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PubMed1999

Sustained antidepressant effect of sleep deprivation combined with pindolol in bipolar depression. A placebo-controlled trial.

Total sleep deprivation (TSD) shows powerful but transient clinical effects in patients affected by bipolar depression. Pindolol blocks the serotonergic 5-HT1A autoreceptor, thus improving the antidepressant effect of selective serotonin reuptake inhibitors. We evaluated the interaction of TSD and pindolol in the treatment of acute episodes of bipolar depression. Forty bipolar depressed inpatients were randomized to receive pindolol 7.5 mg/day or placebo for nine days in combination with three consecutive TSD cycles. Pindolol significantly improved the antidepressant effect of TSD, and prevented the short-term relapse after treatment. The response rate (HDRS scores < 8) at the end of treatment was 15/20 for pindolol, and 3/20 for placebo. Coadministration of pindolol and TSD resulted in a complete response, which could be sustained for six months with lithium salts alone, in 65% of cases. This results suggest a major role for serotonergic transmission in the mechanism of action of TSD, and makes TSD treatment more effective in the treatment of bipolar depression.

Acute Disease↗
PubMed2003

The role of activation in the effect of total sleep deprivation on depressed mood.

The present investigation analyzes if the effect of Total Sleep Deprivation (TSD) on depressive mood in normal subjects is related to participants' activation levels. Reaction time (RT), subjective sleepiness, and depressive mood were assessed among 48 normal subjects who were subjected to 60 h of TSD. Subjects were divided into groups based on his/her depressive mood changes following TSD: subjects with worse response (n = 11), subjects with better response (n = 12), and intermediate group (n = 25). We sought to determine if RT and subjective sleepiness were related systematically to depressive mood changes following TSD. TSD produces a general reduction in activation (i.e., a monotonic increase in RT and subjective sleepiness) modulated by circadian oscillations. Baseline activation (RT) was confirmed partially as a predictor of participants' response to TSD. Subjects with high levels of activation (lower RTs at the baseline) experienced a better response (greater reductions in depressive mood) following TSD. There was no relationship between pre-treatment subjective sleepiness levels and the TSD effect on depressive mood. The results partially support the role of the activation level as a differential moderator of TSD effects on depressive mood in normal subjects.

Adolescent↗
PubMedDate not supplied

[Effect of unusual regimens of daily activity and sleep deprivation on the human functional state and work capacity].

Physiological functions, work capacity and sleep characteristics of six healthy test subjects were studied for 30 days. The test subjects adhered to one of the three different regimens (1--sleep from 2.00 a.m. to 10.00 a.m., 2--sleep from 6.00 p.m. to 2.00 a.m., and 3--sleep from 10.00 a.m. to 6.00 p.m.) which were aggravated by 64 hr or 72 hr vigilance during the experiment. The studies demonstrated general and specific changes in physiological functions, work capacity and sleep closely associated with the fact how far work-rest cycles were shifted and how long they were applied. Prolonged vigilance caused similar changes in physiological functions, work capacity and sleep. The test subjects showed very poor tolerance to an alteration in the work-rest cycle combined with sleep deprivation.

Activities of Daily Living↗
PubMed1985

Recovery of performance during sleep following sleep deprivation in older normal and insomniac adult males.

Groups of 12 normal and insomniac male subjects aged 55 to 71 yr. were sleep deprived for 64 hr. In both groups, the sleep loss was preceded by four baseline sleep nights and followed by four recovery nights. Reaction time, immediate recall, sleepiness, and body temperature were measured at approximately 2300, 0115, 0330, 0530, and 0800 during baseline, deprivation and recovery nights. Significant performance or mood differences were not found between the normal and insomniac males on any measure or at any testing period throughout the study. Performance of both groups declined characteristically during sleep loss while subjective sleepiness increased. As in young adults, degraded performance was restored by 8 hr. of recovery sleep. However, subjective sleepiness did not return to baseline levels until early in the second recovery night. It was concluded that chronic insomnia does not result in group performance deficits similar to those seen after chronic sleep loss; and the restorative function of sleep operates as efficiently in older insomniac subjects (who apparently have reduced need to sleep) as in older normal subjects.

Aged↗
PubMed1993

Immediate early gene expression in brain during sleep deprivation: preliminary observations.

