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PubMed1981

Sensitivity of the stanford sleepiness scale to the effects of cumulative partial sleep deprivation and recovery oversleeping.

The sensitivity of the Stanford Sleepiness Scale (SSS) to short-term cumulative partial sleep deprivation (PSD) and subsequent recovery oversleeping was examined. A repeated-measures design included 7 paid healthy undergraduate volunteers, who were normal sleepers (mean sleep time 7.6 hr), and consisted of the following schedule: (a) pre-baseline; (b)sleep reduction of 40% of 1 night (mean, 4.6 hr) for 5 nights; (c) recovery oversleeping for night 1 (mean, 10.6 Hr) and night 2 (mean, 9.1 hr); (d) post-baseline. Daytime performance testing utilized a 1 hr auditory vigilance task and four short-duration (10 min) tests, two of which have been shown sensitive to total and partial sleep loss effects. Subjects completed SSS forms every min while awake and 1-9 scales of mood and energy upon awakening. Subjective measures were analyzed across conditions for mean all-day and task-related SSS values and mood and energy ratings. A correlational analysis investigated individual correspondences between ratings and performance. Results indicate that SSS is sensitive to deficits in alertness following PSD. However, it generally does not predict individual performance efficiency and therefore cannot act as a substitute for performance measures in studies involving chronic sleep loss.

Adolescent↗

PubMed1986

Sustained antidepressive effect of repeated partial sleep deprivation.

In a naturalistic clinical trial we administered three partial sleep deprivations (PSD) within one week to a diagnostically heterogeneous sample of 30 depressed patients and applied serially three dexamethasone suppression tests (DST). We observed that this PSD treatment induced sustained clinical improvement independently from nosological attribution. Abnormal DST results prior to PSD treatment failed to predict clinical course, and normalized after beneficial response.

Adult↗

PubMedDate not supplied

[Physiological status of the body and prediction of the effectiveness of drug therapy of depression. II. Physiological indicators of the reaction to sleep deprivation].

A study of pulse and breath rate, postural muscle tone and mood has been conducted in 30 patients with endogenous depression before and after night's sleep deprivation. Most patients who did respond to antidepressant treatment rated their mood following the sleepless night higher than on the preceding day. After the sleepless night their rate of breathing increased. In a subgroup of poor responders to the applied treatment breathing rhythm after sleepless night did not change and only a few patients found their mood changed following sleep deprivation. Decreased postural muscles tone was noticed in both subgroups of patients. Effects observed in the study may be related to a decreased anxiety level observed in the patients following treatment regimen.

Adult↗

PubMed1986

REM sleep deprivation antagonizes morphine-induced akinesia and catalepsy.

An examination was made of the effect of REM sleep deprivation (REMSD) on some forms of altered motor activity, such as akinesia and catalepsy, induced by intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) administration of morphine in adult, male Wistar rats. Administration of morphine (25 mg/kg i.p.) induced an akinetic-cataleptic syndrome and decreased spontaneous vertical motor activity (SVMA) in animals allowed undisturbed sleep. REMSD decreased the morphine-induced akinesia and catalepsy that are known to be mediated by an inhibitory mu-opiate system. The locomotor depressant action of morphine was converted to excitation (manifested as increased SVMA and hopping behavior) by REMSD. Similarly, decreased motor activity following i.c.v. administration of morphine (25 micrograms) was replaced by excitation in the form of jumping behavior after REMSD. Naltrexone (1 mg/kg i.p.) blocked the akinetic and cataleptic effects, but not the excitatory effects, of morphine. It is suggested that REMSD is associated with a functional insufficiency of an inhibitory mu-opiate system, thus unmasking the excitatory morphine effects. The proposed insufficiency of an endogenous opioid system might explain an increase in neuronal excitation during REMSD and the therapeutic effect of REM deficiency in some types of depression.

Animals↗

PubMed1983

[Long-term EEG recording in comparison with sleep deprivation and other provocation methods in epilepsy patients].

37 epileptics with routine records without paroxysms were subject to 24 hours mobile long-term EEG registration and independently 24 hours sleep deprivation EEG including hyperventilation and photic stimulation. The anticonvulsive treatment was not changed. In 14 cases we could prove epileptiform discharges (= positive finding) by using both methods, in 13 after sleep derivation (10 at rest, 3 only during hyperventilation) in 7 in the long-term record and in 6 of them both after sleep deprivation and in long-term record. As epileptiform discharges we rated spikes, spikes ans slow waves, epileptic K-complexes, spike and waves and poly spike wave-paroxysms. We refer the small number of positive findings in the mobile long-term EEG mainly to the fact that only 3 EEG canals are disponible until now. Therefore on the one hand it is not definitely possible to distinguish sharp waves from sharp transients physiologically appearing in sleep, on the other hand focal EEG-changes often escape from being recorded.

