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To explore how hypertension affects penile erection, we studied erectile hemodynamics during nocturnal penile tumescence in 3 groups of middle-aged men: hypertensive patients with and without erectile dysfunction, and normotensive controls without erectile problems. The hypertensive patients were not taking antihypertensive medication. Evaluations included standard monitoring of penile circumference change as well as noninvasive monitoring of penile segmental pulsatile blood flow and activity in the bulbocavernosus-ischiocavernosus muscles. Variables differed in how they discriminated among groups. Median amplitude of penile blood flow during rapid eye movement sleep differed significantly among all 3 study groups: controls had the highest amplitudes, patients without erectile problems had lower values and patients with erectile complaints had the lowest values. By contrast, standard measures of nocturnal penile tumescence (that is based on penile circumference change during sleep) only distinguished the patients with erectile problems from the 2 other groups. Density of musculovascular event clusters during rapid eye movement sleep (nearly simultaneous muscle activity burst, blood flow burst and circumference pulsation) distinguished the 2 groups of hypertensive men from controls. The sensitivity of the blood flow measure to changes in the hypertensive men without erectile complaints may indicate that the measure can reveal subclinical signs of developing vasculogenic erectile dysfunction.

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The relationships among penile segmental pulsatile blood flow, pelvic musculovascular events, phases of nocturnal penile tumescence, and sleep stages were studied by all-night polysomnography in 23 healthy middle-aged men. Penile blood flow peaked during maximal tumescence. Bursts of phasic musculovascular activity were more frequent during ascending and maximal tumescence than during detumescence and baseline. Both penile blood flow and the number of musculovascular events increased during REM sleep. These data describe important local aspects of penile erectile mechanisms in normal men. The findings on musculovascular events support the notion that the bulbocavernosus-ischiocavernosus muscles have a role in human penile erection.

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The etiology of erectile failure is not always clear despite the fact that recordings of nocturnal penile tumescence (NPT) are used to detect patients with a significant organic component to their complaint. We recorded electrodermal activity in addition to NPT in 60 impotent patients. Normally more electrodermal activity occurs in stage 2 than in stage REM sleep. Despite a similar total amount of electrodermal activity, organically impotent patients tended to have less electrodermal activity in stage 2 and more in stage REM sleep than those with normal NPT. This difference was due to a subgroup of 15 organically impotent patients with less electrodermal activity in stage 2 than in stage REM sleep. Because of this difference in the pattern of electrodermal activity in relation to sleep stages, the results suggest a central nervous system change is related to impaired erectile capability and abnormal NPT in these cases.

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Thirty male sober alcoholic inpatients received placebo or disulfiram in a random double-blind design in order to evaluate the effects of disulfiram on nocturnal penile tumescence. The amount and frequency of full erections were decreased in the cohort receiving disulfiram. Implications of these results for the role of norepinephrine in penile tumescence are discussed.

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Thirty male alcoholic inpatients received in a random double-blind design placebo (P) or disulfiram 250 mg. (D) at bedtime in order to evaluate the effects of the latter on EEG-EOG sleep patterns. Subjects (S's) had no major medical illness and required no medication for 3 weeks prior to the study. There were 13 disulfiram S's and 17 placebo S's. The total REM time decreased significantly (p less than 0.05) in the D group. Total number of REM episodes decreased and latency to stage 1 REM increased in the disulfiram group. These results are characteristic of sleep patterns induced by the administration of catecholaminergics and opposite to those induced by catecholamine inhibiting agents.

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Narcolepsy is characterized by excessive daytime sleepiness and cataplexy, which may be accompanied by hypnogogic or hypnopompic hallucinations and sleep paralysis. Automatic behavior is a relatively newly recognized symptom of the narcolepsy syndrome. This case report describes a particularly troublesome sort of automatic behavior--shoplifting--in a narcoleptic patient. It illustrates how a sleep-laboratory evaluation was used to confirm the diagnosis of narcolepsy and considers aspects of the treatment of the problem.

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The authors conducted a study of nocturnal penile tumescence (NPT) in 35 diabetic men, aged 33 to 70, who complained of impotence and in 35 age-matched control subjects. EEGs and other measurements showed that the diabetic men as a group exhibited significant reductions in the total amount of NPT and in the amount and frequency of full erection, thus suggesting that impotence in this cohort was organogenic. Although NPT monitoring represents an advance over the less precise traditional procedures for the differential diagnosis of impotence, the authors stress the need for more research in this area.

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In this study it is shown that monitoring of nocturnal penile tumescence (NPT) is an objective method for determining the erectile status of patients who complain of impotence. The characteristics of 11 diabetic patients with abnormal NPT, 11 patients with normal NPT and no medical disorders, and 11 normal men are presented. Also described are several sociodemographic characteristics of the first 100 patients undergoing an NPT evaluation as part of a screen for patients seeking implantation of a penile prosthesis. It is suggested that NPT monitoring should be a component of the differential diagnosis procedure for every patient who complains of impotence and that it provides a tool for the concentrated study of the mechanisms of erection and impotence.

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In a 13-night sleep laboratory study, each of 18 normal young adult males twice received 1 cup of warm water, 1-, 2-, and 4-cup equivalents of regular coffee, a 4-cup equivalent of decaffeinated coffee, and a 4-cup equivalent of caffeine. All beverages were administered 30 min before bedtime according to a balanced Latin-square design. Regular coffee produced dose-related changes in most standard electroencephalogram-electrooculogram (EEG-EOG) sleep parameters, and the 4-cup equivalents of regular coffee and caffeine produced equivalent effects. Decaffeinated coffee had no effect. Regular coffee and caffeine caused rapid eye movement (REM) sleep to shift to the early part of the night and stages 3 and 4 sleep to shift to the later part. Coffee also produced dose-related changes in several subjects estimates of sleep characteristics. These results suggest that coffee and caffeine may be used in normal subjects to induce symptoms mimicking those of insomnia. Such a tool should promote further understanding of insomnia.

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The authors conducted a study of nocturnal penile tumescence (NPT) in 125 healthy males aged 3 to 79 by means of EEG recordings to provide normative data on how general the phenomenon is, its range of charateristics, and how it is related to man's sexual function. The results indicate that NPT occurs consistently in a healthy male population, that its expression is significantly affected by age, that it is related to stage of psychosexual development, and that it is worthy of further investigation. Clinical experience indicates that it is a useful, objective method of discriminating among various types of biogenic and psychogenic impotence.

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In order to determine whether sleep onset per se might precipitate the sleep growth hormone (GH) response, sleep EEG-EOG and plasma GH characteristics were studied in 15 healthy young males (AM) sleeping from 8 AM to 10 AM, when REM sleep is known to predominate, and in 14 subjects (PM) sleeping from 4 PM to 6 PM, when slow-wave sleep (SWS) predominates. PM subjects obtained significantly more SWS and less REM sleep than AM subjects. There was wide individual variability in the level and timing of the GH rise during the naps, but GH release was significantly greater during PM naps than during AM naps for the groups as a whole. The difference between conditions reflected primarily the fact that more subjects exhibited frank GH peaks during PM naps than during AM naps. These results indicate that the occurrence of the sleep GH response is not dependent upon sleep onset, and confirm previous reports of an association between the sleep GH response and SWS.

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