The two-process model of sleep regulation posits that a homeostatic drive to sleep, referred to as Process S, increases with time spent awake. The purpose of this study was to evaluate whether immediate early gene (IEG) expression increases in the brain in proportion to time spent awake, when Process S would be expected to increase. Rats were deprived of sleep by cage tapping, cage rotation and gentle handling beginning at light onset for 45 minutes, 3 hours or 6 hours. At the end of the deprivation periods, deprived animals and an equal number of controls were decapitated, the brains dissected into subregions and frozen. Northern blots were prepared from cortex, thalamus, cerebellum, pons and hypothalamus and hybridized with cDNA probes to five IEG mRNAs; c-fos, c-jun, junB, NGFI-A and NGFI-B. Basal levels of c-fos mRNA were detectable in all brain regions from all animals. Sleep-deprived animals showed higher expression of c-fos mRNA than control animals following 45 minutes and 6 hours of sleep deprivation in all brain regions examined, with the greatest increases observed in the cerebellum. Surprisingly, only the pons and cerebellum showed clear increases at the 3-hour timepoint. In contrast to c-fos, c-jun mRNA was essentially invariant among the animals while junB mRNA was inconsistently elevated. The expression of NGFI-A and NGFI-B was similar to the c-fos pattern but of lesser magnitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

[Studies on the host factors in the outbreak of odontogenic infection--the background factors of patients and the effect of serum after sleep deprivation on PMN chemotaxis].

These studies were carried out to investigate the background factors in the outbreak of acute infection of odontogenic origin. In the clinical study, fifty patients who suffered from acute odontogenic infection were compared with fifty symptom free controls with chronic odontogenic inflammation. The subjects were asked whether they had basal disease or not, and were given a series of questionnaires about the episodes of recent life changes (f.e. busy, decrease of sleeping time, travel etc) to measure the incidence of these background factors. In the experimental study, the effect of serum after 24 hours sleep deprivation on PMN chemotaxis in vitro was studied in six young volunteers. Chemotactic assays were performed with the modified Boyden chamber method. Results obtained were as follows: 1) The basal diseases were observed in 16 cases (32%) with acute odontogenic infection, and in 14 cases (28%) of controls. The incidence was not different statistically between both groups. 2) The incidence of background episodes in the patients were noted in 39 cases (78%) of patients and 10 cases (20%) of the controls (p less than 0.01). The predominant factor in these episodes were busy (36%), and decrease of sleeping time (30%) in the patient group. 3) Serum of all 6 subjects obtained after sleep deprivation showed depressed effects on PMN chemotaxis to chemotactic factor. (P less than 0.05). 4) Pre-exposure levels were regained in five of the six subjects within seven days after terminating the visil. These results suggest that fatigue plays a major role in the susceptibility to acute odontogenic infection by the alternation of PMN chemotaxis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed2001

Opposite changes in adenosine A1 and A2A receptor mRNA in the rat following sleep deprivation.

Extracellular levels of adenosine increase in basal forebrain following prolonged wakefulness. Moreover, perfusion of adenosine into basal forebrain increases sleep. In this study we have examined the adenosine receptor subtypes, A1 and A2A, for changes in the levels of mRNA using RT-PCR and in situ hybridization and the receptor ligand binding efficiency using autoradiography following 3 and 6 h of sleep deprivation. We observed that A1 receptor mRNA levels increased in basal forebrain with no changes in other forebrain areas examined. A1 receptor binding was not affected. A2A receptor mRNA and ligand binding were undetectable in basal forebrain. However, in the olfactory tubercle, A2A mRNA and receptor binding decreased significantly. Based on the significant increase in the A1 but not in A2A receptor, we hypothesize that the effects of sleep deprivation-induced increased adenosine are mediated by A1 receptor in basal forebrain of rats.

Animals↗
PubMed2001

Maintaining alertness and performance during sleep deprivation: modafinil versus caffeine.

RATIONALE: The performance and alertness effects of modafinil were evaluated to determine whether modafinil should replace caffeine for restoring performance and alertness during total sleep deprivation in otherwise healthy adults. OBJECTIVES: Study objectives were to determine (a) the relative efficacy of three doses of modafinil versus an active control dose of caffeine 600 mg; (b) whether modafinil effects are dose-dependent; and (c) the extent to which both agents maintain performance and alertness during the circadian trough. METHODS: Fifty healthy young adults remained awake for 54.5 h (from 6:30 a.m. day 1 to 1:00 p.m. on day 3) and performance and alertness tests were administered bi-hourly from 8:00 a.m. day 1 until 10:00 p.m. day 2. At 11:55 p.m. on day 2 (after 41.5 h awake), subjects received double blind administration of one of five drug doses: placebo; modafinil 100, 200, or 400 mg; or caffeine 600 mg ( n=10 per group), followed by hourly testing from midnight through 12:00 p.m. on day 3. RESULTS: Performance and alertness were significantly improved by modafinil 200 and 400 mg relative to placebo, and effects were comparable to those obtained with caffeine 600 mg. Although a trend toward better performance at higher modafinil doses suggested a dose-dependent effect, differences between modafinil doses were not significant. Performance enhancing effects were especially salient during the circadian nadir (6:00 a.m. through 10:00 a.m.). Few instances of adverse subjective side effects (nausea, heart pounding) were reported. CONCLUSIONS: Like caffeine, modafinil maintained performance and alertness during the early morning hours, when the combined effects of sleep loss and the circadian trough of performance and alertness trough were manifest. Thus, equivalent performance- and alertness-enhancing effects were obtained with drugs possessing different mechanisms of action. However, modafinil does not appear to offer advantages over caffeine (which is more readily available and less expensive) for improving performance and alertness during sleep loss in otherwise normal, healthy adults.

