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PubMed1997

The diagnostic yield of a second EEG after partial sleep deprivation: a prospective study in children with newly diagnosed seizures.

PURPOSE: To assess the diagnostic yield of a repeated EEG (REPEEG) after partial sleep deprivation (SD) in children and adolescents with one or more seizures who previously had had a standard EEG (STDEEG) without epileptiform abnormalities (EAs). In the literature, 32-75% of such REPEEGs after SD were reported to show EA. METHODS: In a prospective, multicentred study, we selected children aged 1 month to 16 years with one or more idiopathic or remote symptomatic newly diagnosed seizures. A REPEEG was recorded in children without EAs in their STDEEG. RESULTS: Of 552 children and adolescents who entered the study, 243 (44%) had a STDEEG without EAs. In 177 (73% of eligible children), REPEEGs were recorded after SD. We found EAs in 61 (34.5%) REPEEGs and new nonepileptiform abnormalities in five (1%). In 552 children in the total cohort, the REPEEG thus added 11% with EAs to the 56% with EAs in the STDEEG. Of REPEEGs, 81% included sleep compared with 20% of STDEEGs. In about half the REPEEGs, EAs occurred during sleep only. One child had tonic-clonic seizures probably related to the SD. CONCLUSIONS: One third of REPEEGs yielded new diagnostic information. Partial, age-dependent SD was highly effective in inducing sleep, which is important because in many cases EAs were found only during EEG recording in sleep. The procedure was safe and convenient.

Adolescent↗
PubMed1978

Sleep deprivation and electroencephalographic abnormalities.

Thirty-three patients suspected of having a seizure disorder had routine electroencephalograms (EEG's) followed by post-sleep deprivation (P-SD) EEG's. The P-SD EEG's revealed abnormalities in 33% of those patients with a normal routine EEG. All of those patients with P-SD activation had histories highly suggestive of a seizure disorder. Most patients with normal P-SD EEG's were not highly suspect for seizures, however, several patients with probable seizures were also normal P-SD. Most patients with abnormal routine EEG's continue to show comparable abnormalities P-SD, with enhancement of abnormality in some cases and diminished abnormality in few cases.

Adolescent↗
PubMedDate not supplied

Worsening of delusional depression after sleep deprivation: case reports.

Five patients (three bipolars and two unipolars) affected by a major depressive episode with psychotic features were treated with total sleep deprivation (TSD) without concurrent psychotropic medication. After TSD we observed a worsening in psychotic as well as in depressive symptoms as rated on the Dimension of Delusional Experience Rating Scale and on Hamilton Rating Scale for Depression, respectively. TSD is known to markedly enhance the activity of brain monoaminergic pathways. Given the interaction between brain serotonergic and dopaminergic systems in delusional depression, it is possible that an enhancement in dopaminergic activity may be responsible of the symptomatological worsening in delusional depressives observed after TSD.

Adult↗
PubMed1980

Effect of repeated sleep deprivation on clinical symptoms and the TRH test in endogenous depression.

Twenty-eight patients with endogenous depression were treated with repeated total sleep deprivation (TSD) as the only treatment. In eight patients complete remission was obtained, but an early relapse occurred in five, and after 6 months only three patients (11%) remained in remission. The remaining group of 20 patients with no or only a partial response to TSD also had a significant reduction of the score on the Hamilton Rating Scale (median 23 versus 17, P less than 0.01). A thyrotropin-releasing hormone (TRH) stimulating test was performed before and after TSD. According to previous studies an increase of the maximal response in serum thyrotropin (TSH) to TRH (delta delta max TSH greater than 2.0 microU/ml), after TSD was taken as a predictor of a favourable long-term outcome. Under blind conditions a correct prognosis was made in all patients (n = 8) from the group of responders. By comparison, only two of the 20 patients from the nonresponding group had a delta delta max TSH greater than 2.0 microU/ml after TSD.

Adult↗
PubMed1994

Chlorpromazine versus sleep deprivation in activation of EEG in adult-onset partial epilepsy.

