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PubMed1985

[Treatment of endogenous depressions by sleep deprivation].

Eighty-six patients with endogenous depression (cyclothymia, manic-depressive psychosis and schizophrenia) were treated by sleep deprivation. The efficacy of this treatment with regard to the structure of the depressive syndrome, the course of the attack and nosological nature is discussed. The author also considers the frequency, sequence and effectiveness of sessions of sleep deprivation in both hospital and outpatient settings. Series of total sleep deprivation were shown to be highly effective in cyclothymia and manic-depressive psychosis with melancholic and anesthetic depression, including cases with a protracted course.

Adult↗
PubMed1990

Sleep stage physiology, mood, and vigilance responses to total sleep deprivation in healthy 80-year-olds and 20-year-olds.

Little is known about sleep and the effects of total sleep loss in the 'old old' (i.e., 80-year-olds). We investigated sleep, mood, and performance responses to acute sleep deprivation in healthy 80-year-olds (n = 10) and 20-year-olds (n = 14). The protocol consisted of three nights of baseline sleep, one night of total sleep deprivation, and two nights of recovery sleep. Mood and vigilance were tested using visual analog scales and a Mackworth clock procedure in the morning and evening of each study day. Daytime sleepiness was measured by five naps on the days following the third and sixth nights. Old subjects had lower sleep efficiency and less delta sleep than young subjects. However, sleep continuity and delta sleep were enhanced in both groups on the first recovery night, indicating that sleep changes in old subjects are at least partially reversible by this procedure. Surprisingly, young subjects had shorter daytime sleep latencies than the old, suggesting a greater unmet sleep need in the former group. Mood and performance were disturbed by sleep loss in both groups, but to a greater extent among the young. This suggests that acute total sleep loss is a more disruptive procedure for the young than for the old.

Adult↗
PubMed1982

[Sleep deprivation as activating procedure in EEG of patients with and without epileptic seizures. II. Focal discharges ].

Of 901 patients investigated 167 showed a focal disturbance in the EEG before and/or after 24-hours sleep deprivation. 459 patients suffered from epileptic seizures, the remainder had non-epileptic attacks or an organic cerebral disease without seizures. Of the 167 focal EEG changes 21.6% were seen only following sleep deprivation. In 9.6% focal changes present before could not be observed anymore following sleep deprivation. There was no significant difference between the three groups of patients mentioned above. The 24-hours sleep deprivation thus represents an activation procedure which may enhance diagnostic information relating to the question of focal EEG disturbances not only in epileptic patients. In the group of patients with epileptic seizures the activation or suppression respectively of the focal disturbance showed some dependence from seizure type and frequency as well as from the type of the focal change (spikes or slow waves). In our material the differences were however not statistically significant. More information could be gained from the waking EEG and from stage 1 than from sleeping stages 2 to 4 according to Rechtschaffen and Kales. Trigger functions could be attributed especially to the transitional phases from wakefulness to sleep and from stage 1 to stage 2 and vice versa particularly associated with arousal reactions. In our short sleep records REM stages could be rarely observed.

Adolescent↗
PubMed1997

The alerting effects of short and long naps in narcoleptic, sleep deprived, and alert individuals.

Eleven narcoleptic patients and 22 age- and gender-matched normal controls participated in a study to determine the alerting effects of differing nap lengths. All narcoleptic patients had been previously diagnosed [mean sleep latency on the multiple sleep latency test (MSLT) < or = 5 minutes with two or more sleep-onset rapid eye movement periods (SOREMPs)]. Healthy, normal subjects with a mean sleep latency on the screening MSLT > or = 8 minutes were randomly assigned to one of two groups (i.e. sleep-deprived and alert). All subjects completed two experimental night and days with at least 5 days between sessions. On the evening prior to each experimental day, narcoleptic and alert subjects spent 8 hours in bed and sleep-deprived subjects spent 0 hours in bed. The following day, all subjects underwent one of two napping conditions, 15 or 120 minutes in bed. Both naps were terminated at noon. Every subject underwent both conditions and the order of conditions was counterbalanced. From 1215 to 1355 hours all subjects underwent a modified MSLT. At 1500 hours, the subjects had a 1-hour nap. The results showed that the 120-minute nap condition was more beneficial than the 15-minute nap. Narcoleptic and sleep deprived subjects were shown to have comparable levels of sleepiness on the modified MSLT. However, a differential response pattern on their latency to sleep was noted on the 1-hour nap. Sleep-deprived subjects were shown to be differentially more alert following a 120-minute nap opportunity. In contrast, for narcoleptic patients the beneficial effects of the nap were lost when tested 3 hours later. These results show that narcoleptic patients benefit from a longer nap but that these benefits are short-lived.

