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PubMedDate not supplied

Decoupling motor memory strategies: effects of sleep deprivation and amphetamine.

The purpose of this study was to examine motor memory strategies using sleep deprivation as a probe. Eighteen healthy men participated in a three-day study in which they underwent repeated testing on a kinesthetic arm position replication task. On the morning of Day 3, after approximately 48 hr sleep deprivation, they ingested either 20 mg d-amphetamine or placebo. Results showed that throughout Day 3 performance remained relatively unimpaired at medial positions for both groups. For positions shifted 25 degrees laterally, accuracy was also relatively unimpaired for the amphetamine group but was compromised for the placebo group. It was concluded that sleep deprivation-induced decrements in positioning ability were due to disruption of kinesthetic memory, a narrowing of attention, or both. Kinesthetic feedback, and encoding and retrieval processes of the spatial reference system were preserved.

Adult↗
PubMedDate not supplied

Relation between responses to repetitive transcranial magnetic stimulation and partial sleep deprivation in major depression.

Repetitive transcranial magnetic stimulation (rTMS) has been found to ameliorate symptoms in major depression. However, its mechanism of action has to be further elucidated and the relationship between responses to rTMS and other antidepressant interventions except electroconvulsive therapy has not been investigated to date. Here we studied in an open trial whether the response to partial sleep deprivation may predict the clinical outcome of rTMS treatment. Thirty-three drug-free patients suffering from a major depressive episode underwent a partial sleep deprivation at least 5 days prior to rTMS and subsequently received 10 sessions of 10 Hz rTMS of the left prefrontal cortex. After rTMS a significant overall improvement of 32% on the Hamilton Rating Scale for Depression was observed. Forty-two percent of patients showed an antidepressant response after rTMS. Amelioration of depression after partial sleep deprivation was inversely correlated with improvement after rTMS. There was no clinically applicable predictive value of the response to partial sleep deprivation for the outcome after rTMS. Apparently, different subgroups of depressed patients respond to both interventions. Further studies are needed to characterize the response to rTMS by means of clinical and biological parameters.

Adult↗
PubMed1990

Partial sleep deprivation to prevent 48-hour mood cycles.

The course of a patient with the phenomenon of 48-h mood cycles, including her response to medication and to systematic partial sleep deprivation, is described. She had only a partial response to tranylcypromine alone. Partial sleep deprivation during the second half of alternate nights successfully prevented depressive mood cycles. Three to four weeks after discontinuing tranylcypromine she lost her ability to sustain this regimen. This case demonstrates an interaction between antidepressant medication and partial sleep deprivation in the prevention of depressive mood cycles.

Combined Modality Therapy↗
PubMed1975

Effects of sleep deprivation on short-term recognition memory.

A probe-recognition short-term memory paradigm was used to inquire into the precise effects of sleep deprivation on human memory. It was found that recognition performance, as measured by d', was generally impaired for each subjects after 24 hr of sleep deprivation. While d' was shown to decrease exponentially as the number of items intervening between the target and the probe increased, this decay rate was not affected by sleep loss. In addition there was confirmation of a previously observed increase in the positive skewness of reaction times after wakefulness. The data were consistent with the hypothesis that sleep deprivation increases the occurrence of lapses, periods of lowered reactive capacity, which prevent the encoding of items in short-term memory.

Adult↗
PubMed1989

Effect of normal sleep and sleep deprivation on interhemispheric correlation during subsequent wakefulness in man.

EEG activity was recorded from the right and left central, temporal, parietal and occipital derivations in 10 volunteers under the following conditions: at night before going to sleep, at night before sleep deprivation, in the morning after waking, in the morning after sleep deprivation and in the morning 48 h after recovery. Interhemispheric correlation and relative power were calculated for EEG samples of 20.48 sec. In the morning after normal sleep interhemispheric correlations were higher in all derivations in comparison to presleep values, while in the morning after sleep deprivation, interhemispheric correlations were lower or similar to predeprivation values in all derivations except the temporal cortex. The relative power of beta was significantly lower after normal sleep and higher after sleep loss, while the relative power of low frequencies was higher in the morning after sleep and lower in the morning after deprivation.

Adult↗
PubMed1986

Effects of one night's sleep deprivation on mood and behavior in panic disorder. Patients with panic disorder compared with depressed patients and normal controls.

The effects of one night's sleep deprivation on mood and behavior were evaluated in 12 patients with panic disorder, ten depressed patients, and ten controls. In contrast to the improvement in symptoms of anxiety and depression shown by the majority of depressed patients, the response of patients with panic disorder as a group did not differ from that of normal controls, although a subgroup did experience noticeable worsening in their symptoms of anxiety, with 40% experiencing panic attacks on the day following sleep deprivation. Electroencephalographic recordings with nasopharyngeal electrodes on the day following sleep deprivation were normal, further suggesting that patients with panic disorder do not have seizure activity characteristic of temporal lobe epilepsy.