We prospectively compared the activating effect of chlorpromazine (CHLP, 50 mg, i.m.) versus sleep deprivation (SD) in 41 patients with a clinical diagnosis of partial epilepsy. Patients were selected on the basis of both seizure onset in adulthood and normal interictal awake EEG recordings. Twenty out of 41 patients (group A) were not yet treated because of either recent onset of epilepsy or misdiagnosis. The remaining 21 patients (group B) were treated with antiepileptic drugs (AED). A control group consisted of 18 healthy, volunteers (group C). All EEG recordings were scored by one observer according to a fixed protocol. In group A, SD and CHLP activated sleep EEG in 12 (60%) and 19 (95%) patients, respectively. This difference reached the limit of statistical significance (P = 0.05, McNemar test). In group B, SD and CHLP activated sleep EEG in 12 (57%) and 13 (62%) patients respectively. There was a significant (P < 0.02, exact Fisher test) intergroup difference (95% vs 62%) with respect to the activating effect of CHLP. No false-positive results were found in 18 control subjects. SD or CHLP activating procedures did not provoke any epileptic seizures in any of the groups. In conclusion, EEG activation by either SD or CHLP is highly specific in the diagnosis of adult-on-set partial epilepsy. Moreover, CHLP is more sensitive than SD in untreated patients, whereas the activating effect of CHLP may be partially attenuated by AED.

Adolescent↗
PubMed1992

Therapeutic sleep deprivation in a depressed patient: prolongation of response with concurrent thyroxine.

A 53-year-old woman with major depression was studied throughout 7 trials of therapeutic sleep deprivation (SD). Under conditions where the patients was either medication-free or receiving antidepressant therapy, improvement with SD was followed by full relapse on returning to sleep. Four SD sessions conducted while the patient was receiving thyroxine each resulted in remission, sustained for several days. These results suggest that the beneficial effects of SD may be mediated by thyroid hormones, or associated activity in the hypothalamic-pituitary-adrenal axis.

Antidepressive Agents↗
PubMed1975

Periodic sleep apnea: chronic sleep deprivation related to intermittent upper airway obstruction and central nervous system disturbance.

Periodic sleep apnea may be due to repeated episodes of upper airway obstruction in patients who have a short thick neck and/or large jowls. Apnea due to complete cessation of breathing may occur to a lesser extent. Anaylsis of the sleep electroencephalogram shows that these patients rarely achieve deep sleep and have less stage 1-REM sleep than normal subjects of comparable age. They are chronically sleep-deprived, a manifestation expressed by daytime somnolence, chronic fatigue and often by personality disturbances marked by paranoia, agitated depression and hostility. The definitive diagnosis of this syndrome may be established by monitoring during sleep, the electroencephalogram, measuring abdominal excursions through a mercury-in-Silastic-strain gauge and recording air flow at the nose by means of a thermocouple. As demonstrated by other investigators, chronic hypoventilation during sleep leads to both pulmonary and systemic arterial hypertension, which may produce generalized cardiac enlargement and congestive heart failure. The abnormalities in the periodic sleep apnea syndrome are abolished by establishing a patent airway either through tracheostomy or weight reduction.

Adult↗
PubMed1995

Sleep deprivation increases brain serotonin turnover in the Djungarian hamster.

Djungarian hamsters well adapted to a short photoperiod were subjected to 4 h of total sleep deprivation (SD) by gentle handling. Tissue concentrations of monoamines and of their metabolites were measured from several brain areas using HPLC with electrochemical detection. The 5-hydroxyindoleacetic acid/5-hydroxytryptamine (5-HIAA/5-HT) ratio was significantly increased after SD in the hippocampus, hypothalamus and brain stem, indicating increased serotonin (5-HT) turnover in those areas, while no changes were found in the frontal cortex and olfactory bulb. Dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) concentrations were elevated in the hypothalamus, while the noradrenaline concentrations did not change in any of the measured areas. We conclude that a short SD, which has been shown to elevate EEG slow-wave activity during recovery sleep, specifically increases 5-HT turnover in the brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1996

Dopamine agonist amineptine prevents the antidepressant effect of sleep deprivation.

In a double-blind study, the effects of the interaction between the administration of amineptine versus placebo and repeated cycles of total sleep deprivation (TSD), which is thought to act through an enhancement in dopaminergic transmission, were analyzed. Twenty-two consecutively admitted patients with bipolar depression formed the study group. Repeated administrations of TSD significantly enhanced perceived mood levels in placebo-treated patients, while amineptine administration blocked the antidepressant action of TSD. Hypothesized changes in brain dopaminergic transmission attributable to amineptine pretreatment are discussed.

Adult↗
PubMed2005

Noradrenergic system interacts with genital reflexes induced by cocaine in paradoxical sleep-deprived male rats.

