A single dose of melatonin prevents the phase delay associated with a delayed weekend sleep pattern.

STUDY OBJECTIVES: This study was designed to test the hypotheses that a delayed weekend sleep pattern may lead to a phase delay of the endogenous circadian rhythm, and that melatonin administration can counteract the phase delay and prevent the sleep and functional impairments associated with this sleep pattern. DESIGN: A within-subject, counterbalanced design was used in which each subject participated in both placebo and melatonin conditions. Subjects' sleep-wake schedules were delayed by two hours on Friday and Saturday to simulate the delayed weekend sleep pattern. Six mg of melatonin or a placebo pill was administered double blind on Sunday late afternoon. SETTING: N/A. PARTICIPANTS: Ten healthy volunteers (mean age = 22.1 years old). MEASUREMENTS AND RESULTS: Salivary dim-light melatonin onset (DLMO) was measured on Friday and Monday nights. Subject's sleep was recorded with polysomnography on Sunday night and their levels of sleepiness, cognitive functioning and mood were assessed on Sunday night and Monday morning. Results show that the delayed weekend sleep pattern caused a 31.6 min delay of the endogenous melatonin rhythm. Melatonin administration counteracted the phase delay of endogenous melatonin onset. On Sunday, melatonin administration increased the sleepiness throughout the evening and reduced sleep onset latency at bedtime. On Monday morning, subjective sleepiness was decreased in the melatonin condition. CONCLUSION: A delayed weekend sleep pattern did show a mild phase-delay effect on the endogenous circadian rhythm. A single dose of melatonin can acutely reverse the weekend drift.

Intracerebral hemodynamics probed by near infrared spectroscopy in the transition between wakefulness and sleep.

Previous imaging studies have shown that cerebral metabolism is gradually reduced at the beginning of sleep. Few studies have examined the sleep state transition periods from wakefulness to sleep and sleep to wakefulness. The current study used the Near Infrared Spectroscopy (NIRS) technique to describe the intracerebral hemodynamics at the frontal pole in the circumscribed period between wakefulness and sleep. Nine healthy young adults were studied during afternoon naps. Optical probes were placed on the forehead and EEG electrodes on the scalp. At sleep onset oxygenated hemoglobin (oxy-Hb) was reduced (P<0.01) and deoxygenated hemoglobin (deoxy-Hb) showed a near significant reduction (P<0.063). At sleep offset there were increases in oxy-Hb (P<0.005) and deoxy-Hb (P<0.05). In 18 of 26 transitions to sleep there was a coordinated fall in both NIRS parameters, we call the Switch Point, that lasted a mean of 3.6 s. In 32 of 36 transitions to wakefulness there was an analogous Switch Point that lasted a mean of 3.4 s. Before and after the Switch Point, changes were small and the relationship between oxy-Hb and deoxy-Hb was a combination of parallel and reciprocal fluctuations. A synchronized, parallel and short-lived change in oxy-Hb and deoxy-Hb is a discrete event in the transition period between wakefulness and sleep. The concentration of these light absorbing molecules is abruptly set to a new level at sleep-wake transitions and probably reflects the different perfusion demands of these states.

Nonpharmacologic treatment of chronic insomnia. An American Academy of Sleep Medicine review.

This paper reviews the evidence regarding the efficacy of nonpharmacological treatments for primary chronic insomnia. It is based on a review of 48 clinical trials and two meta-analyses conducted by a task force appointed by the American Academy of Sleep Medicine to develop practice parameters on non-drug therapies for the clinical management of insomnia. The findings indicate that nonpharmacological therapies produce reliable and durable changes in several sleep parameters of chronic insomnia sufferers. The data indicate that between 70% and 80% of patients treated with nonpharmacological interventions benefit from treatment. For the typical patient with persistent primary insomnia, treatment is likely to reduce the main target symptoms of sleep onset latency and/or wake time after sleep onset below or near the 30-min criterion initially used to define insomnia severity. Sleep duration is also increased by a modest 30 minutes and sleep quality and patient's satisfaction with sleep patterns are significantly enhanced. Sleep improvements achieved with these behavioral interventions are sustained for at least 6 months after treatment completion. However, there is no clear evidence that improved sleep leads to meaningful changes in daytime well-being or performance. Three treatments meet the American Psychological Association (APA) criteria for empirically-supported psychological treatments for insomnia: Stimulus control, progressive muscle relaxation, and paradoxical intention; and three additional treatments meet APA criteria for probably efficacious treatments: Sleep restriction, biofeedback, and multifaceted cognitive-behavior therapy. Additional outcome research is needed to examine the effectiveness of treatment when it is implemented in clinical settings (primary care, family practice), by non-sleep specialists, and with insomnia patients presenting medical or psychiatric comorbidity.

Insomnia.

