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PubMed1980

A study of the diagnostic value of waking and sleep EEGs after sleep deprivation in epileptic patients on anticonvulsive therapy.

One hundred and twenty-seven waking and sleep EEGs were recorded from 102 epileptic patients on anticonvulsant therapy, after sleep deprivation. Epileptiform activity was found in 63% of the patients, or 57% of the records. Since in previously recorded waking EEGs epileptic discharges had been registered in 19%, or 17% respectively, the rate of increase was considerable. The rate of activation was 51% in patients without epileptic activity in their waking EEGS. Two-thirds of the epileptiform activity were already recorded in the waking EEGS, after sleep deprivation, One-third was recorded only during sleep. Epileptic discharges in the different sleep stages ranged from 25% (E) to 48% (C). On the other hand, approximately the same frequency was recorded in the separate sleep stages in patients whose waking EEGS after sleep deprivation showed epileptiform activity. The EEG changes were correlated with the different clinical parameters (type of seizure, frequency and duration of seizures, age at the first seizure and the time of examination, neurological findings, and personality changes).

Adolescent↗
PubMed1993

Regulation of local sweating in sleep-deprived exercising humans.

Thermoregulatory sweating [total body (msw,b), chest (msw,c) and thigh (msw,t) sweating], body temperatures [oesophageal (T(oes)) and mean skin temperature (Tsk)] and heart rate were investigated in five sleep-deprived subjects (kept awake for 27 h) while exercising on a cycle (45 min at approximately 50% maximal oxygen consumption) in moderate heat (T(air) and T(wall) at 35 degrees C). The msw,c and msw,t were measured under local thermal clamp (Tsk,l), set at 35.5 degrees C. After sleep deprivation, neither the levels of body temperatures (T(oes), Tsk) nor the levels of msw,b, msw,c or msw,t differed from control at rest or during exercise steady state. During the transient phase of exercise (when Tsk and Tsk,l were unvarying), the msw,c and msw,t changes were positively correlated with those of T(oes). The slopes of the msw,c versus T(oes) or msw,t versus T(oes) relationships remained unchanged between control and sleep-loss experiments. Thus the slopes of the local sweating versus T(oes) relationships (msw,c and msw,t sweating data pooled which reached 1.05 (SEM 0.14) mg.cm-2.min-1.degree C-1 and 1.14 (SEM 0.18) mg.cm-2.min-1.degree C-1 before and after sleep deprivation) respectively did not differ. However, in our experiment, sleep deprivation significantly increased the T(oes) threshold for the onset of both msw,c and msw,t (+0.3 degrees C, P < 0.001). From our investigations it would seem that the delayed core temperature for sweating onset in sleep-deprived humans, while exercising moderately in the heat, is likely to have been due to alterations occurring at the central level.

Adult↗
PubMed1989

Priming and cued recall in elderly, alcohol intoxicated and sleep deprived subjects: a case of functionally similar memory deficits.

Young, old, alcohol intoxicated, and sleep deprived subjects studied weakly and strongly related word pairs, and were tested in lexical decision priming and cued recall. Results showed memory deficits for old, alcohol intoxicated, and sleep deprived subjects in cued recall of weakly related pairs. In contrast, there were no differences between these three groups and a control group of young subjects in cued recall of strongly related pairs, and there were no differences between groups in priming. This pattern of results is interpreted to support (a) a hypothesis of functional similarities between the memory deficits associated with adult ageing, alcohol intoxication, and sleep deprivation; (b) the notion that memory deficits in these subjects are more likely to occur in tasks which require effortful rather than automatic processes; and (c) the view that the memory deficits observed are due to inefficiencies at both encoding and retrieval.

Adult↗
PubMed2003

Sleep deprivation causes behavioral, synaptic, and membrane excitability alterations in hippocampal neurons.