Different doses of alpha-1, alpha-2, beta-1, and beta-2 adrenoceptor agonists or antagonists were administered to paradoxical sleep-deprived (PSD) rats prior to cocaine administration. Methoxamine reduced the percentage of rats displaying erection, whereas prazosin did not. Yohimbine significantly decreased this percentage. For beta-1 adrenoceptor drugs, both compounds reduced the percentage of rats displaying erection at the highest dose; beta-2 adrenoceptor drugs had no effect. Except for clonidine, all drugs significantly reduced the frequency of erection. Ejaculation was significantly decreased following yohimbine and beta-1 drugs, whereas it was completely abolished by prazosin. The results showed that noradrenergic drugs inhibited genital reflexes in PSD rats, with distinct responses in relation to their respective action over the adrenoceptor.

Adrenergic Agonists↗
PubMed1977

MHPG excretion during sleep deprivation in endogenous depression.

MHPG excretion of 14 endogenously depressive patients and 5 healthy controls was investigated before, during and after a night of sleep deprivation (SD). Patients having a minimum improvement of 40% in the Cronholm-Ottoson rating scale had shown a significantly higher MHPG excretion in the night before SD ( p less than 0.02) as compared to the non-improved group. The MHPG excretion of the night before SD shows a significant negative correlation, both with the depression score according to Cronholm-Ottoson (p less than 0.05) and with the self-rating score according to von Zerssen (p less than 0.005), on the day after SD. No correlation was found between the motor activity measured by pedometer and MHPG excretion. The results are discussed in connection with values found in controls.

Adult↗
PubMed2006

REM sleep deprivation attenuates actin-binding protein cortactin: a link between sleep and hippocampal plasticity.

Rapid eye-movement sleep (REMS) is thought to affect synaptic plasticity. Cortactin is a cytoskeletal protein critically involved in the regulation of actin branching and stabilization including the actin backbone of dendritic spines. Hippocampal cortactin levels, phosphorylation, and processing appear to be altered during learning and long-term potentiation (LTP); consistent with a role for cortactin in the dendritic restructuring that accompanies synaptic plasticity. In this study juvenile male Sprague-Dawley rats were selectively REMS-deprived (RD) for 48 h by the flowerpot method. Cage control (CC) and large pedestal control (PC) animals were used for comparison. Animals were euthanized immediately, or 12 h, after removal from the pedestal. The hippocampus was dissected, flash-frozen, and stored for subsequent Western blot or quantitative RT-PCR analysis of cortactin. Cortactin mRNA/cDNA levels initially rose in PC and RD rats but returned to CC levels by 12 h after removal from the pedestal. Predictably cortactin protein levels were initially unchanged but were up-regulated after 12 h. The PC group had more total and tyrosine-phosphorylated cortactin protein expression than the RD and CC groups. This increase in cortactin was likely due to the exposure of the rats to the novel environment of the deprivation chambers thus triggering plasticity events. The lack of REMS, however, severely hampered cortactin protein up-regulation and phosphorylation observed in the PC group suggesting an attenuation of plasticity-related events. Thus, these data support a functional link between REMS and cytoskeletal reorganization in the hippocampus, a process that is essential for synaptic plasticity.

Actins↗
PubMed2000

Total sleep deprivation combined with lithium and light therapy in the treatment of bipolar depression: replication of main effects and interaction.

The clinical usefulness of total sleep deprivation (TSD) in the treatment of bipolar depression is hampered by a high-rate short-term relapse. Previous literature has suggested that both long-term lithium treatment and light therapy could successfully prevent relapse. We randomized 115 bipolar depressed inpatients to receive three cycles of TSD, alone or in combination with morning light exposure, given at an intensity of 150 or 2500 lux. Forty-nine patients were undergoing long-term treatment with lithium salts (at least 6 months), while 66 patients were taking no psychotropic medication. Mood was self-rated by the Visual Analogue Scale three times a day during treatment. The results showed that both light therapy and ongoing lithium treatment significantly enhanced the effects of TSD on the perceived mood, with no additional benefit when the two treatments were combined. Subjective sleepiness during TSD, as rated by the self-administered Stanford Sleepiness Scale, was significantly reduced by light exposure, and was correlated with the outcome. This study confirms the possibility of obtaining a sustained antidepressant response to TSD in bipolar patients.

