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Montague cites a study that surveyed three groups of men, all of whom were successfully using an ED treatment. One group was on oral medications, one was using injections and a third had surgically implanted pumps.

The most satisfied users were those with the implanted prostheses.

Once implanted, the pumps become “part of their body,” Montague explains.

Works every time.” Pills, even when they work, might be less effective if you’ve had more than a couple drinks or are out of sorts for other reasons. Injections are slightly more reliable than pills but, Montague says, are still subject to variability. Erectile Dysfunction – Symptoms and Treatment Options for ED. Erectile Dysfunction – Symptoms and Treatment Options for ED.

Erectile dysfunction, also known by the acronym ED, is a rarely-discussed but very common medical condition that affects men worldwide. In fact, approximately 1 in 5 men in the United States over the age of 20, roughly 30 million men, suffer from ED.

To understand erectile dysfunction, it is important to understand how erections occur.

Under normal circumstances, psychological or sexual stimulation causes the penile smooth muscles to relax, allowing increased blood flow to the corporal bodies (the two chambers within the shaft of the penis). As the penile arteries expand the penis elongates and clamps down on the venous outflow to maintain the erection. If the arteries are calcified or diseased such as someone with heart disease or vascular disease, blood flow may be compromised. It is important to see your doctor if you have new onset erectile dysfunction as it may be an indication of cardiovascular disease.

The causes of ED are often multifactorial and include such common conditions such as diabetes and heart disease.

Sometimes the condition can be an early warning sign of heart problems and up to 40 percent of ED cases are the result of vascular problems such as atherosclerosis, or plaque buildup in your arteries.

ED can have broad implications on a man’s quality of life and can include difficulties with depression, intimacy, anxiety and self-esteem.

Treatments for ED usually can be classified into five categories. Medications – The most common treatment for ED are the oral prescription medications. These medications are phosphodiesterase-5 inhibitors and are the Viagra’s of the world.

They work by bringing more blood to

the

Injections work well for most people but the man or his partner must be willing to inject the medication into the penis. Prosthesis – For those men who wish to achieve an erection but have failed the previous treatments, a penile prosthesis is the final option.

Penile implants have been used since the 1970s and typically consist of inflatable cylinders that are placed into the corporal bodies of the penis in the operating room. Patient satisfaction is high with penile prostheses and can be a life-changing event for many men and their partners. If you are having difficulty with your erectile function, talk to someone. Talk to your partner, talk to your friends, or talk to your doctor – just know that you are not alone when it comes to this condition. Options are out there so find out if there is a treatment option right for you! Jason Phillips is a specialist in men’s urological health and is available to discuss your options is you suffer from erectile dysfunction. Jason Phillips is a Board Certified Urologist specializing in men’s and women’s urologic health.

Dedicated to providing patients superior care, he has a special interest in treating BPH, urologic cancers, kidney stones, overactive bladder, incontinence, bladder prolapse, and erectile dysfunction. He is trained in minimally invasive technologies including ureteroscopy, Greenlight laser, Urolift, laparoscopic surgery and the da Vinci robotic surgical system.

The treatment of erectile dysfunction in patients with neurogenic disease.

Contributions: (I) Conception and design: All authors; (II) Administrative support: All authors; (III) Provision of study materials or patients: AN Shridharani; (IV) Collection and assembly of data: AN Shridharani; (V) Data analysis and interpretation: All authors; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. Abstract: Erectile dysfunction (ED) related to compromise of the nervous system is an increasingly common occurrence.

This may be due to the multifactorial nature of ED, the myriad of disorders affecting the neurotransmission of erectogenic signals, and improved awareness and diagnosis of ED. Nevertheless, neurogenic ED remains poorly understood and characterized.

Disease related factors such as depression, decreased physical and mental function, the burden of chronic illness, and loss of independence may preclude sexual intimacy and lead to ED as well. The amount of data regarding treatment options in subpopulations of differing neurologic disorders remains scarce except for womens viagra buy men with spinal cord injury.

The treatment options including phosphodiesterase inhibitors, intracavernosal or intraurethral vasoactive agents, vacuum erection devices (VED) and penile prosthetic implantation remain constant.

This review discusses the options in specific neurologic conditions, and briefly provides insight into new and future developments that may reshape the management of neurogenic ED. Keywords: Erectile dysfunction (ED); neurogenic; treatment.

