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PubMed1995

Stimulation of A1 adenosine receptors mimics the electroencephalographic effects of sleep deprivation.

N6-Cyclopentyladenosine (CPA), an A1 adenosine receptor agonist, increased EEG slow-wave activity in nonREM sleep when administered either systemically (0.1-3 mg/kg) or intracerebroventricularly (3.5-10 micrograms) in the rat. The power spectrum of EEG changes (as calculated by Fourier analysis) matched that produced by total sleep deprivation in the rat. The effects of CPA on the nonREM-sleep EEG were dose-dependent. These findings suggest that adenosine is an endogenous mediator of sleep-deprivation induced increases in EEG slow-wave activity, and therefore that increased adenosine release is a concomitant of accumulation of sleep need and may be involved in homeostatic feedback control of sleep expression.

Adenosine↗
PubMed2000

Prefrontal neuropsychological effects of sleep deprivation in young adults--a model for healthy aging?

Neuropsychological testing and brain imaging show that healthy aging leads to a preferential impairment of the prefrontal cortex (PFC). Interestingly, in young adults sleep deprivation (SD) has similar effects. Psychological tasks not so oriented to the PFC are less sensitive both to SD and aging. The PFC is a cortical region working particularly hard during wakefulness, which may make it more vulnerable to "deterioration," whether this is through aging or SD. In these respects SD in young adults may offer a model for aging. No study has directly compared aging with SD. We compared groups comprising (equal sexes): YOUNG (av. 23y), MIDDLE AGED (av. 60y) and OLD (av. 73y). Young were subdivided into SD and non-sleep deprived groups. All participants were carefully screened, were healthy, good sleepers and with a similar educational background. A battery of PFC-oriented, short and straightforward neuropsychological tests was used to compare the effects of 36h of SD in the young group, with findings from the healthy, alert, non-sleep deprived groups. Tests relied on accuracy rather than speed (which took into account the problem of "global slowing" in the older participants), and were administered once (i.e., were novel). Test outcomes were significantly affected by: (1) SD in the young groups, and (2) by age. A non-PFC component of one test was not affected by SD or by age. It was concluded that 36h SD in young adults produces effects on the PFC similar to those found in normal, alert people aged about 60 years. However, it can not be concluded that an aged brain is a sleep-deprived brain.

Adult↗
PubMed2005

Caffeine effects on recovery sleep following 27 h total sleep deprivation.

INTRODUCTION: Caffeine is widely used to reverse alertness and performance decrements. However, caffeine's effects on subsequent recovery sleep and post-recovery performance are not well documented and, therefore, were evaluated. METHODS: Six habitually low (LC: < or = 100 mg x d(-1)) and three habitually high (HC: > or = 400 mg x d(-1)) caffeine users completed a randomized crossover design. After 20 h of wakefulness, repeated doses of caffeine gum [0 (placebo) mg, 100 (low dose) mg, or 300 (high dose) mg] were administered at 03:00, 05:00, and 07:00. At 10:00 (27 h sleep deprivation) subjects slept for 8 h, followed by Psychomotor Vigilance Task (PVT) administration at 33 and 65 min post-awakening. RESULTS: Low dose caffeine increased stage 1 minutes only. However, high dose caffeine impaired sleep maintenance (reduced total sleep time/increased wake) and reduced sleep depth (increased stage 1 minutes/percentage and slow-wave sleep (SWS) latency, and reduced SWS minutes during the first third of the sleep period). With high dose caffeine, LC users had less SWS percentage as compared with HC users. The HC users had reduced stage 2 percentage with high dose caffeine as compared with placebo and low dose caffeine. Caffeine dose and habitual caffeine use did not influence post-recovery sleep PVT performance. DISCUSSION: Caffeine exerts mild deleterious dose-response effects on recovery sleep following total sleep deprivation, primarily early in the sleep period, with potential recovery from these effects after sufficient sleep as suggested by lack of post-recovery sleep performance deficits. Habitual caffeine use appears to minimally reduce caffeine effects.

