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PubMed2003

Is the antidepressive effect of sleep deprivation stabilized by a three day phase advance of the sleep period? A pilot study.

Sleep deprivation (SD) induces a rapid amelioration of mood in about 60 % of depressed patients. After the next night of sleep, however, most patients experience a relapse. Previous studies demonstrated that a six day sleep-phase advance protocol prevents relapses in about 60 % of patients who responded positively to SD. We investigated whether also a three day phase advance of the sleep period might be able to maintain the antidepressant effects of SD. Twenty-eight medicated depressed inpatients, who had a significant improvement after a SD in one night were recruited for this study. The phase advance protocol began on the first day after SD with a bed time from 5:00 p. m. to 12:00 p. m. on the first, from 7:00 p. m. to 2:00 a. m. on the second and 9:00 p. m. to 4:00 a. m. on the third day after SD. Three patients dropped out because of protocol violations. Only ten of the remaining 25 SD responders had a relapse during the three days of phase advance treatment or during the two days after it. Two of the relapsers improved again until day 6, i. e. 68 % showed an improvement of at least 30 % six days after the beginning of the treatment. This study indicates that even a three day phase advance protocol may help to prevent relapses after successful SD.

Circadian Rhythm↗

PubMed1995

Sleep deprivation and c-fos expression in the rat brain.

This study examined the effects of sleep deprivation on the expression of the immediate early gene c-fos in the brain with both in situ hybridization and immunocytochemistry. Rats were manually sleep-derived for 3 h, 6 h, 12 h, and 24 h starting at light onset (08.00 hours), and for 12 h starting at dark onset (20.00 hours). c-Fos expression was found to be higher in sleep-deprived rats with respect to control animals in several brain areas. The increase was evident both in terms of c-fos mRNA and Fos protein, although with a different time course. Among the areas that showed a consistent induction of c-fos were many cortical regions, the medial preoptic area and the posterior hypothalamic area, some thalamic nuclei, and several nuclei of the dorsal pontine tegmentum. The pattern of c-fos expression after sleep deprivation was very similar to that observed after comparable periods of spontaneous wakefulness (Pompeiano et al. 1994). In general, the increase in c-fos expression was not simply proportional to the amount of previous wakefulness. In many areas, the highest levels of c-fos were seen after 3 h of sleep deprivation. These observations are discussed with respect to the homeostatic regulation of sleep and to the functional consequences of wakefulness in specific brain areas.

Journal Article↗

PubMed2000

Effects of sleep and sleep deprivation on interleukin-6, growth hormone, cortisol, and melatonin levels in humans.

The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on circulating concentrations of interleukin-6 (IL-6) in relation to the secretory profiles of GH, cortisol, and melatonin. In 31 healthy male volunteers, blood samples were obtained every 30 min during 2 nights: uninterrupted, baseline sleep and partial sleep deprivation-early night (awake until 0300 h). Sleep was measured by electroencephalogram polysomnography. Sleep onset was associated with an increase in serum levels of IL-6 (P < 0.05) during baseline sleep. During PSD-E, the nocturnal increase in IL-6 was delayed until sleep at 0300 h. Sleep stage analyses indicated that the nocturnal increase in IL-6 occurred in association with stage 1-2 sleep and rapid eye movement sleep, but levels during slow wave sleep were not different from those while awake. The profile of GH across the 2 nights was similar to that of IL-6, whereas the circadian-driven hormones cortisol and melatonin showed no concordance with sleep. Loss of sleep may serve to decrease nocturnal IL-6 levels, with effects on the integrity of immune system functioning. Alternatively, given the association between sleep stages and IL-6 levels, depressed or aged populations who show increased amounts of REM sleep and a relative loss of slow wave sleep may have elevated nocturnal concentrations of IL-6 with implications for inflammatory disease risk.

Adult↗

PubMed1994

The effect of partial sleep deprivation on weight-lifting performance.