Administration, Oral↗
PubMed2004

Rhythms of ghrelin, leptin, and sleep in rats: effects of the normal diurnal cycle, restricted feeding, and sleep deprivation.

To determine the relationships among plasma ghrelin and leptin concentrations and hypothalamic ghrelin contents, and sleep, cortical brain temperature (Tcrt), and feeding, we determined these parameters in rats in three experimental conditions: in free-feeding rats with normal diurnal rhythms, in rats with feeding restricted to the 12-h light period (RF), and in rats subjected to 5-h of sleep deprivation (SD) at the beginning of the light cycle. Plasma ghrelin and leptin displayed diurnal rhythms with the ghrelin peak preceding and the leptin peak following the major daily feeding peak in hour 1 after dark onset. RF reversed the diurnal rhythm of these hormones and the rhythm of rapid-eye-movement sleep (REMS) and significantly altered the rhythm of Tcrt. In contrast, the duration and intensity of non-REMS (NREMS) were hardly responsive to RF. SD failed to change leptin concentrations, but it promptly stimulated plasma ghrelin and induced eating. SD elicited biphasic variations in the hypothalamic ghrelin contents. SD increased plasma corticosterone, but corticosterone did not seem to influence either leptin or ghrelin. The results suggest a strong relationship between feeding and the diurnal rhythm of leptin and that feeding also fundamentally modulates the diurnal rhythm of ghrelin. The variations in hypothalamic ghrelin contents might be associated with sleep-wake activity in rats, but, unlike the previous observations in humans, obvious links could not be detected between sleep and the diurnal rhythms of plasma concentrations of either ghrelin or leptin in the rat.

Animals↗
PubMed2005

Functional brain imaging of a complex navigation task following one night of total sleep deprivation: a preliminary study.

Several neuroimaging studies have demonstrated compensatory cerebral responses consequent to sleep deprivation (SD), but all have focused on simple tasks with limited behavioral response options. We assessed the cerebral effects associated with SD during the performance of a complex, open-ended, dual-joystick, 3D navigation task (simulated orbital docking) in a cross-over protocol, with counterbalanced orders of normal sleep (NS) and a single night of total SD (approximately 27 h). Behavioral performance on multiple measures was comparable in the two sleep conditions. Functional magnetic resonance imaging revealed multiple compensatory SD > NS cerebral responses, including the posterior superior temporal sulcus [Brodmann area (BA) 39/22/37], prefrontal cortex (BA 9), lateral temporal cortex (BA 22/21), and right substantia nigra. Right posterior cingulate cortex (BA 31) exhibited NS > SD activity. Our findings extend the compensatory cerebral response hypothesis to complex, open-ended tasks.

Adult↗
PubMed1998

Pupillographic assessment of sleepiness in sleep-deprived healthy subjects.

Spontaneous pupillary-behavior in darkness provides information about a subject's level of sleepiness. In the present work, pupil measurements in complete darkness and quiet have been recorded continuously over 11-minute period with infrared video pupillography at 25 Hz. The data have been analyzed to yield three parameters describing pupil behavior; the power of diameter variation at frequencies below 0.8 Hz (slow changes in pupil size), the pupillary unrest index, and the average pupil size. To investigate the changes of these parameters in sleep deprivation, spontaneous pupillary behavior in darkness was recorded every 2 hours in 13 healthy subjects from 19:00 to 07:00 during forced wakefulness. On each occasion, comparative subjective sleepiness was assessed with a self-rating scale (Stanford Sleepiness Scale, SSS). The power of slow pupillary oscillations (< or = 0.8 Hz) increased significantly and so did the values of SSS, while basic pupil diameter decreased significantly. Slow pupillary oscillations and SSS did not correlate well in general but high values of pupil parameters were always associated with high values in subjective rating. Our results demonstrate a strong relationship between ongoing sleep deprivation and typical changes in the frequency profiles of spontaneous pupillary oscillations and the tendency to instability in pupil size in normals. These findings suggest that the results of pupil data analysis permit an objective measurement of sleepiness.