The series of cases presented here should illustrate that the complaint "I can't sleep" is deceptively simple. The clinician must be prepared to gather information from many disparate aspects of the patient's history and present circumstances. Diagnostic considerations are complicated further by the significant night-to-night variation in the manifestations of the insomnia. Too often, the result of this hidden complexity is a tendency either to prescribe hypnotic drugs as a first intervention or to give signals to patients with insomnia that not much can be done and that difficulty sleeping is simply a fact of life. The sleep log can help to bring order to the jumble of insomniac experiences. It leads both the clinician and patient away from assigning too much weight to a specific instance, instead allowing more general patterns to be discerned. As order is created out of the factors contributing to the insomnia, a treatment plan can be designed that goes beyond mere symptomatic treatment.

Sleepiness and REM sleep recurrence: the effects of stage 2 and REM sleep awakenings.

Determinants of daytime sleepiness include sleep length, sleep continuity, and circadian factors. Sleep stage composition has not been seen as influencing subsequent daytime functioning; however, earlier studies did not focus explicitly on sleepiness. The present experiment studied the effects of selective sleep-stage restriction on an objective measure of sleep tendency, and explored the relationship between sleepiness and subsequent REM recurrence during REM deprivation. Daytime sleep latency was measured by a modified Multiple Sleep Latency Test prior to and following two nights of awakenings from either REM or Stage 2 sleep in 16 normal young adults. Sleep latency following these awakenings was also measured. REM sleep and Stage 2 awakenings produced comparable levels of sleepiness, both during the Awakening Nights and subsequent daytime Multiple Sleep Latency Testing. Pooling the groups, daytime and nocturnal sleepiness measures were correlated within individuals. In the REM-Awakening Group, Pre-Awakening daytime sleepiness was associated with the tendency for REM sleep to recur following experimental awakenings. Comparable levels of sleepiness may result from nonspecific processes such as sleep curtailment and fragmentation, or alternatively from separate REM and Stage 2 mechanisms. The relationship between REM sleep and sleepiness is discussed in the context of both state and trait models.

Delayed sleep phase syndrome in adolescents.

The delayed sleep phase syndrome is characterized by difficulty in falling asleep at a socially acceptable time of night and an inability to be easily aroused in the morning. Most commonly encountered in adolescents, this condition can produce daytime sleepiness and poor school performance, and it can lead to behavioral problems. The clinical features of the syndrome are described in 22 adolescents. Nine subjects participated in a protocol of polysomnographic recordings to simulate habitual "weekday" and "weekend" sleep patterns. There was a significant increase in total sleep time (p less than 0.005) and REM sleep (p less than 0.001) during the "weekend" sleep period. A multiple sleep latency test was performed between the two nights to assess daytime sleep tendency. Daytime sleepiness was maximal in the morning, with a tendency for greater alertness as the day progressed. The reduced amount of REM sleep during the "weekdays" plus the tendency for sleepiness in the mornings may contribute to the behavioral and educational difficulties seen in these patients. Recognition of this syndrome enables a specific sleep schedule change to be made that effectively treats the problem.

A behavioral perspective on insomnia treatment.

The major behavioral treatments of insomnia--progressive relaxation, biofeedback, cognitive approaches, stimulus control instructions, chronotherapy, and sleep restriction therapy--are described. The basis of these interventions are conceptualized as issuing from the interdependence of sleep and wakefulness, the temporal organization of sleep-wake processes, cognitive effects on arousal, the role of perpetuating factors in chronic insomnia, and conditioning. A pilot study of the conditioning of rapid sleep onset with the aid of a hypnotic provides a preliminary demonstration of the application of conditioning to the pharmacotherapy of sleep. It is predicted that the commonly accepted view of sleep latency as solely reflecting physiological sleep tendency, will require modification to include the effects of conditioning. The current pattern of hypnotic usage, an issue of widespread concern, is subjected to a behavioral analysis based on a new model of conditioned tolerance. The intermittent administration of placebo within a hypnotic regimen is predicted to be especially beneficial in sustaining hypnotic efficacy.

Treatment of chronic insomnia by restriction of time in bed.

A treatment of chronic insomnia is described that is based on the recognition that excessive time spent in bed is one of the important factors that perpetuates insomnia. Thirty-five patients, with a mean age of 46 years and a mean history of insomnia of 15.4 years, were treated initially by marked restriction of time available for sleep, followed by an extension of time in bed contingent upon improved sleep efficiency. At the end of the 8-week treatment program, patients reported an increase in total sleep time (p less than 0.05) as well as improvement in sleep latency, total wake time, sleep efficiency, and subjective assessment of their insomnia (all p less than 0.0001). Improvement remained significant for all sleep parameters at a mean of 36 weeks after treatment in 23 subjects participating in a follow-up assessment. Although compliance with the restricted schedule is difficult for some patients, sleep restriction therapy is an effective treatment for common forms of chronic insomnia.

Dynamics of REM sleep in narcolepsy.

