Showing papers on "Non-rapid eye movement sleep published in 2003"

The Cumulative Cost of Additional Wakefulness: Dose-Response Effects on Neurobehavioral Functions and Sleep Physiology From Chronic Sleep Restriction and Total Sleep Deprivation

Abstract: OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness were near-linearly related to the cumulative duration of wakefulness in excess of 15.84 h (s.e. 0.73 h). CONCLUSIONS: Since chronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation, it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults. Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits, which may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign. Physiological sleep responses to chronic restriction did not mirror waking neurobehavioral responses, but cumulative wakefulness in excess of a 15.84 h predicted performance lapses across all four experimental conditions. This suggests that sleep debt is perhaps best understood as resulting in additional wakefulness that has a neurobiological "cost" which accumulates over time.

Shift work and disturbed sleep/wakefulness.

Abstract: Of the many health-related effects of shift work, disturbed sleep is the most common. This review describes the main observed effects of the three principal shifts (night, morning and afternoon) on patterns of sleep and wakefulness. The mechanism of sleep disruption in relation to circadian rhythms and the specific impact of aspects of shift organization (speed and direction of rotation) are discussed. The most troublesome acute symptoms are difficulty getting to sleep, shortened sleep and somnolence during working hours that continues into successive days off. These are only partially amenable to amelioration by manipulating shift patterns. However, there is no clear indication that chronic sleep problems result from long-term shift work.

The alpha2-adrenoceptor agonist dexmedetomidine converges on an endogenous sleep-promoting pathway to exert its sedative effects.

Abstract: BackgroundThe authors investigated whether the sedative, or hypnotic, action of the general anesthetic dexmedetomidine (a selective α2-adrenoceptor agonist) activates endogenous nonrapid eye movement (NREM) sleep-promoting pathways.Methodsc-Fos expression in sleep-promoting brain nuclei was assessed

The corticothalamic system in sleep.

Abstract: The transition from wakefulness to NREM sleep is associated with typical signs of brain electrical activity, characterized by prolonged periods of hyperpolarization and increased membrane conductance in thalamocortical (TC) neurons, with the consequence that incoming messages are inhibited and the cerebral cortex is deprived of signals from the outside world. There are three major oscillations during NREM sleep. Spindles are generated within the thalamus, due to thalamic reticular (RE) neurons that impose rhythmic inhibitory sequences onto TC neurons, but the widespread synchronization of this rhythm is governed by corticothalamic projections. There are two types of delta activity: clock-like waves generated in TC neurons by the interplay between two hyperpolarization-activated inward currents; and cortical waves that survive extensive thalamectomy. The hallmark of NREM sleep activity is the slow oscillation, generated intracortically, which has the virtue of grouping the other types of sleep activities, thus leading to a coalescence of different rhythms that can only be observed in intact-brain animals and humans. Far from being epiphenomena, with no functional role, NREM sleep oscillations, particularly spindles and their experimental model augmenting responses, produce synaptic plasticity in target cortical neurons and resonant activity in corticothalamic loops, as in "memory" processes. Upon brain arousal, spindles are blocked by inhibition of RE neurons, the spindles' pacemakers; clock-like delta rhythm is obliterated by depolarization of TC neurons; and the cortically generated slow oscillation is abolished by selective erasure of its hyperpolarizing components. Fast (beta and gamma) oscillations are roduced by the depolarizing effects of mesopontine cholinergic neurons acting on TC neurons and nucleus basalis neurons acting on cortical neurons.

Sleepwalking and Sleep Terrors in Prepubertal Children: What Triggers Them?