Adult↗
PubMed2005

[Preparation of polyclonal and monoclonal antibodies against CRF and change of CRF in the sleep-deprived rat brain].

AIM: To produce polyclonal and monoclonal antibodies against corticotropin-releasing factor (CRF) and to study the changes of CRF in sleep-deprived rat brain with the antibodies acquired. METHODS: Commercial CRF was linked to bovine throglobulin (BTG) and bovine serum albumin (BSA) respectively to produce immunogen and embedding antigen. New Zealand rabbits and BALB/c mice were immunized with the BTG-CRF immunogen to produce polyclonal and monoclonal antibodies, respectively. The acquired antibodies were appraised with ELISA and immnohistochemical staining. The characterized antibodies were used to observe the changes of CRF in the rat brain 48 h after sleep deprivation. RESULTS: CRF polyclonal antibody and 9 clones of monoclonal antibodies were obtained with high titer, affinity and specificity. Among them, the polyclonal antibody and 2 monoclonal antibodies (1D10, 2F4) were excellent in immunocytochemical staining. The CRF-like immunoreactive substances were found more strongly expressed in the neurons of paraverticular hypothalamic nucleus (PVN), central subnucleus of amygdala (CeA), oval subnucleus of bed nucleus of stria terminalis (BNSTov), and nucleus of solitary tract (NTS) in sleep-deprived rat brain. While they were much weaker and even absent in the control. CONCLUSION: The polyclonal and monoclonal antibodies against CRF were successfully produced for immunocytochemical studies. The results indicate that CRF may play an important role in stress-responsive modulation during sleep deprivation. PVN, CeA and BNSTov are integral part of brain circuit related to the stress modulation.

Animals↗
PubMed2003

Variable-interval reinforcement schedule value influences responding following REM sleep deprivation.

The effects of rapid-eye movement sleep deprivation (REMSD) in rats were studied in relation to variable-interval (VI) reinforcement schedule value. Initially, lever pressing was maintained on a VI 30-s schedule of food pellet delivery. After a baseline was established, rats were repeatedly exposed to 96 hr of REMSD and control conditions of an equivalent duration. Responding decreased following REMSD but not after exposure to control conditions. Lever pressing was then maintained on a VI 15-s schedule of food pellet delivery and exposure to the REMSD and control conditions was repeated. Under this condition following repeated REMSD exposures, rates of lever pressing became similar to baseline responding. A VI 30-s schedule of food pellet delivery was then reinstated and REMSD and control conditions were repeated. Lever pressing following exposure to the REMSD condition decreased for 3 of 4 rats. Results suggest that VI schedule value influences the effects of REMSD on responding.

Animals↗
PubMed2005

Changes in hypothalamic corticotropin-releasing hormone, neuropeptide Y, and proopiomelanocortin gene expression during chronic rapid eye movement sleep deprivation of rats.