Although the function of sleep remains elusive, several lines of evidence suggest that sleep has an important role in learning and memory. In light of the available data and with the prevalence of sleep deprivation (SD), we sought to determine the effect of SD on neuronal functioning. We found that the exposure of rats to 72 hr of primarily rapid eye movement SD impaired their subsequent performance on a hippocampus-dependent spatial learning task but had no effect on an amygdala-dependent learning task. To determine the underlying cellular level mechanisms of this hippocampal deficit, we examined the impact of SD on several fundamental aspects of membrane excitability and synaptic physiology in hippocampal CA1 pyramidal neurons and dentate gyrus granule cells. We found that neuronal excitability was severely reduced in CA1 neurons but not in granule cells and that the production of long-term potentiation of synaptic strength was inhibited in both areas. Using multiple SD methods we further attempted to differentiate the effects of sleep deprivation from those associated with the nonspecific stress induced by the sleep deprivation methods. Together these data suggest that failure to acquire adequate sleep produces several molecular and cellular level alterations that profoundly inhibit hippocampal functioning.

Amygdala↗
PubMed2005

Effects of sleep deprivation on cardiac autonomic and pituitary-adrenocortical stress reactivity in rats.

A demanding life style, often associated with restricted time for sleep, is a growing problem in our society and may become a major health issue in the near future. Since the physiological stress system plays a critical role in coping with a challenge, it is important to know whether this system is affected by sleep loss. Although some information is available concerning the effect of sleep loss on the basal activity of the two main limbs of the stress system, the sympathetic-adrenomedullary (SAM) and the hypothalamic-pituitary-adrenocortical (HPA) axes, little is known about the effect of sleep loss on the subsequent response to a stressor. This study investigated the effects of sleep deprivation on cardiac autonomic and HPA axis (re)activity, under baseline conditions and in response to an acute emotional stressor (15-min of restraint). Rats were subjected to 48 h of sleep deprivation by placing them in slowly rotating wheels. Electrocardiographic recordings were performed via radiotelemetry and autonomic balance was quantified via time-domain indexes of heart rate variability. HPA axis activity was examined by collecting blood samples which were analyzed for plasma ACTH and corticosterone concentrations. The results show that sleep deprivation produced a tonic increase of heart rate and HPA axis activity. When the animals in a state of sleep debt were exposed to an acute restraint stress, a blunted parasympathetic antagonism was observed following sympathetic activation, together with an increased susceptibility to cardiac arrhythmias. The HPA axis response to restraint stress was also altered, but while pituitary ACTH response was attenuated, adrenal corticosterone release was unchanged, indicating an increased adrenocortical sensitivity to ACTH. The data show that sleep deprivation not only affects the baseline activity of the stress system, but it also alters its response to a subsequent stressor.

Adrenocorticotropic Hormone↗
PubMed1993

Expression of Egr-1 in the brain of sleep deprived rats.

In previous research, rats subjected to prolonged sleep deprivation have shown disturbances of thermoregulation, hormonal and metabolic changes in apparent response to the thermoregulatory problems, lesions on the tail and paws, and eventual death. To search for alterations of functional activity in brain, the expression of the immediate early gene Egr-1 was examined by immunocytochemistry and Northern blotting in rats subjected to total sleep deprivation (TSD) for 10 days. Controls included yoked stimulus-control (TSC) rats, surgically implanted but otherwise undisturbed control rats, and unoperated control rats. Photographs of immunoreacted coronal sections from four sets of rats were ranked blindly for 25 brain regions. TSD rats showed tendencies for regionally specific increases in Egr-1-like immunoreactivity in dorsal raphe, lateral habenula, superior colliculus, and ventral periaqueductal grey. However, most regions showed no differences in Egr-1-like immunoreactivity between TSD and control rats. Neither was there a difference in whole brain Egr-1 mRNA by Northern blot in two additional sets of rats. Thus, this study, like previous studies of brain histology, amines, adrenoceptors, and glucose utilization, does not provide positive support for the hypothesis that sleep protects the central nervous system against massive global damage, fatigue, or dysfunction.

Animals↗
PubMed1997

[Pro-psychotic change of binocular depth inversion by sleep deprivation].