Abstract: Objectives. To evaluate the clinical presentation and polysomnography of prepubertal children with repetitive sleep terrors and sleepwalking, to compare them with a control group, and to evaluate the treatment of associated sleep disorders. Methods. Patients with complaint of sleep terrors with or without sleepwalking were studied retrospectively. A control group was also recruited. Each subject received a standardized evaluation, which included the following: 1) Pediatric Sleep Questionnaire; 2) interview regarding child’s medical and sociofamilial history, orthodontic history, schooling, psychological difficulties, medication intake, and family history of medical and sleep disorders; 3) general pediatric physical examination and neurologic, otolaryngological, and craniofacial examination by a specialist; 4) obtaining medical history on variables relevant to early life sleep disorders; 5) polysomnography, which included electroencephalogram (EEG; C3/A2, Fp1/T1, T1/O1, O1/C3, C4/A1, Fp2/T2, T2/O2, O2/C4), chin and leg electromyelogram, right and left electro-oculogram, and electrocardiogram (modified V2 lead); respiration was monitored with a nasal cannula/pressure transducer system, mouth thermistor, chest and abdominal bands, pulse oximeter, and neck microphone; respiratory effort was monitored with calibrated esophageal manometry; variables were collected on a computerized sleep system; and 6) available family members with a positive history of sleep terrors and sleepwalking received clinical evaluations similar to those used for index cases; they also underwent ambulatory monitoring with an Edentrace system, which monitors heart rate, body position, oro-nasal flow, chest impedance, breathing noises (neck microphone), and pulse oximetry. Movements are deduced from artifact, and leg movements may be recorded on one channel if the equipment is preset for such recording. Subjects used logs to record “lights out” time, “lights on” time, nocturnal awakenings, and other events that occurred during the night. All original and follow-up recordings were rescored by 2 of 4 randomly selected specialists who were blind to subject identity. Mann-Whitney U test was used for group comparison. Nonparametric χ 2 test was used to compare percentages of symptoms in symptomatic children versus control children. Results. Eighty-four children (5 with sleep terrors and 79 with both sleep terrors and sleepwalking) and 36 normal control children formed the studied population. All subjects were Tanner stage 1 (prepubertal). None of the control children had any parasomnias. Fifty-one (61%) of 84 children with parasomnia had a diagnosis of an additional sleep disorder: 49 with sleep-disordered breathing (SDB) and 2 with restless leg syndrome (RLS). Twenty-nine of the children with both parasomnia and SDB had a positive family history of parasomnias, and 24 of the 29 also had a positive family history of SDB. Of the 51 children with associated sleep disorders, 45 were treated. Forty-three of 49 children with SDB were treated with tonsillectomy, adenoidectomy, and/or turbinate revision, and 2 of 2 children with RLS were treated with Pramipexole, a dopamine agonist, at bedtime. Treatment of the precipitating sleep disorder eliminated parasomnias in all 45 children. In all 43 children who received surgery, polysomnography performed 3 to 4 months later indicated the disappearance of SDB. The recordings also showed an absence of confusional arousals. The number of EEG arousals significantly decreased from a mean of 9 ± 2.6 EEG arousals ≥3 seconds/hour during total sleep time to 3 ± 1.5. The number of EEG arousals ≥3 seconds during the first sleep cycle of slow wave sleep (stage 3–4 non–rapid eye movement sleep) decreased from 4 ± 1.4 to 1 ± 0.2. In all surgically treated cases, parents also reported subsequent absence of the parasomnia. The 2 symptomatic children who were treated with Pramipexole had a complete absence of confusional arousals on the follow-up recording and reported no parasomnia since treatment. The periodic limb movement syndrome arousal index (number of EEG arousals associated with periodic limb movement/hour) decreased from 11 and 16 to 0 and 0.2, respectively. Parasomnia persisted in the 6 children who were untreated for SDB. Surgeons had refused to perform surgery on these children because of lack of data on the relationship between parasomnia and SDB-related tonsil and adenoid enlargement. Conclusion. Children with chronic parasomnias may often also present SDB or, to a lesser extent, RLS. Furthermore, the disappearance of the parasomnias after the treatment of the SDB or RLS periodic limb movement syndrome suggests that the latter may trigger the former. The high frequency of SDB in family members of children with parasomnia provided additional evidence that SDB may manifest as parasomnias in children. Children with parasomnias are not systematically monitored during sleep, although past studies have suggested that patients with sleep terrors or sleepwalking have an elevated level of brief EEG arousals. When children receive polysomnographies, discrete patterns (eg, nasal flow limitation, abnormal respiratory effort, bursts of high θ or slow α EEG frequencies) should be sought; apneas are rarely found in children. Children’s respiration during sleep should be monitored with nasal cannula/pressure transducer system and/or esophageal manometry, which are more sensitive than the thermistors or thermocouples currently used in many laboratories. The clear, prompt improvement of severe parasomnia in children who are treated for SDB, as defined here, provides important evidence that subtle SDB can have substantial health-related significance. Also noteworthy is the report of familial presence of parasomnia. Studies of twin cohorts and families with sleep terror and sleepwalking suggest genetic involvement of parasomnias. RLS and SDB have been shown to have familial recurrence. RLS has been shown to have genetic involvement. It remains to be investigated whether a genetic factor directly influences sleep terror and sleepwalking or instead influences other disorders that fragment sleep and lead to confusional arousals. Additional studies are needed to investigate the association between SDB and non–rapid eye movement parasomnias in the general population.

