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).
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
Oral PDE5i remains the first line treatment for NED from SCI. Three of the four PDE5i currently available in the U.S., avanafil excluded, have been investigated in the SCI, and all of the more recent studies have shown improvements in erectile function based on IIEF score compared to placebo when included (59-63). Other studies have also shown significant improvements in the IIEF score when compared to baseline (64-69). Furthermore, treatment efficacy when compared to placebo occurs despite LOI or American Spinal Injury Association (ASIA) score characterizing impairment related to the injury (59,61).
Between 10 and 88% of patients diagnosed with cancer experience sexual problems following diagnosis and treatment. The prevalence varies according to the location and type of cancer, and the treatment modalities used. Sexuality may be affected by chemotherapy, alterations in body image due to weight change, hair loss or surgical disfigurement, hormonal changes, and cancer treatments that directly affect the pelvic region.

Other factors leading to erectile dysfunction are diabetes mellitus, which is a well-known cause of neuropathy).[2] 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.[2] Screening for cardiovascular risk factors, such as smoking, dyslipidemia, hypertension, and alcoholism is helpful.[2]

Your Ro physician may recommend trying the medication under different circumstances. Using the medication the first time can be anxiety provoking so they may suggest using it alone until you are familiar with its effect or side effects. If you’ve been prescribed ED medication on the Ro platform, please contact a physician if you have any questions. You are not alone. Use every tool you can and asking questions when you need answers is one of them.
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.
Robbins, C. L., Schick, V., Reece. M., Herbenick, D., Sanders, S. A. Dodge, B., & Fortenberry J. D., (2011, December 1). Prevalence, frequency, and associations of masturbation with partnered sexual behaviors among US adolescents. JAMA Pediatrics, 165(12), 1087–1093. Retrieved from https://jamanetwork.com/journals/jamapediatrics/fullarticle/1107656
Low-intensity extracorporeal shock wave therapy has been proposed as a new non-invasive treatment for erectile dysfunction caused by problems with blood vessels. Shock wave therapy machines are now available in some medical practices in Australia. Although there is some evidence that it may help a proportion of men with erectile dysfunction, more research is needed before clear recommendations on its use can be made.
Additionally, the physiologic processes involving erections begin at the genetic level. Certain genes become activated at critical times to produce proteins vital to sustaining this pathway. Some researchers have focused on identifying particular genes that place men at risk for ED. At present, these studies are limited to animal models, and little success has been reported to date. [4] Nevertheless, this research has given rise to many new treatment targets and a better understanding of the entire process.

