This penile tumescence monitor is placed at the base and near the corona of the penis. It is connected to a monitor that records a continuous graph depicting the force and duration of erections that occur during sleep. The monitor is strapped to the leg. The nocturnal penile tumescence test is conducted on several nights to obtain an accurate indication of erections that normally occur during the alpha phase of sleep.

Nearly every primary care physician, internist and geriatrician now understand that many older men retain an interest in sexual activity as they age. Some primary care physicians think that sexual potency in older men is the norm, and that if it is lacking, it is ‘all in the head.’ This viewpoint has not been supported by current literature. The Massachusetts Male Aging Study (MMAS) found that 52% of men between 40 and 70 years old reported having some form of erectile dysfunction (ED).1 The reality is that ED is a natural part of ageing and that the prevalence increases with age. In the MMAS, they found that roughly 50% of men at 50 years old, 60% of men at 60 years old and 70% of men at 70 years old had ED. Thus, nearly all men who live long enough should develop ED. The myths that surround the problems of impotence or ED confound the attempts of patients to receive treatment and the attempts of physicians to help them.1


Normal erectile function depends on the release of NO and endothelial-dependent vasodilation of the penile arteries. The ‘artery size’ hypothesis, first described by Dr Montorsi, offers an explanation why men are more likely to develop ED before a myocardial infacrtion. It is believed that atherosclerosis affects all vascular beds equally but smaller arteries are more likely to become occluded than larger arteries.31 32 The penile arteries are 1–2 mm while the coronary arteries are 3–4 mm. Thus, the same degree of endothelial dysfunction and atherosclerosis is more likely to occlude blood flow in the penile arteries compared with the coronary arteries. The penile arteries therefore serve as a sensitive indicator for subsequent CVD. This theory is supported by the fact that ED occurs approximately 3 years prior to cardiac symptoms in virtually all patients with chronic coronary syndrome whereas patients with acute coronary syndrome have a much lower prevalence of sexual dysfunction.32
Surgery of the penile venous system, generally involving venous ligation, has been reported to be effective in patients who have been demonstrated to have venous leakage. However, the tests necessary to establish this diagnosis have been incompletely validated; therefore, it is difficult to select patients who will have a predictably good outcome. Moreover, decreased effectiveness of this approach has been reported as longer term followups have been obtained. This has tempered enthusiasm for these procedures, which are probably therefore best done in an investigational setting in medical centers by surgeons experienced in these procedures and their evaluation.
Jump up ^ Reepmeyer JC, Woodruff JT (2007). "Use of liquid chromatography-mass spectrometry and a chemical cleavage reaction for the structure elucidation of a new sildenafil analogue detected as an adulterant in an herbal dietary supplement". Journal of Pharmaceutical and Biomedical Analysis. 44 (4): 887–93. doi:10.1016/j.jpba.2007.04.011. PMID 17532168.
Normal erectile function depends on the release of NO and endothelial-dependent vasodilation of the penile arteries. The ‘artery size’ hypothesis, first described by Dr Montorsi, offers an explanation why men are more likely to develop ED before a myocardial infacrtion. It is believed that atherosclerosis affects all vascular beds equally but smaller arteries are more likely to become occluded than larger arteries.31 32 The penile arteries are 1–2 mm while the coronary arteries are 3–4 mm. Thus, the same degree of endothelial dysfunction and atherosclerosis is more likely to occlude blood flow in the penile arteries compared with the coronary arteries. The penile arteries therefore serve as a sensitive indicator for subsequent CVD. This theory is supported by the fact that ED occurs approximately 3 years prior to cardiac symptoms in virtually all patients with chronic coronary syndrome whereas patients with acute coronary syndrome have a much lower prevalence of sexual dysfunction.32
Most older men suffer not ED but erection dissatisfaction. Starting around age 50 (often earlier among smokers and/or diabetics), erections change. In some men, the process is gradual, in others, it happens more quickly. Either way, older men lose the ability to raise erections solely from sexual fantasies. Direct fondling of the penis becomes necessary. When erections appear, they rise more slowly and do not become as firm as they were during men’s thirties and forties. And minor distractions may cause wilting—the doorbell or an ambulance siren. These changes alarm many men, who jump to the conclusion that they must have ED. If you can still raise erection durings masturbation, you don’t. What you have is erection dissatisfaction.