This study examined the effects of partial sleep deprivation on submaximal and maximal weight-lifting tasks and on subjective states pre- and post-activity. Eight male subjects (aged 18-24 years) were restricted to a nightly ration of 3 h sleep for 3 successive nights after baseline measures on the first day. A 4 day period where normal sleep was permitted fulfilled a control condition, the normal and sleep-deprived conditions being counterbalanced and separated by 10 days. The weight-lifting tasks consisted of biceps curl, bench press, leg press, and dead lift. For each exercise a submaximal load, corresponding to a fixed value on a category ratio scale of exertion, was determined for 20 repetitions; the maximal lift for that exercise was then obtained. A profile of mood states and subjective sleepiness were determined at each test occasion, tests being conducted in the evening of each day. There was no significant effect of sleep loss on performance of maximal biceps curl (p < 0.05) but a significant effect was noted on maximal bench press, leg press, and dead lift (p < 0.001). Trend analysis indicated decreased performance in submaximal lifts for all the 4 tasks: the deterioration was significant after the second night of sleep loss (p < 0.01). Performing the lifts had little influence on sleepiness ratings which increased linearly with successive days of sleep loss. Mood states of confusion, vigour, and fatigue were affected significantly by the sleep deprivation regimen (p < 0.001), but there was no significant effect of sleep loss or anger, tension, and depression (p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Sleep deprivation decreases mu and delta opioid receptor binding 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 rat displayed particular behavior characterized by wakefulness, a high degree of motor and exploratory activity, increased alertness and reactivity to environmental stimuli. Our previous results indicated that this behavior was antagonized by the administration of the opioid receptor antagonist naloxone and increased by opioid agonists. In this paper we show that concomitantly with this behavior, a decreased Bmax of mu and delta opioid receptors is present in the limbic system of these animals. These data suggest an active role of limbic mu and delta receptors in the generation of arousal and insomnia related to sleep deprivation induced stress.

Animals↗

PubMed1993

[Regularly employed inpatient group sleep deprivation therapy assessed by nursing staff and patients].

The antidepressive efficacy of sleep-deprivation therapy has been well known for more than 20 years and has repeatedly been demonstrated in clinical trials. In spite of its proven merits, the method is rarely used as an established element of antidepressant therapy in Swiss psychiatric hospitals. This study includes 56 depressive patients having had a total of 341 partial sleep-deprivation treatments at the psychiatric hospital of Königsfelden (CH). The results suggest that sleep-deprivation therapy could be incorporated on an large scale in the clinical treatment of depression.

Adult↗

PubMed2004

Differential effects of rapid eye movement sleep deprivation and immobilization stress on blood lymphocyte subsets in rats.

OBJECTIVES: There is growing evidence of the relationship between sleep and the immune response. Studies aimed at elucidating the function of rapid eye movement (REM) sleep have found it difficult to separate the effects due to REM sleep deprivation and the effects due to the stress produced by the deprivation procedure. It has been claimed that immobilization is the main stressor that the animals have to face during the deprivation process. In this study, we analyzed the effects of short-term (24 h) and long-term (240 h) REM sleep deprivation on the distribution of lymphocyte subsets in the peripheral blood of rats. In addition, these effects were compared with those obtained after both short- and long-term stress by immobilization. METHODS: Lymphocyte population bearing surface markers such as CD5 (T cells), CD45RA (B cells), CD4 (T helper/inducer cells), CD8 (T suppressor/cytotoxic cells) and CD161 (NK cells) were analyzed using monoclonal antibodies. Lymphocyte subsets were assessed by flow cytometry. RESULTS: Both short- and long-term REM sleep deprivation decreased the percentage of T lymphocytes and induced a significant increase in NK cells. Short-term immobilization induced only a significant increase in the percentage of B lymphocytes and a decrease in the percentage of T lymphocytes, while long-term immobilization did not elicit any change. CONCLUSION: The present results support the notion that REM sleep deprivation and immobilization stress each exert particular effects on the immune system. These data suggest that the characteristics of the immune response will depend on the nature of the behavioral manipulation.