Adolescent↗
PubMed1988

Nocturnal TSH and prolactin secretion during sleep deprivation and prediction of antidepressant response in patients with major depression.

In order to test the hypothesis that changes in the hypothalamic-pituitary axis during sleep deprivation are related to the antidepressant effects of this procedure, we measured thyroid-stimulating hormone (TSH) and prolactin levels in 32 depressed patients at 2:00 AM during a night before, during, and after total sleep deprivation (TSD). TSH levels increased significantly (p less than 0.05) during TSD, and prolactin levels decreased significantly (p less than 0.0001). When we divided the patients into responder and nonresponder groups based on a 30% reduction in the Hamilton Rating Scale, there was no difference between the two groups in their hormone levels on the baseline, TSD, or recovery nights. Changes in prolactin or TSH were not correlated with clinical improvement when the two groups were considered together or in the responder/nonresponder groups separately. Baseline values of both hormones were significantly (p less than 0.01) correlated with their respective levels during TSD and recovery sleep. These findings indicate that the relative levels of nocturnal TSH and prolactin are stable even within acutely depressed individuals and that changes in their levels are not related to the clinical response to sleep deprivation.

Adult↗
PubMedDate not supplied

[Comparative evaluation of seizure provocation methods with sleep deprivation and Brietal in epileptics].

In 10 patients with suspected epilepsy in whom routine EEG investigations failed to demonstrate changes the sleep deprivation method and intravenous injection of 1% Brietal solution were used as provocation methods. The efficiency of both methods was compared. In cases in which sleep deprivation provoked appearance of pathological changes Brietal gave a similar result but evoked more frequently the manifestation of focal changes. In cases in which sleep deprivation was ineffective Brietal provoked slight changes in some cases only. Both methods may be used for provocation and Brietal may be more suitable in cases with suspected focal lesions.

Adolescent↗
PubMed1987

Sleep deprivation effects in older endogenous depressed patients.

In a drug-free group of 15 older endogenous depressed inpatients, all-night sleep deprivation (SD) was associated with a significant decrease in Hamilton depression scores and in Profile of Mood States self-ratings of depression. Six of 15 patients (40%) were responders to SD, as evidenced by greater than or equal to 30% improvement in Hamilton ratings. While symptomatic improvement was short-lived (8 of 15 patients worsened after 1 night of recovery sleep), five patients showed further improvement after 1 night of recovery sleep. The final two patients had an increase in Hamilton ratings after sleep deprivation, with a return to baseline values after 1 night of recovery sleep. Responders (but not nonresponders) showed significant improvement in sleep latency, sleep efficiency, and slow wave sleep during recovery sleep (as did controls). The SD Hamilton depression rating (at 9 a.m. after all-night sleep deprivation) showed a significant inverse correlation with the increase in slow wave sleep (SWS) minutes and in SWS % from baseline to first recovery night. Responders also had significantly larger increases in SWS minutes than did nonresponders (53.8 vs. 7 minutes). Similarly, the % change in Hamilton depression ratings was predicted by baseline Stage 4 sleep. These findings suggest that there is a mutual interaction between the process of sleep regulation and the symptoms of depression. They also confirm a prediction from the two-process model of sleep regulation--namely, that improved sleep initiation and maintenance and increased SWS, attained by SD, are associated with clinical improvement.

Affect↗
PubMed2006

The effects of total sleep deprivation on brain functional organization: mutual information analysis of waking human EEG.