Biochemical regulation of non-rapid-eye-movement sleep.

Abstract: The concept, that sleep regulatory substances (sleep factors) exist, stems from classical endocrinology and is supported by positive transfer experiments in which tissue fluids obtained from sleepy or sleeping animals elicited sleep when injected into recipient animals. The transfer experiments concluded with the identification of four sleep factors: delta sleep-inducing peptide (DSIP), uridine, oxidized glutathione, and a muramyl peptide. A physiological sleep regulatory role, however, has not been determined for these substances. In contrast, transfer experiments did not play a part in the development of the strong experimental evidence that implicated the currently known sleep factors in sleep regulation. These substances include adenosine, prostaglandin D2 (PGD2), growth hormone-releasing hormone (GHRH), interleukin-1 (IL1) and tumor necrosis factor (TNF). They promote non-REMS in various species, inhibition of their action or endogenous production results in loss of spontaneous sleep, and their synthesis and/or release display variations correlating with sleep-wake activity. Although the source of these substances vary they all enhance sleep by acting in the basal forebrain/anterior hypothalamus--preoptic region. It is also characteristic of these substances that they interact in multiple ways often resulting in mutual stimulation or potentiation of each other. Finally, there is a third group of substances whose significance in sleep regulation is less clear but for which there are two or more lines of evidence suggesting that they may have a role in modulating non-REM sleep (NREMS). This group includes oleamide, cortistatin, cholecystokinin (CCK), insulin, and nitric oxide (NO). More sleep regulatory substances are likely to be discovered in the future although it is a long and difficult process requiring multiple laboratories to generate sufficient convincing data to implicate any one of them in sleep regulation.

Sleep states alter activity of suprachiasmatic nucleus neurons.

Abstract: The timing of sleep and wakefulness in mammals is governed by a sleep homeostatic process and by the circadian clock of the suprachiasmatic nucleus (SCN), which has a molecular basis for rhythm generation. By combining SCN electrical activity recordings with electroencephalogram (EEG) recordings in the same animal (the Wistar rat), we discovered that changes in vigilance states are paralleled by strong changes in SCN electrophysiological activity. During rapid eye movement (REM) sleep, neuronal activity in the SCN was elevated, and during non-REM (NREM) sleep, it was lowered. We also carried out selective sleep deprivation experiments to confirm that changes in SCN electrical activity are caused by changes in vigilance state. Our results indicate that the 24-hour pattern in electrical activity that is controlled by the molecular machinery of the SCN is substantially modified by afferent information from the central nervous system.

Sleep and Dreaming: The reinterpretation of dreams: An evolutionary hypothesis of the function of dreaming

Abstract: Several theories claim that dreaming is a random by-product of REM sleep physiology and that it does not serve any natural function. Phenomenal dream content, however, is not as disorganized as such views imply. The form and content of dreams is not random but organized and selective: during dreaming, the brain constructs a complex model of the world in which certain types of elements, when compared to waking life, are underrepresented whereas others are over represented. Furthermore, dream content is consistently and powerfully modulated by certain types of waking experiences. On the basis of this evidence, I put forward the hypothesis that the biological function of dreaming is to simulate threatening events, and to rehearse threat perception and threat avoidance. To evaluate this hypothesis, we need to consider the original evolutionary context of dreaming and the possible traces it has left in the dream content of the present human population. In the ancestral environment human life was short and full of threats. Any behavioral advantage in dealing with highly dangerous events would have increased the probability of reproductive success. A dream-production mechanism that tends to select threatening waking events and simulate them over and over again in various combinations would have been valuable for the development and maintenance of threat-avoidance skills. Empirical evidence from normative dream content, children's dreams, recurrent dreams, nightmares, post traumatic dreams, and the dreams of hunter-gatherers indicates that our dream-production mechanisms are in fact specialized in the simulation of threatening events, and thus provides support to the threat simulation hypothesis of the function of dreaming.

