Poor recovery sleep after sleep deprivation in delayed sleep phase syndrome

To clarify disturbances in sleep regulation in patients with delayed sleep phase syndrome (DSPS), we studied three patients with DSPS and seven healthy controls. Sleep propensity and melatonin rhythms after 24-h sleep deprivation were investigated under dim light condition by using the ultra-short sleep-wake schedule. The sleep propensity curves displayed clear differences between DSPS patients and the controls. During the subjective day when melatonin was not produced, recovery sleep after the sleep deprivation did not occur in DSPS patients, while recovery sleep occurred during the subjective day in controls. This suggests that DSPS may involve problems related to the homeostatic regulation of sleep after sleep deprivation.     

Acute sleep deprivation reduces amygdala-kindled seizure thresholds in cats

It is well known that sleep loss activates human and experimental epilepsy. Because sleep deficits are also common among epileptics, it is possible that sleep loss enhances seizures by worsening these spontaneous sleep abnormalities. We examined this hypothesis by documenting the effects of acute (72 h) sleep deprivation on seizures in fully kindled cats. We have reported elsewhere sustained decrements in both slow-wave sleep (SWS) and rapid-eye-movement (REM) sleep with the development of amygdala kindling in this species. In the present experiment, eight cats underwent an A₁ B₁ A₂ paradigm in which sleep state physiology (12-h polygraphic recordings) and seizure thresholds were examined in both an experimental (sleep deprivation) and control (nonsleep deprived) sequence of conditions, with order of presentation counterbalanced. Sleep deprivation was produced by a modification of the “flower pot” procedure and involved placing the cat on a small platform over water so as to prevent REM sleep. In the control sequence, cats underwent the same procedure except the platform was large enough to allow normal SWS and REM sleep. A significant reduction in both REM and SWS sleep occurred exclusively during the experimental B₁ condition and was accompanied by a significant reduction in seizure threshold for partial or generalized tonic-clonic convulsions. These findings indicated that this procedure, thought to influence only REM sleep, also disrupts SWS; further, this generalized disruption of sleep reduced kindled seizure thresholds, perhaps by compounding existing sleep deficits. Collectively, these observations again suggest that the integrity of both SWS and REM sleep may be an important consideration in the etiology of amygdala-kindled seizures.     

White blood cells and cortisol after sleep deprivation and recovery sleep in humans

Sleep deprivation (SD) has enriched our treatment programme for major depression. SD has been demonstrated to modify different host defence activities. There is some evidence that there are reciprocal relationships between immune function and increased hypothalamic-pituitary-adrenocortical (HPA) axis activity in depression. We therefore investigated the number of leukocytes, granulocytes, monocytes, lymphocytes, B cells, T cells, helper T cells, cytotoxic T cells, NK cells and salivary cortisol in 10 healthy men before and after total SD (TSD) as well as after recovery sleep. Blood samples were drawn on 3 consecutive days at 7 am, 1 pm and 7 pm, respectively. Comparison of the 7 am values by contrast analysis yielded significant differences for granulocytes (p = 0.044) and NK cells (p = 0.001) after SD and recovery sleep. NK cells decreased and granulocytes increased after SD and after recovery sleep. Significant differences between single points in time across the day were found for granulocytes (p = 0.022), monocytes (p = 0.031), T cells (p = 0.005), helper T cells (p = 0.004), cytotoxic T cells (p = 0.005) and NK cells (p = 0.017). No significant difference could be detected for leukocytes, lymphocytes and B cells counts. These results favour the thesis that SD and recovery sleep lead to changes in the distribution of peripheral leukocytes, especially in a reduction of NK cells after SD and recovery sleep. The cortisol rhythm was affected neither by SD nor recovery sleep.     

Impact of sleep deprivation and subsequent recovery sleep on cortisol in unmedicated depressed patients