Phosphodiesterase inhibitors: This class of medications includes sildenafil, tadalafil, and vardenafil. They work by inhibiting an enzyme called phosphodiesterase type 5 (PDE-5), allowing more blood to enter the penis and helping to produce an erection. These medications are often taken before sex and will cause an erection only when the man is sexually stimulated.
Penile blood flow is measured using a Doppler probe and a 2.5 cm blood pressure cuff. Systolic pressures in the right and left corpora cavernosa are measured and the penile–brachial index is calculated taking a ratio of penile systolic pressure to brachial systolic pressure. These measures should be repeated before and after 3 minutes of exercising the pelvic and leg muscles. In normal men, the PBI should be 0.9 or greater. Ratios between 0.7 and 0.9 suggest vascular impotence; a ratio below 0.6 is diagnostic. Pelvic arteriography can be done if revascularization is considered.
This statement is more than five years old and is provided solely for historical purposes. Due to the cumulative nature of medical research, new knowledge has inevitably accumulated in this subject area in the time since the statement was initially prepared. Thus some of the material is likely to be out of date, and at worst simply wrong. For reliable, current information on this and other health topics, we recommend consulting the National Institutes of Health's MedlinePlus http://www.nlm.nih.gov/medlineplus/.
First realize that this is normal, and just because it happened once does not mean it will happen again (but freaking out about it could make it happen again). Then Skyler tells people to completely ditch the idea that sex is a goal-oriented act with orgasm being the big finish. Instead, take a pleasure-oriented mentality where various sex acts are done because they feel good — not because it's part of series of steps to get you to climax. This helps take away some of the anxiety, because when you're not so focused on the performance, it's not that big of a deal if there's a little bit of stage fright, she says. There's plenty of other things you can do while hanging out with a non-erect penis!
Normal erectile function depends on the release of NO and endothelial-dependent vasodilation of the penile arteries. The ‘artery size’ hypothesis, first described by Dr Montorsi, offers an explanation why men are more likely to develop ED before a myocardial infacrtion. It is believed that atherosclerosis affects all vascular beds equally but smaller arteries are more likely to become occluded than larger arteries.31 32 The penile arteries are 1–2 mm while the coronary arteries are 3–4 mm. Thus, the same degree of endothelial dysfunction and atherosclerosis is more likely to occlude blood flow in the penile arteries compared with the coronary arteries. The penile arteries therefore serve as a sensitive indicator for subsequent CVD. This theory is supported by the fact that ED occurs approximately 3 years prior to cardiac symptoms in virtually all patients with chronic coronary syndrome whereas patients with acute coronary syndrome have a much lower prevalence of sexual dysfunction.32
PDE 5 inhibitors are broken down primarily by enzyme, cytochrome P450enzyme CYP3A4. Medications that decrease or increase the activity of CYP3A4 may affect levels and effectiveness of PDE 5 inhibitors. Such drugs include medications for the treatment of HIV (protease inhibitors) and the antifungal medications ketoconazole and itraconazole. Thus caution is recommended.
Impotence, also called erectile dysfunction, in general, the inability of a man to achieve or maintain penile erection and hence the inability to participate fully in sexual intercourse. In its broadest sense the term impotence refers to the inability to become sexually aroused; in this sense it can apply to women as well as to men. In common practice, however, the term has traditionally been used to describe only male sexual dysfunctions. Professional sex therapists, while they identify two distinct dysfunctions as forms of impotence, prefer not to use the term impotence per se. Thus, because of its pejorative connotation in lay usage and because of confusion about its definition, the word impotence has been eliminated from the technical vocabulary in favour of the term “erectile dysfunction.”