Sleep and Dreaming: A review of mentation in REM and NREM sleep: “Covert” REM sleep as a possible reconciliation of two opposing models

Abstract: Numerous studies have replicated the finding of mentation in both rapid eye movement (REM) and nonrapid eye movement (NREM) sleep. However, two different theoretical models have been proposed to account for this finding: (1) a one-generator model, in which mentation is generated by a single set of processes regardless of physiological differences between REM and NREM sleep; and (2) a two-generator model, in which qualitatively different generators produce cognitive activity in the two states. First, research is reviewed demonstrating conclusively that mentation can occur in NREM sleep; global estimates show an average mentation recall rate of about 50% from NREM sleep--a value that has increased substantially over the years. Second, nine different types of research on REM and NREM cognitive activity are examined for evidence supporting or refuting the two models. The evidence largely, but not completely, favors the two-generator model. Finally, in a preliminary attempt to reconcile the two models, an alternative model is proposed that assumes the existence of covert REM sleep processes during NREM sleep. Such covert activity may be responsible for much of the dreamlike cognitive activity occurring in NREM sleep.

Slowing of electroencephalogram in rapid eye movement sleep behavior disorder

Abstract: Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by a loss of atonia and an increase in phasic muscle activity during REM sleep, leading to complex nocturnal motor behaviors. Brainstem structures responsible for the pathogenesis of RBD are also implicated in cortical activation. To verify the hypothesis that electroencephalogram (EEG) activation will be impaired in RBD, we performed quantitative analyses of waking and REM sleep EEG in 15 idiopathic RBD patients and 15 age- and gender-matched healthy subjects. During wakefulness, RBD patients showed a considerably higher theta power in frontal, temporal, and occipital regions with a lower beta power in the occipital region. The dominant occipital frequency was significantly lower in RBD. During REM sleep, beta power in the occipital region was lower in RBD. This study shows for the first time an impaired cortical activation during both wakefulness and REM sleep in idiopathic RBD, despite an absence of changes on sleep architecture compared with controls. EEG slowing in these patients may represent an early sign of central nervous system dysfunction, perhaps paralleled by subclinical cognitive deficits. The topographical distribution of EEG slowing and possible pathophysiological mechanisms are discussed in light of the known association between RBD and neurodegenerative disorders.

The effects of pramipexole in REM sleep behavior disorder

Abstract: The authors evaluated the effects of pramipexole, a dopaminergic D2-D3 receptor agonist, on eight patients with idiopathic REM sleep behavior disorder. Five patients reported a sustained reduction in the frequency or intensity of sleep motor behaviors, which was confirmed by video recording, although no change was observed for the percentage of phasic EMG activity during REM sleep. Surprisingly, a decrease in the percentage of time spent with REM sleep muscle atonia was observed with treatment. The treatment did not modify the indexes of periodic leg movements.

Periodic limb movement disorder of sleep in children.

Abstract: To characterize periodic limb movement disorder (PLMD) in a cohort of prepubertal children we examined sleep-related identifiable differences between children with PLMD and attention-deficit/hyperactivity disorder (ADHD), PLMD alone, and age-matched controls. Children were selected from a chart review of all children referred to a pediatric sleep medicine center and from a community survey of 5-7-year-old-children. Polysomnography (PSG) and parental report data from all children identified as having periodic limb movement index (PLMI) >5 were reviewed and compared with a cohort of age-matched controls. A total of 8.4% of children in the clinic-referred sample, and 11.9% of the children recruited from the community had PLMI >5. Of those, 44.4% were identified as having ADHD. Children with PLMD had significantly lower percentage of rapid eye movement (REM) than control children (P < 0.001). Children in the PLMD/ADHD group had a significantly greater number of arousals associated with PLM (PLMa) than children with PLMD only (P < 0.05). While a relationship between ADHD and PLMD was observed, it was weaker than previous reports (Chervin, R. D. et al. Sleep, 2002; 25: 213; Chervin, R. D. and Archbold, K. H. Sleep, 2001; 24: 313; Picchietti et al. J. Child Neurol., 1999; 13: 588; Picchietti et al. Mov. Disord., 1999; 14: 1000; Picchietti and Walters Sleep, 1999; 22: 297). Children in the PLMD/ADHD group were more likely to have PLMas than were children with PLMD only. We postulate that rather than a direct relationship between ADHD and PLMD, this link may be mediated by the presence of reduced REM sleep and more importantly by the sleep fragmentation associated with PLM-induced arousals.

