The commonest cause of prolonged impotence is an anxiety or depression state. These closely related conditions can be diagnosed by the criteria. Other psychological factors such as disinterest in the sexual partner, fear of sexual incompetence, marital discord, deviant sexual attitudes, worry, fatigue, and ill health often operate in various combinations to reduce sexual impulse. The central issue in the evaluation of impotence is to separate those instances due to psychological factors from those due to organic causes. Usually, the separation can be made on the basis of history. From early childhood through the eighth decade, erections occur during normal sleep. This phenomenon, termed nocturnal penile tumescence (NPT), occurs during rapid eye movement sleep, and the total time of NPT averages 100 min per night. Consequently, if the impotent man gives a history of turgid erections under any circumstances (often when awakening in the early morning), the psychic, efferent neurologic, and circulatory systems that mediate erection are intact, and dysfunction is probably due to a psychiatric disorder. In these patients the physical and laboratory examinations should be limited. (Occasional patients with sensory neuropathy may have nocturnal erections.)
If the history of nocturnal erections is questionable, measurements of NPT can be made with the use of a strain gauge attached to a recorder. Alternatively, the penis can be wrapped with gummed, perforated paper; failure to break the perforations on three successive nights suggests absence of nocturnal erections. Although false-negative and false-positive results are possible, these procedures help to differentiate psychogenic and organic impotence. Interestingly, psychogenically impotent men may experience longer and more frequent nocturnal erections than do normal men. Other factors in favor of organic impotence include a similar degree of erectile dysfunction under all circumstances, onset not associated with any particular psychiatric symptomatology, a previous uninterrupted period of normal erectile function, and persistent sexual desire.
Having deduced an organic cause, the fundamental problem is the differential diagnosis of the etiology. The history should be probed for symptoms of diabetes mellitus, symptoms of peripheral neuropathy or bladder dysfunction, symptoms referable to the vascular system such as intermittent claudication, and symptoms of local disease such as a history of priapism. A thorough drug history should be obtained, and inquiry concerning past operations that may have produced neurologic damage should be made.
Physical examination should include a thorough genital examination to identify abnormalities of the penis. The testes should be palpated for size and abnormal masses; if the length is less than 3.5 cm, hypogonadism should be considered. Evidence of feminization such as gynecomastia and abnormal body hair distribution should be sought. All pulses should be palpated, including the penile pulse, which can be felt by pressing both corpora between the thumb and forefinger and palpating to either side of the midline. However, because only a portion of the superficial dorsal arteries reach the corpus cavernosum, normal dorsal pulse pressures do not exclude the presence of deep cavernous arterial occlusion. If there is an indication from either history or physical examination of a vascular etiology, a Doppler procedure or arteriography may be indicated.
The neurologic exam should measure anal sphincter tone, perineal sensation, and the bulbocavernosus reflex. This reflex is elicited by squeezing the glans penis and noting the degree of anal sphincter constriction. An examination for peripheral neuropathy, including distal muscle weakness, loss of tendon reflexes in the legs, and tests for impairment of vibratory, position, tactile, and pain sensation should also be performed. In the absence of a concomitant neurogenic bladder, electromyographic sacral signal tracing of the bulbocavernosus reflex may be a useful ancillary procedure for detection of localized peripheral neuropathy; the methodology involves measurement of bulbocavernosus response latencies following electrical stimulation of the glans. Although this procedure has not been studied exhaustively, improvement by revascularization surgery is unlikely if the test is abnormal.
Laboratory evaluation is probably of minimal value. Measurement of serum testosterone in the absence of evidence of feminization or hypogonadism is seldom helpful.