Animals↗

PubMed1998

Does the sedation resulting from sleep deprivation and lorazepam cause similar cognitive deficits?

It is notoriously difficult to assess the contribution of the sedative effects of benzodiazepines to the cognitive impairments that they produce. The purpose of the present experiment was to determine whether a similar pattern of cognitive impairment would be seen in conditions when subjects felt equally sleepy as the result of sleep deprivation. The effects of a sedative dose of lorazepam (2.5 mg) in healthy volunteers was therefore compared with the effects of acute sleep deprivation (a night on-call) in a group of junior doctors and the effects of chronically disturbed sleep due to snoring. Lorazepam, acute sleep deprivation, and chronic sleep disturbance all significantly increased subjective sedation. In addition, lorazepam significantly impaired performance in two tests of psychomotor speed and caused significant anterograde amnesia. Semantic and short-term memory were not impaired by lorazepam, nor was there any impairment in executive function. The only deficit found following acute sleep deprivation was in a test of semantic memory, generating examples from a difficult category. The only significant deficit in the group suffering from chronically disturbed sleep, compared with age-matched controls, was in executive function, and there was a nearly significant impairment in sustained attention. These results suggest that, despite the common factor of increased subjective sedation, the profile of cognitive impairment in the two sleep deprivation groups are neither similar to each other nor to that seen following an acute dose of lorazepam.

Adult↗

PubMed2005

Acute sleep deprivation in the thoracic surgical resident does not affect operative outcomes.

BACKGROUND: There is an increasing trend toward work hour restrictions for doctors world wide. These reforms have been inspired, in part, by the assertion by some that the fatigued physician is more prone to making errors. Interestingly, there is very little in the way of objective data with regard to the effects of sleep deprivation on patient outcomes. We have recently studied this in attending surgeons. The present study focused on thoracic surgical residents. Our hypothesis was that acute sleep deprivation would not lead to an increase in operative times or complications. METHODS: A retrospective review of all cases performed by thoracic surgical residents at the University of Virginia from January 1994 to March of 2004 was done. Complication rates of cases performed by "sleep deprived" (SD) residents were compared with cases done when the residents were "not sleep deprived" (NSD). A resident was deemed sleep deprived if he or she performed a case the previous evening that started between 10 pm and 5 am or ended between the hours of 11 pm and 7:30 am. RESULTS: A total of 7,323 cases were recorded in the STS database over the 10-year period examined. Two hundred and twenty-nine of these cases (3%) were performed by SD residents. Mortality rates for coronary artery bypass operations showed no significant differences (2.1% [SD = 3 of 141 patients] vs 3.1% (NSD = 143 of 4452 patients), p = 0.63). A comparison of operative, neurologic, renal, infectious, and pulmonary complications as well as cardiopulmonary bypass times, cross-clamp times, the use of blood products, and length of stay also demonstrated no significant differences between groups. CONCLUSIONS: Acute sleep deprivation in thoracic surgical residents does not affect operative efficiency, morbidity, or mortality in cardiac surgical operations.

Cardiac Surgical Procedures↗

PubMed1988

Reversal of the increase in apomorphine-induced stereotypy and aggression in REM sleep deprived rats by dopamine agonist pretreatments.

REM sleep deprivation (REMSD) induces augmented responses to dopaminergic agonists. Prolonged administration of neuroleptics induces a similar state, probably by the production of supersensitivity of dopaminergic receptors. Such a supersensitive state could be induced by REMSD as a result of impairment of dopamine neurotransmission. In order to test this hypothesis, bromocriptine, nomifensine, amphetamine, L-dopa, imipramine and electroconvulsive shock (ECS) were administered to rats during REMSD, and aggressive and stereotyped behaviors were measured. Amphetamine and L-dopa pretreatment attenuated the increases in apomorphine-induced stereotypy and aggression in REMSD rats, but ECS selectively reduced apomorphine-induced aggression. The other drugs tested were ineffective on both behavioral tests. Such a selective action may reflect different effects of ECS on different dopaminergic systems such as those involved with stereotypy and aggression. The results suggest that REMSD induces an increase in dopaminergic sensitivity which may be reversed by pretreatment with some dopaminergic agonists.

