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Long-term sleep deprivation by hypothalamic stimulation in cats.

Several techniques were developed to prevent sleep in animals in order to examine the biological role fulfilled by sleep; however, most were either stressful or difficult to accomplish routinely, especially in such a large animal as the cat. Electrical stimulation of activating structures in the brain presents a very attractive alternative to peripheral stimulation used by the usual sleep deprivation methods although it has been rarely tried. The paper describes a microcomputer-based system used to achieve sleep deprivation in cats by stimulating the hypothalamic predatory area with short trains. During control days and deprivation the electrocorticogram (EEG), electromyogram (EMG) and electrooculogram (EOG) were continuously digitalized by the computer in 5 s epochs and the integrated power of the 4 usual frequency bands of the EEG (alpha, beta, delta, theta) as well as the variance of EMG and EOG signals were calculated. Criteria for stimulus delivery were based on the integrated power of the delta band and on the variance of EMG but the flexibility of the computer ensures that any other parameter can be used to achieve total or selective sleep deprivation.

Animals↗

Effect of sleep deprivation on the performance of simulated laparoscopic surgical skill.

BACKGROUND: Resident work hours may impact patient care. We hypothesized that "call-associated" acute sleep deprivation has no effect on technical dexterity as measured on a minimally invasive surgery trainer, virtual reality (MIST VR) surgical simulator. METHODS: Thirty-five surgical residents were prospectively evaluated pre-call (rested), on-call (rested), and post-call (acutely sleep deprived). Participants completed questionnaires regarding sleep hours and level of fatigue. Technical skill was assessed using the MIST VR. Speed, errors, and economy of motion were automatically recorded by the MIST VR computer simulator. Data were analyzed by paired Student t test and analysis of variance. RESULTS: Estimated hours of sleep and subjective indicators of fatigue were different between rested and sleep-deprived residents. The number of errors and time to complete all tasks increased at the post-call assessment. CONCLUSIONS: Resident work schedules lead to sleep deprivation and fatigue. Call-associated sleep deprivation and fatigue are associated with increased technical errors in the performance of simulated laparoscopic surgical skills.

Adult↗

[Sleep deprivation (wakefulness therapy) as an antidepressant].

In this complete survey of publications concerning therapeutic sleep deprivation (including reports of a conference held in 1985) first the practical management and especially the advantages of sleep deprivation of the second half of the night are explained. After discussing the psychological conditions and methods of therapeutic evaluation the treatment results in endogenous depression (melancholia), the effectiveness of repetition and of combination with antidepressive pharmacotherapy, the comparison with electroconvulsive therapy and the predictors are described. Sleep deprivation is indicated in nearly every therapeutic situation, including drug-resistant melancholia, furthermore in severe neurotic depression and in depressive states of schizophrenic patients. Side effects are unimportant, and complications are almost absent. In addition psychophysiological, neuroendocrinological and biochemical investigations are reported, as far as they concern either the mechanism of action of sleep deprivation or chronobiological hypotheses of depression.

Antidepressive Agents↗

REM sleep deprivation decreases apomorphine-induced stimulation of locomotor activity but not stereotyped behavior in mice.

1. Effects of rapid eye movement (REM) sleep deprivation on central dopaminergic system were investigated by testing the behavioral responses to apomorphine and brain dopamine metabolism in mice. 2. REM sleep deprivation for 48 hr significantly suppressed apomorphine.HCl (3.0 and 6.0 mg/kg, i.p.)-stimulated spontaneous locomotor activity without affecting the intensity of stereotyped behavior. 3. Neither the latency of nociceptive response in a hot-plate test nor the duration of pentobarbital-induced sleep was changed by REM sleep deprivation. 4. Dopamine turnover in the striatum and the nucleus accumbens of REM sleep-deprived mice was significantly higher than that of control animals. 5. These results suggest that REM sleep deprivation may decrease the function of postsynaptic dopamine receptor in the mesolimbic but not nigrostriatal dopaminergic system.

3,4-Dihydroxyphenylacetic Acid↗

Sleep deprivation effects on the activity of the hypothalamic-pituitary-adrenal and growth axes: potential clinical implications.