Chronic rapid eye movement (paradoxical) sleep deprivation (REM-SD) of rats leads to two conspicuous pathologies: hyperphagia coincident with body weight loss, prompted by elevated metabolism. Our goals were to test the hypotheses that 1) as a stressor, REM-SD would increase CRH gene expression in the hypothalamus and that 2) to account for hyperphagia, hypothalamic gene expression of the orexigen neuropeptide Y (NPY) would increase, but expression of the anorexigen proopiomelanocortin (POMC) would decrease. Enforcement of REM-SD of adult male rats for 20 d with the platform (flowerpot) method led to progressive hyperphagia, increasing to approximately 300% of baseline; body weight steadily declined by approximately 25%. Consistent with changes in food intake patterns, NPY expression rapidly increased in the hypothalamic arcuate nucleus by d 5 of REM-SD, peaking at d 20; by contrast, POMC expression decreased progressively during REM-SD. CRH expression was increased by d 5, both in mRNA and ability to detect neuronal perikaryal staining in paraventricular nucleus with immunocytochemistry, and it remained elevated thereafter with modest declines. Taken together, these data indicate that changes in hypothalamic neuropeptides regulating food intake are altered in a manner consistent with the hyperphagia seen with REM-SD. Changes in CRH, although indicative of REM-SD as a stressor, suggest that the anorexigenic actions of CRH are ineffective (or disabled). Furthermore, changes in NPY and POMC agree with current models of food intake behavior, but they are opposite to their acute effects on peripheral energy metabolism and thermogenesis.

Animals↗
PubMed1989

Sleep deprivation in the rat: VII. Immune function.

Immune function studies were performed on splenic lymphocytes obtained from rats subjected to total or paradoxical sleep deprivation. Spleen cell counts, in vitro lymphocyte proliferation responses to mitogens, and in vitro and in vivo plaque-forming cell responses to antigens were obtained. Sleep-deprived rats were roughly equivalent to both their yoked controls and home-cage controls in all assays. The results do not support the hypothesis that sleep deprivation results in immune suppression as measured by the above-mentioned parameters.

Animals↗
PubMed1990

Sleep deprivation and cognitive testing in internal medicine house staff.

There is increased concern about the effects of sleep deprivation on physician performance. We administered four standard tests of cognitive function to 23 university hospital house staff. Each physician served as his or her own control, and the tests were administered at rest, after a night on call, and after a night of sleep for recovery. The study was designed so that normal learning would minimize any deterioration in the post-on-call test performance. Statistically significant deterioration occurred in 3 of the 4 tests after a night on call. Even physicians acclimated to sleep deprivation on a regular, every-third-or-fourth-night basis showed functional impairment. The results have implications for patient care under conditions where house staff are stressed by sleep deprivation and prolonged fatigue.

Clinical Competence↗
PubMed2004

Increased hypocretin-1 levels in cerebrospinal fluid after REM sleep deprivation.

Rat cisternal (CSF) hypocretin-1 in cerebrospinal fluid was measured after 6 or 96 h of REM sleep deprivation and following 24 h of REM sleep rebound. REM deprivation was found to increase CSF hypocretin-1 collected at zeitgeber time (ZT) 8 but not ZT0. Decreased CSF hypocretin levels were also observed at ZT8 after 24 h of REM sleep rebound. These results suggest that REM sleep deprivation activates and REM sleep rebound inhibits the hypocretin system. Increased hypocretin tone during REM deprivation may be important in mediating some of the effects of REM sleep deprivation such as antidepressant effects, hyperphagia and increased sympathetic activity.

Animals↗
PubMed1999

Alterations in monoamine neurotransmitters and dendritic spine densities at the medial preoptic area after sleep deprivation.

The experiments were conducted on 24 adult male Wistar rats to find out the alterations in the levels of monoamines and dendritic spine densities in the medial preoptic area and cortex after total sleep deprivation. Noradrenaline was reduced in the medial preoptic area, though there was no significant change in the cortex. Dopamine and serotonin were decreased both in the medial preoptic area and in the cortex. Dendritic spine counts in the medial preoptic area and the motor cortex were increased after total sleep deprivation. Enhanced release of the monoamines and their subsequent breakdown during sleep deprivation could be responsible for the decreased levels of the transmitters. An increase in synaptic activity, resulting in the enhanced release of the transmitters, might be responsible for the increased spine density after total sleep deprivation. Localized changes in noradrenaline levels at the medial preoptic area suggest its involvement in sleep genesis and maintenance, though its possible contribution to other functions like thermoregulation and reproduction cannot be ruled out. As the available literature does not indicate a role for serotonin and dopamine at the medial preoptic area in sleep regulation, these changes may represent their participation in non-sleep functions.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Sleep deprivation in the rat: VI. Skin changes.

