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Using several measures of sexual activity, 24 male and 30 female Sprague-Dawley rats were subjected to a pretreatment test and 3 posttests (immediate and Recovery Days 4 and 7) following REM sleep deprivation in a water tank. With careful controls, sexual activity was not significantly affected by the sleep treatments. Data do not support motivational hypotheses.
Four cases are described in which observation of the response to forty hour sleep deprivation was used in resolving the differential diagnosis between depression and dementia. In each case it was possible to conduct psychometric assessment of cognitive ability during the period of improvement of the clinical state. The utility of this approach and some of the difficulties associated with its use are discussed.
The Djungarian hamster (Phodopus sungorus) is a markedly photoperiodic rodent which exhibits daily torpor under short photoperiod. Normative data were obtained on vigilance states, electroencephalogram (EEG) power spectra (0.25-25.0 Hz), and cortical temperature (TCRT) under a 16:8 h light-dark schedule, in 7 Djungarian hamsters for 2 baseline days, 4 h sleep deprivation (SD) and 20 h recovery. During the baseline days total sleep time amounted to 59% of recording time, 67% in the light period and 43% in the dark period. The 4 h SD induced a small increase in the amount of non-rapid eye movement (NREM) sleep and a marked increase in EEG slow-wave activity (SWA; mean power density 0.75-4.0 Hz) within NREM sleep in the first hours of recovery. TCRT was lower in the light period than in the dark period. It decreased at transitions from either waking or rapid eye movement (REM) sleep to NREM sleep, and increased at the transition from NREM sleep to waking or REM sleep. After SD, TCRT was lower in all vigilance states. In conclusion, the sleep-wake pattern, EEG spectrum, and time course of TCRT in the Djungarian hamster are similar to other nocturnal rodents. Also in the Djungarian hamster the time course of SWA seems to reflect a homeostatically regulated process as was formulated in the two-process model of sleep regulation.
1. The authors examined the effect of total sleep deprivation (SD) in combination with nortriptyline in 20 patients with major depressive disorder (MDD). Patients underwent a 36-hour SD procedure followed by nortriptyline started on the evening after SD, with ratings for two weeks. 2. Eleven (55%) patients were responders; they showed a rapid and sustained remission after SD, whereas non-responders demonstrated the delayed results expected with nortriptyline. 3. High initial depression scores and absence of depersonalization were associated with response to SD, while being female and middle insomnia were associated with response to the combined regimen. 4. The combination of SD with antidepressants proves to be an effective and safe treatment modality.
Data from recent laboratory studies indicate that nocturnal sleep periods reduced by as little as 1.3 to 1.5 hours for 1 night result in reduction of daytime alertness by as much as 32% as measured by the Multiple Sleep Latency Test (MSLT). Other data document that 1) 17%-57% of normal young adults have MSLT latencies of < or = 5.5 minutes, whereas < or = 50% have MSLT values of > or = 10 minutes and 2) 28%-29% of young adults reported normally sleeping < or = 6.5 hours on each weeknight. More extensive reduction of daily sleep amount is seen in nightshift workers. A minimum of 2%-4% of middle-aged adults have hypersomnolence associated with sleep apnea. Together, these data show that significant sleep loss exists in one-third or more of normal adults, that the effects are large and replicable and that similar effects can be produced in just 1 night in the laboratory. In light of the magnitude of this sleep debt, it is not surprising that fatigue is a factor in 57% of accidents leading to the death of a truck driver and in 10% of fatal car accidents and results in costs of up to 56 billion dollars per year. A recent sleep extension study suggests that the average underlying sleep tendency in young adults is about 8.5 hours per night. By comparison, the average reported sleep length of 7.2-7.4 hours is deficient, and common sleep lengths of < or = 6.5 hours can be disastrous. We must recognize the alertness function of sleep and the increasing consequences of sleepiness with the same vigor that we have come to recognize the societal impact of alcohol.
During 26 consecutive nights, electroencephalographic recordings and/or actigraphs were used to monitor the nighttime sleep of 10 asymptomatic healthy sleepers (mean age = 23.6 years). The schedule comprised: 7 nights of baseline sleep, 14 nights of extended sleep (up to 10 hr/night), and 5 nights of recovery sleep. During extended sleep, subjects slept significantly longer (approximately 1 hr), but sleep latency and interim wakefulness deteriorated. Extended sleep produced no improvements to self-rated mood or subjective sleepiness. Vigilance tests showed a small but significant reduction in reaction time following extended compared with both baseline and recovery nights. Ability to detect target tones did not change significantly. Multiple Sleep Latency Test scores during extended sleep showed small (about 1 min) reductions. These findings give little support to the view of chronic sleep deprivation in the average 7.5-hr sleeper.