To examine what is known about the demographics, etiology, risk factors, pathophysiology, diagnostic assessment, treatments (both generic and cause-specific), and the understanding of their consequences by the public and the medical community, the National Institute of Diabetes and Digestive and Kidney Diseases and the Office of Medical Applications of Research of the National Institutes of Health, in conjunction with the National Institute of Neurological Disorders and Stroke and the National Institute on Aging, convened a consensus development conference on male impotence on December 7-9, 1992. After 1 1/2 days of presentations by experts in the relevant fields involved with male sexual dysfunction and erectile impotence or dysfunction, a consensus panel comprised of representatives from urology, geriatrics, medicine, endocrinology, psychiatry, psychology, nursing, epidemiology, biostatistics, basic sciences, and the public considered the evidence and developed answers to the questions that follow.
This is one of many types of constricting devices placed at the base of the penis to diminish venous outflow and improve the quality and duration of the erection. This is particularly useful in men who have a venous leak and are only able to obtain partial erections that they are unable to maintain. These constricting devices may be used in conjunction with oral agents, injection therapy, and vacuum devices.

Another approach is vacuum therapy. The man inserts his penis into a clear plastic cylinder and uses a pump to force air out of the cylinder. This forms a partial vacuum around the penis, which helps to draw blood into the corpora cavernosa. The man then places a special ring over the base of the penis to trap the blood inside it. The only side effect with this type of treatment is occasional bruising if the vacuum is left on too long.


Penile blood flow is measured using a Doppler probe and a 2.5 cm blood pressure cuff. Systolic pressures in the right and left corpora cavernosa are measured and the penile–brachial index is calculated taking a ratio of penile systolic pressure to brachial systolic pressure. These measures should be repeated before and after 3 minutes of exercising the pelvic and leg muscles. In normal men, the PBI should be 0.9 or greater. Ratios between 0.7 and 0.9 suggest vascular impotence; a ratio below 0.6 is diagnostic. Pelvic arteriography can be done if revascularization is considered.
Your boyfriend is having a pretty normal problem but because guys are so insecure, they almost never talk about it. That silence often makes guys, especially young guys, panicky — like they’re the only ones in the world dealing with this problem. That freaks them out even more, and that anxiety feeds on itself in a fairly classic and unfortunately common pattern: When a guy has trouble getting it up, he gets so down that the impotence gets worse before it gets better. Anxiety-driven impotence can be a vicious cycle: Quite unlike his dick, the problem just grows and grows.
My boyfriend has a hard time getting and staying hard. It's obviously a difficult situation to talk about, but he says he feels pressure when he's with me (versus previous random hookups he wasn't invested in), so he psyches himself out. When we do have sex, I'm almost always really satisfied and I care a lot about him, both things I express in and outside of the bedroom. But the situation seems to be only getting worse. We've stopped having sex during the week because our busy lives mean we don't have an hour or more to devote to sex (which is sometimes what it takes), or we can't have sex at all because of what he's experiencing. I'm afraid this is going to continue to get worse, not only sexually but emotionally in our relationship. How can I help him fix this, and reassure him in the meantime that I care about him and want to support him?
Inside the cell, NOS catalyzes the oxidation of L-arginine to NO and L-citrulline. Endogenous blockers of this pathway have been identified. The gaseous NO that is produced acts as a neurotransmitter or paracrine messenger. Its biologic half-life is only 5 seconds. NO may act within the cell or diffuse and interact with nearby target cells. In the corpora cavernosa, NO activates guanylate cyclase, which in turn increases cyclic guanosine monophosphate (cGMP). Relaxation of vascular smooth muscles by cGMP leads to vasodilation and increased blood flow.
Some men should not take PDE5 inhibitors. They can cause hypotension (abnormally low blood pressure that can lead to fainting and even shock) when given to patients who are taking nitrates (medications taken for heart disease). Therefore, patients taking nitrates daily should not take any of the PDE5 inhibitors. Nitrates relieve angina (chest pain due to insufficient blood supply to the heart muscle because of narrowing of the coronary arteries); these include nitroglycerine tablets, patches, ointments, sprays, and pastes, as well as isosorbide dinitrate and isosorbide mononitrate. Other nitrates such as amyl nitrate and butyl nitrate also are in some recreational drugs called "poppers."
