Impotence or, more clinical, erectile dysfunction is the inability to maintain an erection of the penis for satisfactory sexual intercourse regardless of the capability of ejaculation.
According to a recent survey, the Massachusetts Male Aging Study, 52% of men beyond 40 years of age may have some degree of erectile failure. Unfortunately, only a small percentage of men seek medical help.
Penile erection is managed by two different mechanisms. The first one is the reflex erection, which is achieved by directly touching the penile shaft and the second is the psychogenic erection, which is achieved by erotic stimuli. The first one uses the peripheral nerves and the lower parts of the spinal cord, whereas the second one uses the limbic system of the brain. Neural signals originating in the limbic system of the brain are transmitted through spinal cord to the thoracolumbar erection center in the spine. Psychogenic erection is associated with either fantasy or viewing erotic material. Reflex erection occurs when signals triggered by touching the penile shaft are carried through the pudendal nerve to S4-5 in the lower spinal cord. Stimulation of S4-5 sends parasympathetic signals to the penis and leads to reflex erection. Both mechanisms augment each other during sex. In both conditions an intact neurologic system is required for a successful and complete erection. Stimulation of penile shaft by the nervous system gives rise to the secretion of nitric oxide (NO), which causes the relaxation of smooth muscles of corpora cavernosa (the main erectile tissue of penis), subsequently giving rise to penile erection.
Although neural signals are crucial, the vigor of a man?s erection is ultimately determined by vascular events governing the flow of blood into the corpora cavernosa. The force with which blood flows into the corpora cavernosa is mediated by an intriguing intracavernosal chemistry sequence involving the enzyme nitric oxide synthase (NOS), nitric oxide (NO), and a second enzyme (adenylate cyclase), which helps generate the cyclic guanosine monophosphate needed to maximize intracavernosal blood flow and increase the pressure within the corpora cavernosa.
The main neurotransmitter produced seems to be NO, the endothelium-derived relaxing factor. This agent causes relaxation of the arterioles and cavernosal smooth muscle of the penis, which allows increased blood flow and increases the intracorporeal pressure to approximate the systolic pressure. The dilated corpora compress the venous outflow channels against the elastic tissue of the tunica albuginea, an action that prevents venous leakage and further increases the intracavernosal pressure to above systolic blood pressure. Just before ejaculation, the ischiocavernosal and pubocavernosal muscles contract to increase intracavernosal pressure further; the response is ejaculation.
Additionally, adequate levels of testosterone (produced by the testes) and an intact pituitary gland are required for the development of a healthy male erectile system. As can be understood from the mechanisms of a normal erection, impotence may develop due to hormonal deficiency, disorders of the neurologic system, lack of adequate penile blood supply or psychological problems.
The role of testosterone in male sexual function remains complex and
controversial. Men acquire full sexual and reproductive competence at
adolescence when, in response to pulsatile pituitary luteinizing hormone
(LH) secretion, Leydig cell testosterone production surges to adult
levels as coincidental pulsatile pituitary folliclestimulating hormone (FSH)
secretion initiates and maintains
the orderly process of spermatogenesis in testicular Sertoli cells. Thereafter, the role of testosterone becomes unclear. Some men with below-normal testosterone levels can still have nocturnal erections, but for fully satisfactory sexual and erectile function, a ?normal? quotient of
testosterone must be present in the bloodstream.
As testosterone levels decline, so does a man?s sexual function. Two actions of testosterone?one central and the other peripheral?are thought to be critical. Testosterone is the main hormonal mediator of a man?s libido. As testosterone levels decline, sexual desire decreases. Testosterone also has a critical role in stabilizing the levels of intracavernosal NOS, the enzyme responsible for triggering the NO cascade required to have an erection. Thus, the man with inadequate circulating testosterone will have a dampened libido and suboptimal erectile function. Anything that interferes with hypothalamic pulsatile LH release or reduces the number of Leydig cells available to respond to LH will result in decreased production of testosterone.
