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PubMed2006

Neuroimaging of sleep and sleep disorders.

Herein are presented the results of research in the area of sleep neuroimaging over the past year. Significant work has been performed to clarify the basic mechanisms of sleep in humans. New studies also extend prior observations regarding altered brain activation in response to sleep deprivation by adding information regarding vulnerability to sleep deprivation and regarding the influence of task difficulty on aberrant responses. Studies in sleep disorder medicine have yielded significant findings in insomnia, depression, and restless legs syndrome. Extensive advances have been made in the area of sleep apnea where physiologic challenges have been used to probe brain activity in the pathophysiology of sleep apnea syndrome.

Depressive Disorder↗
PubMed2005

Intermittent hypoxia causes REM sleep deficits and decreases EEG delta power in NREM sleep in the C57BL/6J mouse.

BACKGROUND AND PURPOSE: Obstructive sleep apnea (OSA) severely impairs sleep architecture. We hypothesized that both intermittent hypoxia (IH) and non-hypoxic arousals of OSA result in significant disruption of non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS). PATIENTS AND METHODS: Polysomnography was performed in C57BL/6J mice (n=5) exposed to IH (cycling of FIO2 from 20.9 to 5.0%) or sleep fragmentation (SF: high flow air blasts) throughout the 12-h light phase over 5 consecutive days. RESULTS: Both IH and SF induced arousals from sleep. On Day 1 of exposure, total NREMS during the light phase decreased comparably during IH (44.1+/-7.8%/12h, P<0.05) and SF (43.7+/-3.3%/12h, P<0.05) but returned to baseline levels of 62.0+/-7.8%/12h by Day 5 of exposure under both conditions. During IH, however, the electroencephalographic (EEG) delta power of NREMS remained impaired throughout the 5-day period of IH with a nadir of 65.4+/-5.6% relative to baseline (P=0.01), and REMS was effectively abolished during the light phase. In contrast, SF did not cause a significant reduction in either EEG delta power or REMS during the light phase. CONCLUSIONS: Thus, hypoxic exposure, but not arousals, caused overall deficits in the EEG delta power of NREMS and marked deficits in the total amount of REMS. We propose that hypoxic arousals may have a more severe impact on sleep architecture in patients with OSA than non-hypoxic arousals.

Animals↗
PubMed1986

L-tryptophan administered to chronic sleep-onset insomniacs: late-appearing reduction of sleep latency.

The effects of 3 g L-tryptophan on sleep, performance, arousal threshold, and brain electrical activity during sleep were assessed in 20 male, chronic sleep-onset insomniacs (mean age 20.3 +/- 2.4 years). Following a sleep laboratory screening night, all subjects received placebo for 3 consecutive nights (single-blind), ten subjects received L-tryptophan, and ten received placebo for 6 nights (double-blind). All subjects received placebo on 2 withdrawal nights (single-blind). There was no effect of L-tryptophan on sleep latency during the first 3 nights of administration. On nights 4-6 of administration, sleep latency was significantly reduced. Unlike benzodiazepine hypnotics, L-tryptophan did not alter sleep stages, impair performance, elevate arousal threshold, or alter brain electrical activity during sleep.

Adult↗
PubMed1996

Low-dimensional dynamic self-organization in delta-sleep: effect of partial sleep deprivation.

Studies on extended data including 37 electroencephalographic (EEC) records of delta-sleep, each 10(3) s long (six subjects: up to seven nights per subject, comprising normal sleep, partial deprivation and recovery), confirmed earlier conclusions that rare episodes of low-dimensional dynamic self-organization, with life-times between 10 and 20 s, are present in stage 4 sleep. Particular care was taken of the Theiler correction which, in some delta-sleep signals, required the deletion of trajectory points covering nearly one pseudo-period. The percentage of segments showing an episode, i.e. the attractor probability, decreased with a change in sleep conditions either deprivation or recovery prior to the next deprivation. Repetition of deprivation over three nights resulted in an adaptation process, manifested by an increase in attractor probability. After the sharp decrease in probability observed when recovery was established prior to the next deprivation, and on return to normal conditions of sleep at 2200 hours, the probability was immediately close to that observed in normal baseline sleep conditions free of any interference. The observation of a definite effect of sleep deprivation and recovery upon the number of stage 4 attractors observed provides a line of approach to the physiological significance of the probability of such attractors.

