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.
Self-injection of these agents has been of enormous benefit because they represent the most effective way to achieve erections in a wide variety of men who otherwise would be unable to achieve adequate rigid erections. The need for intact nerve pathways to the penile tissue is not needed. The locally injected medication directly relaxes the arteriole vessels and penile cavernosal tissue. Thus, this therapy is not dependent on sexual stimulation.
The severity of ED has been correlated with the extent of CVD. Banks et al reported that the risk of future CV events increased progressively according to ED severity.28 This was shown in both men with and without known CVD at baseline and after controlling for confounders. Solomon and colleagues found an inverse correlation between international index of erectile function (IIEF) scores and plaque burden seen on coronary angiography.29 In addition, Yaman et al demonstrated a significant correlation between ED severity on IIEF questionnaires and coronary artery calcification.30
Iatrogenic hypotension can occur in men in neurodegenerative disease using sildenafil (49). Hussain et al. placed men with PD and MSA on sildenafil and recorded blood pressure before and after. Half of the 12 MSA patients developed postural hypotension, while none of the twelve PD patients did. Since MSA can be difficult to distinguished diagnostically from PD, baseline blood pressure measurements prior to prescribing the medication and seeking medical assistance if symptomatic hypotension occurred was recommended for all patients with PD, and MSA. Of note, none of the men with MSA who developed hypotension discontinued sildenafil use due to its effectiveness at improving their erections.
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.
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.
What you need to know about delayed ejaculation Delayed ejaculation is a sexual disorder that can be distressing for a man and his partner and may disrupt a relationship. There are many reasons why delayed ejaculation occurs, including tissue damage, age, drugs, and the side effects of medication. They may be physiological or psychological. Find out how to get help. Read now

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.
Now, there are lots of ways that you can reduce stress and anxiety in your life. One of those things you can do is exercising daily. Now, it doesn’t mean getting into a gym all the time, but it can just be doing sit-ups at home, long walks at the grocery store, bicycling, and if you can afford the gym, getting there maybe two to three days a week. But don’t forget, a healthy body equals a healthy mind. Meditation, yoga, breathing exercises– now, here’s where you can take a few moments to be centered and communicate with your inner self, peace. Healthy eating– now, taking control of the intake of what goes into your body makes you to start feeling better and looking better. That wellness is the opposite of anxiety. And treating issues and tackling things that are weighing you down, taking that very first step is liberating.
If you have symptoms of ED, it’s important to check with your doctor before trying any treatments on your own. This is because ED can be a sign of other health problems. For instance, heart disease or high cholesterol could cause ED symptoms. With a diagnosis, your doctor could recommend a number of steps that would likely improve both your heart health and your ED. These steps include lowering your cholesterol, reducing your weight, or taking medications to unclog your blood vessels.
Factors that mediate contraction in the penis include noradrenaline, endothelin-1, neuropeptide Y, prostanoids, angiotensin II, and others not yet identified. Factors that mediate relaxation include acetylcholine, nitric oxide (NO), vasoactive intestinal polypeptide, pituitary adenylyl cyclase–activating peptide, calcitonin gene–related peptide, adrenomedullin, adenosine triphosphate, and adenosine prostanoids.

A CVA can occur anywhere through the brain, midbrain, brainstem and spinal cord leading to varying degrees of SD depending on location. A decline in libido, erection and ejaculation are frequent in men who have had a CVA, with a reported prevalence of ED that varies from 17% to 48% (28,29). Right hemispheric infarcts seem to affect erections more so than left-sided ones. The exact effects of CVA on sexual function are complex and multifactorial, as disability, psychological and emotional status can affect sexual function aside from the location of the CVA.
Alprostadil is injected into the side of penis with a very fine needle. It's of great value to have the first shot in the doctor's office before doing this on your own. Self-injection lessons should be given in your doctor's office by an experienced professional. The success rate for getting an erection firm enough to have sex is as high as 85% with this treatment. Many men who do not respond to oral PDE5 inhibitors can be ‘rescued' with ICI.
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