Erectile dysfunction affects millions of men. Although for some men erectile function may not be the best or most important measure of sexual satisfaction, for many men erectile dysfunction creates mental stress that affects their interactions with family and associates. Many advances have occurred in both diagnosis and treatment of erectile dysfunction. However, its various aspects remain poorly understood by the general population and by most health care professionals. Lack of a simple definition, failure to delineate precisely the problem being assessed, and the absence of guidelines and parameters to determine assessment and treatment outcome and long-term results, have contributed to this state of affairs by producing misunderstanding, confusion, and ongoing concern. That results have not been communicated effectively to the public has compounded this situation.
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.
Despite the accumulation of a substantial body of scientific information about erectile dysfunction, large segments of the public -- as well as the health professions -- remain relatively uninformed, or -- even worse -- misinformed, about much of what is known. This lack of information, added to a pervasive reluctance of physicians to deal candidly with sexual matters, has resulted in patients being denied the benefits of treatment for their sexual concerns. Although they might wish doctors would ask them questions about their sexual lives, patients, for their part, are too often inhibited from initiating such discussions themselves. Improving both public and professional knowledge about erectile dysfunction will serve to remove those barriers and will foster more open communication and more effective treatment of this condition.
Causes contributing to erectile dysfunction can be broadly classified into two categories: organic and psychologic. In reality, while the majority of patients with erectile dysfunction are thought to demonstrate an organic component, psychological aspects of self-confidence, anxiety, and partner communication and conflict are often important contributing factors.
The patient and partner must be well informed about all therapeutic options including their effectiveness, possible complications, and costs. As a general rule, the least invasive or dangerous procedures should be tried first. Psychotherapy and behavioral treatments and sexual counseling alone or in conjunction with other treatments may be used in all patients with erectile dysfunction who are willing to use this form of treatment. In patients in whom psychogenic erectile dysfunction is suspected, sexual counseling should be offered first. Invasive therapy should not be the primary treatment of choice. If history, physical, and screening endocrine evaluations are normal and nonpsychogenic erectile dysfunction is suspected, either vacuum devices or intracavernosal injection therapy can be offered after discussion with the patient and his partner. These latter two therapies may also be useful when combined with psychotherapy in those with psychogenic erectile dysfunction in whom psychotherapy alone has failed. Since further diagnostic testing does not reliably establish specific diagnoses or predict outcomes of therapy, vacuum devices or intracavernosal injections often are applied to a broad spectrum of etiologies of male erectile dysfunction.
You should talk to your doctor about possible treatments. You may want to talk to other patients who have had the treatment planned for you. You also may want to seek a second doctor's opinion about surgery before making your decision. You may find it difficult to talk to your doctor about impotence. You will want to find a doctor who treats this condition and will help you feel comfortable talking about the problem and choosing the best treatment. You can also get more information by contacting your local National Kidney Foundation affiliate.
In fact, one common reason many younger men visit their doctor is to get erectile dysfunction medication. Often, men with erectile dysfunction suffer with diabetes or heart disease, or may be sedentary or obese, but they don’t realize the impact of these health conditions on sexual function. Along with erectile dysfunction treatment, the doctor may recommend managing the illness, being more physically active, or losing weight.
A study published in May 2014 in The Journal of Sexual Medicine found that some men can reverse erectile dysfunction with healthy lifestyle changes, such as exercise, weight loss, a varied diet, and good sleep. The Australian researchers also showed that even if erectile dysfunction medication is required, it's likely to be more effective if you implement these healthy lifestyle changes.
Erections are more complicated than you think. Your brain, nerves, heart, blood vessels, and a whole lot of hormones have to work together perfectly or nothing happens. It’s a lot to ask, and sometimes things break down. And while ED happens to most guys at some point in their lives, erectile dysfunction isn’t something you can just ignore and hope it goes away.
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