Binocular depth inversion represents an illusion of visual perception. Such inversion does not occur in all cases, especially when objects with a higher degree of familiarity (e.g. photographs of faces) are displayed. Cognitive factors are assumed to override the binocular disparity cues of stereopsis. We tested the hypothesis that during sleep deprivation the human CNS is unable to correct the implausible perceptual information. Measurements of binocular depth inversion in perception of 3D objects were taken in sleep-deprived medical staff and healthy volunteers. The binocular depth inversion scores were highly elevated in the sleep-deprived group in comparison to the healthy volunteers. The data demonstrate a strong impairment of binocular depth inversion after sleep deprivation and support the view that sleep deprivation may be accompanied by a disorganisation of the interaction between sensory input and generation of perceptual hypotheses.

Adult↗
PubMed1990

The biological basis of an antidepressant response to sleep deprivation and relapse: review and hypothesis.

Sixty-one papers involving over 1,700 subjects have documented that over half of depressed patients experience an antidepressant response to sleep deprivation. Eighty-three percent of unmedicated depressed patients who had an antidepressant response to sleep deprivation relapsed after one night of sleep. Short naps can also activate severe relapses. The authors suggest that these phenomenological observations concerning relapse with a night of sleep or with naps after successful sleep deprivation would be compatible with the existence of a sleep-associated depressogenic process.

Circadian Rhythm↗
PubMed1996

The effect of REM sleep deprivation on somatostatin and growth hormone-releasing hormone gene expression in the rat hypothalamus.

Growth hormone-releasing hormone (GHRH) and somatostatin (SRIF) have been implicated as sleep factors. We studied how the hypothalamic SRIF/GHRH system is affected by possible feedback regulation resulting from REM sleep deprivation at the level of gene expression and how this is reflected in serum growth hormone (GH) content. Male rats were deprived of REM sleep on small platforms for 24 or 72 h, and one group was allowed a rebound sleep of 24 h after 72 h deprivation. Animals maintained on large platforms and animals taken directly from their home cages served as controls. In situ hybridization was made from 20 microm cryosections through the periventricular, paraventricular and arcuate hypothalamic nuclei using oligonucleotide probes for GHRH and SRIF. The number of cells expressing SRIF or GHRH was counted. Serum GH was measured by means of radioimmunoassay in similarly treated rats. Fewer cells expressed GHRH in the paraventricular nucleus of animals subjected to 24 and 72 h of REM sleep deprivation than in home control animals. A similar trend was observed in the arcuate nucleus. The number of cells expressing SRIF was elevated in the arcuate nucleus after 24 h of REM sleep deprivation but not after 72 h. In the periventricular nucleus the number of cells expressing SRIF was higher after 72 h of deprivation when compared to expression in animals maintained on large platforms. Serum GH levels were decreased in animals maintained on either small or large platforms. It is concluded that the expression of the SRIF and GHRH genes is modulated by REM sleep deprivation.

Animals↗
PubMedDate not supplied

Clinical effects of sleep deprivation and clomipramine in endogenous depression.

Three groups of ten hospitalized endogenously depressed patients were treated with clomipramine alone (CL), a combination of sleep deprivation and clomipramine (CL/SD), and a combination of sleep deprivation and placebo (PL/SD), respectively. The sleep deprivation (SD) regime consisted of two deprivations per week. Measurements by self, blind and nurse ratings were taken twice daily during the experimental period of 15 days. Self and blind ratings indicate that, on average, over the entire experimental period, CL/SD was the most effective treatment in alleviating depression. The results of the PL/SD treatment were not significantly different from those of CL. In contrast, the nurse ratings did not differentiate significantly between the CL/SD and CL groups. Hamilton depression ratings indicated significantly less depression after one week of treatment with CL/SD relative to the treatment with CL alone. After the second week, however, no such differential clinical gain was found for the CL/SD group. It is concluded that SD in combination with clomipramine as compared with CL alone induces a faster onset of improvement in depression.

Clomipramine↗
PubMed1999

Exercise-induced changes in plasma atrial natriuretic peptide and brain natriuretic peptide concentrations in healthy subjects with chronic sleep deprivation.