The discovery of sleep onset REM periods (SOREMPs) in narcolepsy first suggested the important role of REM sleep in the disorder. We have conducted a series of studies exploring factors that affect the onset and termination of REM sleep in narcolepsy. Following a preliminary study of REM sleep deprivation, we compared the sleep onset response of narcoleptic and normal subjects to awakenings at REM sleep onsets and awakenings during NREM sleep. In addition, we have investigated the relationship of these awakenings to daytime sleepiness. We have demonstrated that an index of the REM sleep process predicts the sleepiness of both normal and narcoleptic subjects. The finding of increased frequency of SOREMPs following both REM and NREM sleep awakenings in the narcoleptic patient suggests that accelerated triggering and inertia of the REM sleep process are pathophysiological mechanisms of the disorder.

Predictive value of Müller maneuver in selection of patients for uvulopalatopharyngoplasty.

Uvulopalatopharyngoplasty (UPPP) is an effective treatment for some patients with obstructive sleep apnea syndrome (OSAS). A major difficulty has been to select those patients who will have a good response to UPPP. Fiberoptic nasopharyngoscopy with Müller Maneuver (FNMM) was applied in preoperative evaluation of patients with OSAS to identify those in whom greatest pharyngeal collapse was in the region of the tonsillar fossae and soft palate. Those with pharyngeal changes on FNMM who were considered most likely to respond to surgery underwent UPPP. Comparison of pre and postoperative polysomnography reveals significant (p less than .001) improvement in indices of severity of OSAS The mean apnea index (apneas per hour) was diminished by 72%. Eighty-seven percent of patients had greater than 50% reduction in apnea index. Preoperative selection of OSAS patients by FNMM increases the likelihood of success of UPPP.

Patterns of daytime sleepiness in narcoleptics and normals: a pupillometric study.

Pupil diameter was measured in light and dark conditions every half hour for 6.5-10 h in 3 normal controls and 3 narcoleptics. Mean pupillary diameter was significantly smaller in the narcoleptic group than in the normal group. Pupil activity was correlated with pupil diameter only in the dark condition in narcoleptics. Pupil diameter varied with a circa 90 min periodicity in the narcoleptics but not in the normal controls. These results indicate firstly, that one-time assessment of pupil size is insufficient; and secondly, that the appearance of these rhythms may be the result of a defect in arousal mechanisms of narcoleptics which usually play an inhibitory role.

Delayed sleep phase syndrome. A chronobiological disorder with sleep-onset insomnia.

We describe a new syndrome called "delayed sleep phase insomnia." Thirty of 450 patients seen for a primary insomniac complaint had the following characteristics: (1) chronic inability to fall asleep at a desired clock time; (2) when not on a strict schedule, the patients have a normal sleep pattern and after a sleep of normal length awaken spontaneously and feel refreshed; and (3) a long history of unsuccessful attempts to treat the problem. These patients were younger than the general insomniac population and as a group did not have a specific psychiatric disorder. Six patients' histories are described in detail, including the successful nonpharmacological chronotherapy regimen (resetting the patients' biological clock by progressive phase delay). Delayed sleep phase insomnia is proposed to be a disorder of the circadian sleep-wake rhythm in which the "advance" portion of the phase response curve is small.

Theoretical and technical problems in the measurement of nocturnal penile tumescence for the differential diagnosis of impotence.

Theoretical and technical problems in using Nocturnal Penile Tumescence (NPT) measurements for the differential diagnosis of impotence are discussed and possible solutions are offered: 1) The basic assumption that NPT measurements can distinguish psychogenic from organic impotence has never been demonstrated in patients shown to be psychogenically and organically impotent independent of the NPT measurements themselves. Studies attempting to do this are necessary to determine definitively the limits of the clinical applicability of this important diagnostic tool. 2) Evidence is presented showing that though a direct observation of one of the patient's fullest erections is required for an adequate NPT evaluation, this is not always done. The danger of misdiagnosis if this step is omitted is illustrated with a case report. 3) Disagreements in the literature about NPT criteria for diagnosing psychogenic impotence are discussed and criteria are suggested that are based on demonstrating the intactness of the physiological mechanisms required for erection rather than on values recorded in normal subjects.

Impaired nocturnal erections and impotence following transurethral prostatectomy.

A case of impotence with significantly impaired nocturnal penile tumescence (NPT) following transurethral resection of the prostate (TURP) is described. The patient was studied with polysomnographic recording including measurements of NPT for three consecutive nights at nine months after surgery and showed a total absence of full erections. Possible causes of his impotence are discussed. It is concluded that the total clinical picture strongly suggests that the erectile dysfunction was a result of physiologic complications of the surgery. Methodologic problems in past work are discussed, and the need for detailed diagnostic studies is stressed. The sleep studies that should be a part of this comprehensive evaluation are described.

The differential diagnosis of impotence. The measurement of nocturnal penile tumescence.

The literature on nocturnal penile tumescence (NPT) and impotence is briefly reviewed. Available evidence suggests that measurement of NPT provides objective data, which when combined with a thorough clinical evaluation can be helpful in distinguishing psychogenic from organic impotence in approximately 80% of those patients who present this differential diagnostic problem. Further research is needed to determine whether some psychogenically impotent patients may have impaired NPT. The interdisciplinary evaluation employed at our center is described, and clinical material illustrating the usefulness of this technique is presented. The potential errors that can result from the use of portable NPT monitoring devices are discussed.