Adult↗
PubMed2000

Effects of amphetamine and modafinil on the sleep/wake cycle during experimental hypersomnia induced by sleep deprivation in the cat.

Modafinil is a newly discovered waking substance now being used in the treatment of hypersomnia and narcolepsy. We have shown previously in the cat that, unlike amphetamine, modafinil induces long-lasting wakefulness (W) without behavioral excitation and subsequent sleep rebound, and that its waking effect does not depend on endogenous catecholamines. To further characterize the awakening properties of modafinil and current psychostimulants in experimental models of hypersomnia, we examined the effect of oral administration of placebo, modafinil (5 mg kg-1) or amphetamine (1 mg kg-1) on the sleep/wake cycle and power spectral density (PSD) in cats after an 18-h water-tank sleep deprivation period. We found that the placebo had no effect on the dynamics of sleep recovery, while both modafinil and amphetamine induced suppression of cortical slow activity and a waking state lasting 6-8 h. After the amphetamine-induced waking period, both deep slow wave sleep (SWS2) and paradoxical sleep (PS) occurred in greater amounts than after placebo and the PSD during SWS was also increased. Thus, the cumulative time spent in W during a 48-h period was similar to that with placebo, indicating enhanced sleep rebound. In contrast, after the modafinil-induced W, the occurrence and evolution of SWS2 or PS, as well as the PSD during SWS, were similar to those seen with placebo during the same period, so that the total time spent in W in a 48-h period remained significantly higher than the control level, indicating no additional sleep rebound. These results indicate that modafinil is effective against somnolence and hypersomnia and does not produce a subsequent increase in sleep and suggest that the pharmacological profile of modafinil is different from that of amphetamine.

Amphetamine↗
PubMed1981

[All-night polygraphic recordings in the child with suspected epileptic seizures, in spite of normal routine and post-sleep deprivation EEGs (author's transl)].

Normal standard EEGs and normal or borderline EEGs after sleep deprivation in children with one or several suspected epileptic seizures are relatively frequent. All-night polygraphic recordings were performed on 31 children, aged 3-11, who fall into this category, in order to demonstrate epileptiform activity. Three of the recordings were normal, whereas 8 were borderline and 20 showed unequivocal epileptiform activity. The rate of sleep activation is discussed according to the types of epilepsies, the age at the first seizure, the frequency of the seizures, and the position of the seizures within the sleep-waking cycle.

Child↗
PubMed2004

Distribution of CNT2 and ENT1 transcripts in rat brain: selective decrease of CNT2 mRNA in the cerebral cortex of sleep-deprived rats.

Nucleoside transport processes regulate the levels of adenosine available to modulate neurotransmission, vascular tone and other physiological events. However, although equilibrative transporter transcripts or proteins have been mapped in the central nervous system of rats and humans, little is known about the presence and distribution of the complete family of nucleoside transporters in brain. In this study, we analysed the distribution of the transcript encoding the high affinity adenosine-preferring concentrative transporter CNT2 in the rat central nervous system and compared it with that of the equilibrative transporter ENT1. Furthermore, we evaluated the changes in expression of these two transporters in a situation of increased extracellular levels of adenosine, such as sleep deprivation. CNT2 mRNA was widespread in rat brain, although most prevalent in the amygdala, the hippocampus, specific neocortical regions and the cerebellum. The distribution of CNT2 mRNA only partially overlapped that of ENT1. Most of the cells labelled were neurones. Total sleep deprivation dramatically diminished the amounts of CNT2 mRNA, whereas ENT1 mRNA remained unchanged. This specific decrease in CNT2 transcript suggests a new physiological role for the transporter in the modulation of extracellular adenosine levels and the sleep/wakefulness cycle.

Animals↗
PubMed1998

Effect of modafinil on plasma melatonin, cortisol and growth hormone rhythms, rectal temperature and performance in healthy subjects during a 36 h sleep deprivation.