OBJECTIVE: One night of sleep deprivation induces a transient improvement in about 60% of depressed patients. Since depression is associated with abnormalities of the hypothalamic-pituitary-adrenal (HPA) axis, the authors measured cortisol secretion before, during, and after therapeutic sleep deprivation for 1 night. METHOD: Fifteen unmedicated depressed inpatients participated in a combined polysomnographic and endocrine study. Blood was sampled at 30-minute intervals during 3 consecutive nights before, during, and after sleep deprivation. Saliva samples were collected at 30-minute intervals during the daytime before and after the sleep deprivation night. RESULTS: During the night of sleep deprivation, cortisol levels were significantly higher than at baseline. During the daytime, cortisol levels during the first half of the day were higher than at baseline in the patients who responded to sleep deprivation but not in the nonresponders. During recovery sleep, cortisol secretion returned to baseline values. CONCLUSIONS: This study demonstrated a significant stimulatory effect of 1 night of sleep deprivation on the HPA axis in unmedicated depressed patients. The results suggest that the short-term effects of antidepressant treatments on the HPA axis may differ from their long-term effects. A higher cortisol level after sleep deprivation might transiently improve negative feedback to the hypothalamus or interact with other neurotransmitter systems, thus mediating or contributing to the clinical response. The fast return to baseline values coincides with the short clinical effect.     

Estradiol treatment modulates spontaneous sleep and recovery after sleep deprivation in castrated male rats

Exogenous estradiol (E) is used occasionally to treat the side effects associated with androgen-deprivation in men, but its effects on sleep patterns have received little attention. We examined whether E modulates sleep patterns and recovery from sleep loss in castrated male rats. Adult male rats were castrated and implanted subcutaneously with Silastic tubes containing either oil (Cast + Oil) or E (Cast + E). Sham-operated male rats (Intact) were implanted with oil-filled tubes. All rats were also implanted with EEG and EMG electrodes for sleep/wake recordings. After two weeks, polysomnographic recordings were made before, during, and following 6 h of sleep deprivation (SD). At baseline, the Cast + Oil group showed sleep and EEG patterns similar to those in the Intact group. Compared to these groups, the Cast + E group spent more time awake during the dark (active) phase, and showed higher EEG theta power (a measure of cortical activation) during wake and rapid eye movement (REM) sleep in both the light and dark phases. Following SD, the Cast + E group showed a larger increase from baseline in REM sleep amount, compared to the Cast + Oil group. The Cast + Oil group showed prolonged rebound in non-REM sleep and EEG delta power, and reduced REM sleep rebound, compared to the other two groups. These results indicate that E treatment in castrated male rats promotes baseline wakefulness during the active phase, and facilitates recovery of REM sleep after acute sleep loss. The possible benefit of E treatment for improving sleep quality in androgen-deprived men remains to be investigated.     

The diagnostic value of the short sleep EEG and other provocative methods following sleep deprivation

Summary One hundred and eighty-five EEGs recorded after deprivation of sleep for 24h were evaluated. Valuable diagnostic information was found in 59% of the EEG recordings; 24% of the EEGs contained seizure activity. The duration of the stages of sleep and the frequency of seizure activity, paroxysmal sharp wave groups and localizing findings were analyzed. The sleep stages A to C (based on the Loomis scale) were reached for about equal duration by an EEG recording of 30–40 min; sleep stage D was reached only shortly and stage E was not observed. Pathological EEG findings appeared for the most part in the sleep stages A and B. Localized findings were pronounced in stage C. No significant differences pertaining to the occurrence and form of EEG patterns were found between patient groups with primary generalized seizures, psychomotor seizures or those with unclarified disturbances of consciousness. The combination of the short sleep EEG following 24h of sleep deprivation with subsequent use of the additional provocative methods of hyperventilation, photostimulation and hydration, yielded, in all, new information in 50% of the patients. Each of these additional methods contributed nearly equally to this information.

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Zusammenfassung Es wurden 185 EEGs nach 24h Schlafentzug ausgewertet. Hiervon enthielten 110 EEGs (59%) diagnostisch weiterführende Befunde. In 24% fand sich Krampfaktivität. Es wurden die Dauer der Schlafstadien, die Häufigkeit des Auftretens von Krampfaktivität, paroxysmalen Steilwellengruppen und Lokalbefunden analysiert. Die Schlaftiefen A bis C (nach Loomis) wurden während einer EEG-Ableitung von 30–40 min gleichmäßig lang, Stadium D nur kurz, Stadium E nicht erreicht. Pathologische EEG-Befunde traten überwiegend in den Schlafstadien A und B auf. Lokalbefunde fanden sich besonders im Stadium C. Zwischen den Patientengruppen mit primär generalisierten Anfällen, psychomotorischen Anfällen sowie Zuständen ungeklärter Bewußtseinsstörung fand sich kein signifikanter Unterschied hinsichtlich Auftreten und Ausprägung der EEG-Veränderungen. Die regelmäßig durchgeführte Hyperventilation und Fotostimulation und die Flüssigkeitsbelastung, die nur bei negativen Vorbefunden zusätzlich durchgeführt wurde, ergaben zusammen in 50% eine neue Information.