Adult↗
PubMed2003

[Expression changes of nitric oxide synthase mRNA of hypothalamus after sleep deprivation in rats].

OBJECTIVE: To study the effects of rapid eye movement sleep (REMS) deprivation on the expression of mRNA coding for neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) of hypothalamus in rats. METHOD: Flower pot technique was adopted to deprive the REMS of Sprague-Dawley rats for 24 h, 48 h and 72 h respectively. The expression of mRNA coding for nNOS or iNOS of hypothalamus in rats was assayed by reverse-transcription polymerase chain reaction (RT-PCR). RESULT: The amount of nNOS mRNA was significantly higher in 24 h REMS deprivation group (P<0.01), then the amount was lowered in 48 h deprivation group and became significantly lower in 72 h deprivation group than that in the control group (P<0.05). There was low expression of iNOS mRNA of hypothalamus in rats, and there was no difference in the expression of iNOS mRNA among 24 h, 48 h REMS deprivation and the control groups. But the expression was significantly increased in 72 h REMS deprivation group (P<0.01). CONCLUSION: Deprivation of REMS increased the expression of nNOS and iNOS mRNA of hypothalamus. Excessive nitric oxide (NO) might be a major factor resulting in not only the sleep rebound phenomenon but also the injury of human function caused by sleep loss directly or indirectly by other sleep factors.

Animals↗
PubMed1967

Rapid eye movement sleep deprivation: a central-neural change during wakefulness.

Three adult cats were deprived of rapid eye movement sleep for six separate periods of up to 32 days. Animals were allowed normal amouints of sleeping time during which rapid eye movement sleep was interrupted, whenever it occurred, by human observers who continually monitored the animals and their electrocortical activity. Cortical responses evoked by pairs of acoustic clicks were recorded during wakefulness. Recovery functions derived from these data were facilitated during periods of deprivation of rapid eye movement sleep and returned to base-line values when animals were allowed normal amounts of this sleep phase. This change was noted repeatedly within, as well as between, subjects. It did not occur during control periods when non-rapid eye movement sleep was interrupted on identical schedules, nor did it occur when the cats were deprived of all sleep for 22 hours a day for 5 days.

Animals↗
PubMed2004

Over-expression of inducible heat shock protein 70 in the gastric mucosa of partially sleep-deprived rats.

BACKGROUND: Previous findings have demonstrated increased expression of inducible heat shock protein 70 (iHSP70) in the gastric mucosa of rats exposed to partial sleep deprived (PSD). The purpose of this study was to investigate the functional role of iHSP70 and its relationship with acid secretion in the stomachs of PSD animals. METHODS: A slowly rotating drum was used to induce PSD in male Sprague-Dawley rats with or without omeprazole treatment. Gastric mucosal samples were harvested for iHSP70 mRNA and protein analysis with RT-PCR and Western blotting, respectively. Enzyme immunoassay was used to determine plasma gastrin level and gastric acidity was measured by titration. The modulating effect of PSD on 0.6 M hydrochloric acid (HCl)-induced gastric damage was also evaluated. RESULTS: PSD increased plasma gastrin, gastric acidity and expression of iHSP70, while significantly reducing HCl-induced gastric damage. Omeprazole administration decreased gastric acidity and reversed iHSP70 over-expression in PSD rats. CONCLUSIONS: PSD increases gastric acidity which enhances expression of mucosal iHSP70. Over-expression of iHSP70 may be a protective homeostatic response of the stomach to stress induced by PSD and acid secretion.

Animals↗
PubMed2003

Effect of paradoxical sleep deprivation and stress on passive avoidance behavior.

Previous studies have shown that several types of stress can induce memory impairment. However, the memory effects of paradoxical sleep deprivation (PSD), a stressor in itself, are unclear. We therefore compared passive avoidance behavior of rats undergoing PSD and PSD stress yoked-control (PSC) using the "reversed flowerpot method." When rats were kept isolated on a PSC platform for 24 h immediately after criterion training, retention trials showed impaired aversive memory storage. When delayed for 24 h after criterion training, PSC stress did not disrupt retention performance. In rats subjected to PSD, either immediately or 24 h after criterion training, there was no disruption of aversive memory consolidation. These results suggest that, during stress, paradoxical sleep plays a role in erasing aversive memory traces, in line with the theory that we "dream in order to forget."

Analysis of Variance↗