Modafinil is an alerting substance which has been used successfully to treat narcolepsy. Nothing is known about its effect on hormone secretions. For this purpose, eight healthy young men were enrolled in a double blind trial to test the effects of modafinil on daily plasma melatonin, cortisol and growth hormone (GH) rhythms. Blood was sampled for hormone assays, every hour during the daytime and every 30 min during the nighttime. In addition, rectal temperature and mental performances were determined during the study which comprised 3 sessions, two weeks apart: a 24 h control session including a night with sleep (S1) and two 48 h sessions S2 and S3 with a sleep-deprived night (N1) followed by a recovery night (N2). Modafinil (300 mg x 2) or placebo were randomly attributed during N1 at 22 h and 8 h. As expected, performance was improved after modafinil administration and body temperature was maintained or increased. Plasma melatonin and cortisol profiles were similar after modafinil and placebo administration. The levels observed during the recovery and the control nights (N2) displayed no difference. For GH, during both sleep deprived nights, secretion was dramatically reduced compared with the control one, although the number of secretory episodes was unchanged. These data show that the alerting property of modafinil is not related to an alteration of hormone profiles and suggest that the acute modafinil administration is devoid of short-term side-effects.

Adult↗
PubMed1985

REM sleep deprivation decreases the grooming and shaking behaviour induced by enkephalinase inhibitor or opiate withdrawal.

Intraventricular administration of enkephalinase inhibitor, phosphoramidon (1 X 10(-8)-5.6 X 10(-7) moles ICV) induced a behavioural syndrome consisting of excessive grooming with the body scratching as the most prominent symptom and wet-dog-shakes (WDS). The frequency of the phosphoramidon-induced WDS and body scratching were decreased by the pretreatment with the opiate receptor blocking agent, naltrexone (2.9 X 10(-6) moles/kg IP). Both the phosphoramidon-induced WDS in naive rats and naloxone-precipitated withdrawal WDS were decreased in REM sleep deprived rats compared with animals allowed normal sleep (control and stress groups). The results are discussed in light of a possible functional insufficiency of endorphinergic system during REMSD. It has been suggested that this insufficiency might be a background to the increased neuronal excitability during REMSD.

Animals↗
PubMed1994

On the ability to self-monitor cognitive performance during sleep deprivation: a calibration study.

The antagonistic effects of extensive sleep deprivation (SD) on human cognitive performance are well documented. However, one aspect of human performance that has not been investigated with respect to its susceptibility to SD is the 'meta-cognitive' ability to self-monitor overt performance. In the present study, 16 male subjects participated in an experiment requiring sustained cognitive work during a three day period. One of the cognitive tasks required the mental addition of rapidly presented numbers. On each trial, subjects reported the sum and then provided a subjective confidence rating to indicate the degree of certainty in their response. As expected, performance on the sequential addition task deteriorated with increasing fatigue and returned to baseline following a recovery sleep. However, calibration analyses, which quantify a number of properties of the relationship between subjective and overt performance, revealed that the correlation between confidence and performance (calibration), the ability to differentiate correct from incorrect judgments (resolution), and validity of subjective 'certainty', were all unaffected by SD. Hence, in the absence of external feedback from the environment, people have access to fairly reliable internal feedback about their performance during periods of sustained and vigilant cognitive activity.

Journal Article↗
PubMed2003

Behavioral and subjective effects of marijuana following partial sleep deprivation.

This study tested whether performance would be more impaired when marijuana use followed partial sleep deprivation (PSD) than when marijuana use followed a typical night of sleep. Seven recreational marijuana users (mean 15 of last 30 days) completed six test sessions in a double-blind randomized within-subject design. Each session began with an overnight stay in a sleep laboratory. Bed and wake times were calculated from mean data on individual sleep diaries. Time-in-bed was either regular (mean=8.2 h) or shortened (first 65% of regular time-in-bed deprived). At 3 and 5 h after waking, daytime sleepiness was measured with self-report questionnaires and a sleep latency test. Approximately 6.5 h after waking, subjects smoked a marijuana cigarette (0.003, 2, or 3.5% delta-9 tetrahydrocannabinol [THC]). Test batteries were completed 2, 62, and 122 min after smoking ended. Sleepiness was significantly greater following PSD than after regular sleep. Following regular sleep, heart rate increases with active THC doses were comparable, but heart rate with 2% THC was significantly less elevated following PSD. Ratings of "impaired" and "stoned" increased with both THC doses after regular sleep and were further increased with 3.5% THC after PSD. High-potency marijuana increased body sway similarly across sleep conditions. There were no significant effects of marijuana or PSD, alone or in combination, on brake latency. Thus, while PSD increased the dose-dependence of THC effects on heart rate and subjective impairment, it did not enhance the effects of marijuana on standing balance and brake latency.

Adult↗