In the Massachusetts Male Aging Study, a community-based survey of men between 40 and 70 years of age, 52% of respondents reported some degree of ED: 17% mild, 25% moderate, and 10% complete. Although the prevalence of mild ED remained constant (17%) between the ages of 40 and 70, there was a doubling in the number of men reporting moderate ED (from 17% to 34%) and a tripling in the number of men reporting complete ED (from 5% to 15%). Among the major predictors of ED are diabetes mellitus, heart disease, hypertension, and decreased high-density lipoprotein level. There is a higher prevalence of ED in men who have undergone radiation or surgery for prostate cancer. The psychological correlates of ED include depression and anger (Feldman et al, 1994). In the National Health and Social Life Survey in men aged 18-59, other male sexual dysfunctions were also found to be highly prevalent: premature ejaculation (28.5%), lack of sexual interest (15.8%), anxiety about sexual performance (17%), and lack of pleasure in sex (8.1%) (_{Laumann et al, 1994}).

Classification & Pathogenesis

A new classification of ED has been recommended by the International Society of Impotence Research (Lizza and Rosen, 1999,

Table 37-3). In the 1950s, 90% of cases of ED were believed to be psychogenic. Most authors now believe that mixed organic and psychogenic ED is the most common.

Psychological Disorders

Many psychologic conditions (performance anxiety, strained relationship, lack of sexual arousal, depression, and schizophrenia) can either cause or aggravate ED. The pathogenesis of psychogenic ED is still speculative. The most cited include imbalance of central neurotransmitters, over-inhibition of spinal erection center by the brain, inadequate NO release, and sympathetic overactivity.

Neurogenic Disorders

ED can be caused by disease or dysfunction of the brain, spinal cord, or cavernous and pudendal nerves. In men with spinal cord injury, the degree of erectile function depends on the nature, location, and the extent of the lesion. Peripheral neuropathy as seen in diabetes mellitus, chronic alcohol abuse, or vitamin deficiency may affect the nerve endings and result in a deficiency of neurotransmitters. Direct injury to the cavernous or pudendal nerves from trauma or radical prostatic or rectal surgery also can cause disruption of the neural pathway and result in ED.

Hormonal Disorders

Hypogonadism due to hypothalamic or pituitary tumors, estrogen or antiandrogen therapy, or orchiectomy can suppress sexual interest and nocturnal erections. However, these patients may achieve varying degree of erections during visual sexual stimulation (_{Bancroft and Wu, 1983}), and thus, the erectile ability is preserved. Similarly, ED resulting from hyperprolactinemia is probably caused by suppressed sexual interest. Hyperthyroidism, hypothyroidism, Cushing syndrome, and Addison disease are all reported to cause decreased libido and ED. Whether the hormonal disturbance or other factors are responsible for the ED needs further investigation.

Arterial Disorders

Although arteriogenic ED may be due to trauma or may be congenital, most often it is part of a generalized systemic arterial disease. The distribution and severity of the disease, however, differ from person to person. Some patients with severe arterial disease may still be potent as long as the arterial flow exceeds the venous flow; conversely, some patients with minimal arterial disease may be partially or completely impotent because of relatively large venous outflow, cavernous smooth-muscle dysfunction, or inadequate neurotransmitter release.

Arterial disease can be classified as extra- or intrapenile arterial insufficiency. Extrapenile arterial disease is amenable to surgical repair and comprises diseases of the internal pudendal artery, internal and common iliac arteries and aorta, the pelvic steal syndrome, and pelvic trauma. Intrapenile arterial disease such as that resulting from aging, arteriosclerosis, or diabetes mellitus does not respond well to currently available surgical techniques.

Cavernosal Disorders

Cavernous (venous) impotence can be divided into 5 types according to cause: In type 1, large veins exit the corpus cavernosum (this type is probably congenital); in type 2, venous channels are enlarged as a result of distortion of the tunica albuginea (as in Peyronie disease or the weakening associated with aging); in type 3, the cavernous smooth muscle is unable to relax because of fibrosis, degeneration, or dysfunction of gap junctions; in type 4, there is inadequate neurotransmitter release (in neurologic or psychological impotence or endothelial dysfunction); and in type 5, there is abnormal communication between the corpus cavernosum and the spongiosum or glans (congenital, traumatic, or consequent to shunt procedure for priapism) (_{Lue, 2000}). Electron microscope studies of cavernous erectile tissue obtained during implantation of penile prostheses reveal a high incidence of smooth-muscle atrophy, fibrous replacement, and endothelial disruption in patients with diabetes mellitus and atherosclerosis (_{Mersdorf et al, 1991}). Studies of penile tissue obtained by needle biopsy have also revealed changes in the smooth muscle-collagen ratio, decreased endothelium, and diminished elastic fibers in impotent patients and impaired smooth-muscle relaxation in diabetic patients (_{Saenz de Tejada et al, 1989; Sattar et al, 1995}).