All rats subjected to total or paradoxical sleep deprivation by the disk apparatus developed severe ulcerative and hyperkeratotic skin lesions localized to the plantar surfaces of their paws and to their tails. Yoked control rats only occasionally developed similar appearing lesions, which were always much less severe than in deprived rats. The deprived rat lesions could not be explained by pressure, disk rotation, water immersion, infection, necrotizing vasculitis, tyrosinemia, protein deficiency, or reduced rates of mitosis. Thus, although paw and tail lesions constitute a very reliable and severe symptom of total or selective sleep deprivation in the rat that potentially could yield insights into the pathogenic mechanisms induced by sleep loss, the mediation of the lesions remains unknown.

Animals↗
PubMed2004

Methylphenidate does not improve cognitive function in healthy sleep-deprived young adults.

BACKGROUND: Abuse of methylphenidate, a treatment of attention-deficit/hyperactivity disorder, is reported to be increasing among students for the purpose of improving cognition. METHODS: A single capsule, containing methylphenidate (20 mg) or placebo, was administered to healthy young adults orally following 24 hours of sleep deprivation. Measurements included percent change in score from sleep-deprived baseline on four standardized tests of cognitive function: Hopkins Verbal Learning, Digit Span, Modified Stroop, and Trail Making tests. Measurements also included percent changes in blood pressure and heart rate from sleep-deprived baseline and plasma methylphenidate concentration. RESULTS: Differences in cognitive test performance were not observed between intervention groups. In subjects receiving methylphenidate, mean percent changes from baseline for systolic blood pressure and heart rate were increased relative to placebo between 90 and 210 minutes following capsule administration (maximum increases of 9.45% and 11.03%, respectively). The timing of peak differences in physiologic measures did not correlate with peak serum methylphenidate concentrations. Exit questionnaire ratings of "capsule effect" and perceived performance on the postcapsule administration of the most challenging cognitive test were both higher (p = .044 and p = .009, respectively) for the methylphenidate group than for the placebo group. CONCLUSIONS: Cognitive improvement among sleep-deprived young adults was not observed following methylphenidate administration. Benefits perceived by abusers may relate to increased confidence and sense of well-being, as well as to sympathetic nervous system stimulation. Moreover, methylphenidate administration results in physiologic effects that could be harmful to certain individuals.

Adult↗
PubMed1992

Effect of sleep deprivation on the EEG of learning-impaired children with absence seizures.

Learning-impaired children can present with a clinical history suggesting additional problems, including attention deficit disorder and absence seizures. Physicians use clinical judgment in diagnosing the former, but rely heavily on the electroencephalogram (EEG) to diagnose the latter. Most clinicians are reluctant to treat patients with anticonvulsants without seeing 3 Hz spike-and-wave discharges in an EEG. We studied 21 learning-impaired and 7 control children, ages 5 through 12 years, with normal baseline EEGs. All had an additional EEG recorded after 24 hour sleep deprivation. Nine learning-impaired children had a history compatible with absence seizures; 8 of them showed spike-and-wave discharges after sleep deprivation. Of the 12 learning-impaired children with no history of absence seizures, 2 showed spike-and-wave discharges after sleep deprivation. These results are significant (p less than 0.001). Of the 7 controls, none had epileptiform activity following sleep deprivation. Our results show that routine EEGs may be falsely negative in patients with absence seizures, and that sleep deprivation is a potent activator.

Cerebral Cortex↗
PubMed1977

Comparative study of efficacy of waking and sleep recordings following sleep deprivation as an activation method in the diagnosis of epilepsy.

In the present work, on the basis of an unselected collection of patients suspected of epilepsy, the diagnostic value of waking and sleep recordings each after 24 h sleep deprivation are compared with one another. Indicative findings of epilepsy were found in 16.7% of the cases in the waking EEG after sleep deprivation. In the sleep EEG after sleep deprivation this amounted to 57.1%. These figures speak for the advantage of the second method. The result is highly significant with a chi2 value of 13.01 (p less than 0.01).

Adolescent↗
PubMed2003

Functional reactivity of central cholinergic systems following desipramine treatments and sleep deprivation.