Aggression↗

PubMed1994

Autoradiographic analysis of D1 and D2 dopaminergic receptors in rat brain after paradoxical sleep deprivation.

Previous work had shown that paradoxical sleep deprivation (PSD) results in potentiation of several apomorphine-induced behaviors, leading to the suggestion that PSD induces an upregulation of brain dopamine receptors. In this study, quantitative receptor autoradiography was used to verify whether PSD does, in fact, induce alterations in D1 or D2 receptor binding, and to investigate the regional brain specificity of such effects. After 96 h of PSD, [3H]SCH-23390 binding to D1 receptors was examined in 30 different brain areas of 10 experimental and 10 cage control rats. [3H]Spiperone was used to label D2 sites in adjacent tissue sections. Results revealed a 39% increase in [3H]SCH-23390 binding in the entorhinal cortex of PSD rats (p < 0.05), but no other changes in any of the remaining 29 brain areas examined. In contrast, [3H]spiperone binding was significantly elevated in the n. accumbens (+45%) and in all subregions of the caudate-putamen (range: +13% to +23%). These results, thus, provide evidence that PSD increases D2 but not D1 receptor binding in brain. The present results also suggest that upregulated D2 receptors can account for the previously reported changes in apomorphine-induced behaviors after PSD.

Animals↗

PubMed1996

Changes in monoamines and their metabolite concentrations in REM sleep-deprived rat forebrain nuclei.

Rapid eye movement sleep deprivation (REMSD) is a potent stressor in rats. Behavioral abnormalities such as passive and active avoidance, locomotor activity, problem solving, sensory information processing, and the development of adaptive copping strategy in response to repeated stress are among the earliest obvious symptoms of REMSD, the mechanism for which remain largely unknown. The aim of this study was to determine whether 96 h of REMSD causes changes in monoamine neurotransmitters concentrations in rat forebrain regions (frontal cortex, FC; parietal cortex, PC, and striatum) that are involved in mediating higher brain functions such as attentional mechanisms, sensory information processing, and locomotor activity, which are severely affected in REMSD conditions. Rats were subjected to 96 h of REMSD using inverted flower pot water tank technique. To account for the stress associated with water tanks, a tank control group (TC) was included where the animals could reside comfortably on a large pedestal in the water tank. Regional brain concentrations of norepinephrine (NE), dopamine (DA), dihydroxyphenyacetic acid (DOPAC), L-3,4-dihydroxyphenylalanine (L-DOPA), homovanillic acid (HVA), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (HIAA) were determined by electrochemical detection using high-performance liquid chromatography. The concentrations of serotonin and its metabolite, HIAA, was reduced in the frontal and parietal cortexes of REMSD rats compared with TC or cage control (CC) group. NE, DA, DOPAC, and HVA concentrations in FC and PC of REMSD animals were remained unchanged compared with TC or CC rats. A significant increase in the concentrations of DA metabolites was observed in the striatum of REMSD rats when compared with CC and TC rats. There was a 29 and 31% increase in the concentration of striatal DA in REMSD group compared to the TC and CC groups, respectively; however, these percentages were not statistically different. Striatal NE, 5-HT, and HIAA concentrations were not significantly different among the three groups. These results suggest that 96 h of REMSD alters dopaminergic and serotonergic systems in different locations in rat brain. The effect of REMSD on the serotonergic systems are localized in the cerebral cortex, whereas dopaminergic metabolism is increased in the striatum.

Animals↗

PubMed2005

Effects of sleep deprivation on Color-Word, Emotional, and Specific Stroop interference and on self-reported anxiety.