Recent observations have shown that plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) correlate with cardiac function or prognosis in heart failure patients. However, relatively little is known about changes in their plasma concentration during commonly occurring physiological states such as fatigue. Therefore, this study was designed to examine the physiological changes of plasma ANP and BNP concentrations using a chronic sleep-deprivation model. Bicycle ergometer cardiopulmonary exercise tests were performed in 10 healthy volunteers (mean age: 22.7 years). Blood samples for measuring ANP and BNP were drawn during the resting state and immediately after each exercise test. Cardiac output (CO) was measured during the exercise test by the impedance method. The study conditions were designed as follows: (A) a day following a period of normal sleep (control state) and (B) a day preceded by 1 month during which sleep lasted <60% of normal (chronic sleep-deprived state). Results were as follows. (1) Peak oxygen uptake and peak CO decreased during the sleep-deprived state compared with the control state. (2) There was no difference between peak heart rates measured during exercise under the 2 conditions. (3) Plasma ANP concentration during exercise increased significantly during the control state, whereas only a tendency toward increase was observed during the sleep-deprived state. (4) Plasma BNP concentration during exercise tended to increase in the control state compared with the resting state, whereas there was no difference in plasma BNP between after exercise and resting state in the sleep-deprived state. These results indicate that changes of ANP or BNP induced by exercise tended to be decreased by chronic sleep deprivation.

Adult↗
PubMed2005

Effects of age on recovery of body weight following REM sleep deprivation of rats.

Chronically enforced rapid eye (paradoxical) movement sleep deprivation (REM-SD) of rats leads to a host of pathologies, of which hyperphagia and loss of body weight are among the most readily observed. In recent years, the etiology of many REM-SD-associated pathologies have been elucidated, but one unexplored area is whether age affects outcomes. In this study, male Sprague-Dawley rats at 2, 6, and 12 months of age were REM sleep-deprived with the platform (flowerpot) method for 10-12 days. Two-month-old rats resided on 7-cm platforms, while 10-cm platforms were used for 6- and 12-month-old rats; rats on 15-cm platforms served as tank controls (TCs). Daily changes in food consumption (g/kg(0.67)) and body weight (g) during baseline, REM-SD or TCs, and post-experiment recovery in home cages were determined. Compared to TCs, REM-SD resulted in higher food intake and decreases in body weight. When returned to home cages, food intake rapidly declined to baseline levels. Of primary interest was that rates of body weight gain during recovery differed between the age groups. Two-month-old rats rapidly restored body weight to pre-REM-SD mass within 5 days; 6-month-old rats were extrapolated by linear regression to have taken about 10 days, and for 12-month-old rats, the estimate was about 35 days. The observation that restoration of body weight following its loss during REM-SD may be age-dependent is in general agreement with the literature on aging effects on how mammals respond to stress.

Adaptation, Physiological↗
PubMed1991

Alterations in the morning plasma levels of hormones and the endocrine responses to bicycle exercise during prolonged strain. The significance of energy and sleep deprivation.

The relative significance of physical exercise, energy and sleep deprivation for the morning levels of hormones and the endocrine response to short-term bicycle exercise were investigated in 24 male cadets during a 5-day military training course. Significant increases in the morning levels of noradrenaline, adrenaline, and dopamine, and a decrease in PRL were ascribed mainly to physical strain. Cortisol and hGH increased, whereas insulin and glucose decreased mainly due to energy deficiency. Pulse rate after the bicycle test was unchanged and similar in all groups in spite of increased catecholamine responses. The increased catecholamine response was mainly due to physical strain. The cortisol response to the bicycle test was increased in all groups, and energy deficiency caused slower postexercise recovery. The incremental hGH response to the exercise test was unchanged in the energy-deficient subjects but abolished in the well-fed subjects. The results suggest that the endocrine responses during long-lasting exhausting strain were mainly due to physical exertion and energy deficiency, whereas sleep deprivation did not play any major role.

Adult↗
PubMed1980

Relationship between sleep deprivation and urinary MHPG levels.