Correlation between electroencephalography and heart rate variability during sleep.

Abstract: It is known that autonomic nervous activities change in correspondence with sleep stages. However, the characteristics of continuous fluctuations in nocturnal autonomic nerve tone have not been clarified in detail. The study aimed to determine the possible correlation between the electroencephalogram (EEG) and autonomic nervous activities, and to clarify in detail the nocturnal fluctuations in autonomic nerve activities. Overnight EEGs and electrocardiograms of seven healthy males were obtained. These EEGs were analyzed by fast Fourier transformation algorithm to extract delta, sigma and beta power. Heart rate and heart rate variability (HRV) were calculated in consecutive 5-min epochs. The HRV indices of low frequency (LF), high frequency (HF) and LF/HF ratio were calculated from the spectral analysis of R-R intervals. The sleep stages were manually scored according to Rechtschaffen and Kales' criteria. Low frequency and LF/HF were significantly lower during non-rapid eye movement (NREM) than REM, and were lower in stages 3 and 4 than in stages 1 and 2. Furthermore, delta EEG showed inverse correlations with LF (r = - 0.44, P < 0.001) and LF/HF (r = - 0.41, P < 0.001). In contrast, HF differed neither between REM and NREM nor among NREM sleep stages. Detailed analysis revealed that correlation was evident from the first to third NREM, but not in the fourth and fifth NREM. Delta EEG power showed negative correlations with LF and LF/HF, suggesting that sympathetic nervous activities continuously fluctuate in accordance with sleep deepening and lightening.

Effect of testosterone on the apneic threshold in women during NREM sleep.

Abstract: The hypocapnic apneic threshold (AT) is lower in women relative to men. To test the hypothesis that the gender difference in AT was due to testosterone, we determined the AT during non-rapid eye mo...

Sleep regulation in adenosine A2A receptor-deficient mice.

Abstract: Adenosine is proposed to be an endogenous sleep-promoting substance based on the results of a variety of pharmacologic and behavioral experiments.1 For example, sleep is induced in rats after administration of metabolically stable adenosine analogues, such as N6-l-(phenylisopropyl)-adenosine, adenosine-5′-N-ethylcarboxamide, and cyclohexyladenosine,2,3⇓ which are agonists for adenosine A1 receptor (A1R) or A2A receptors (A2ARs). Caffeine is considered to inhibit sleep by acting as an antagonist of adenosine receptor.4 Adenosine content is increased in the basal forebrain, one of the sleep centers, after sleep deprivation and is proposed to be a sleep substance accumulating in the brain during prolonged wakefulness.5 Most previous studies on sleep regulation by adenosine have focused on the A1R-mediated pathway1,6⇓ because A1R is widely distributed in the CNS, whereas A2AR is localized mainly in the striatum, nucleus accumbens, and olfactory bulb. However, we found that A2AR is also important in sleep regulation by using several A1R and A2AR agonists, including N6-cyclopentyladenosine (CPA) and 2-(4-(2-carboxyethyl)phenylethylamino)-adenosine-5′- N -ethylcarboxamideadenosine (CGS 21680).7-12⇓⇓⇓⇓⇓ CGS 21680 is highly selective for the A2AR (Ki = 14 nmol/L), having a much lower affinity for the A1R (Ki = 2,600 nmol/L), whereas CPA is selective for the A1R (Ki = 0.6 nmol/L) and has a lower affinity for the A2AR (Ki = 462 nmol/L).13,14⇓ We investigated the molecular mechanism of induction of non-REM (NREM) sleep by prostaglandin (PG) D2, which is also known as a potent endogenous sleep-promoting substance.15-17⇓⇓ In the course of this study, Satoh et al.7 found that PGD2 …