OBJECTIVES: Although several studies have shown that sleep deprivation is associated with increased slow wave sleep during the recovery night, the effects of sleep deprivation on cortisol and growth hormone (GH) secretion the next day and recovery night have not been assessed systematically. We hypothesized that increased slow wave sleep postsleep deprivation is associated with decreased cortisol levels and that the enhanced GH secretion is driven by the decreased activity of the HPA axis. DESIGN AND SUBJECTS: After four consecutive nights in the Sleep Laboratory, 10 healthy young men were totally deprived of sleep during the fifth night, and then allowed to sleep again on nights six and seven. Twenty-four hour blood sampling was performed serially every 30 minutes on the fourth day, immediately following the previous night of sleep and on the sixth day, immediately after sleep deprivation. MEASUREMENT: Eight-hour sleep laboratory recording, including electroencephologram, electro-oculogram and electromyogram. Plasma cortisol and GH levels using specific immunoassay techniques. RESULTS: Mean plasma and time-integrated (AUC) cortisol levels were lower during the postdeprivation nighttime period than on the fourth night (P < 0.05). Pulsatile analysis showed significant reduction of both the 24 h and daytime peak area (P < 0.05) and of the pulse amplitude (P < 0.01), but not of the pulse frequency. Also, the amount of time-integrated GH was significantly higher for the first 4 h of the postdeprivation night compared to the predeprivation night (P < 0.05). Cross-correlation analyses between the absolute values of the time-series of each hormone value and percentage of each sleep stage per half hour revealed that slow wave sleep was negatively correlated with cortisol and positively correlated with GH with slow wave sleep preceding the secretion of these hormones. In contrast, indices of sleep disturbance, i.e. wake and stage 1 sleep, were positively correlated with cortisol and negatively correlated with GH. CONCLUSION: We conclude that sleep deprivation results in a significant reduction of cortisol secretion the next day and this reduction appears to be, to a large extent, driven by the increase of slow wave sleep during the recovery night. We propose that reduction of CRH and cortisol secretion may be the mechanism through which sleep deprivation relieves depression temporarily. Furthermore, deep sleep has an inhibitory effect on the HPA axis while it enhances the activity of the GH axis. In contrast, sleep disturbance has a stimulatory effect on the HPA axis and a suppressive effect on the GH axis. These results are consistent with the observed hypocortisolism in idiopathic hypersomnia and HPA axis relative activation in chronic insomnia. Finally, our findings support previous hypotheses about the restitution and immunoenhancement role of slow wave (deep) sleep.

Adult↗

[EEG after sleep deprivation in patients with suspected epilepsy].

BACKGROUND: The purpose of this study was to investigate to what extent sleep deprivation provokes epileptiform discharges in EEG in patients with suspected epilepsy. MATERIAL AND METHODS: Data from 189 adults and children with unspecified seizures who had had EEG after sleep deprivation were evaluated retrospectively. Previous standard EEGs were without epileptiform discharges. The patients' final diagnosis were collected from the medical records. RESULTS: 13% of the patients demonstrated epileptiform activity in their sleep deprivation EEG, and significantly more epileptiform activity was found in patients with generalized tonic-clonic seizures and absences. None of the patients with a history of syncope showed epileptiform activity. The activation rate was higher in patients with an abnormal standard EEG compared to those with a normal standard EEG. The sensitivity of sleep deprivation EEG in this study was 35%, specificity 98% and positive predictive value 92%. INTERPRETATION: Sleep deprivation EEG seems to have greatest diagnostic value in patients with generalized tonic-clonic seizures, absences and abnormal standard EEG.

Adolescent↗

Sleep deprivation in junior doctors--house officers in Singapore.

House officers are known to endure marked levels of sleep deprivation in administration of their duties. We aim to establish sleep patterns of local house officers while on the job and the impact it might have on their mood and sleepiness state. We also studied their sleep during their final year of medical school and pre-university for identification of any prior sleep deprivation. Questionnaires were used to assess sleep and mood change. Sleepiness levels on the day after call were assessed using the Stamford Sleepiness Scale. Subjects were found to sleep a median of only 1.0 (+/- 2.0) h per night on call and 6.0 h (+/- 1.0) per non-call night. They suffered median of 5 interruptions (+/- 5) during sleep on one night call. Night call was found to adversely affect mood in 89.5% of the subjects while daytime sleepiness levels following call were found to increase the more the time spent at work after call. Subjects were found to have had 6.5 h (+/- 1.0) of sleep per night during final year of medical school and 8.0 h (+/- 1.0) in final year of pre-university. House officers enter the profession chronically sleep-deprived. The call schedule and general work regime further add to the existent sleep deprivation and may have adverse consequences on patient care and doctor's health. This calls for measures to be instituted for provision of proper sleep and work hours for them.