     

Changes in cognitive processing following short-term cumulative partial sleep deprivation and recovery oversleeping

Abstract

The effects on cognitive processing of 1 and 5 cumulative nights of partial sleep deprivation (PSD) and 1 and 2 nights of subsequent recovery oversleep was studied using an anagrams test and the Wisconsin Card Sorting Test. Seven paid undergraduate volunteers (5 male; 2 female) aged 18–23 who had normative 6.5–8.0 hr sleep patterns participated. They followed an 8-day schedule of morning and afternoon testing sessions consisting of 2 days in each of the experimental conditions: prebase-line, PSD, recovery sleep, and postbaseline. Sleep duration was calculated relative to individual habitual by subtracting 40% per night (PSD) and adding 40% and 20%, respectively (recovery sleep). On the anagrams test, results showed exaggerated time of day differences during both sleep manipulation conditions. Card-sorting performance was characterized by lesser efficiency of cognitive strategies (> non-perseverative errors) during recovery sleep and tendency towards perseveration with sleep loss. Results were discussed with particular reference to hypothesized neural substrates and clinical implications.     

Ocular dominance of cortical cells in cats dark-reared into maturity after short postnatal monocular deprivation

We studied the preservation of the early monocular deprivation effect by rearing kittens in complete darkness for long periods (9.5 to 20 months) after a monocular deprivation period of 4 weeks that was initiated at the age of 1 month (MDDR cats). For comparison, four groups of kittens were used: monocularly deprived as those described above and then reared in normal light conditions (MDN), monocularly deprived at the age of 1 month (MD), and dark-reared (DR) or normally light-reared (NOR) from birth. Recordings from the visual cortex of MDDR and MDN cats showed that there was a clear preference for cells driven only by the experienced eye compared with the deprived eye. This preference was found whether, subsequent to the monocular deprivation period, these cats were dark- or light-reared (P less than 0.005 for MDDR and MDN compared with NOR cats). The difference between the MDDR, MDN, and MD groups of cats was reflected in the proportions of binocularly driven cells; the largest number of binocularly driven cells was found in the MDDR cats. There was no bias toward either eye in the ocular dominance distribution of cortical cells in cats that were reared in total darkness (DR) or in the light under normal conditions (NOR). We thus conclude that the long-term dark period during development did not erase the effect of early monocular deprivation on the cat visual cortex provided that the latter lasted 4 weeks prior to the dark period.     

Quantitative analysis of recovery curves

It is assumed that recovery curves may be produced either by a dynamic process caused by a feedback mechanism or by a linear compensation process which is independent of previous compensation. Based on this assumption, 3 types of recovery functions are derived. Two behavior functions correspond to each of these types of recovery curves, one starting at a low level and the other at a high level. For each of the resulting 6 types of behavior curves, examples of real data have been reported in literature. Elementary parameter estimates are provided and substantial interpretations of the parameters are given. Behavior measures are derived for the data from an illustrative example, and 1 of the 6 behavior curves is fitted to this data. By additionally taking into account a physical repair function which is assumed to cause a certain delay in recovery, it is shown that an even better fit can be achieved.     

睡眠剥夺及睡眠恢复后大鼠中缝核群星形胶质细胞的反应及其与神经元的关系

目的探索睡眠剥夺及睡眠恢复后大鼠脑干中缝核群星形胶质细胞的反应及其与神经元的关系。方法采用小平台水环境法建立大鼠睡眠剥夺模型,20只大鼠分为睡眠剥夺12h组,睡眠剥夺12h恢复睡眠3h组及大平台对照组和正常单独饲养组,每组5只,用免疫组化的方法测量glial fibrillary acidic protein(GFAP)和Fosprotein在脑干中缝核群的表达。结果睡眠剥夺后GFAP-like immunoreaction(LI)星形胶质细胞和FosLI神经元在中缝核群各核有明显表达,睡眠恢复后表达明显减少,两者的变化趋势基本一致。结论睡眠剥夺影响GFAPLI星形胶质细胞和FosLI神经元的表达,提示星形胶质细胞和神经元可能共同参与睡眠调节。     

Quantitative analysis of the effects of slow wave sleep deprivation during the first 3 h of sleep on subsequent EEG power density