The effects of 24 h sleep deprivation (SD) on central thyroid hormone metabolism were investigated in rat frontal cortex. SD induced a significant rise in the activity of iodothyronine type II 5'-deiodinase (5'D-II), which catalyzes the conversion of thyroxine (T4) to triiodothyronine (T3) in the rat central nervous system (CNS). Tissue concentrations of T4 remained unchanged, whereas levels of T3 increased to more than 150% of the corresponding levels measured in control rats. Serum concentrations of T4 and T3 were also significantly enhanced by SD--an effect that has previously been described in depressed patients having undergone the same procedure. These results suggest that SD can dramatically increase T3 concentrations (and possibly function) in rat CNS. Whether or not these findings are of relevance in regard to the well-known antidepressant effect of SD in psychiatric patients with major depressive disorders remains to be established.
We investigated the use and possible mechanisms mediating the increased energy expenditure (EE) previously described for rats subjected to total or paradoxical sleep deprivation. Bomb calorimetry of wastes showed that during deprivation the efficiency of energy utilization was not reduced. Estimates of CO2 production by the doubly labelled water method of indirect calorimetry correlated with EE estimated from the caloric value of food, weight change, and wastes and confirmed an increase in EE during deprivation. Core temperatures decreased during the later stages of deprivation, suggesting the hypothesis that excessive heat loss may have required increased EE to protect body temperature. The increased EE could not be explained by the metabolic cost of increase wakefulness, water exposure, or motor activity; an increase in resting EE was indicated. The contribution of the hypothalamic-pituitary-adrenal axis, thyroid gland, and sympathoadrenal system to the mediation of the EE increases was evaluated by measuring the plasma levels of their hormones. Results appear to rule out the first as a mediator. Evidence for the other two was equivocal.
BACKGROUND: To elucidate significance of physical signs seen in excessive television-game (TVG) players complaining of unexplained persistent symptoms, a cross-sectional cohort study was designed. METHODS: A total of 1143 school children, aged between 6 and 11-years-old, and their parents were included in the study. Questionnaires were sent to guardians asking the number of hours that their children watched TV, TVG, and slept. All children were examined to check for three physical signs, black rings in the skin under the eye (BR), muscle stiffness in the shoulder (MS), and displacement of the scapula associated with muscle stiffness in the shoulder (DS/MS) by inspection and palpitation. RESULTS: The three signs, BR, MS and DS/MS, were present in 165 (14.4%), 229 (20.0%) and 72 (6.2%) children, respectively. Boys had greater frequencies of two signs than girls (BR, 19.6% vs 8.9%, P<0.01; MS, 26.1% vs 13.6%, P<0.01), respectively. Boys spent more time on TVG playing than girls (1.1+/-0.7 h/day vs 0.4+/-0.6 h/day, P<0.0001), respectively. Excessive TVG players, who spent > or = 1 h/day for TVG had greater frequencies of two signs, BR and MS, than those of non-TVG-players (18.9% vs 13.0%, P<0.05; 25.6% vs 14.4%, P<0.01), respectively. The TVG playing time correlated with two signs, BR (P=0.0143) and MS (P=0.0048). Furthermore, sleep deprivation related to three signs, BR (P=0.0078), MS (P<0.0001) and DS/MS (P=0.0290). CONCLUSIONS: Excessive TVG playing links to the occurrence of BR and MS. Other factors, which cause sleep deprivation, may underlie in the occurrence of the three signs. The amount of time spent on TVG playing should be regulated to < 1.0 h/day.