Neurogenic erectile dysfunction (NED) is a traditional classification of erectile dysfunction (ED) encompassing disorders impairing erections via neurologic compromise or dysfunction. The disorders compromising erections may act centrally, peripherally or both.

The prevalence of neurogenic ED has been suspected to be between 10% and 19% of all causes of ED (1,2). However, several classically defined neurogenic processes may affect several components of the normal pathway to achieve erection e.g., multiple sclerosis (MS), diabetes mellitus, iatrogenic surgical and spinal cord injury.

Each disease state has its own unique characteristics that require acknowledgement to fully

understand

Much of the emphasis on erectile pathophysiology has been placed on penile smooth muscle function and cavernosal hemodynamics.

The neuroanatomy and neurophysiology of erection can be characterized but its full extent is poorly understood. Neurologic disease does not always reproducibly affect erections in a uniform manner compared to other types of sexual dysfunction (SD).

This offers many obstacles to understanding the role the nervous systems plays in SD and consequently obscures what treatment options readily optimize erections specific to the neurologic insult.

Treatment strategies for ED usually target the corporal smooth muscle to augment its relaxation or replace its function via prosthesis implantation. Nevertheless, to treat ED related to a neurologic disorder, assessments of function and disease related factors are recommended, as ED in these men is often multifactorial in origin.

A comprehensive understanding of the neural pathways for erection is necessary for assessing whether neurogenic ED exists and how to appropriately address the ED.

As stated previously, neurologic disease may affect multiple neural pathways leading to ED, sensation deficits and ejaculatory dysfunction. 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. The sympathetic pathway originates from the 11 th thoracic to the 2 nd 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).

Parasympathetic pathways originate from the intermediolateral cell columns of buy uprima the 2 nd , 3 rd and 4 th sacral spinal cord segments.

Preganglionic fibers pass through the pelvic plexus where they coalesce with sympathetic fibers from the superior hypogastric plexus. The cavernous nerves that innervate the penis arise from the portion of the pelvic plexus.

The pelvic plexus also contains nerves that innervate the rectum, bladder and urinary sphincter and the nerve projections can be damaged during radical excision of the bladder, prostate and rectum, leading to iatrogenic ED (4). 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. The somatosensory pathways for erections originate in the penile skin, glans and urethra. Glans afferent sensory free nerve endings are 10-fold more than their corpuscular receptors, and are derived from A ? and unmyelinated C fibers. The nerve endings coalesce to form the dorsal penile nerve along with other sensory nerve fibers. Through the pudendal nerve they enter the S2-4 nerve roots to terminate on spinal neurons and interneurons.

Nerve bundles within the dorsal nerve contain nitric oxide (NO) synthase, found typically in autonomic nerves, and stimulation of the sympathetic chain can leak to evoked potentials from the dorsal nerve and vice versa (10-12).

Somatomotor penile innervation originates in Onuf’s nucleus in the S2-4 spinal segments.

These nerves travel to the ischiocavernosus and bulbocavernosus muscles when activated lead to contraction necessary for the rigid-erection phase. Several animal studies show that stimulation of the somatomotor pathways may also be under sympathetic control, and adrenergic stimulation may lead to contraction of these muscles during ejaculation (13,14). Somatomotor spinal reflexes may also be initiated by genital stimulation. For instance, the well-known bulbocavernosus reflex is evidence this reflex exists; however the clinical significance of its absence in the neurological assessment of ED has not been substantiated (15). 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).

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.

The supraspinal pathways are likely activated via central neural activation during sexual arousal.

Positron emission tomorgraphy (PET), and functional magnetic resonance imaging (fMRI) have led to a greater understanding to which center are activated during arousal.

These imaging studies measure increases in cerebral blood flow or changes in cerebral activity buy addyi on a real-time basis. Studies are performed when male subject are aroused by visual cues (usually sexual explicit photos or videos) and compared to images obtained during exposure to sexually neutral cues differences can be measured. Several studies have identified that the inferior frontal lobes, inferior temporal lobes and insular gyrus, and occipital lobes are involved with processing arousal cues, although each are likely to process different stimuli (20-23).

Spinal cord injury (SCI) 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).

Cerebrovascular accident (CVA/stroke) 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

The cause of ED is likely multifactorial, with neurologic, endocrine, iatrogenic, psychiatric and psychosocial factors leading to varying degrees of ED (31).