A 5-day study, forming the initial part of two 32-day clinical trials and involving 22 unipolar depressed inpatients, was designed to determine the relationship between response to sleep deprivation and 24-hour urinary MHPG levels. A statistically significant, positive relationship was noted between the sleep deprivation, modified total HAM-D scores and MHPG levels at postsleep deprivation, indicating that the greater the severity of depression during sleep deprivation the higher were the MHPG levels after the sleep deprivation period.

Adult↗
PubMed1980

Rapid-eye-movement sleep deprivation decreases the density of 3H-dihydroalprenolol and 3H-imipramine binding sites in the rat cerebral cortex.

The high affinity binding sites for 3H-imipramine (3H-IMI) and 3H-dihydroalprenolol (3H-DHA) in the rat cerebral cortex were studied after 2,4 48 and 72 h of rapid-eye-movement (REM) sleep deprivation. Both the Kd and Bmax values for 3H-IMI and 3H-DHA binding remained unaffected after 24 or 48 h of REM sleep deprivation. After 72 or REM sleep deprivation there was a significant reduction in the Bmax for 3H-IMI and 3H-DHA binding with a concomitant increase in the apparent affinities. The reduction in high affinity 3H-IMI and 3H-dihydroalprenolol binding sites observed 72 h after REM sleep deprivation could be related to the antidepressant effects of REM sleep deprivation in man.

Alprenolol↗
PubMed1984

Episodic excitation and changes in aggressive behavior induced by apomorphine in rats subjected to REM sleep deprivation.

Behavioral changes induced by apomorphine in normal, pseudodeprived (control) and REM sleep-deprived AM-2/TOR inbred rats were investigated. Deprived rats exhibited aggressive behavior for nearly 30 min in the absence of administration of drug, this effect not being observed in normal or control rats. The administration of apomorphine (1, 2 and 5 mg/kg) 5 min before the test elicited short periods of aggressive behavior in normal and control rats, but decreased the total duration of aggressive behavior in deprived rats. However, the deprived rats exhibited a more intense aggressive behavior, since the frequency of real fighting events was enhanced. The administration of apomorphine to deprived rats elicited stereotyped behavior. Enhancement of stereotyped behavior by increasing the dose was correlated with a reduction in the duration of aggressive behavior. Apomorphine also induced short episodes of intense excitability, manifested by increased locomotor activity, jumping and vocalization. This behavioral response was termed "episodic excitation". Deprived rats were significantly more sensitive to apomorphine-induced episodic excitation than normal and control rats. The episodic excitation, stereotyped and aggressive behavior displayed by deprived rats, injected with apomorphine, alternated with time. The results demonstrate increased responsiveness to apomorphine after deprivation of REM sleep. The possible mechanism for such interaction is discussed.

Aggression↗
PubMed1999

[Effect of awakening and sleep deprivation in triggering idiopathic generalized epilepsy].

The facilitating effect of awakening and sleep deprivation on seizure production and EEG abnormalities is characteristic of idiopathic generalized epilepsies (IGE). This effect is particularly patent in awakening epilepsy. Paroxysmal events occurring in non-REM sleep, related to spindle production during transitional periods or awakening are characteristic of IGE. Because IGEs are particularly sensitive to sleep, sleep deprivation, and awakening, the association of these three conditions is particularly helpful in exploration protocols, especially when no wakefulness abnormalities are seen on the EEG. These observations in IGE suggest a dysfunction of awakening control systems. Awakening epilepsies may be differentiated from sleep-induced seizures observed in other IGE and in partial epilepsies.

Cerebral Cortex↗
PubMed1993

Sodium diclofenac inhibits hyperthermia induced by paradoxical sleep deprivation: the possible participation of prostaglandins.

Sodium diclofenac inhibits hyperthermia induced by paradoxical sleep deprivation (PSD), which suggests the participation of prostaglandins. The temperature of paradoxical sleep-deprived rats increased from the first to the fourth day of deprivation. This hyperthermia was blocked on the second, third, and fourth days by daily administration, twice a day, of 10 mg/kg of sodium diclofenac, a potent prostaglandin synthesis inhibitor. In the dose of 10 mg/kg, a decrease of temperature was observed only on the second and third days of PSD. These data suggest the participation of prostaglandins in modulating the increase in temperature during PSD.

Animals↗