This study examined the effects of acute and chronic desipramine, 24-h total sleep deprivation (TSD) and 96-h REM sleep deprivation (REMSD) on physostigmine-induced hypothermia, analgesia and behaviour. The effects of acute and chronic desipramine treatment on oxotremorine-induced hypothermia were also examined. Intraperitoneal administration of physostigmine (0.5 mg/kg i.p.) induced hypothermia, analgesia, purposeless chewing movements (chewing) and head tremors. While atropine given in a low dose (1.0 mg/kg i.p. 15 min prior) did not antagonize the hypothermia, chewing and head tremor associated with physostigmine (0.5 mg/kg i.p.), a higher dose of atropine (10 mg/kg i.p. 15 min prior) decreased physostigmine-induced hypothermia, chewing and head tremor behaviour. Chronic (10 or 20 mg/kg i.p. daily for 10 days and withdrawn 24 h prior, chronic DMI) and acute (10 mg/kg, i.p. + 60 min prior, acute DMI) desipramine treatments abolished physostigmine (0.5 mg/kg i.p.)-induced hypothermia compared with saline pretreatment. Interestingly atropine (1 mg/kg i.p. 15 min prior) reversed the inhibitory effect of chronic DMI on hypothermia induced by physostigmine. Acute but not chronic DMI decreased physostigmine-induced chewing and head tremor behaviour. Atropine (1 mg/kg i.p. 15 min prior) increased the inhibitory action of acute DMI on physostigmine-induced chewing behaviour. Acute DMI (10 mg/kg i.p.) decreased oxotremorine (0.1 mg/kg i.p.)-induced hypothermia, while chronic DMI increased the hypothermic effect of oxotremorine. TSD and REMSD did not alter physostigmine (0.5 mg/kg i.p.)-induced hypothermia; however, REMSD and stress decreased physostigmine-induced analgesia and chewing.It is suggested that chronic desipramine treatment decreased physostigmine-induced hypothermia by causing hypersensitivity of pre-synaptic muscarinic receptors, whereas acute desipramine decreased the sensitivity of post-synaptic muscarinic receptors

Adrenergic Uptake Inhibitors↗
PubMed1991

Sleep deprivation, epilepsy and the ability to operate a motor vehicle.

This study is based upon 207 examinations for the evaluation of the ability to operate a motor vehicle in persons with transient disturbances of the cerebral function. In 26 persons, the EEG was repeated after sleep deprivation. There was EEG activation with transient disturbances in seven cases (not present in the routine EEG). In five individuals, there were transient disturbances in the routine EEG as well as after sleep deprivation. No abnormalities were recorded in 14 persons. No driver's license could be granted in five patients with unequivocal spike wave complexes or spike wave paroxysms following sleep deprivation. In two patients, however, the permission to drive could be granted. These patients showed spike wave patterns in the routine EEG, but no seizures had occurred for several years and their performance in the experimental-psychological evaluation (with simulator) were superior. In persons with suspected and clinically obscure cerebral attacks, as well as in persons with known seizure disorder but seizure-free for several years, the EEG after sleep deprivation must be regarded as a highly informative test which may crucially influence the decision. The method of activation corresponds with a type of stress with which the motorist must deal frequently. This test can be carried out on an outpatient basis and with negligible iatrogenic damage.

Adult↗
PubMed1986

Increased aggression after rapid eye movement sleep deprivation in Wistar rats is not influenced by reduction of dimensions of enclosure.

Twelve female and twelve male Wistar rats were assigned to home groups, platform-control groups, and rapid eye movement sleep deprivation groups. The deprivation was performed with the cuff-pedestal method. Rats were tested in pairs in a shrinking chamber to increase proximity of the rats and to provoke interaction between them. An increase in boxing behavior was noted in the sleep-deprived groups. The result confirms that deprivation of rapid eye movement sleep increases aggressive behavior in the rat. However, this behavior is not influenced by the area of the testing arena. The sleep-deprived females explored each other more than the controls; the males' behavior did not differ in this respect. The amount of genital exploration decreased with diminishing area of enclosure, whereas boxing was not area dependent.

Aggression↗