Adolescent↗
PubMed1987

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

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. Spectral 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.

Acoustic Stimulation↗
PubMed1997

Positron emission tomography studies of sleep and sleep disorders.

Using positron emission tomography (PET) it is possible to perform an in vivo study of cerebral physiological and biochemical processes in man. Employing this technique in sleep studies, decreased cerebral metabolic rates for glucose during slow wave sleep compared with those seen during wakefulness were first demonstrated, whereas similar rates of cerebral glucose metabolism were observed during paradoxical sleep and wakefulness. More recently, regional modifications of cerebral blood flow during sleep have also been demonstrated. During slow wave sleep, cerebral blood flow is decreased particularly in the prefrontal cortex. Rapid eye movement sleep is characterized by activation of the pons, thalami, amygdaloid complexes and a number of cortical areas (e.g. the anterior cingulate cortex). Although data remain incomplete, a variety of sleep disorders, including narcolepsy, fatal familial insomnia and continuous spike-and-wave discharges during slow sleep have been investigated. These results are briefly reviewed.

Brain↗
PubMed1997

The GABAA agonist THIP produces slow wave sleep and reduces spindling activity in NREM sleep in humans.

Recent studies in the rat demonstrated that systemic administration of muscimol and THIP, both selective GABAA receptor agonists, elevates slow wave activity in the EEG during non-rapid eye movement (NREM) sleep. In this placebo-controlled study, we assessed the influence of an oral dose of 20 mg THIP on nocturnal sleep in young healthy humans. Compared to placebo, THIP increased slow wave sleep by about 25 min. Spectral analysis of the EEG within NREM sleep revealed significant elevations in the lower frequencies (< 8 Hz) and reductions in the spindle frequency range (approximately 10-16 Hz). In accordance with previous findings in the rat, these data imply that GABAA agonists promote deep NREM sleep, without suppressing REM sleep. These effects are opposite to those induced by agonistic modulators of GABAA receptors such as benzodiazepines and are at variance with established mechanisms according to which GABAA agonists and modulatory agonists would have similar effects. The sleep response to GABAA agonists is highly similar to that evoked by sustained wakefulness, suggesting that GABAA receptors may be implicated in the homeostatic regulation of sleep.

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↗
PubMed1991

Recovery within day-time sleep after slow wave sleep suppression.

Six subjects had their SWS activity suppressed by acoustic stimulation during a day-time (11.00 h) recovery sleep after a 4 h night sleep (03.00-07.00 h). Sleep was disturbed for a period corresponding to 90% of the duration of a preceding undisturbed baseline sleep (also at 11.00 h and preceded by a 4 h night sleep) and thereafter allowed to continue undisturbed until spontaneous awakening. The results showed that SWS and EEG power density were significantly reduced during suppression and that full recovery occurred before spontaneous awakening. The disturbed sleep was significantly longer than the baseline sleep. The increase in duration consisted mainly of SWS, stage 2 and REM. The results suggest that the suppression of SWS activity caused a need for an extension of sleep in order to allow recovery.

Adult↗
PubMed1995

Sleep-wake cycle abnormalities in fatal familial insomnia. Evidence of the role of the thalamus in sleep regulation.

Alterations in sleep organization were longitudinally studied in 6 new cases of fatal familial insomnia (FFI) by 24 h polygraphic recording. All patients showed an early reduction in sleep spindles and K complexes, and a drastic reduction in total sleep time and disruption of the cyclic sleep organization. Complete abolition of NREM sleep and persistence of only brief residual periods of REM sleep without atonia were features characteristic of the 3 patients with a short (less than 1 year) clinical course, and lacking in the 3 cases with a longer (more than 2 years) disease course. In the latter, sudden transitions from waking to NREM or REM sleep occurred, sometimes recurring periodically. Our findings confirm that impairment of sleep-wake regulation is a consistent distinctive feature of FFI.

Adult↗
PubMed1992

The 5-HT1A antagonist (-)-alprenolol fails to modify sleep or zimeldine-induced sleep-waking effects in rats.