Adult↗
PubMed1977

Sleep deprivation deficits and their reversal by d- and l-amphetamine.

Vigilance performance, waking EEG patterns and mood were studied before and after one night of sleep deprivation in normal males. The effects of d-amphetamine 10 mg, l-amphetamine 10 mg and placebo on these measures were compared. Changes were found in all three measures after one night of sleep-deprivation. d-Amphetamine was more powerful than l-amphetamine in reversing sleep deprivation effects on vigilance and on waking EEG.

Adult↗
PubMed1998

The effect of one night's sleep deprivation on temperature, mood, and physical performance in subjects with different amounts of habitual physical activity.

Eleven healthy males were studied twice. On one occasion (control, C), they slept (night 1) and then underwent a battery of tests at 4 h intervals from 06:00 day 1 to 02:00 day 2; then, after a normal sleep (night 2), they were tested from 10:00 to 22:00 on day 2. On the second occasion (sleep deprivation, SD), the subjects remained awake during night 1. Each battery of tests consisted of measurements of tympanic membrane temperature, profile of mood states (POMS), muscle strength, self-chosen work rate (SCWR), perceived exertion, and heart rate (HR) while exercising on a stationary cycle ergometer. Subjects also kept a diary of their activities during the two days and answered a questionnaire about their habitual physical activity. Results showed a significant negative effect of sleep deprivation on most mood states on day 1, but no effect on the other variables. By day 2, mood had tended to recover, though muscle strength tended to be worse in both control and sleep-deprivation experiments. There was also a more general tendency for negative effects to be present at the end of day 1 (02:00) or at the beginning of day 2 (10:00). There was limited support for the view that subjects who were habitually more active showed less negative effects after sleep deprivation and responded less adversely to the poor sleep achieved on the university premises (night 2). These results stress the considerable interindividual variation in the responses to sleep loss and, therefore, the difficulty associated with giving general advice to individuals about work or training capability after sleep loss.

Adult↗
PubMed1998

Female exposure to high G: performance of simulated flight after 24 hours of sleep deprivation.

BACKGROUND: Ground-based research has investigated the loss of cognitive function in the extreme conditions of G-induced loss of consciousness, however, little is known about pilots' abilities to maintain cognitive performance throughout prolonged conscious exposure in the high-G environment. The effects of fatigue and G layoff on performance during exposure to high G are mostly unknown for the female population. METHODS: This research was conducted on the centrifuge Dynamic Environment Simulator. Active-duty personnel (8 male and 8 female) were trained to fly the F-16 simulation while 30 performance measures were recorded. Performance was re-evaluated after 24 h of sleep deprivation. RESULTS: Neither male nor female overall performance was affected significantly by sleep status, although individual tasks showed sensitivity; call-sign reaction time was longer by 33%, and missile survival was less likely. Also, when sleep deprived, perceived effort and physical demand were higher while perceived performance was lower. No differences in performance were found in either gender due to lay-off, although some physiologic deconditioning was apparent. Women commanded and endured the same amount of G load as men, however, on average they could not perform the tracking task quite as well. CONCLUSIONS: Sleep deprivation (24 h) produced sensations of fatigue and frustration, but overall performance was not reduced. The ability of personnel to complete a complex defensive maneuver was reduced when they were sleep deprived. The women that we tested apparently could not optimize the tracking task as well as their male counterparts when Gz was in the simulation. None of these results were sufficient to suggest that women should not be allowed to compete for flying assignments in high-performance aircraft.

Aerospace Medicine↗
PubMed1997

Effects of REM sleep deprivation on the d-amphetamine-induced self-mutilating behavior.

It is well known that self-mutilating behavior (SMB) is developed in rats and humans during the daily treatment with d-amphetamine. Accordingly, in this work it was found that the daily treatment with 7.5 mg/kg d-amphetamine induced in rats a progressive appearance of SMB. Lower doses (5.0 mg/kg) were uneffective and higher doses (10 mg/kg) produced a pattern of SMB in which the mutilation induced at the beginning of the d-amphetamine administration disappears completely as the treatment progresses. Interestingly, it was also found that REM sleep deprivation (48 h) potentiated significantly the SMB induced by the daily administration of 7.5 mg/kg d-amphetamine, and to lesser extent, the SMB induced by the daily treatment with 10 mg/kg d-amphetamine. R(+)-SCH-23390 a D1 dopamine (DA) receptor antagonist blocked completely or abolished the SMB induced by 7.5 mg/kg d-amphetamine in REM sleep deprived rats while (+/-)-sulpiride a D2 DA receptor antagonist had only a partial blocking effect. Haloperidol a D1/D2 DA receptor antagonist behaved as a D1 antagonist. Our results indicate that REM sleep deprivation enhances the SMB induced by the daily administration of d-amphetamine and suggest the involvement of D1 DA receptors in the mechanism underlying the SMB. A role of REM sleep deprivation is also suggested in the appearance of self-mutilating episodes in d-amphetamine addicts.