The device consists of an acrylic cylinder placed over the penis that uses a lubricant to achieve a good seal between the penile body and cylinder. An erection is then achieved by creating a vacuum inside the cylinder with a pump connected to the cylinder. Once an erection is achieved, a constriction band is applied to the base of the penis to maintain the erection. The cylinder can then be removed and the patient can engage in intercourse with the constriction band at the base of the penis maintaining the erection. The band can remain on for approximately 30 minutes and then must be removed. The erection produced by the device differs from a normal erection likely because of venous occlusion from the constriction band resulting in generalized swelling of the entire penis, with probable preservation of arterial inflow.
Approximately 95% of penile implant surgeries are successful in producing erections that enable men to have sexual intercourse. Moreover, patient satisfaction questionnaires show that up to 90% of men who have undergone penile implants say they would choose the surgery again, and overall satisfaction ratings are higher than those reported by men using oral medication or penile injection therapy.
The role of the endothelium in erectile function became clearer with the observation that the phosphodiesterase type 5 (PDE5) inhibitor, sildenafil, enhanced erectile function. Erection occurs with the release of nitric oxide (NO) from the vascular endothelial cells.17 The reduction in endothelial cell production of NO results in the negative impact on the smooth muscles in the corporal bodies and results in less relaxation of the smooth muscle cells with decrease in blood supply and resulting ED. A similar phenomenon is well known to impact the coronary arterial system resulting in CVD.
Centrally active compounds such as apomorphine have been used in men with ED whose cardiovascular comorbidity may prohibit PDE5i use, or in men who have concurrent apomorphine use for its anti-parkinsonian properties. Unfortunately, its side effect profile and poor effectiveness compared to other ED treatments have impaired its mainstream utilization (118). It is suspected that the side effects of apomorphine relate to its D2 receptor affinity. D4 receptor agonists, such as ABT-724 and azulenylmethylpiperazines, may not have the same associated side effects and show potent pro-erectile effects in animal models compared to apomorphine (32,119).
The sympathetic pathway originates from the 11th thoracic to the 2nd lumbar spinal segments and goes via the white rami to enter the sympathetic chain ganglia. Subsequently nerves travel through the lumbar splanchnic to inferior mesenteric and superior hypogastric nerves to the pelvic plexus. The T10 through T12 segments are most often the origin of sympathetic fibers, and the sympathetic chain ganglia that innervate the penis are located in the sacral and caudal ganglia (3).
L-arginine, an amino acid that is naturally present in the body and helps make nitric oxide, supports a successful erection. Nitric oxide is responsible for making the blood vessels relax, which helps sustain an erection for men. A 1999 study, observed the effects of six weeks of high-dose (5 grams/day) orally administered nitric oxide (NO) donor L-arginine on men with organic ED. Thirty-one percent of those who took 5 grams/day of L-arginine experienced significant improvements in sexual function. Burns told Medical Daily, “l-arginine and deer antler velvet” have been the most popular go-to natural treatments for men.
However, in contrast, a recent systematic review of published studies, the authors concluded that overall, the addition of testosterone to PDE-5 inhibitors might benefit patients with ED associated with testosterone levels of less than 300 ng/dL (10.4 nmol/L) who failed monotherapy. [20] A limitation of existing studies are their heterogeneous nature and methodological drawbacks.
The pathogenesis of organic ED is related to dysfunction of the endothelium. Endothelial cells can become injured through a variety of mechanisms, most of which cause oxidative stress on the tissues. Many of these causes of oxidative stress are related to lifestyle issues which lead to hypertension, diabetes and dyslipidaemia (figure 1). Endothelial cell dysfunction results in reduction of endothelium-dependent vasorelaxation as well as increased adhesion of leukocytes to the endothelium. Endothelial cell injury then leads to a variety of sequelae, including ED, other types of vasoconstriction, atherosclerosis and thrombus formation.18
Yes, it's possible to cure erectile dysfunction. The first step is to find out what's causing it. For some men, it's as simple as changing medications. Some drugs - those that treat high blood pressure or depression, for example - can make erections fizzle. So can alcohol and recreational drugs. Other causes are also treatable, including hormonal imbalances, hypertension, high cholesterol, obesity, diabetes and smoking, all of which can impede blood flow to the penis. For some men, ED is all in their heads, so consulting a mental health practitioner to help resolve anxiety, depression or learn techniques for dealing with stress can take the "dys" out of 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.
Centrally active compounds such as apomorphine have been used in men with ED whose cardiovascular comorbidity may prohibit PDE5i use, or in men who have concurrent apomorphine use for its anti-parkinsonian properties. Unfortunately, its side effect profile and poor effectiveness compared to other ED treatments have impaired its mainstream utilization (118). It is suspected that the side effects of apomorphine relate to its D2 receptor affinity. D4 receptor agonists, such as ABT-724 and azulenylmethylpiperazines, may not have the same associated side effects and show potent pro-erectile effects in animal models compared to apomorphine (32,119).
For best results, men with ED take these pills about an hour or two before having sex. The drugs require normal nerve function to the penis. PDE5 inhibitors improve on normal erectile responses helping blood flow into the penis. Use these drugs as directed. About 7 out of 10 men do well and have better erections. Response rates are lower for Diabetics and cancer patients.