The effect of 5-day sleep deprivation (SD) on cholesterol metabolism, together with triglyceridaemia, was studied in seven healthy male volunteers. A 3-day control period was followed by 5 days (120 h) complete SD and 4 days recovery. Blood was collected at 9 a.m. and at 9 p.m. Vastus lateralis muscle biopsy was performed during the control period, on the 5th day of SD, and on day 3 of recovery. The value of muscle cholesterol was related to the non-collagen protein content. The plasma triglycerides (TG) varied in a circadian biorhythm, the amplitude of which declined gradually during SD. The morning triglyceridaemia was significantly decreased on days 3-5 of SD (35%-79% of initial values). On days 4 and 5 of SD, plasma cholesterol fell significantly to 78% and 88% of control values, respectively. The ratio of its esterified to unesterified fractions remained unchanged throughout SD. Basal activity of lecithin cholesterol acyltransferase (LCAT) showed no diurnal biorhythm; on the last 2 days of SD, LCAT activity fell significantly to 71%-80%. In contrast, the decrease in fractional esterification rate (FER) was insignificant. In the vastus lateralis muscle, total cholesterol (TC) was decreased by 40% at the end of SD, the reduction being greater for cholesterol esters (CE) (by 63%) than for free cholesterol (FC) (by 36%). The relative proportion of CE significantly decreased from an initial 14.7% to 9.2% on the last day of SD. During recovery after SD, plasma cholesterol and TG slowly returned to normal. LCAT activity and FER recovered quickly, within 48 h.(ABSTRACT TRUNCATED AT 250 WORDS)
Norepinephrine, acetylcholine and GABA levels alter during rapid eye movement (REM) sleep and its deprivation. Increased synthesis of those neurotransmitters is necessary for their sustained release. Hence, in this study, the concentrations of tyrosine hydroxylase (TH), choline acetyl transferase (ChAT) and glutamic acid decarboxylase (GAD), the enzymes responsible for their synthesis, were immunohistochemically estimated within the neurons in locus coeruleus, laterodorsal tegmentum and pedunculopontine tegmentum and medial preoptic area in REM sleep deprived and control rats. It was observed that as compared to controls, deprivation increased TH and GAD significantly in the locus coeruleus only, while in other areas, they remained unchanged. The findings help explaining the mechanism of increase in neurotransmitter levels in the brain after REM sleep deprivation and their significance has been discussed.
Rats treated with phosphoramidon (an enkephalinase-inhibitor 250 micrograms, i.c.v.), morphine (20 micrograms i.c.v.) or subjected to cold-water-swim (CWS, animals forced to swim in water at 5 degrees C for 5 min) showed consistent analgesia. The antinociceptive effect of phosphoramidon, morphine and CWS was antagonised by REM sleep deprivation (REMSD). It is suggested that normal duration of REM sleep is of importance for the anti-nociceptive activity of endogenous and exogenous opiates.
According to a recent experimental study published in the Lancet, sleep debt, frequently imposed by the life habits of industrialized countries, results in profound metabolic (impaired glucose tolerance) and endocrine (increased sympathetic activity and evening cortisol levels) alterations, which mimic those of normal ageing and may have pathophysiological consequences in the long term. Another study recently published in the International Journal of Obesity demonstrated a significant positive relationship between the duration of shift-work and body mass index or waist to hip ratio, a marker of visceral adiposity. One may thus hypothesize that chronic sleep deprivation could predispose to the metabolic syndrome and increase the cardiovascular risk.
Variations occurring in cortical nitric oxide (NO) release were analysed with a voltametric method in rats (i) placed in control conditions, (ii) while being paradoxical sleep deprived (PSD), or (iii) recovering from a PSD. Activities of neuronal (nNOS) and inducible (iNOS) NO-synthases as well as nNOS expression were also determined in several brain regions. In baseline conditions, circadian variations in nNOS expression and activity were maximal during the dark period and minimal during the light one for all the structures analysed (frontal cortex, pons and medulla). In the same way, cortical NO release occurred through a circadian rhythm exhibiting maxima and minima during dark and light periods, respectively. In the same experimental conditions, iNOS activity did not exhibit time-dependent changes. The correlative changes observed in baseline conditions between NO release, nNOS expression and activity within the frontal cortex were disrupted during PSD and subsequent recovery. Still again, iNOS activity remained unchanged. Results obtained point out that the tight coupling existing in control conditions between nNOS expression-activity and NO release is disrupted by a PSD and remains affected during the subsequent 24 h recovery. Their significance is discussed.