Animals↗
PubMed1994

Yield of sphenoidal recording in sleep-deprived outpatients.

We retrospectively reviewed the results of sphenoidal recordings performed after sleep deprivation in 101 consecutive outpatients whose prior scalp EEGs failed to show epileptiform discharges (EDs). These patients were suspected of having seizures of temporal lobe origin. Blinded reviews of the recordings by two electroencephalographers showed a tendency for sphenoidal recording to detect EDs at a higher rate than scalp recording, but the difference did not reach statistical significance (p = 0.06). However, EDs appeared exclusively at sphenoidal electrodes in 11 patients and exclusively at scalp electrodes in 3. The probability of detecting EDs with combined scalp and sphenoidal recordings was greater when spells were characterized by focal symptoms or signs. Except in three patients, initial EDs occurred during the first 30 min of recording. We recommend that post-sleep-deprivation recording be performed initially with scalp and other noninvasive electrodes (such as anterior temporal, ear, or cheek electrodes). If no EDs occur after 30 min, sphenoidal electrode insertion and recording may then be considered, especially in patients with spells characterized by focal signs or symptoms.

Adolescent↗
PubMed1988

Physical performance and physiological responses following 60 hours of sleep deprivation.

The effect of 60 h of sleep deprivation (SD) upon physical performance and physiological responses to exercise was examined in 11 male subjects. The experiment consisted of two conditions separated by at least 10 d. In the experimental condition (E) subjects remained awake for 60 h and in the control condition (C) the same subjects had 7 h of sleep per night. In both conditions subjects reported to the laboratory on the evening prior to d 1 and slept for 7 h. Physical performance testing was carried out on d 1 and again on d 3 after either two nights of sleep or two nights of SD. Results obtained on d 3 are expressed relative to d 1, the control day. Maximal isometric and isokinetic muscular strength and endurance of selected upper and lower body muscle groups, performance of the Wingate Anaerobic Power Test, simple reaction time, the blood lactate response to cycle exercise at 70% VO2max, and most of the cardiovascular and respiratory responses to treadmill running at 70% and 80% VO2max, were not significantly altered as a result of SD. These results suggest that sleep loss of up to 60 h will not impair the capability for physical work, a finding of considerable importance in sustained military operations which frequently involve the combination of both physical and mental tasks.

Adult↗
PubMed2005

Endocrinological and catecholaminergic alterations during sleep deprivation and recovery in male rats.

Since previous data of our group showed increased concentrations in HPA axis hormones in sleep deprived rats, we hypothesized that this augmentation could produce effects in other hormonal systems, particularly in the sexual system. Considering that little is known about how the hormonal system changes during the recovery period after sleep deprivation (SD), our objective was to examine from what point SD alters sexual and stress-related hormones along with plasma catecholamine concentrations during 4 days. We also sought to verify the time course of their recovery after an equivalent period of recovery sleep. Rats were deprived of sleep by the platform technique for 1-4 days and were allowed to recover for the same period. Plasma catecholamines [dopamine (DA) and noradrenaline (NOR)], testosterone, estrone, progesterone, prolactin, corticosterone and adrenocorticotropic hormone (ACTH) concentrations were measured. Comparisons between groups showed that the SD procedure used in the present study produced marked alterations in almost all studied hormones from 24 h of SD, except for estrone and prolactin (which required 96 h of SD to become altered). Testosterone and estrone decreased, whereas progesterone, prolactin, corticosterone, ACTH, DA and NOR increased. During recovery period, progesterone, prolactin and corticosterone concentrations returned to control levels, whereas testosterone, estrone, NOR and DA did not. In addition, after 48 h of recovery ACTH and NOR decreased below control concentrations, remaining low until 96 h of sleep recovery. Thus, SD showed long lasting, differential effects upon these neurochemicals suggesting that each has its own pattern of responses to SD as well as variable periods of recovery.

Adrenocorticotropic Hormone↗
PubMed1995

The effects of drugs acting at GABA-benzodiazepine-barbiturate receptor complex on the behaviour of sleep-deprived mice.