Adult↗

Sleep deprivation increase the expression of inducible heat shock protein 70 in rat gastric mucosa.

AIM: To investigate if sleep deprivation is able to increase the expression of inducible heat shock protein 70 in gastric mucosa and its possible role in mucosal defense. METHODS: Rats for sleep disruption were placed inside a computerized rotating drum, gastric mucosa was taken from rats with 1, 3 and 7d sleep deprivation. RT-PCR, immunohistochemistry and Western blotting were used to determine the expression of heat shock protein 70. Ethanol (500mL.L(-1), i.g.) was used to induce gastric mucosa damage. RESULTS: RT-PCR, Western blotting and immunostaining confirmed that the sleep deprivation as a stress resulted in significantly greater expression of inducible heat shock protein 70 in gastric mucosa of rats. After the 500mL.L(-1) ethanol challenge, the ulcer area found in the rats with 7d sleep deprivation (19.15 +/- 4.2)mm(2) was significantly lower (P<0.01) than the corresponding control (53.7 +/- 8.1) mm(2). CONCLUSION: Sleep deprivation as a stress, in addition to lowering the gastric mucosal barrier, is able to stimulate the expression of inducible heat shock protein 70 in gastric mucosa of rats, the heat shock protein 70 may play an important role in gastric mucosal protection.

Animals↗

The expression of m1-m3 muscarinic receptor mRNAs in rat brain following REM sleep deprivation.

We used in situ hybridization histochemistry to study the effects of REM sleep deprivation on m1-m3 muscarinic receptor mRNA expression in the rat brain. REM sleep deprivation for 72 h did not affect m1 receptor mRNA expression. However, we found significantly increased m3 receptor mRNA expression in the pontine nuclei and nucleus accumbens-bed nucleus of the stria terminalis region of REM sleep-deprived rats compared with controls. Paradoxically, we found significantly decreased m2 receptor mRNA expression in the pontine nuclei of REM sleep-derived rats vs controls. The present findings implicate these structures in the cholinergic effector pathways of REM sleep, although the type and magnitude of the effects of these structures on REM sleep may vary with different receptor subtypes.

Animals↗

Effects of chronic sleep deprivation on autonomic activity by examining heart rate variability, plasma catecholamine, and intracellular magnesium levels.

Chronic sleep deprivation is associated with cardiovascular events. In addition, autonomic activity determined from the levels of the heart rate variability (HRV), plasma catecholamine, and intracellular magnesium (Mg) are important in the pathophysiology of cardiovascular events. This study therefore aimed to determine the effects of chronic sleep deprivation on autonomic activity by examining the HRV, plasma catecholamine, and intracellular magnesium levels. Thirty (30) healthy male college students ranging in age from 20 to 24 years of age (average 22 +/- 1 years; mean +/- SD) with no coronary risk factors such as hypertension, diabetes mellitus, hyperlipidemia or a family history of premature coronary artery disease (CAD) were included in the study. Over a 4-week period, the volunteers' plasma levels of epinephrine, norepinephrine, and erythrocyte-Mg were measured. The study was made during the 4 weeks before and immediately after college finals exams. HRV, obtained from 24-hour ambulatory ECG monitoring, included time and frequency domain indices. The HRV indices and erythrocyte-Mg decreased while norepinephrine increased during chronic sleep deprivation. It is concluded that chronic sleep deprivation causes an autonomic imbalance and decreases intracellular Mg, which could be associated with chronic sleep deprivation-induced cardiovascular events.

Adult↗

The impact of sleep deprivation and task difficulty on networks of fMRI brain response.