Adolescent↗

PubMed2002

Increase in amino acids in the pons after sleep deprivation: a pilot study using proton magnetic resonance spectroscopy.

Total sleep deprivation (TSD) is an efficient method to relieve depression. An involvement of GABAergic and glutamatergic neurotransmission in the pathophysiology of depression and the mechanism of action of TSD has been suggested. To directly assess the content of GABA, glutamate (Glu) and glutamine (Gln) before and after TSD, we estimated their concentrations in four brain regions in six healthy subjects using proton magnetic resonance spectroscopy. The unresolved estimate of GABA, Glu and Gln, as well as GABA and Gln were increased in the pons after 24 h of TSD, the effect being prominent in three subjects. There were no significant changes in the hypothalamus, thalamus or parietooccipital cortex. These preliminary data support earlier animal data and indirect findings in humans suggesting that GABA and Gln, especially in the pontine structures, may play a key role in the mechanism of TSD.

Adult↗

PubMed1994

The repeatability of posturographic measurements and the effects of sleep deprivation.

The repeatability of posturographic measurements and the effects of sleep deprivation on them were investigated in 23 volunteers over a period of four months. Postural stability was studied by evaluating body sway velocity and the maximal and average vibration-induced shifts of the centre of pressure in the anterio-posterior and lateral directions. The posturographic test was performed with and without exposure of the calf muscles to vibration. Subjects were tested both with their eyes open and closed, and the measurements were performed weekly during the first month and once every month thereafter. The interindividual results differed more than the intraindividual ones, indicating that posturographic measurements are most suitable for functional monitoring in one person's tests. The dispersion of the results did not diminish with time, nor did the body sway decrease. The findings suggest that no learning takes place in nontrained persons. In the second part of the research, measurements were performed twice after the subjects had been awake the previous night or 24 hours. Postural stability did not deteriorate in this situation.

Adult↗

PubMed2000

[Effects of sleep deprivation on human performance].

Objective. To investigate the effects of sleep deprivation (SD) on human performance. Method. 8 healthy male college students participated the test. During 26 h of continuous awakeness (from 6:00 to 8:00 the next day), the volunteers were demanded to perform a battery of tests at 9 different time (7:00, 12:00, 16:00, 20:00, 0:00, 2:00, 4:00, 6:00, 8:00). The tests include: (1) single task: aural Oddball response, the response time (RT1) and correct rate (CR1) were recorded; (2) dual tasks: manual tracking and aural Oddball response, the response time (RT2), tracking error (ER) and correct rate (CR2) were recorded; (3) The Stanford sleepiness scale and subjective ratings of task difficulty access. Result. SD had significant effects on CT1, CT2 and ER (P=0.0001, P=0.00001, P=0.0004 respectively); SD increased RT1, RT2, ER at night time. SD had significant effects on SR, SSS score (P=0.0001, P=0.0000 respectively); SD increased SR, SSS score at night time. Since the subjects changed their response strategy, CR1 and CR2 were not influenced by SD at night time. Conclusion. SD has significant effects on response time, tracking error, subjective difficulty of cognitive tasks and subjective sleepiness.

Adult↗

PubMed1984

Swimming immobility of REM sleep deprived rats reared in different environments.

This study tested the hypothesis that environmental rearing treatments which alter the REM sleep levels of rats affect swimming immobility, an adaptive, REM sleep sensitive behavior. At weaning, 72 female Sprague-Dawley rats were maintained in either an enriched, an impoverished, or a social control environment for 32-33 days. They were then placed in either a REM sleep depriving platform-in-water condition or in one of two control conditions (large platform or dry control) for 4 days before being scored for swimming immobility during a 10-min swimming test. A 3 (environments) X 3 (platforms) ANOVA revealed a main effect for environments, F(2,63) = 5.20, p less than 0.01. Enriched rats exhibited a behavioral advantage over impoverished rats under the large platform control condition, F(1,63) = 6.58, p less than 0.025, and under the dry control condition, F(1,63) = 6.14, p less than 0.025. However, under the REM depriving condition, their behavioral advantage was virtually eliminated, F(1,63), p less than 1. The conclusion that the REM sleep levels of the rat groups probably determined their swimming immobility scores is discussed.

Adaptation, Physiological↗

PubMed2000

Differential effect of short-term REM sleep deprivation on NGF and BDNF protein levels in the rat brain.

