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PubMedDate not supplied

Effect of sleep deprivation on neuroendocrine response to a serotonergic probe in healthy male subjects.

Neuroendocrine responses to stimulation with a selective serotonin reuptake inhibitor (citalopram) were measured to investigate the effects of all-night sleep deprivation on serotonergic function in healthy male subjects (n = 7). We studied citalopram-stimulated prolactin and cortisol plasma concentrations in a placebo-controlled cross-over protocol following sleep and sleep deprivation. Citalopram infusion (20 mg i.v. at 14:20-14:50 h) after a night of undisturbed sleep prompted robust increases in both plasma prolactin and cortisol concentrations. Following a night of sleep deprivation, by contrast, the citalopram-induced prolactin response was blunted, but the cortisol response was not significantly altered. This differential response pattern relates to the distinct pathways through which serotonin may activate the corticotrophic and the lactotrophic systems. While an unchanged cortisol response does not indicate (but also does not refute the possibility of) an altered serotonergic responsivity following sleep deprivation, the suppressed prolactin response could reflect a downregulation of 5-HT1A or 2 receptors. An alternative, not mutually exclusive, explanation points to the possibility that sleep deprivation activates the tubuloinfundibular dopaminergic system, the final inhibitory pathway of prolactin regulation.

Adult↗
PubMedDate not supplied

Variability of the averaged evoked potentials in healthy subjects after 24-hour sleep deprivation.

Variability of the averaged evoked visual potentials in healthy subjects after 24-hour sleep deprivation. Acta Physiol. Pol., 1977, 28 (1): 61-69. The authors evaluated the effects of 24-hour sleep deprivation on visual evoked potentials in 20 pilots aged 20 to 40 years, clinically healthy and with normal bioelectric cerebral activity. A slight reduction in the latency time of components was observed, mainly in the non-specific part of the visual evoked potentials, and a rise in the P3-N4 amplitude. An analysis of the duration of potential components suggests that sleep deprivation causes disturbances in the equilibrium between the processes of excitation and inhibition from non-specific structures (with increased excitation). All parameters assessed may evidence increased excitation of the central nervous system after activation with insomnia + light flashes, and may be useful for extending the diagnostic possibilities in cases of borderline pathological changes in cerebral bioelectric activity.

Adult↗
PubMed1999

Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications.

The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.

Adult↗
PubMed2006

Modafinil activates cortical and subcortical sites in the sleep-deprived state.

UNLABELLED: SUBJECT OBJECTIVES: To assess the effect of the wake-promoting drug modafinil on working memory and brain activation in the executive network, following a single night of sleep deprivation. DESIGN: Randomized, placebo-controlled, 4-arm, double-blind evaluation of a single 200-mg dose of modafinil on working memory (1-, 2-, and 3-back)-related functional brain activation and performance following overnight sleep deprivation. SETTING: General Clinical Research Center, Biomedical Imaging Center. SUBJECTS: Eight medication-free men, aged 21 to 35 years. INTERVENTIONS: Overnight sleep deprivation, single-dose 200-mg modafinil, functional magnetic resonance imaging MEASUREMENTS AND RESULTS: Brain activation patterns and regional signal intensity based on the blood-oxygen level-dependent signal were assessed. The following reaction times were used as measures of performance: (1) attention in the scanner before functional scanning, (2) "back" responses during the active-task block, and (3) attention during the baseline task block. Contrast of activation maps among conditions revealed sleep-deprivation and drug effects, and their interactions. Performance in the deprived state was enhanced by modafinil only at an intermediate (2-back) level of task difficulty and was associated with the recruitment of increased cortical activation volumes. Strong and consistent individual differences in performance were noted on the working memory tasks. CONCLUSIONS: Modafinil effectively counters the adverse effects of overnight sleep deprivation on working memory but only when task difficulty is moderate, recruiting extensive areas in the executive network to do so. Interindividual differences in working-memory performance are stable trait characteristics.

Adult↗
PubMed1998

REM sleep deprivation increases the levels of tyrosine hydroxylase and norepinephrine transporter mRNA in the locus coeruleus.

The present study was conducted to determine the effects of REM sleep deprivation on the levels of tyrosine hydroxylase (TH) and norepinephrine transporter (NET) mRNA in the locus coeruleus (LC) of rats. The animals were deprived of REM sleep for 1, 3 or 5 days, then killed and changes in the mRNA levels were determined using in situ hybridization. The levels of both TH and NET mRNA increased in animals deprived of REM sleep for 3 days or longer whereas no change in these messages were observed in the LC of control animals. REM sleep deprivation has been used as a mode of treatment for major depression. Others have shown that treatment with tricyclic antidepressants also results in increased levels of TH and NET mRNA in LC. Our results suggest that the antidepressant effect of REM sleep deprivation and tricyclic antidepressants may share similar molecular changes in the norepinephrine system.