Sleep deprivation can affect the waking electroencephalogram (EEG) that may reflect functional organization of the brain. We examined the effect of total sleep deprivation (TSD) on functional organization between different cortical areas from the waking EEG. Waking EEG data were recorded from 18 healthy male volunteers with eyes closed after 8-h night's sleep and after 24 h of TSD. The averaged cross mutual information (A-CMI) after 24 h of TSD were compared to before TSD. 24 h of TSD yielded the decreased A-CMIs in the inter-hemispheric C3-F4, C3-F8, and C3-C4 pairs: therefore, the electrodes that contribute to pairs with significant decrease of A-CMI were C3, F4, F8, and C4. The decreased A-CMIs between C3 and right frontal and central brain areas after 24 h of TSD may reflect the changes of cortico-cortical functional organization by homeostatic process during TSD. Our results of the frontal-area-related A-CMI decreases may support that the frontal brain regions are related to the homeostatic deterioration of brain function due to TSD.

Adult↗
PubMed1992

Response to sleep deprivation in three women with postpartum psychosis.

BACKGROUND: Postpartum psychotic disorders are rare and poorly understood phenomena occurring after approximately 1 in 2000 births. Increasing attention has been given to the concept of postpartum psychosis as an affective spectrum disorder. We sought to characterize the responses to sleep deprivation of three women with postpartum psychotic and mood symptoms. METHOD: Three hospitalized postpartum women with no prior history of psychotic disorder were treated according to a partial sleep deprivation protocol. Each patient was awakened at 2:00 a.m. and kept awake until 9:00 p.m. the following night. A full and an abbreviated Hamilton Rating Scale for Depression (HAM-D) were completed for each patient before and after partial sleep deprivation. RESULTS: Two of the three patients became transiently manic and the third became hypomanic after sleep deprivation. HAM-D scores decreased drastically for each patient. After recovery sleep, each patient de-escalated but required further treatment with mood-stabilizing agents. CONCLUSION: These findings suggest that postpartum psychosis in our patients may represent a variant of bipolar affective disorder.

Adult↗
PubMed2002

The value of sleep deprivation as a diagnostic tool in adult sleepwalkers.

OBJECTIVE: Adult somnambulism can result in injury to the sleeper and to others. Attempts to induce sleepwalking episodes in the sleep laboratory have yielded mixed results. Having shown that sleepwalkers have lower slow-wave activity power than control subjects, the authors hypothesized that an enhanced pressure of the homeostatic process underlying sleep regulation could affect the disorder's characteristics even further. Therefore, the effects of 38 hours of sleep deprivation in adult sleepwalkers and control subjects were investigated. METHODS: Ten adult somnambulistic patients and 10 sex- and age-matched control subjects were studied in the sleep laboratory. After a screening night, participants were monitored during 1) one night of baseline recording, and 2) one recovery night in which subjects slept ad libitum immediately after the sleep deprivation protocol. Behavioral manifestations were assessed for frequency and complexity using a 3-point scale of increasing complexity. RESULTS: None of the control subjects had any behavioral manifestations on either of the two nights. Conversely, sleepwalkers showed a significant increase in the frequency and complexity of the somnambulistic episodes during the recovery night compared with baseline. Somnambulistic patients had a greater number of awakenings from slow-wave sleep than control subjects on both nights, but there was no significant increase during the recovery night. CONCLUSION: Sleep deprivation can be an effective tool for inducing somnambulistic episodes in the laboratory, thereby facilitating the diagnosis of sleepwalking.

Adult↗
PubMed1990

Sleep deprivation increases dopamine D1 receptor antagonist [3H]SCH 23390 binding and dopamine-stimulated adenylate cyclase in the rat limbic system.

Sleep deprivation induced by the platform technique is considered to be a heavy stressful situation in rats. At the end of the sleep deprivation period (72 h) the rats displayed particular behaviour characterized by wakefulness, a high degree of motor and exploratory activity, increased alertness and reactivity to environmental stimuli. Our previous results indicated that this behaviour was potently antagonized by the administration of the D1-selective antagonist SCH 23390. In this paper we show that concomitantly to this behaviour, an increased number of D1 receptors associated with an increased dopamine-stimulated adenylate cyclase activity is present in the limbic system but not in the striatum of these animals. These data suggest an active role of limbic D1 receptors in the generation of arousal and insomnia related to sleep deprivation induced stress.