Usually, both mechanisms are at work to cause erections, but as men
age, they derive less stimulation from the higher centers and need to
rely more on direct penile stimulation hence, the requirement of aging
men to practice extended foreplay. The mechanisms involved are complex
and may be related to decreased production of or responsiveness to NOS, the enzyme that produces NO.
Erections, once achieved through fantasy and foreplay, are more fragile as men age. Older men must maintain their focus; if they become distracted by thinking of work or other activities, detumescence may occur. The telephone ringing may be enough to cause detumescence.
As men age, the absolute number of Leydig cells decreases by about
40%, and the vigor of pulsatile LH release is dampened. In association
with these events, the free testosterone level declines approximately
1.2% per year and may be associated with commensurate increases
in serum LH levels. Most aging men with subnormal levels of testosterone, however, have low or inappropriately normal levels of LH. Some clinicians believe that ageappropriate but lowered levels of free testosterone (in comparison with those in young men) are not contributory to sexual dysfunction. Nevertheless, some clinical studies have substantiated positive responses to testosterone therapy in men with borderline low levels of free testosterone.
- Diseases of the blood vessels (vascular disease) e.g. arteriosclerosis, hypertension, high cholesterol.
- Diabetes can damage both blood vessels and nerves.
- Neurologic disorders affect the nervous system and include multiple sclerosis, Parkinson's disease and spinal cord injury with paralysis.
- Deficiencies of the endocrine system for example, low levels of testosterone or thyroid hormone often cause poor quality erections. Excessive production of prolactin by the pituitary gland may contribute to a low testosterone level and lack of desire.
- Substance abuse affects erectile function as well. Illegal drugs
and the excessive use of alcohol or cigarettes can seriously damage
the blood vessels and nerves involved in a normal erection.
A few causes of impotence may be iatrogenic (medically caused). Various medications intended to control blood pressure or to modify central nervous system response, may inhibit erection by denying blood supply or by altering nerve activity. Surgical intervention for a number of different conditions may remove anatomical structures necessary to erection, damage nerves, or impair blood supply. Radical pelvic surgery may also result in impotence. Surgical procedures involving the prostate gland the bladder or colon may sever the nerves involved in erectile response. Radiation treatment in this area can also affect the erectile process.
Erectile dysfunction is characterised by the inability to maintain erection. Normal erections during sleep and in the early morning suggest a psychogenic cause, while loss of these erections may signify underlying disease, often cardiovascular in origin. Other causes leading to erectile dysfunction are diabetes mellitus (causing neuropathy) or hypogonadism (decreased testosterone levels due to disease affecting the testicles or the pituitary gland).
There are no formal tests to diagnose erectile dysfunction. Some blood tests are generally done to exclude underlying disease.`
Treatment depends on the cause. Testosterone supplements may be used
for cases with hormonal deficiency. However, usually the cause is lack
of adequate penile blood supply as a result of age-dependent damage of
inner walls of blood vessels. Previously, medical substances (e.g.
apomorphine) were used to be directly injected into the erectile tissue
of penile shaft to treat impotence. In some cases refractory to the
medical treatment, a penile implant (penile prosthesis) could be
advised. After the discovery of orally active agents that increase the
efficacy of NO, which dilates the blood vessels of corpora cavernosa,
more conservative methods were started to be used.
Sildenafil citrate (Viagra?) is an oral agent that blocks specific phosphodiesterases. NO acts on blood vessels by increasing the levels of cyclic guanosine monophosphate, which is required for dilation of the vessels. Phosphodiesterases block this substance and reduce the effect of NO on erectile tissue. By using sildenafil, NO's effects are increased and a more sustained penile erection can be achieved. Other agents with less side effects and holding promise as an effective oral treatment for penile erectile dysfunction are currently being developed. Two newer drugs now available for the treatment of erectile dysfunction are tadalafil (Cialis?) and vardenafil (Levitra?). These agents have a similar mode of action to Sildenafil.
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