Sleep and waking in rats were studied for 8 h following administration of a selective 5-hydroxytryptamine (5-HT) reuptake inhibitor (zimeldine), a putative 5-HT1A antagonist (L(-)-alprenolol hydrogene tartrate monohydrate [(-)-alprenolol]) and a combination of (-)-alprenolol and zimeldine. Consistent with earlier findings, zimeldine gave a biphasic effect on sleep and waking. Waking was increased during the first 3 h, followed by a small decrease. Deep slow-wave sleep (SWS-2) showed the opposite trend. An initial decrease in SWS-2 was followed by an increase after around 3 h. Rapid eye movement sleep was markedly suppressed and latencies to sleep increased after zimeldine. (-)-Alprenolol had no effects on the different sleep and waking stages or latencies to sleep. The 5-HT1A antagonist also failed to modify the effects of zimeldine administration. The behavioral syndrome induced by a selective 5-HT1A agonist [8-hydroxy-2-(di-n-propyl-amino)-tetralin (8-OH-DPAT)] was clearly antagonized by administration of (-)-alprenolol, indicating that (-)-alprenolol was an efficient 5-HT1A blocker. The data indicate that the sleep-waking effects of zimeldine cannot easily be explained by stimulation of 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1984

Ontogenesis of circadian sleep-wakefulness rhythms and developmental changes of sleep in the altricial rat and in the precocial guinea pig.

Ontogenesis of circadian sleep-wakefulness rhythms and other developmental changes of sleep were examined in the altricial rat and in the precocial guinea pig. Circadian sleep-wakefulness rhythms began to emerge on the 4th-4.5th week after birth in rats born and raised not only under light-dark (LD) 12:12 h lighting schedule but also under a constant light condition. Only ultradian rhythms were recognized in the rat up to 2.5-3.5 weeks after birth. Unlike the rat, the guinea pig did not develop significant diurnal and circadian sleep rhythms during the course of its growth. Sleep-wakefulness rhythms of the 1-week-old infant guinea pig were very similar to those of the adult. During the development of the altricial rat the periods of slow wave sleep (SWS) and paradoxical sleep (PS) cycles, and the amounts of SWS per day increased. On the other hand, the amounts of PS per day and the length of the PS episodes decreased. For the guinea pig, however, these parameters of sleep were apparently constant throughout development.

Aging↗
PubMed1983

The effect of sleep deprivation on sleep in rats with suprachiasmatic lesions.

The effect of 24-h sleep deprivation on sleep was investigated in rats whose circadian rest-activity rhythms were extensively disrupted by bilateral lesions of the suprachiasmatic nuclei (SCN). Sleep deprivation caused an increase in total sleep, REM sleep and the slow wave sleep fraction of non-REM sleep. It is concluded that the homeostatic component of sleep regulation is morphologically and functionally distinct from the circadian component.

Animals↗
PubMed1984

Little sleep-promoting effect of three sleep substances diurnally infused in unrestrained rats.

Delta-sleep-inducing peptide (2.5 nmol), prostaglandin D2 (0.36 nmol) and uridine (10 pmol) were intraventricularly infused for 10 h at daytime in otherwise saline-infused freely moving male rats. In contrast to a nocturnal infusion which may result in marked sleep-promoting effects, such a diurnal infusion brought about almost no change in sleep parameters. It is postulated that the requirement of sleep in rats might be fully achieved at the environmental light period to cancel the effect of the exogenously administered sleep substances. It is proposed that an endogenous sleep substance should be characterized by a property not to cause excessive sleep at the time when sleep is physiologically saturated.

Animals↗
PubMed1993

Sleep homeostasis in the guinea pig: similar response to sleep deprivation in the light and dark period.

In the guinea pig, sleep and slow-wave activity (SWA) are evenly distributed over 24 h in contrast to the sleep pattern in other rodents where a daily preference for sleep and a decline of SWA within the main sleep period is typical. SWA is regulated as a function of prior waking and is assumed to reflect sleep intensity. We investigated sleep homeostasis and its possible circadian modulation by performing sleep deprivation (SD) at two phases of the light-dark cycle. SD induced an increase in SWA which was similar under both conditions. We conclude that sleep is homeostatically regulated in the guinea pig and is not subject to a circadian modulation.

Animals↗
PubMed2005

Antero-posterior functional coupling at sleep onset: changes as a function of increased sleep pressure.