Animals↗
PubMed2000

Oculomotor impairment after 1 night of total sleep deprivation: a dissociation between measures of speed and accuracy.

OBJECTIVES: The present study examined the effects of 40 h of sleep deprivation and of time-of-day on saccadic and smooth pursuit oculomotor performance. METHODS: Nine normal subjects slept for 3 consecutive nights in the laboratory (one adaptation, one baseline, one recovery). Baseline and recovery were separated by a period of 40 h of continuous wakefulness, during which subjects were tested every 2 h. Oculomotor performance assessed at the following hours: 10:00, 12:00, 14:00, 16:00, 18:00, 20:00, 22:00, of both the days preceding and following the sleep deprivation night, as well as at 24:00, 02:00, 04:00, 06:00 and 08:00 h during the deprivation period. RESULTS: Saccade latency increased and peak velocity decreased significantly during the post-deprivation day; saccadic accuracy was unaffected. As regards smooth pursuit performance, phase (a measure of accuracy) was not affected by sleep loss, while velocity gain significantly decreased during the day that followed the sleep deprivation night. Significant time-of-day effects on the considered oculomotor variables except saccadic accuracy were also found, indicating an overall performance impairment during the night. CONCLUSIONS: It is concluded that 40 h of sleep deprivation significantly impaired diurnal performance in pursuit and saccadic tasks. This performance worsening is limited to the measures of speed, while accuracy is not affected by sleep loss. A significant operational relevance of these results is suggested, since saccadic velocity has recently been found to be negatively correlated with simulator vehicle crash rates.

Adult↗
PubMed2001

Pattern analysis of sleep-deprived human EEG.

Progress during the past decade in non-linear dynamics and instability theory has provided useful tools for understanding spatio-temporal pattern formation. Procedures which apply principle component analysis (using the Karhunen-Loeve decomposition technique) to the multichannel electroencephalograph (EEG) time series have been developed. This technique shows localized changes of cortical functioning; it identifies increases and decreases of the activity of localized cortical regions over time while the subject performs a simple task or test. It can be used to demonstrate the change in cortical dynamics in response to a continuous challenge. Using 16 EEG electrodes, the technique provides spatio-temporal information not obtained with power spectrum analysis, and includes the weighted information given with omega complexity. As an application, we performed a pattern analysis of sleep-deprived human EEG data in 20 healthy young men. Electroencephalograph recordings were performed on subjects for <2 min, with eyes closed after normal sleep and after 24 h of experimentally-induced sleep deprivation. The significant changes in the eigenvector components indicated the relative changes of local activity in the brain with progressive sleep deprivation. A sleep deprivation effect was observed, which was hemispherically correlated but with opposite directional dynamics. These changes were seen in the temporo-parietal regions bilaterally. The application of the technique showed that the simple test task was performed with a limited unilateral hemispheric involvement at baseline, but needed a much larger cortical participation with decreased frontal activity and increased coherence and bilateral hemispheric involvement. The calculations performed demonstrated that the same weighted changes as those obtained with omega complexity were shown, but the technique had the added advantage of showing the localized directional changes of the principle eigenvector at each studied electrode, pointing out the cortical localized region affected by the sleep deprivation and toward which direction the environmental challenge induced the spatial change. This methodology may allow the evaluation of changes in local dynamics in brain activity in normal and pathological conditions.

Adult↗
PubMed1988

Total sleep deprivation in patients with obsessive-compulsive disorder.

Total sleep deprivation was performed in 16 patients with obsessive-compulsive disorder. Overall, no effect was observed on either mood or obsessive-compulsive behaviour. However, individual patients showed worsening, improvement or no change in obsessive-compulsive symptoms, independent of mood response, across the 3 days of sleep deprivation.

Adult↗
PubMed1986

Sleep deprivation as a method of EEG activation. Observation on the incidence of positive responses.

Sleep deprivation is known to be one of the principal mechanisms to activate epileptogenic activity in the EEG recording and indeed it is one of the most common activation techniques in EEG practice. It is generally recognized that about one third of patients with seizures presenting a normal or borderline normal routine EEG may be expected to exhibit an abnormal paroxysmal recording after sleep deprivation. In the present study it was estimated that activation, by sleep deprivation, of a normal EEG into a record with abnormal paroxysmal activity, may be expected to be even higher with selection of patient population. The incidence of such activation was found to be 23% among patients presenting a history of attacks with variable clinical paroxysmal manifestations with or without impairment of consciousness, but in whom the overall picture could not be judged typically epileptic upon historical grounds alone. However, the incidence of activation was found to increase up to 57% among patients with attacks judged by history to be typical as to their epileptic nature. This higher incidence of activation appears to parallel the higher incidence of underlying abnormality as revealed by CAT scanning.