The aim of this study was principally to assess the impact of sleep deprivation on interference performance in short Stroop tasks (Color-Word, Emotional, and Specific) and on subjective anxiety. Subjective sleepiness and performance on a psychomotor sustained attention task were also investigated to validate our protocol of sleep deprivation. Twelve healthy young subjects were tested at four-hourly intervals through a 36-h period of wakefulness under a constant routine protocol. Analyses of variance for repeated measurements revealed that self-assessment of sleepiness on a visual analogue scale as well as mean reaction time performance on the sustained attention task, both for the first minute and for 10 min of testing, were worsened by sleep deprivation. Analyses revealed an increase in self-reported anxiety scores on the STAI questionnaire but did not reveal any significant effect after sleep deprivation either on indexes of interference or on accuracy in Stroop tasks. However, analyses showed sensitivity to circadian effect on verbal reaction times in the threat-related (Emotional) and sleep-related (Specific) Stroop tasks. We concluded that 36 h of prolonged wakefulness affect self-reported anxiety and Emotional Stroop task resulting in a cognitive slowing. Moreover, total sleep deprivation does not affect interference control in any of the three short Stroop tasks.

Adolescent↗

PubMed1990

Total and partial sleep deprivation in clomipramine-treated endogenous depressives.

Improvement in depression after total sleep deprivation (TSD) is, as a rule, followed by relapse after subsequent ad libitum sleep. This study is addressed to the question of how nocturnal partial sleep following TSD affects this relapse. Thirty endogenously depressed patients participated in the study. During the night after TSD, subjects were allowed sleep during one of three periods, i.e., unlimited sleep (11:00 p.m.-8:00 a.m.), early partial sleep (11:00 p.m.-3:00 a.m.), or late partial sleep (4:00 a.m.-8:00 a.m.). The hypothesis that partial sleep deprivation on the night following TSD prevents relapse has to be rejected. Relapse was inversely related to a drop in minimum rectal temperature during the night with unlimited or partial sleep, compared with minimum rectal temperature on the previous night.

Body Temperature Regulation↗

PubMed2005

Is the sleep-deprivation EEG a burden for both child and parent?

BACKGROUND AND PURPOSE: Inducing sleep deprivation is supposed to increase interictal epileptic discharges on EEGs from children suspected of having epilepsy. Although it is supposed that depriving a child from sleep is a burden for both child and parent, this assumption has not been investigated in any study so far. METHODS: To analyze the perception of the sleep deprivation procedure, we developed two questionnaires, one for the parent and one for the child over ten years of age at the time of the SDEEG. These questionnaires were sent to parents of all 179 patients and 47 children (older than ten) from which a SDEEG was obtained because of suspected epilepsy. A total of 103 questionnaires were returned by the parents and 18 by the children. The extent to which the SDEEG turned out to be inconvenient was assessed with regard to issues that covered the psychological and physical impact of the SDEEG. RESULTS: Our results showed that the whole procedure of the SDEEG proved to be a burden for 18.6% of the parents and 23.5% of the children. 49.6% of the parents reported complaints including their child- like fatigue, illness and in 2 cases even an increase in seizure frequency. Overall, 47.1% of the children described having symptoms the next day. These consisted mainly of fatigue. CONCLUSION: Our survey shows that the SDEEG places a notable burden on both parent and child. This should be taken into consideration before requesting an SDEEG.

Attitude to Health↗

PubMed1996

Effects of chronic treatment with zimelidine and REM sleep deprivation on the regulation of raphe neuronal activity in a rat model of depression.