It is well known that REM sleep is associated with memory consolidation, especially, procedural skill learning. Neurotrophic factors are known to be involved in synaptic plasticity. We therefore investigated the effects of selective REM sleep deprivation (RSD) on NGF and BDNF proteins in the hippocampus, cerebellum and brainstem in the rat. NGF and BDNF were detected by an ELISA. Our findings show that 6 h RSD affected the NGF and BDNF protein levels in different manner. In the cerebellum and brainstem, BDNF was significantly decreased, while NGF was not changed. Conversely, in the hippocampus, NGF was significantly decreased while BDNF was not changed. This study indicates that REM sleep may be associated with the secretion of neurotrophic factors and thus contribute to the memory functions.

Animals↗

PubMed1991

Effects of sleep deprivation on the limbic system and the frontal lobes in affective disorders: a study with Tc-99m-HMPAO SPECT.

We studied 10 patients with melancholia before and after sleep deprivation and 8 controls with Tc-99m-hexamethylpropylenamineoxime (HMPAO) single photon emission computed tomography (SPECT). All depressed subjects showed relative hypoperfusion in the left anterolateral prefrontal cortex under both conditions. Only responders showed relative hyperperfusion in parts of the limbic system and a reduction of blood flow in these regions after sleep deprivation.

Adult↗

PubMed2002

Effect of sleep deprivation on spike-wave discharges in idiopathic generalised epilepsy: a 4 x 24 h continuous long term EEG monitoring study.

The aim of the study was to investigate the effect of sleep and sleep deprivation on spike-wave discharges (SWD) in an idiopathic generalised epileptic patient population by continuous long term cassette EEG monitoring for 4 x 24 h. In ten patients with idiopathic generalised epilepsy, showing SWD during awake state and in sleep as well, EEG and sleep polygraphy was recorded for 4 x 24 h. Sleep was deprived during the second 24 h. Awake state, NREM1, NREM2, NREM3+4 and REM sleep duration and number of SWD episodes were evaluated in 4 min intervals by visual scoring. For analysing the effect of 'day' and 'night', 'vigilance' and 'sleep deprivation' (SD) on the density variables multi-way ANOVAs were carried out in different designs. SWD densities for different vigilance states were not significantly different during 'day' and 'night' in 24 h without SD or rebound after SD. Sleep had an activating effect SWD densities being the highest during NREM1 and NREM2. There was an increase of SWD densities in all vigilance states after SD, but SWD densities remained the highest in NREM1 andNREM2. Our results support the view that sleep dependent rather than sleep independent mechanisms cause activation of SWD after SD in generalised epilepsy. We assume that fine graded vigilance fluctuations, that are more frequent after SD, have an essential role in SWD activation in superficial sleep or even in wakefulness.

Adult↗

PubMed1992

The timing of partial sleep deprivation in depression.

In 26 major depressed and 4 schizoaffective inpatients (according to the RDC) early and late partial sleep deprivation (PSD) were carried out. For most of the patients (N = 25) this was done in a balanced crossover design. Residual sleep, starting at 21:00 or 2:00 respectively, was recorded polygraphically. Total sleep time was held constant between the 2 conditions (168 +/- 46 min in early sleep, 173 +/- 28 min in late sleep). Mood ratings with 5 different measures on the 2 days following each PSD revealed significant therapeutic effects from both procedures with only minor differences between them. Thus, sleep reduction as such and not the time at which it takes place (first or second half of the night) appears to be the therapeutic agent in PSD.

Adult↗

PubMedDate not supplied

Sleep deprivation and hypothalamic-pituitary-adrenal (HPA) axis activity in depressed patients.

In the present study we investigated HPA axis activity in depressed patients treated with partial sleep deprivation (PSD) in order to identify endocrinological characteristics related to PSD responsiveness. Thirty-three drug-free patients (14 men, 19 women) suffering from major depression according to DSM-IV criteria were treated with PSD. Response to PSD was defined as a reduction of at least 30% according to the 6-item version of the Hamilton Depression Scale (6-HAMD). Subsequently, the combined dexamethasone-suppression/CRH-stimulation test (DEX/CRH test) was performed. Patients were pretreated with 1.5 mg dexamethasone (DEX) at 23:00 h and challenged with 100 microg corticotropin-releasing hormone (CRH) the following day. Postdexamethasone cortisol concentrations (before CRH administration) served as parameters for the DST status (dexamethasone suppression test). The cortisol stimulation after CRH was used as measurement for the DEX/CRH test status. Of the depressive patients, 54.5% (18 out of 33) responded to PSD. DST suppressors (postdexamethasone cortisol levels < 15 ng/ml) showed a significantly greater reduction in 6-HAMD scores after PSD than DST nonsuppressors. Furthermore, a significant negative correlation between postdexamethasone cortisol levels and reduction in 6-HAMD scores after PSD could be established. However, there was no relationship between the cortisol stimulation following CRH challenge and response to PSD. Although the combined DEX/CRH challenge test is a more sensitive marker for HPA axis dysregulation in depression than the standard DST, the negative feedback of the HPA system reflected by the DST status is apparently more closely associated with response to partial sleep deprivation in major depressive disorder.