Summary The relation between EEG power density during slow wave sleep (SWS) deprivation and power density during subsequent sleep was investigated. Nine young male adults slept in the laboratory for 3 consecutive nights. Sepctral analysis of the EEG on the 2nd (baseline) night revealed an exponential decline in mean EEG power density (0.25–15.0 Hz) over successive nonrapid eye movement — rapid eye movement sleep cycles. During the first 3 h of the 3rd night the subjects were deprived of SWS by means of acoustic stimuli, which did not induce wakefulness. During SWS deprivation an attenuation of EEG power densities was observed in the delta frequencies, as well as in the theta band. In the hours of sleep following SWS deprivation both the power densities in the frequency range from 1 to 7 Hz and the amount of SWS were enhanced, relative to the same period of the baseline night. Both the amount of EEG energy accumulating subsequent to SWS deprivation and its time course could be predicted accurately from the EEG energy deficit caused by SWS deprivation. The data show that the level of integral EEG power density during a certain period after sleep onset depends on the amount of EEG energy accumulated during the preceding sleep rather than on the time elapsed since sleep onset. In terms of the two-process model of sleep regulation (Borbély 1982; Daan et al. 1984) this finding indicates that EEG power density reflects the rate of decay of the regulating variable, S, rather than S itself, as was originally postulated.     

The clinical response to total sleep deprivation and recovery sleep in geriatric depression: potential indicators of antidepressant treatment outcome

The clinical response to antidepressant treatment in late-life depression is often delayed and highly variable. Better indicators of antidepressant efficacy are needed early in the course of treatment, so that augmentation strategies or alternative treatments may be initiated. The goal of this study was to evaluate whether the change in the Hamilton depression rating scale (HDRS) after 36 h of total sleep deprivation (TSD) and recovery sleep predicted clinical outcome after 12 weeks of antidepressant treatment, and whether greater predictive value was observed in certain aspects of depressive symptomology. Fifteen elderly patients diagnosed with major depression underwent combined treatment with an initial 36 hours of TSD and a 12-week trial with the antidepressant paroxetine. Six HDRS subscores were evaluated with respect to how the changes after TSD and after one night of recovery sleep correlated with HDRS scores after 12 weeks of treatment. A significant correlation was obtained between the change in the core depressive symptomology subscale from baseline to recovery sleep and the HDRS score at 12 weeks, but the correlation was not significant when evaluating the change from baseline to TSD. These results indicate that the decrease in symptoms after recovery sleep compared with baseline levels (indicating the persistence of the antidepressant response), rather than the symptom reduction after TSD, has greater predictive value with respect to treatment outcome.     

Topographical changes in N1-P2 amplitude upon awakening from recovery sleep after slow-wave sleep deprivation.

OBJECTIVES: To assess auditory evoked potentials (AEPs) before sleep and upon 3 awakenings during an undisturbed baseline night and to compare them to AEPs during a night characterized by a recuperative increase in the amount of slow-wave sleep (SWS) as a consequence of two consecutive nights of selective SWS deprivation. METHODS: Ten male subjects slept in the laboratory for 6 consecutive nights. The first 2 nights were undisturbed. The 3rd night was considered as baseline. During the 4th and 5th nights, selective SWS deprivation was obtained by means of acoustic stimulation. The 6th night was a recovery. The data reported here were collected during the baseline and the recovery night. Subjects were awakened 3 times: after 2 h, 5 h (nocturnal awakenings) and 7.5 h (final morning awakening) of sleep, respectively. All the awakenings were carried out from stage 2. The AEP recordings were carried out in bed, while subjects were performing a simple auditory reaction time task. RESULTS: The amplitude of the N1-P2 complex decreased upon the first awakening of the baseline night as compared to pre-sleep wakefulness levels; during the recovery night, the decrease of N1-P2 amplitude was present also upon the second and final awakening. N1 latency increased upon the two nocturnal awakenings regardless of the night, while P2 latency was not affected. Moreover, the N1-P2 amplitude increased during recovery at the frontal midline derivation as compared to baseline, while it decreased at Pz and Oz. CONCLUSIONS: The N1-P2 amplitude and, to a lesser extent, the N1 latency, are sensitive in showing a state of brain deactivation during the sleep-wake transition. The decrease of N1-P2 amplitude at the parieto-occipital locations during recovery is coherent with the hypothesis of a functional link between SWS amount and cortical hypoarousal upon awakening. The unexpected increase of the same variable at Fz can be interpreted as the effect of a compensatory effort of the frontal areas for the increased homeostatic drive for sleep during the recovery night.