
Think of erectile dysfunction as your body’s “check engine light.” The blood vessels in the penis are smaller than other parts of the body, so underlying conditions like blocked arteries, heart disease, or high blood pressure usually show up as ED before something more serious like a heart attack or stroke. ED is your body’s way of saying, “Something is wrong.” And the list of things that cause erectile dysfunction can include:
The first stem cell study for the treatment of ED was published in 2004. This study used embryonic stem cells to treat ED. At this time, there is a total of 36 published basic studies assessing stem cell therapy for ED, with two clinical trials. The mechanism of action of stem cells is to generate angiogenesis with subsequent increase in cavernosal smooth muscle cells within the corporal bodies.46
With sex therapy, your counselor looks at the sexual problems you and your partner are having. Sex therapy works with problems such as performance anxiety, which means that you worry so much about whether you will be able to have sex that you are not able to. It also helps when you have erection problems that are not due to physical or drug problems, or premature ejaculation (you come too quickly). It may help you to reach orgasm or to learn to relax enough to avoid pain during sex. Counseling can help you to adjust to the treatment you and your doctor choose.
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 ED within medicine is covered by andrology, a sub-field within urology. Research indicates that ED is common, and it is suggested that approximately 40% of males experience symptoms compatible with ED, at least occasionally.[38] The condition is also on occasion called phallic impotence.[39] Its antonym, or opposite condition, is priapism.[40][41]
Nerves originating in the spinal cord and peripheral ganglia innervate the penis. There are autonomic (parasympathetic and sympathetic), and somatic separate and integrated pathways. The autonomic pathways neurons originate in the spinal cord and peripheral ganglia from the sympathetic and parasympathetic systems, respectively. They merge to form the cavernous nerves that travel alongside the prostate, enter the corpora cavernosa and corpus spongiosum to affect the neurovascular events required for tumescence and detumescence. The somatic nerves send sensory information from the penile skin, glans, and urethra via the dorsal penile nerve and pudendal nerve to the spinal cord. The somatic nerves also initiate contraction of the ischio- and bulbocavernosus muscles.
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. The odds depend 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.
medicines called alpha-blockers such as Hytrin (terazosin
HCl), Flomax (tamsulosin HCl), Cardura (doxazosin
mesylate), Minipress (prazosin HCl), Uroxatral (alfuzosin HCl),
 Jalyn (dutasteride and tamsulosin HCl), or Rapaflo (silodosin).
Alpha-blockers are sometimes prescribed for prostate
problems or high blood pressure. In some patients, the use
of Sildenafil with alpha-blockers can lead to a drop in blood pressure or to fainting
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.
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 cavernosa, similar to those found elsewhere in the body, are contributing factors. Other risk factors associated with aging include depression, sleep apnea, and low HDL levels.

Oral therapies via the PDE5i sildenafil, vardenafil, and tadalafil have been proven to be generally safe and effective in select NED populations. The majority of the treatment effectiveness data has been generated in the SCI population. Data regarding the use of PDE5i outside of the SCI population is lacking (58). Furthermore, the ED that exists in the population with neurologic disorders is often multifactorial and may be caused by psychogenic, psychosocial, hormonal, medication-related and disability-related factors. A careful evaluation of each patient must be performed to isolate these factors prior to initiating vasoactive therapy.


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