The effects of the benzodiazepine receptor agonist diazepam, the benzodiazepine receptor antagonist flumazenil and the benzodiazepine receptor inverse agonist ethyl-8-azido-5,6-dihydro-5-methyl-6-oxo-4H-imidazo-[1,5-a][1-4] benzodiazepine-3-carboxylate (RO 15-4513) on the locomotor activity and the behaviour of animals in the plus-maze test were studied in sleep-deprived mice. The effects of convulsants acting at GABA-benzodiazepine-barbiturate receptor complex-bicuculline, picrotoxin and pentylenetetrazole, were also studied. Sleep deprivation of mice for 24 hr using the platform technique caused behavioural excitation that was reflected by an increase in the locomotor activity. Administration of diazepam (0.5 and 2.0 mg/kg), flumazenil (5.0 and 10.0 mg/kg) and RO 15-4513 (1.0, 2.0 and 3.0 mg/kg) either did not affect (in low doses) or inhibited (in high doses) locomotions of control animals. The inhibition of locomotor activity by these drugs was greater in sleep-deprived animals. In the plus-maze test, diazepam in a dose of 2.5 mg/kg had an anxiolytic effect in control mice that was reflected by an increase in the percentage of entries onto and the percentage of time spent on the open arms of the plus-maze. In contrast, in sleep-deprived animals, diazepam did not induce anxiolytic action at any dose tested. In the highest dose (2.5 mg/kg) diazepam produced a sedative effect that was reflected by a decrease in the total number of entries made onto the open and into the closed arms of the plus-maze.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1982

Effects of REM sleep deprivation and desipramine on beta-adrenergic binding sites in rat brain.

Rats were subjected to REM sleep deprivation by the flower pot method for 7 days. Another group of rats received either desipramine (10 mg/kg, i.p.), a tricyclic antidepressant, or saline (i.p.) once daily for 7 days. beta-Adrenergic receptor sensitivity in rat brain cortices was assessed by determining the maximum number of [3H]dihydroalprenolol binding sites by Scatchard analysis. Administration of desipramine caused a 26% reduction in beta-adrenergic receptor density (P less than 0.01) while REM sleep deprivation reduced beta-adrenergic receptor density by 13%, which was not statistically significant.

Animals↗
PubMed1992

Effect of REM sleep deprivation on molecular forms of acetylcholinesterase in rats.

Since REM sleep deprivation was reported to increase the activity of acetylcholinesterase, an attempt was made to investigate whether the different forms of enzyme could be affected selectively. The flower pot method was used for deprivation and suitable control experiments were conducted. The bound and the soluble forms, if affected would show an increase or a decrease, respectively, on REM deprivation. The former is affected first in the pons while the latter in the medulla. The findings support the pontomedullary cholinergic mechanism for the generation of REM sleep. Though there may be a possibility of conversion of the free to the bound form, the increase in the latter was more than the decrease in the former.

Acetylcholinesterase↗
PubMed1986

REM sleep deprivation (REMSD) antagonizes naloxone-precipitated withdrawal in acute morphine-dependent rats.

In rats allowed undisturbed sleep (control and stress) the administration of naloxone (10 mg/kg, s.c.) to morphine (7.5 mg/kg, s.c. 90 min prior) pretreated animals precipitated a jumping behaviour. REM sleep deprivation (REMSD 96 h, prior) significantly decreased the frequency of the naloxone-precipitated jumping behaviour compared with control and stressed animals. In second animal model for morphine withdrawal, naloxone (10 mg/kg, s.c.) provoked myoclonic twitch activity (MTA) in rats previously exposed to morphine (7.5 mg/kg, s.c., 90 min prior). The intensity of naloxone-induced MTA in REM sleep deprived rats was significantly lower compared to stressed animals, but it is not different from the control group. It is suggested that REMSD interferes with a neural mechanism involved in the development of acute dependence. Results are discussed in light of a possible functional insufficiency of a mu-opioid system during REMSD.

Animals↗
PubMed2006

Nocturnal sustained attention during sleep deprivation can be predicted by specific periods of subjective daytime alertness in normal young humans.

In our 24-h society, nocturnal sleep-related accidents are common. Because all individuals are not equal in their responses to sleep loss, it is very important to identify predictors of vulnerability to sleep deprivation in normal subjects. We investigated the performance of a cognitive test of sustained attention, electroencephalogram theta/alpha power, subjective sleepiness, and two circadian markers (core temperature and melatonin) in 18 healthy men (nine morning types and nine evening types, 21.4 +/- 1.9 years) during a 36-h sleep deprivation in a constant routine protocol. Sleep need (self-reported) and baseline sleep structure were also investigated. Nighttime performance impairment was defined as the difference between the mean nocturnal number of lapses (00:00-07:30 [corrected] hours) and the mean diurnal number of lapses (07:30-20:30 hours) expressed as a percentage. Feeling fully alert in the morning just after awakening and/or sleepy in early afternoon were the only two factors (Multiple R > 0.80, > 60% of explained variance) which better predicted the decrease in performances of nocturnal operational tasks requiring sustained attention.

Adult↗