Experts often treat psychologically based impotence using techniques that decrease anxiety associated with intercourse. The patient's partner can help apply the techniques, which include gradual development of intimacy and stimulation. Such techniques also can help relieve anxiety during treatment of physical impotence. If these simple behavioral methods at home are ineffective, a doctor may refer an individual to a sex counselor.
Following a detailed discussion about the history of erectile dysfunction and its risk factors, your doctor will examine the testicles and penis to help determine the cause of erectile dysfunction. Your doctor will check reflexes and pulses in the area to see if problems with blood vessels or nerves are contributing to the erectile dysfunction. If necessary, your doctor will order tests to help diagnose erectile dysfunction.
MSA is a neurodegenerative disease of undetermined etiology, where ED is an early prominent sign occurring in 40% of men at the time of diagnosis (46,47). ED occurs in the majority of patients and the exact cause of it is unknown (48). Like PD, MSA likely affects the dopaminergic pathways within the brain essential for arousal (49). Orthostatic hypotension (OH) as a causal factor has been refuted by evidence that sildenafil can overcome reduced filling pressures, and the ED usually precedes the development of OH (46,49,50). Similar to other neurologic disorders that lead to ED, other disease related factors such as psychosocial stress, the burden of chronic illness, changed appearance, fatigue, decreased fine motor movement of fingers, immobility and diminished self-esteem due to loss of independence may contribute as well (51).
Erosion of the prosthesis, whereby it presses through the corporal tissue into the urethra, may occur. Symptoms and signs may include pain, blood in the urine, discharge, abnormal urine stream, and malfunction. If the prosthesis erodes into the urethra, a physician must remove it. If the other cylinder remains intact, it can be left in place. A physician leaves a catheter in place to allow the urethra to heal.
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 Aδ 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. The dorsal nerve is not purely somatic, however. 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).
Since endothelial dysfunction, CVD and ED are closely associated in epidemiological studies, the question for clinicians is whether to recommend the man presenting with ED undergo a cardiovascular (CV) evaluation. Clearly, based on numerous studies, ED can be considered at least a ‘marker’ for possible further vascular disease or CVD.15 In their report, Vlachopoulos and coworkers make the point that the man presenting with ED, the clinician, is offered an opportunity to attempt to improve the health of the man by addressing lifestyle modification, and consider further vascular evaluation owing to the clear relationship between endothelial dysfunction, ED and CVD.19
ED varies in men with seizure disorders, occurring in 3% to 58% of men with epilepsy (30). The cause of ED is likely multifactorial, with neurologic, endocrine, iatrogenic, psychiatric and psychosocial factors leading to varying degrees of ED (31). ED can occur in periods surrounding active seizures (ictal) or in the periods unrelated to seizure activity (post-ictal) as well (32).
There are so many potential reasons a man might develop erectile dysfunction (ED), it's nearly impossible to generalize the best ways to treat it. What works for one man may not work for another simply because they are having problems for different reasons. That said, it may encouraging to hear that there are a variety of options that may be considered, from psychological counseling to lifestyle changes, medications to treatments and devices.
Neurogenic ED remains difficult to diagnose and treat effectively. It is important to realize that many men with neurologic disorders may have ED related to disease related factors separate from the insult to the neuro-erectile pathway. These disease related factors must be addressed prior or simultaneously with pharmacologic and/or surgical therapy to effectively treat their SD. As awareness of the complexities of normal sexual function increase so will the recognition of SD in this population. This movement will lead to improved quality of life in men with neurologic disorders, as proven by the strong link between sexual function and quality of life.
Arterial vascular diseases account for nearly half of all cases of ED in men older than 50 years of age. Arterial vascular disease includes atherosclerosis (fatty deposits on the walls of arteries, also called hardening of the arteries), which may affect the heart (history of heart attacks, angina, coronary artery disease, myocardial infarct) or blood vessels in the legs, peripheral vascular disease (problems with blood circulation to the legs), as well as other areas of the body including blood vessels supplying blood to the penis and high blood pressure. Prolonged tobacco use (smoking) is considered an important risk factor for ED because it is associated with poor circulation and reduced blood flow in the penis. This is related to microvascular damage (stiffening of the artery as well as smaller caliber vessel size secondary to endovascular atherosclerotic plaques).
A physical cause can be identified in about 80% of cases. These include cardiovascular disease, diabetes mellitus, neurological problems such as following prostatectomy, hypogonadism, and drug side effects. Psychological impotence is where erection or penetration fails due to thoughts or feelings; this is somewhat less frequent, in the order of about 10% of cases. In psychological impotence, there is a strong response to placebo treatment.
Individuals at higher risk for priapism (painful erection lasting longer than six hours), including men with sickle cell anemia, thrombocytopenia (low platelet count), polycythemia (increased red blood cell count), multiple myeloma (a cancer of the white blood cells), and history of blood clots (for example, deep venous thrombosis [DVT]) or hyperviscosity (thick blood) syndrome are at increased risk for priapism with MUSE.
The other 5 percent of prostheses are either pump devices in which the saline is permanently in the prosthesis, not in a separate reservoir (urologists may recommend this for men who have had multiple surgeries); or a pair of semi-rigid, malleable rods implanted in the penis, which render it hard at all times. The patient manually shifts the penis into an erect position for sex.
Tadalafil shares the common side effects of the PDE5 inhibitors, however, due to its effect on PDE11, another phosphodiesterase located in muscle, tadalafil has been associated with muscle aches. Back pain and muscle aches occur in less than 7% of men taking tadalafil and in most patients will go away without treatment within 48 hours. When treatment was necessary, acetaminophen (Tylenol) and nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Motrin, Advil) or naproxen (Aleve) were effective. Rarely do the muscle aches and back pain cause men to stop using tadalafil.