Diagnosis, Differential↗
PubMed1992

Changes in the waking EEG as a consequence of sleep and sleep deprivation.

Electroencephalographic (EEG) activity was monopolarly recorded during resting wakefulness in 10 volunteers under the following conditions: at night before going to sleep, at night before total sleep deprivation, in the morning after waking, in the morning after sleep deprivation and at night after having slept during the day. Absolute and relative power and inter- and intrahemispheric correlation were established. After diurnal and nocturnal sleep as compared to sleep deprivation, we obtained the following significant results: interhemispheric correlations were higher; intrahemispheric correlations were lower; absolute power of alpha 2, beta 1 and beta 2 was lower; and relative power of alpha 2 and beta 2 was lower. EEG changes as a consequence of sleep or lack of sleep are dependent on prior sleep and/or wakefulness and not on circadian phase. EEG activity during wakefulness is a sensitive parameter and a useful tool to assess the consequences of sleep on brain functional organization.

Adult↗
PubMed1982

48-hour sleep-wake cycles in manic-depressive illness: naturalistic observations and sleep deprivation experiments.

Wrist motor activity and sleep were monitored longitudinally in 15 rapidly cycling and 52 nonrapidly cycling manic-depressive patients. The majority of patients experienced one or more consecutive 48-hour sleep-wake cycles (alternate nights with no sleep) when they switched out of depression into mania of hypomania. During a depressive phase, nine rapidly cycling patients were asked to simulate a 48-hour sleep-wake cycle by remaining awake for 40 hours (one night's total sleep deprivation). Eight switched out of depression, and seven were rated as manic or hypomanic; indicating that sleep loss (such as occurs with spontaneous 48-hour sleep-wake cycles) may help to trigger switches from depression to mania. The 48-hour sleep-wake cycles in patients may depend on a mechanism that is normally present in all humans, since normal persons also spontaneously experience near-48 hour sleep-wake cycles in certain experimental conditions.

Adult↗
PubMed2003

Clinical caveat: prior sleep deprivation can affect the MSLT for days.

It is common practice to forcibly awaken patients from an all-night polysomnographic study prior to performance of a multiple sleep latency test (MSLT); either for reasons of protocol or for the convenience of the laboratory personnel. We report a case of a young woman who, by formal sleep study criteria, received the erroneous diagnosis of narcolepsy due to the effects of severe sleep deprivation, and document that the effects of prior sleep deprivation require more than one night of ad libitum sleep. Forced awakening prior to MSLT may permit sleep deprivation or delayed sleep phase syndrome to masquerade as narcolepsy or idiopathic central nervous system (CNS) hypersomnia.

Adult↗
PubMed1981

Sleep deprivation: effects on circadian rhythms of rat brain neurotransmitter receptors.

Specific binding of ligand to rat forebrain alpha- and beta-adrenergic, muscarinic cholinergic, opiate, benzodiazepine, and striatal dopamine receptors was measured at 4-hour intervals during the last 13 hours of a 24-hour sleep deprivation period, and during the first 11 hours of the recovery sleep period. In non-sleep-deprived controls a 24-hour rhythm in binding was evident. The minor differences between the sleep deprivation group and the control group consisted mainly in a reduced amplitude of the 24-hour rhythm under the sleep deprivation schedule. The results indicate that neither the 24-hour forced locomotion nor the subsequent prominent sleep rebound is accompanied by marked changes in the number of neurotransmitter receptors and their circadian rhythms.

Animals↗
PubMed1992

Prediction of sleep deprivation outcome by diurnal variation of mood.

This study investigates whether response to total sleep deprivation in depressed patients may be predicted by the presence of diurnal variation of mood. Diurnal variation was measured with two different self-rating scales in 140 untreated depressed patients. Sleep deprivation responders manifest a higher percentage of diurnal variation than nonresponders, with a pattern of improved mood in the evening. Patients with marked diurnal variation respond better to sleep deprivation than those with little. The symptom of diurnal variation is a potential marker for a patient's likelihood to respond to different therapies.

Adult↗
PubMed2003

Effects of one night's sleep deprivation on anaerobic performance the following day.