Vigilance states, electroencephalogram (EEG) power spectra (0.25-25.0 Hz), and cortical temperature (TCRT) of 10 rats were obtained during a baseline day, a 24-h sleep deprivation (SD) period, and 2 days of recovery (recoveries 1 and 2). EEG power density in waking gradually increased in most frequencies during the SD period. Non-rapid-eye-movement (NREM) sleep was enhanced on both recovery days, and rapid-eye-movement sleep was enhanced only on recovery 1. In the initial 4 h of recovery 1, EEG slow-wave activity (SWA; mean power density 0.75-4.0 Hz) in NREM sleep was elevated relative to baseline, and the number of brief awakenings (nBA) was reduced. In the dark period of recovery 1 and the light period of recovery 2, SWA was below baseline, and nBA was increased. During the entire recovery period, SWA and nBA, both expressed as deviation from baseline values, were negatively correlated. During the SD period, TCRT was above baseline, and in the initial 16 h of recovery 1 it was below baseline. Whereas TCRT was negatively correlated with NREM sleep, no significant correlation was found between TCRT and SWA within NREM sleep. It is concluded that SD causes a short-lasting intensification of sleep, as indicated by the enhanced SWA and the reduced nBA, and a long-lasting increase in sleep duration. The different time courses of SWA and TCRT suggest that variations in NREM sleep intensity are not directly related to changes in TCRT.
Slow-wave sleep (SWS) has been theorized to be an intense form of nonREM sleep, but selective deprivation of SWS or Stage 4 sleep has not been shown to cause greater decrements in alertness or performance, compared to deprivation or disruption of the other stages of sleep. The present experiment examined the effects of marked SWS deprivation (SD) for two nights, a control sleep disruption (CD) condition in which minutes of SWS were preserved, and a no sleep disruption (ND) condition. Daytime sleepiness was assessed with the multiple sleep latency test (MSLT) and performance was evaluated with the simulated assembly line task (SALT), neither of which was used in previous studies of SWS or Stage 4 sleep deprivation. In agreement with prior studies, two nights of SD did not cause greater daytime sleepiness than did CD, although sleepiness in both conditions was increased compared to the ND condition. In addition, neither SD nor CD caused declines in performance or mood. However, post hoc analysis suggests an interaction between SWS and sleep duration, such that sufficient SWS may tend to prevent adverse effects of mild sleep loss on waking function.
One night of total or partial sleep deprivation (SD) produces temporary remissions in 40-60% of patients with major depression. Two unmedicated patients with major depression and a matched control received quantitative perfusion MR images at baseline and after one night of partial SD (PSD). A reduction > or =30% in the 17-item Hamilton Depression Rating Scale (omitting sleep and weight loss items) defined antidepressant response. Theory, techniques, strengths and weaknesses of quantitative perfusion MRI are described in detail. At baseline, the responder exhibited elevated perfusion covering ventral anterior cingulate/medial frontal cortex; the control's maximal perfusion area was markedly smaller. The nonresponder's perfusion was lowest of all, particularly ventrally. PSD decreased perfusion over much of the responder's hyperperfused area but did not change the nonresponder's scan. These preliminary findings are consistent with previous SD studies using PET and SPECT.
Selective deprivation of paradoxical (or rapid eye movements) sleep (REMS) in protein malnourished young male rats, results in circadian and homeostatic alterations. By means of electrocorticographic recordings, we have examined the sleep-wake cycle as a functional maturity index, and its circadian and homeostatic mechanisms in prenatal (PM) and chronically (CM) protein malnourished young male rats. The effects of rapid eye movements sleep-deprivation (REMS-D), by the platform technique in a "conflict experiment" (i.e. recovery from REMS-D begun during the circadian phase of activity), revealed that in PM animals, wake (WAK) was increased significantly during recovery days 1 and 2 (RD1, RD2); and slow wave sleep (SWS) was reduced significantly during these days. Prenatal protein-malnutrition altered the phase of WAK and REMS rhythms, and the amplitude of SWS rhythm was decreased. The REMS compensatory increase after REMS-D (REMS rebound) was confined to the first 4-h block of the activity phase in all experimental groups and 24 h later another REMS rebound was displayed in PM animals. The paradoxical sleep-rebound in CM animals was significantly higher than control and PM rats and it was only shown at the first 4-h block after REMS-D. Before and after REMS-D the circadian distribution of both sleep states, and the electrocortical frequency bands showed different circadian phases at the same day-time in control, PM and CM rats. The aforementioned indicates that protein malnutrition exerts important effects on the circadian and homeostatic mechanisms driving sleep. Therefore, the temporal structure of the malnourished rats may not allow proper synchronization of some sleep parameters, particularly REMS, to the environmental time cues.