Adenylyl Cyclases↗
PubMed2004

Effects of sleep deprivation, nicotine, and selenium on wound healing in rats.

Effects of sleep deprivation (SD), nicotine, and selenium (Se) on wound healing were studied in 50 male rats (Sprague-Dawley strain). Full-skin-thickness burns were produced in animals. Then, SD, nicotine, and Se administrations were applied to animals in different groups. Wound healing was assessed by pathological analysis of wound by counting fibroblasts, capillary vessels, polymorphonuclear leucocytes (PNLs), and by measuring radiolabeled immunoglobulin G (IgG) amount in wound area by radio-pharmaceutical and immunoscintigraphic procedures. The number of fibroblasts and capillary vessels were higher in control and Se groups than in sleep deprivation and nicotine groups, and the number of PNLs and the radiolabeled polyvalent IgG levels were higher in SD and nicotine groups than in control and Se groups. The results suggest that SD and nicotine may delay wound healing and that Se supplementation may accelerate wound healing by preventing nicotine-induced oxidative stress and lipid peroxidation.

Animals↗
PubMed1989

Effects of brief naps on mood and sleep in sleep-deprived depressed patients.

To determine the effects of brief naps on mood and electroencephalographic (EEG) sleep in sleep-deprived depressed patients, data from 19 hospitalized patients with depression were analyzed; all were kept awake from 0700h until the following day, when they were allowed 10-min naps at either 0830h or 1500h. Six of the patients showed a clinically significant improvement (greater than 40% change) on the Hamilton Rating Scale for Depression (HRSD) before the nap after all-night sleep deprivation, and the group as a whole showed a significant improvement on the HRSD, the Profile of Mood States, and the Brief Psychiatric Rating Scale subscale for depression. Naps did not alter mood in the responders, but did improve measured depression on the HRSD in the non-responders. Morning and afternoon naps did not differ significantly in their effects on mood or nap sleep. On the recovery sleep, patients who were classified as responders after the nap showed a significantly greater increase in delta (Stage 3 + 4) sleep compared with baseline than nonresponders.

Affect↗
PubMed2005

Accelerating symptom-reduction in late-life depression: a double-blind, randomized, placebo-controlled trial of sleep deprivation.

OBJECTIVE: Authors tested the hypothesis that one night of total sleep deprivation (TSD) would accelerate antidepressant response to paroxetine, as compared with TSD+placebo (PBO) and paroxetine-alone, in late-life major depression. METHODS: Eighty elderly outpatients with current episodes of non-psychotic, non-bipolar major depression were randomly assigned to one of three treatment conditions: TSD+paroxetine (N = 27), TSD + PBO (N = 27), and paroxetine-only (N = 26). Primary outcome was percentage of subjects in each condition who demonstrated early response (Hamilton Rating Scale for Depression scores [Ham-D: 17-item] of < or = 10) or remission (score of < or = 7) on Day 14. RESULTS: Response rates after 14 days were 22% in subjects randomly assigned to the TSD + paroxetine condition, 41% in TSD + PBO, and 46% in paroxetine alone. Remission rates after 14 days were 11% in TSD+paroxetine, 22% in TSD + PBO, and 38% in paroxetine. After adjusting for baseline depression severity, there were no statistically significant differences in response or remission rates. CONCLUSION: Contrary to the study hypothesis, one night of total sleep deprivation did not accelerate onset of antidepressant response to paroxetine pharmacotherapy of late-life depression. The data suggest, rather, that the two interventions might have counteracted each other.

Aged↗
PubMed2003

Effect of 38 h of total sleep deprivation on the waking EEG in women: sex differences.