Electrophysiological investigations on the mechanism of action of antidepressants have shown that both deprivation of rapid eye movement (REM) sleep and chronic treatment with antidepressants render serotoninergic (5-HT) neurons less sensitive to the inhibitory effect of 5-HT reuptake blockers in the rat. It was of interest to test whether the same mechanisms could be evidenced in a possible experimental model of depression. The latter consisted of rats which had been treated neonatally with clomipramine and exhibited at adult age behavioural and sleep alterations which resemble the human disorder. Recording the electrophysiological activity of 5-HT neurons in the nucleus raphe dorsalis (NRD) revealed that both chronic treatment with zimelidine and REM sleep deprivation induced a hyporeactivity of these neurons to the inhibitory effect of citalopram in "normal" rats. However, in rats which had been treated neonatally with clomipramine, 5-HT neurons were hyporeactive to the effect of this 5-HT reuptake blocker already under baseline conditions, and no further modification could be induced by chronic zimelidine administration or REM sleep deprivation. It can be hypothesized that adaptive phenomena at the serotoninergic NRD level are not a relevant element to explain the mechanism of action of anti-depressants in the present model of depression, while they have been considered as a crucial event in "normal" rats.

Animals↗

PubMed1993

Sleep deprivation is a less potent agent than clomipramine in increasing firing rate in lateral septal neurons in the rat.

Acute injection of clomipramine or a 24-hour period of sleep deprivation produces an increased firing rate in lateral septal neurons of the rat. However, it is unknown whether changes in firing rate in lateral septal neurons also appear after repetitive treatments. This study explored and compared the effects of long-term clomipramine with those of sleep deprivation from 1 to 4 days in the firing rate of lateral septal neurons. The firing rate increased after both treatments; however, maximal effects occurred on different days. Clomipramine (1.25 mg/kg, i.p., twice a day) produced a stable, increased firing rate after 20 days of treatment. Twenty-four hours of total sleep deprivation produced changes in firing rate comparable to 10 days of clomipramine treatment. Changes in firing rate did not appear when animals were exposed to 12 h of sleep deprivation alternated with 12 h in housing cages. Therefore, it is concluded that 24 h of total sleep deprivation is a less effective treatment than clomipramine for producing changes in firing rate in lateral septal neurons.

Animals↗

PubMed2003

Cardiorespiratory responses to submaximal incremental exercise are not affected by one night's sleep deprivation during the follicular and luteal phases of the menstrual cycle.

The purpose of the study was to investigate the effects of one night's sleep deprivation on the cardiorespiratory responses to exercise during the follicular and luteal phases of the menstrual cycle. We have studied nine, healthy females aged 24-35 years with regular menstrual cycles. Each subject performed spirometric tests at rest and then an incremental exercise testing during 11-13 days of follicular phase and 22-24 days of luteal phase following one normal night's sleep or one night's sleep loss. Compared with resting values exercise produced significant increases in cardiorespiratory variables including oxygen uptake (VO2), carbon dioxide production (VCO2), tidal volume (VT), respiratory rate (RR), minute ventilation (VE), systolic blood pressure, heart rate (HR) and respiratory quotient (R). However, it did not alter significantly diastolic blood pressure, end-tidal PO2 (PETO2), end-tidal PCO2 (PETCO2) and arterial oxygen saturation (SaO2). Spirometric variables which include forced vital capacity (FVC), forced expiratory volume in one s (FEV1), FEV1/FVC%, forced expiratory volume in three s (FEV3), forced expired flow from 25-75% of FVC (FEF 25-75%), forced expired flow at 25% of FVC (FEF 25%), forced expired flow at 50% of FVC (FEF 50%), forced expired flow at 75% of FVC (FEF 75%), forced expired flow from 75-85% of FVC (FEF 75-85%), peak expiratory flow (PEF), expiratory reserve volume (ERV), inspiratory capacity (IC) and maximal voluntary ventilation (MVV) and cardiorespiratory variables were not different between the cycle phases after one normal night's sleep or one night's sleep deprivation. Neither menstrual cycle phase nor sleep deprivation affected spirometric and cardiorespiratory parameters. We suggest that one night's sleep deprivation does not produce alterations in spirometric parameters and cardiorespiratory responses to submaximal incremental exercise during the follicular and luteal phases.

Adult↗