The use of the directed transfer function (DTF), an advanced computational analysis of electroencephalogaphic (EEG) data, which provides an estimation of the direction of the information flow underlying cortico-cortical functional coupling, has shown that the presleep period is characterized by posterior-to-anterior functional cortical coupling, while at sleep onset there is an inversion of that direction. This finding supported the idea that anterior cortical areas first synchronize sleep EEG activity. The aim of the present study was to assess the changes of functional coupling between anterior and posterior midline cortical areas during the sleep onset process when sleep pressure is heightened by a selective slow-wave sleep (SWS) deprivation. The hypothesis was that the anterior-to-posterior direction of the cortical functional coupling at sleep onset is enhanced by SWS deprivation. Ten normal right-handed male students slept for six consecutive nights in the laboratory (1: adaptation, 2: baseline, 3: baseline with awakenings, 4 and 5: SWS deprivations, 6: recovery), with standard polysomnographic recordings. The DTF was computed on data recorded during nights two and six from anterior (Fz(A1)) and posterior (Pz(A1), Oz(A1)) derivations. Results showed that, during the recovery night, the anterior-to-posterior direction of functional cortical coupling is already present in the presleep period, indicating that SWS deprivation advances the shift to an anterior-to-posterior directionality of functional cortical coupling, possibly as a consequence of heightened sleep pressure. These findings support the notion that a spread of synchronizing signals from associative prefrontal to posterior areas play a role in the wake-sleep transition.

Adult↗
PubMed2005

Gender difference in sleep profile of severely obese patients with obstructive sleep apnea (OSA).

OBJECTIVES: Few papers addressed the gender difference in the polisomnographic features of obstructive sleep apnea (OSA). In this paper we investigated the sleep architecture and the nocturnal respiratory pattern in a group of severely obese women with OSA compared with a group of men with OSA matched by age and weight. DESIGN: A cross-sectional study. SETTING: Primary-care setting. SUBJECTS, MAIN OUTCOME MEASURES: Anthropometric parameters, respiratory function data and a full night polisomnography were evaluated in a group of 45 obese subjects, 20 females and 25 males, with a previous diagnosis of OSA. RESULTS: The group of the severely obese women with OSA presented greater disturbances of the sleep architecture than the group of the men does (wake time after sleep onset 92.6+/-52.4 vs 58.2+/-45.2 min, P<0.05; total wake time 104.8+/-51.4 vs 67.8+/-47.4, P<0.05; number of awakenings 15.5+/-3.6 vs 10.2+/-6.215, P<0.001; OSA that occurred almost exclusively during REM sleep (REM OSA) 35% vs 4%, P<0.05) and a reduced sleep efficiency (69.6+/-15.9 vs 80.3+/-14.0%, P<0.05). CONCLUSIONS: Severely obese women with OSA, even with milder OSA, present greater disturbances of the sleep architecture with a more severe sleep disruption and more frequently REM OSA in comparison with men matched by age and weight.

Adult↗
PubMed2002

Non-linear EEG measures during sleep: effects of the different sleep stages and cyclic alternating pattern.

The objective of this work was to study the non-linear aspects of sleep EEG, taking into account the different sleep stages and the peculiar organization of its phasic events in ordered sequences (CAP) by applying a series of new non-linear measures (non-linear cross prediction or NLCP), which appear more reliable for the detection and characterization of non-linear structures in experimental data than the commonly used correlation dimension. Eight healthy subjects aged 18-20 years participated in this study. Polysomnography was performed in all subjects; signals were sampled at 128 Hz and stored on hard disk. The C3 or C4 derivation was used for all the subsequent computational steps, which were performed on EEG epochs (4096 data points) selected from sleep stage 2 (S2) and slow-wave sleep (SWS), in both CAP and non-CAP (NCAP) conditions. Also, epochs from sleep stage 1 (S1), REM and wakefulness preceding sleep were recorded. The dynamic properties of the EEG were assessed by means of the non-linear cross-prediction test, which uses three different 'model' time series in order to predict non-linearly the original data set (Pred, Ama, and Tir). Pred is a measure of the predictability of the time series, and Ama and Tir are measures of asymmetry, indicating non-linear structure. The non-linear measures applied in this study indicate that sleep EEG tends to show non-linear structure only during CAP periods, both during S2 and SWS. Moreover, during CAP periods, non-linearity can only be detected during the phase A1 subtypes (and partially A2) of CAP. The A3 phases show characteristics of non-stationarity and bear some resemblance to wakefulness. Based on the results of this study, sleep might be considered as a dynamically evolving sequence of different states of the EEG, which we could track by detecting non-linearity, mostly in association with CAP. Our results clearly show that detectable non-linearity in the EEG is closely related to the occurrence of the phase A of CAP.

Adolescent↗