Adrenocorticotropic Hormone↗

PubMed2006

Improved anatomic delineation of the antidepressant response to partial sleep deprivation in medial frontal cortex using perfusion-weighted functional MRI.

This study used functional magnetic resonance imaging (fMRI) to clarify the sites of brain activity associated with the antidepressant effects of sleep deprivation (SD). We hypothesized: 1) depressed responders' baseline ventral anterior cingulate (AC) perfusion will be greater than that of nonresponders and controls; 2) following partial sleep deprivation (PSD), ventral AC perfusion will significantly decrease in responders only. Seventeen unmedicated outpatients with current major depression and eight controls received perfusion-weighted fMRI and structural MRI at baseline and following 1 night of late-night PSD. Talairach-transformed gray matter masks were merged with Talairach Daemon-based region of interest (ROI) templates. Baseline left ventral AC (LVAC) perfusion was greater in responders than nonresponders. There was no difference involving the medial frontal cortex. Responders' LVAC perfusion dropped from baseline to PSD scans compared with nonresponders and controls, as did perfusion in the right dorsal AC. In the patient group as a whole, decrease in LVAC perfusion from baseline to PSD scans correlated directly with the decrease in the modified 17-item Hamilton Depression Rating Scale (HDRS17) between baseline and PSD conditions. These data--the first using fMRI--show greater anatomic specificity than previous findings of SD and depression in linking decreased brain activity in this area with clinical improvement.

Adolescent↗

PubMed1993

Antidepressant response to sleep deprivation as a function of time into depressive episode in rapidly cycling bipolar patients.

Three patients with treatment-resistant rapidly cycling bipolar disorder were studied with multiple sleep deprivations (SD) during several depressive episodes to assess the effect of phase or duration of a depressive episode on SD response. There was little response to SD early in a depressive episode, but responses were often robust late in an episode, sometimes triggering its termination. In 2 subjects, the duration of antidepressant response to SD increased linearly as time into episode increased. Neither the number of SD given in an episode nor the medication status of the patients appeared to account for the observed increases in antidepressant response. These results suggest that the neurobiological substrates underlying depression may change over the course of an episode, resulting in an increased responsivity to sleep deprivation later compared with earlier in the course of an episode in rapidly cycling patients. The generalizability of these findings to unipolar patients remains to be explored.

Adult↗

PubMed1985

Effects of previous REM sleep deprivation on the acquisition of different topographies of discriminated avoidance in the rat.

The effects of REM sleep deprivation (REMSD) for 96 h on discriminated avoidance learning were tested in rats using three different task topographies:in a jumping-box, in a shuttle-box and bar-pressing. The same stimulus relationship and the same methodological controls with regard to the avoidance schedules and to the platform technique were employed. REMSD facilitated the acquisition of the jumping-box response, which was detectable at the end of the third session. REMSD did not interfere in the acquisition of the shuttle-box response since both the experimental and control groups met the criterion by concluding the eighth session without any observable difference in the analyzed parameters. With bar-pressing, neither group reached the learning criterion (80% of avoidance responses throughout two consecutive sessions). We have related these results to the existing hypothesis that REM sleep stimulates the coding of all complex sequences of motor behavior which are necessary for innate behaviors and concluded that the reimbursement of the REM sleep debt after testing facilitated only the acquisition of the jumping-box response through a reprogramming of the motor organization of this innate behavior.

Animals↗

PubMed1987

Total sleep deprivation and Parkinson disease.

Twelve Parkinson disease (PD) patients were submitted to a single night of total sleep deprivation (SD). Disease duration had a median of 5.1 years and all were using either anticholinergic or L-Dopa or the combination of both drugs. After SD there was an improvement of rigidity, bradykinesia, gait and posture disturbances and functional disability that remained significant for 2 weeks. No effect was observed on tremor. Concerning depressive symptoms, a significant difference was noted, that remained for one week. These results suggest that SD may be an useful procedure to improve PD symptomatology. It is discussed a possible change of dopaminergic receptors, induced by SD, to explain the improvement.

Adult↗