Sleep and Dreaming: The case against memory consolidation in REM sleep

Abstract: We present evidence disputing the hypothesis that memories are processed or consolidated in REM sleep. A review of REM deprivation (REMD) studies in animals shows these reports to be about equally divided in showing that REMD does, or does not, disrupt learning/memory. The studies supporting a relationship between REM sleep and memory have been strongly criticized for the confounding effects of very stressful REM deprivation techniques. The three major classes of antidepressant drugs, monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), and selective serotonin reuptake inhibitors (SSRIs), profoundly suppress REM sleep. The MAOIs virtually abolish REM sleep, and the TCAs and SSRIs have been shown to produce immediate (40-85%) and sustained (30-50%) reductions in REM sleep. Despite marked suppression of REM sleep, these classes of antidepressants on the whole do not disrupt learning/memory. There have been a few reports of patients who have survived bilateral lesions of the pons with few lingering complications. Although these lesions essentially abolished REM sleep, the patients reportedly led normal lives. Recent functional imaging studies in humans have revealed patterns of brain activity in REM sleep that are consistent with dream processes but not with memory consolidation. We propose that the primary function of REM sleep is to provide periodic endogenous stimulation to the brain which serves to maintain requisite levels of central nervous system (CNS) activity throughout sleep. REM is the mechanism used by the brain to promote recovery from sleep. We believe that the cumulative evidence indicates that REM sleep serves no role in the processing or consolidation of memory.

β1-adrenergic antagonists and melatonin reset the clock and restore sleep in a circadian disorder, Smith-Magenis syndrome

Abstract: First described by Smith et al 1 in 1982, Smith-Magenis syndrome (SMS) is a contiguous gene syndrome ascribed to interstitial deletions of chromosome 17p11.2. Clinical features include infantile hypotonia, characteristic craniofacial appearance, brachydactyly, short stature, ocular anomalies, deep, hoarse voice, early speech delay, mental retardation, and behavioural disturbances.2,3 Behavioural problems include hyperactivity, attention deficit, self-injury, temper tantrums, and major sleep disturbance.4 These symptoms have a major impact on the children and their families. The diagnosis is based on high resolution karyotype analysis and fluorescence in situ hybridisation (FISH).5 Sleep disturbances occur in all cases and are predictive of maladaptive behaviour, increased by mental retardation and cognitive delay. The specific pattern of sleep disturbance in SMS includes early sleep onset, frequent awakenings, and early waking.6,7 Moreover, “sleep attacks” at the end of the day are consistent features of the disease and may represent the endogenous sleep onset of the patients. The children could therefore be regarded as having a sleep phase advance. Normally, melatonin secretion increases soon after onset of darkness, peaks at midnight, and gradually falls during the second half of the night. Interestingly, all SMS patients display a phase shift of their circadian rhythm of melatonin, with a diurnal secretion of the hormone8–10 (fig 1). Tantrums and tiredness occur when melatonin rises in the morning and children have naps and sleep attacks when melatonin peaks at midday and in the evening. Sleep is fragmented with prolonged nocturnal awakenings and early waking when melatonin is low during the night (fig 1). This clinical and biological sleep phase advance supports the existence of an aberrant biological clock in SMS. Figure 1 (A) Inversion of serum melatonin rhythm in SMS (solid lines) as compared to age matched controls (dotted lines). (B) Sleep-wake patterns correlated with melatonin …

Prefrontal cortex: links between low frequency delta EEG in sleep and neuropsychological performance in healthy, older people.

Abstract: Low frequency (< 1 Hz) delta EEG in sleep is of increasing interest as it indicates cortical reorganization, especially in the prefrontal cortex (PFC). Other research shows that delta power in sleep is positively linked to waking cerebral metabolic rate. Such findings suggest that < 1 Hz activity may reflect waking performance at neuropsychological tests specific to the PFC. We investigated this unexplored area. Sleep EEGs (Fp1-F3, Fp2-F4, O1-P3, O2-P4) were recorded in 24 healthy 61-75-year-olds. We found significant associations between 0.5-1.0 Hz power from the left frontal EEG channel, in the first non-REM period, and performance at tasks more specific to the left PFC (e.g., nonverbal planning and verbal fluency). This association was absent from the posterior channels. Neither age nor response times were confounding factors. This potential sleep EEG marker for PFC neuropsychological function in healthy, older people also points to further uses of the sleep EEG in understanding the role of sleep.