Erectile Dysfunction
Cindy Meston, Ph.D., Alessandra Rellini, Ph.D., & Christopher Harte, B.A.

DEFINITION, DIAGNOSIS, AND PREVALENCE

ED is defined in the DSM-IV-TR as the inability to reach or maintain adequate erection of the penis to engage in intercourse. Patients are diagnosed with ED when their erectile difficulties are exclusively psychogenic in nature, or are caused by a combination of psychological and medical factors. Men of all ages occasionally have difficulty obtaining or maintaining an erection, but true erectile disorder is more common after age 50 years. Laumann, Paik, & Rosen (1999) reported approximately 7% of men aged 18-29 years have erectile problems compared to 18% of men aged 50-59 years. Level of education and ethnicity are not associated with erectile difficulties, but married men are less likely to report erectile problems compared to never married or divorced men (Laumann et al.). It has been estimated that approximately 60-80% of ED cases are of organic etiology. Even when the etiology is organic, however, anxiety, self-confidence, and relationship factors can contribute to the maintenance or exacerbation of the condition.

Back to top

FACTORS ASSOCIATED WITH ERECTILE DYSFUNCTION

Erection is caused by increased blood pressure in the corpora cavernosa (the sinusoid of the erectile tissue) via increased blood inflow and decreased blood outflow. The increment of blood inflow is regulated by the relaxation of the smooth muscles surrounding the arterioles, a phenomenon that allows the arteriole to dilate. Smooth muscle relaxation has been attributed to an increase in parasympathetic activity which causes a release of the neurotransmitters acetylcholine, vasoactive intestinal polypeptide, and nitric oxide. Nitric oxide causes a greater amount of cyclic guanosine monophosphate (cGMP) to be available in the smooth muscles, and this causes the smooth muscles to relax. Normally, cGMP is broken down by enzymes known as phosphodiesterases (PDEs). However, this may be circumvented by inhibiting the activity of these enzymes. Viagra (sildenafil) and other drugs used to treat ED inhibit PDE type 5. In doing so, these drugs enhance the concentration of cGMP, allowing for greater smooth muscle relaxation and therefore improved erection. Detumescence (i.e., loss of erection) occurs with the release of catecholamines during orgasm and ejaculation.

Surgery, metabolic disorders such as diabetes mellitus, alcoholism, hypothyroidism, infectious diseases such as HIV and other viral infections, and pelvic pathologies such as systemic lupus, and vascular problems associated with atherosclerosis and hypertension are all potential causes of ED. Drugs that decrease dopamine or reduce testosterone production are also implicated in ED. These include antihypertensive medications, antipsychotic drugs, anxiolitics, antiandrogens, anti-cholesterol agents, and drugs used to regulate heart rate. Antiparkinsonian medications increase dopamine and facilitate erection.

The major psychological contributors to ED as identified by Barlow’s (1986) model of sexual dysfunction are anxiety, negative expectations, and spectatoring. Men who are anxious about not being able to have an erection tend to focus on themselves and how they are “performing” more than on what gives them pleasure. This spectatoring increases anxiety which, physiologically, inhibits the relaxation of the smooth muscles necessary for erection and, psychologically, leads to a negative mood state and a focus on negative expectancies. Since the result is impaired erectile responding, the man’s fears of not being able to perform are confirmed and they are likely to repeat the process in subsequent sexual situations. By contrast, men with normal erectile responding approach sexual situations with positive expectancies, and a focus on erotic cues. Consequently, they become aroused and are able to obtain and sustain an erection which creates a positive feedback loop for future sexual encounters.

Back to top

ASSESSMENT AND TREATMENT OF ERECTILE DYSFUNCTION

The assessment of ED includes identifying the situation(s) surrounding the onset of ED and the potential beliefs that were formed at that time. Beliefs may be specific to the relationship (i.e., a feeling of inadequacy with one specific partner) or generalize to all situations. In cases where ED is the result of a vascular problem, laboratory assessments that measure genital blood inflow and outflow during sexual stimulation may be helpful. Blood outflow can be measured by injecting agents such as papaverine into the penile corpora cavernosa. The substance relaxes the smooth muscles at the base of the penis, which, in presence of normal blood outflow, produces penile erection even without sexual stimulation. When the drug fails to provide the expected erection, it is considered evidence for impairment in vascular mechanisms. Measurement of nocturnal penile erections which are expected to increase during the REM sleep cycle in sexually healthy men, is another commonly used technique for assessing potential vascular causes of ED. Assays of free and bioavailable serum testosterone are used to rule out abnormal hormone levels.

Treatments for ED include vacuum devices and constriction rings, intracavernosal injections, intraurethral pharmacotherapy, topical pharmacotherapy, oral pharmacotherapy, and penile implants. Vacuum constriction devices are the most safe and least expensive ED treatment. These consist of a tube that is placed over the penis, and a vacuum pump that draws blood into the penile arteries. A constriction ring is placed at the base of the penis to prevent blood outflow so that the erection is maintained until completion of the sexual act. Intracavernosal injections refer to medications such as papaverine, phentolamine, and prostaglandin E 1 that are be injected into the corpus cavernosum of the penis to induce erection. These all act to dilate penile capillaries, allowing blood to flow into the penis. Although intracavernosal injections are effective in approximately 70-90% of patients, a large percentage of users discontinue treatment due to the inconvenience, cost, and/or invasiveness of treatment.

Without a doubt, the most popular and effective pharmacological treatments for ED are phosphodiasterase type 5 (PDE 5) inhibitors such as sildenafil (Viagra), verdanafil (Levitra), and tadalafil (Cialis). In fact, since Viagra was introduced to the market in 1998, many of these other rather cumbersome and involved treatments have become less popular. Viagra has been estimated to successfully treat 2/3 of men with ED, is well tolerated by a variety of patients, and is an effective treatment for both organic and psychogenic ED. However, despite these drugs’ success with facilitating erection, one study reported between 40 and 80% of men with ED who began treatment with Viagra stopped taking the medication (Leiblum, 2002). Some men discontinue Viagra use because, although it enhances their ability to have an erection, this is not always enough to restore overall sexual desire and satisfaction which may be more closely intertwined with psychological and relational factors. In a recent study (Melnik & Abdo, 2005) that compared the effects of six months treatment with Viagra to psychotherapy or Viagra plus psychotherapy, psychotherapy alone outperformed Viagra in terms of improving the severity of ED. The psychotherapy aimed at developing realistic and positive expectations for the sexual relationship and encouraged patients to explore the emotional components linked to ED.

Penile implants are generally considered a last resort treatment technique when tissue damage or deterioration is severe or when other treatments have failed. This may be the case in men with severe diabetes mellitus or who have had radical prostatectomy. Implants can be hydraulic, semirigid or soft silicone and consist of two or three cylinders placed in the space normally occupied by the spongy tissue in the penis. The patient’s ability to ejaculate after the implant surgery remains in tact, however the implant does not restore sensitivity or sexual drive that may have been present prior to the onset of ED. Implant surgeries usually result in decreased penis size which may dissuade some men from undergoing surgery.

Back to top