Previous fMRI research has found altered brain response after total sleep deprivation (TSD), with TSD effects moderated by task difficulty. Specific models of the impact of sleep deprivation and task difficulty on brain response have yet to be developed. Differences in networks of fMRI measured brain response during verbal encoding in sleep deprived and well-rested individuals were examined with structural equation modeling (SEM). During fMRI scanning, 23 healthy volunteers memorized words either easy or difficult to recall, 12 (well-rested) and 36 hours (sleep deprived) after awaking. A priori models that linked specified regions of interest were evaluated, with the focus on the extent to which two left parietal regions interacted with the left inferior frontal gyrus (Model 1) or with the right inferior frontal gyrus (Model 2). Task difficulty, not TSD, determined which model fit the brain response data; Model 2 fit best for hard words before and after TSD, whereas Model 1 fit best for easy words. TSD altered the patterns of interaction within each of the best fitting models: prefrontal interactions with the left inferior parietal lobe were diminished and intra-parietal interactions increased. Sleep deprivation and item difficulty produce different effects on brain networks involved in verbal learning.

Adult↗

Exercise after sleep deprivation.

The influence of acute sleep loss on subsequent exercise remains poorly defined. To investigate this question, six subjects performed cycle ergometer exercise daily in a 3-d series that included 30 h without sleep before day 2, and then unlimited sleep before day 3. Each day 8 min of exercise was performed at each of three constant external work loads that required approximately 25%, 50%, and 75% of the VO2max. On days 2 and 3 after sleep loss, exercise at all work loads resulted in unchanged O2 uptake (VO2), CO2 production (VO2), CO2 production (VCO2), ventilation (VE), heart rate, and arterial blood perssure, when compared with the equivalent day in a control series. Despite these unchanged physiological variables, ratings of preceived exertion were increased significantly during moderate and heavy exercise on day 2 (P less than 0.05), but returned to control levels on day 3. In further experiments on six additional subjects, sleep loss failed to alter VO2max, while it significantly reduced peak exercise heart rate (P less than 0.05). These results suggest that acute sleep deprivation primarily alters the psychological responses to moderate and heavy exercise.

Adult↗

Thyroid function and response to 48-hour sleep deprivation in treatment-resistant depressed patients.

BACKGROUND: Clinical depression is associated with abnormalities of the hypothalamic-pituitary-thyroid axis. Changes in thyroid function during sleep deprivation may be related to its antidepressant effects. METHODS: Levels of thyroid-stimulating hormone, tri-iodothyronine, tri-iodothyronine uptake, thyroxine, and free thyroxine were measured before, during, and after a 48-hour sleep deprivation in nine treatment-resistant depressed patients. Clinical state was assessed every 4 hours. A retrospective study of 26 similar patients was added for cross-validation. RESULTS: Significant increases in thyroid-stimulating hormone and tri-iodothyronine during sleep deprivation were not correlated with clinical improvement. Sleep deprivation responders had lower tri-iodothyronine uptake levels than nonresponders in both the prospective (p <.02) and the retrospective (p <.03) samples. CONCLUSIONS: The lower tri-iodothyronine uptake values in responders may identify a subgroup of depressed patients who respond to sleep deprivation by virtue of some abnormality of the hypothalamic-pituitary-thyroid axis that is temporarily corrected by sleep deprivation.

Adult↗

Thyroid and adrenomedullary reactions during sleep deprivation.

The possible influence of a 48 h period of sleep deprivation on the serum concentrations of total and unbound 3,5,3',5'-thyroxine (T4) and 3,5,3'-triiodothyronine (T3), and of total 3,3',5'-triiodothyronine (reverse T3, rT3) was studied in 12 young male volunteers. In addition, plasma concentrations of TSH and the urinary excretion of noradrenaline and adrenaline were examined. Both total S-T4, S-T3 and S-rT3, and unbound S-T4 and S-T3 (unbound rT3 was not calculated) were significantly enhanced following sleep deprivation. P-TSH showed a numerical but statistically not significant increase, while the catecholamines remained unaltered. The results suggest that sleep deprivation provokes enhanced secretion of thyroid hormone(s), supposedly via increased secretion of TSH.

Adrenal Medulla↗

The effect of sleep deprivation on median nerve somatosensory evoked potentials.

The purpose of the study was to determine the effect of one night's sleep deprivation on the early and middle-latency median nerve (MN) somatosensory evoked potentials (SEPs). In 20 healthy volunteers, SEPs in response to electrical stimulation of the MN at the wrist were recorded for the 100-ms post-stimulus period, before and after one night of sleep deprivation. The P14 latency was significantly prolonged after sleep deprivation. We found significant increases in the amplitudes of the early parietal (N20-P24) and the frontal middle-latency (P45-N60) components following sleep deprivation. Our results indicate that somatosensory processing is altered after sleep deprivation.