The purpose of this study was to determine the effect of one night's sleep deprivation on anaerobic performance in the morning and afternoon of the following day. Thirteen healthy males were studied twice in a balanced, randomized design. The experiment consisted of two conditions 1 week apart. In the sleep deprivation condition (SDN) subjects remained awake overnight and in the control condition (reference night, RN) the same subjects slept at home, retiring between 2230 and 2330 hours, as decided individually, and rising at 0500 hours. In both conditions, activity, sleep and diet were monitored by actimetry and daily activity and dietary diaries. Physical performance testing was carried out at 0600 hours and at 1800 hours after the one night of sleep and the one night of sleep deprivation. At each test occasion, subjects were measured for maximal power ( P(max)), peak power ( P(peak)) and mean power ( P(mean)). Blood lactate concentrations were measured at rest, at the end of the force-velocity ( F- V) test, just before and just after the Wingate test and again 5 min later. Oral temperatures were measured every 2 h. In both conditions, the results showed a circadian rhythm in temperature. Analysis of variance revealed a significant (sleep x time of day of test) interaction effect on P(peak), P(mean) and P(max). These variables improved significantly from morning to afternoon after RN and SDN. The reference night was followed by a greater improvement than the SDN. Up to 24 h of waking, anaerobic power variables were not affected; however, they were impaired after 36 h without sleep. Analysis of variance revealed that blood lactate concentrations were unaffected by sleep loss, by time of day of testing or by the interaction of the two. In conclusion, sleep deprivation reduced the difference between morning and afternoon in anaerobic power variables. Anaerobic performances were unaffected after 24 h of wakefulness but were impaired after 36 h without sleep.

Adaptation, Physiological↗
PubMed1996

The relationship between sleep deprivation and the nocturnal decline of blood pressure.

Blood pressure (BP) has a circadian pattern with a 10% to 15% drop in systolic and diastolic BP comparing nighttime and daytime averages. The mechanism and the "reason" for the decline of nocturnal blood pressure has not been described. If the nocturnal decline is a restorative physiologic process we reasoned that sleep deprivation would increase the nocturnal drop. Thus, we tested the hypothesis that there is a compensatory decline in nocturnal sleep blood pressure after a period of nocturnal sleep deprivation. Twenty-four house staff personnel (normotensive and not taking any BP medications) with a mean age of 29.3 years were recruited for this study (13 men and 11 women). Subjects were randomly assigned to have 24-h BP monitoring after being sleep deprived (on call with 3 +/- 1.3 h of sleep) or after a normal night's sleep (7.3 +/- 0.8 h). There was no significant difference in hours asleep or time to bed or time awake for both 24-h studies. Subjects had similar activities for both monitoring intervals. The percent change in day awake versus night asleep mean values for systolic BP, diastolic BP, and mean arterial pressure for sleep deprived and normal night's sleep intervals were compared using paired t tests. None of these paired parameters were significantly different despite a subjectively "deeper" sleep postcall. In conclusion, sleep deprivation does not appear to result in a compensatory decline in nocturnal blood pressure. Thus, the "reason" for the normal nocturnal decline in blood pressure remains to be explored.

Adult↗
PubMed1988

Auditory evoked potentials and total sleep deprivation in depressed patients.

Cortical auditory evoked potentials (latencies N1 and P2, N1-P2 amplitude, and amplitude/stimulus intensity function) were studied before and after 1 night's total sleep deprivation in 20 drug-free depressed inpatients. Responders to sleep deprivation showed an augmenting pattern on the non-dominant hemisphere and a reducing pattern on the dominant hemisphere. The interhemispheric difference in auditory cortex was also apparent in the group of patients who failed to respond to sleep deprivation, but with values pointing in the opposite direction. The augmenting pattern shown by responders in the nondominant hemisphere may be a predictor of therapeutic response to sleep deprivation and to subsequent treatment with drugs influencing serotonergic pathways.

Adult↗
PubMed2005

Less effective executive functioning after one night's sleep deprivation.

The prefrontal cortex (PFC) is affected negatively by sleep deprivation (SD) and executive functioning is largely dependent on activity in the PFC. Earlier studies have focused on subsystems of executive functioning, and tests of executive functioning have shown both low reliability and low validity. In the present study, 11 healthy volunteers were sleep deprived and compared with 11 healthy controls in a study on effects of one night's SD on integrative executive functioning. Following SD, the performance of subjects on an ecologically valid test, the modified Six Elements Test, was significantly impaired. There were no group differences on psychomotor vigilance, verbal or visuo-spatial working memory. This extends previous knowledge of performance effects of SD, and may be of special importance for individuals with cognitive work tasks.

Adult↗