38 h of sleep deprivation in women resulted in decreased alpha, increased theta and increased intrahemispheric correlation during rest and increased theta and reaction time during task. F3-O1 coherent activity was selectively decreased consistent with the role of sleep for recovery of frontal functions. Sleep deprivation effects were milder in women than in men, however, recovery was not complete suggesting that women need more sleep than men to recover.

Adult↗
PubMed2003

One night of total sleep deprivation impairs implicit learning in the serial reaction task, but not the behavioral expression of knowledge.

Implicit sequence learning in the serial reaction task suffers from total sleep deprivation. The authors compared implicit-learning scores in a sleep-deprivation (SD) group (n = 12) and a control group (n = 6). Both groups were tested immediately after learning a 1st sequence; a delayed test was conducted on the next day (after a night without sleep in the SD group). Immediately after the delayed test a 2nd sequence was learned, followed by an immediate test and a delayed test toward the end of the experiment. In the SD group implicit-learning scores were reduced in both tests of the 2nd sequence, but in neither test of the 1st sequence. Thus, 1 night of total sleep deprivation impairs the acquisition of implicit sequence knowledge, but not its behavioral expression.

Adult↗
PubMed2004

Comparison of clonidine to sleep deprivation in the potential to induce spike or sharp-wave activity.

OBJECTIVE: This study aimed to investigate previously observed side effects, i.e. increased epileptic activity during clonidine medication. The safety and effectiveness of clonidine as spike inducing agent compared to sleep deprivation were tested. METHODS: Patients suffering from drug-resistant localization related epilepsy took part in 3 magnetoencephalography (MEG) sessions. One session was recorded without any activating measures. The other two sessions were either performed after sleep deprivation or after medication with clonidine. Target parameter was the number of spikes or sharp-waves during a 30 min recording period. RESULTS: About 67% of the patients showed increased spike activity after clonidine, whereas sleep deprivation increased the number of spikes in 33%, and 29% of the patients did not show any activation at all. Clonidine was most effective in temporal lobe epilepsy, when the focus was located in the right hemisphere, and when clonidine serum concentrations were ranging between 0.6 and 1.0 ng/ml. CONCLUSIONS: This study showed for the first time that clonidine can be considered an effective spike or sharp-wave inducing drug that is superior to the potency of sleep deprivation. SIGNIFICANCE: The administration of clonidine increases the probability of recording ictal and interictal epileptic activity during limited acquisition time.

Action Potentials↗
PubMed1994

Effects of sleep on the antidepressant response to sleep deprivation.

The effect of a 90-min nap period on mood was studied in 22 sleep-deprived patients with a diagnosis of major depression. All patients remained awake from 7 AM until 12 noon the following day at which time they were permitted to nap while being monitored by sleep encephalography. Fifteen subjects showed a significant response to sleep deprivation as defined by a 35% improvement on the Hamilton Rating Scale for Depression. After the nap a relapse of depressive symptoms occurred which was significantly related to the amount of non-rapid eye movement sleep time.

Adult↗
PubMed2006

The relation between EEG prefrontal asymmetry and subjective feelings of mood following 24 hours of sleep deprivation.

Several studies have investigated the relationship between asymmetrical EEG activity over the frontal cortex and mood. This study aimed at investigating the association between state fluctuations in frontal alpha EEG asymmetry and state changes followed by 24 h of sleep deprivation (SD). Our results show that sleep deprivation caused a significant alteration in the asymmetry values. Activation shifted from the left hemisphere, before SD, to the right hemisphere, after SD, in all frontal electrode pairs. In addition, according to the self-rating scale of SD-related mood effects, subjects became significantly less alerted and active, and sleepier. According to these results, increased right prefrontal activation might be potentially associated with the negative mood states typically seen after sleep deprivation, although the causal relationship is still uncertain. However, more studies will be necessary to establish the viability of EEG asymmetry and the cerebral lateralization hypothesis to explain the SD-related affective changes.

Adult↗