Adult↗

Cardiopulmonary regulation after rapid-eye-movement sleep deprivation.

Arterial blood pressure, chest movement, electroencephalogram, and electromyogram were monitored in six normotensive Sprague-Dawley rats for 4 h/day 3 days before and 4 days after 114 h of rapid-eye-movement (REM) sleep deprivation. During recovery sleep immediately after REM sleep deprivation (RD), there was a significant increase in the amount of time spent in REM sleep. During this rebound in REM sleep, there was a significant rise (26%) in heart rate in wakefulness, non-REM sleep, and REM sleep during the first 4 h after RD. Systolic blood pressure was also significantly elevated (14%) but only during wakefulness before recovery sleep. Rats with the greatest waking systolic blood pressure after RD had the lowest REM sleep rebound in the 4 h immediately after RD (r = -0.885, P less than 0.05). The rise in heart rate, systolic blood pressure, and REM sleep time evident on day 1 immediately after RD was absent on recovery days 2-4. The respiratory rate tended to be higher throughout the recovery period in every state of consciousness; however, these values never reached the level of significance. In the initial recovery sleep period, regulation of heart rate was more disrupted by REM sleep deprivation than either arterial blood pressure or respiratory rate.

Animals↗

Hypersynchronous delta waves and somnambulism: brain topography and effect of sleep deprivation.

STUDY OBJECTIVES: Hypersynchronous delta activity (HSD) is usually described as several continuous high-voltage delta waves (> or = 150 microV) in the sleep electroencephalogram of somnambulistic patients. However, studies have yielded varied and contradictory results. The goal of the present study was to evaluate HSD over different electroencephalographic derivations during the non-rapid eye movement (NREM) sleep of somnambulistic patients and controls during normal sleep and following 38 hours of sleep deprivation, as well as prior to sleepwalking episodes. DESIGN: N/A. SETTING: Sleep disorders clinic. PATIENTS: Ten adult sleepwalkers and 10 sex- and age-matched control subjects were investigated polysomnographically during a baseline night and following 38 hours of sleep deprivation. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: During normal sleep, sleepwalkers had a significantly higher ratio of HSD over the time spent in stage 2, 3 and 4 on frontal and central derivations when compared with controls. Sleep deprivation resulted in a significant increase in the ratio of the time in HSD over the time in stage 4 on the frontal lead in both groups and on the central lead in controls. There was no evidence for a temporal accumulation of HSD prior to the episodes. CONCLUSIONS: HSD shows a clear frontocentral gradient across all subjects during both baseline and recovery sleep and has relatively low specificity for the diagnosis of NREM parasomnias. Increases in HSD after sleep deprivation may reflect an enhancement of the homeostatic process underlying sleep regulation.

Adult↗

Habitual sleep length and patterns of recovery sleep after 24 hour and 36 hour sleep deprivation.

Five long sleepers (LS) and 5 short sleepers (SS) were selected from 310 medical students. Nine regular sleepers (RS) were used as a control. The sleep was recorded during 3 reference nights, one recovery night after a 36 h sleep deprivation (R2), one morning sleep after a 24 h sleep deprivation (D1) and the night following D1(R1). According to previous data slow wave sleep (SWS) amounts were the same in the 3 groups while stage 2 and paradoxical sleep (PS) amounts increased with the sleep duration. The hourly distribution of intervening wakefulness and SWS were similar for all groups. When compared to RS or SS the hourly distribution in LS of PS was lower until the sixth hour. As a function of experimental conditions, sleep patterns of LS were the most affected. In R2 the sleep of LS more closely resembled that of RS or SS than in reference nights, while in R1 LS' sleep was the most disturbed. Morning sleep durations were very similar for all groups, but in LS intervening wakefulness was increased and PS was decreased when compared to RS and SS. Negative correlations (Spearman rank test) were found between the morning increase of body temperature after a sleep-deprived night and both TST and PS durations. In all recorded sleep periods, SWS amounts were positively correlated with prior wakefulness duration and the PS amount with TST.

Adult↗