Showing papers on "Slow-wave sleep published in 2005"
TL;DR: The fading of consciousness during certain stages of sleep may be related to a breakdown in cortical effective connectivity, as measured by transcranial magnetic stimulation and high-density electroencephalography.
Abstract: When we fall asleep, consciousness fades yet the brain remains active. Why is this so? To investigate whether changes in cortical information transmission play a role, we used transcranial magnetic stimulation together with high-density electroencephalography and asked how the activation of one cortical area (the premotor area) is transmitted to the rest of the brain. During quiet wakefulness, an initial response (approximately 15 milliseconds) at the stimulation site was followed by a sequence of waves that moved to connected cortical areas several centimeters away. During non-rapid eye movement sleep, the initial response was stronger but was rapidly extinguished and did not propagate beyond the stimulation site. Thus, the fading of consciousness during certain stages of sleep may be related to a breakdown in cortical effective connectivity.
1,337 citations
TL;DR: The functions of mammalian sleep remain unclear, but theories suggest a role for non-rapid eye movement sleep in energy conservation and in nervous system recuperation.
Abstract: The functions of mammalian sleep remain unclear. Most theories suggest a role for non-rapid eye movement (NREM) sleep in energy conservation and in nervous system recuperation. Theories of REM sleep have suggested a role for this state in periodic brain activation during sleep, in localized recuperative processes and in emotional regulation. Across mammals, the amount and nature of sleep are correlated with age, body size and ecological variables, such as whether the animals live in a terrestrial or an aquatic environment, their diet and the safety of their sleeping site. Sleep may be an efficient time for the completion of a number of functions, but variations in sleep expression indicate that these functions may differ across species.
901 citations
01 Jan 2005
TL;DR: In this article, a nightly pattern of sleep in mature humans sleeping on a regular schedule includes several reliable characteristics: sleep begins in NREM and progresses through deeper NREM stages (stages 2, 3, and 4 using the classic definitions, or stages N2 and N3 using the updated definitions) before the first episode of REM sleep occurs approximately 80 to 100 minutes later.
Abstract: Normal human sleep comprises two states—rapid eye movement (REM) and non–REM (NREM) sleep— that alternate cyclically across a sleep episode. State characteristics are well defined: NREM sleep includes a variably synchronous cortical electroencephalogram (EEG; including sleep spindles, Kcomplexes, and slow waves) associated with low muscle tonus and minimal psychological activity; the REM sleep EEG is desynchronized, muscles are atonic, and dreaming is typical. A nightly pattern of sleep in mature humans sleeping on a regular schedule includes several reliable characteristics: Sleep begins in NREM and progresses through deeper NREM stages (stages 2, 3, and 4 using the classic definitions, or stages N2 and N3 using the updated definitions) before the first episode of REM sleep occurs approximately 80 to 100 minutes later. Thereafter, NREM sleep and REM sleep cycle with a period of approximately 90 minutes. NREM stages 3 and 4 (or stage N3) concentrate in the early NREM cycles, and REM sleep episodes lengthen across the night. Age-related changes are also predictable: Newborn humans enter REM sleep (called active sleep) before NREM (called quiet sleep) and have a shorter sleep cycle (approximately 50 minutes); coherent sleep stages emerge as the brain matures during the first year. At birth, active sleep is approximately 50% of total sleep and declines over the first 2 years to approximately 20% to 25%. NREM sleep slow waves are not present at birth but emerge in the first 2 years. Slow-wave sleep (stages 3 and 4) decreases across adolescence by 40% from preteen years and continues a slower decline into old age, particularly in men and less so in women. REM sleep as a percentage of total sleep is approximately 20% to 25% across childhood, adolescence, adulthood, and into old age except in dementia. Other factors predictably alter sleep, such as previous sleep-wake history (e.g., homeostatic load), phase of the circadian timing system, ambient temperature, drugs, and sleep disorders. A clear appreciation of the normal characteristics of sleep provides a strong background and template for understanding clinical conditions in which “normal” characteristics are altered, as well as for interpreting certain consequences of sleep disorders. In this chapter, the normal young adult sleep pattern is described as a working baseline pattern. Normative changes due to aging and other factors are described with that background in mind. Several major sleep disorders are highlighted by their differences from the normative pattern.
813 citations
TL;DR: Hcrt cells discharge in active waking and have moderate and approximately equal levels of activity during grooming and eating and maximal activity during exploratory behavior, suggesting that these cells are activated during emotional and sensorimotor conditions similar to those that trigger cataplexy in narcoleptic animals.
796 citations
TL;DR: The potential role of CRH in circadian-dependent alerting, aside from its role in the stress response, is discussed, as is the role the HPA axis plays in secondary effects of primary sleep disorders.
Abstract: The hypothalamic-pituitary-adrenal (HPA) axis plays important roles in maintaining alertness and modulating sleep. Dysfunction of this axis at any level (CRH receptor, glucocorticoid receptor, or mineralocorticoid receptor) can disrupt sleep. Herein, we review normal sleep, normal HPA axis physiology and circadian rhythm, the effects of the HPA axis on sleep, as well as the effects of sleep on the HPA axis. We also discuss the potential role of CRH in circadian-dependent alerting, aside from its role in the stress response. Two clinically relevant sleep disorders with likely HPA axis dysfunction, insomnia and obstructive sleep apnea, are discussed. In insomnia, we discuss how HPA axis hyperactivity may be partially causal to the clinical syndrome. In obstructive sleep apnea, we discuss how HPA axis hyperactivity may be a consequence of the disorder and contribute to secondary pathology such as insulin resistance, hypertension, depression, and insomnia. Mechanisms by which cortisol can affect slow wave sleep are discussed, as is the role the HPA axis plays in secondary effects of primary sleep disorders.
742 citations
TL;DR: Maturational changes of homeostatic sleep regulation are permissive of the sleep phase delay in the course of adolescence as well as aspects of sleep homeostasis.
Abstract: STUDY OBJECTIVES:
To examine the effects of total sleep deprivation on adolescent sleep and the sleep electroencephalogram (EEG) and to study aspects of sleep homeostasis.
DESIGN: Subjects were studied during baseline and recovery sleep after 36 hours of wakefulness.
SETTING: Four-bed sleep research laboratory.
PARTICIPANTS: Seven prepubertal or early pubertal children (pubertal stage Tanner 1 or 2 = Tanner 1/2; mean age 11.9 years, SD +/- 0.8, 2 boys) and 6 mature adolescents (Tanner 5; 14.2 years, +/- 1.4, 2 boys).
INTERVENTIONS: Thirty-six hours of sleep deprivation.
MEASUREMENTS: All-night polysomnography was performed. EEG power spectra (C3/A2) were calculated using a Fast Fourier transform routine.
RESULTS:
In both groups, sleep latency was shorter, sleep efficiency was higher, non-rapid eye movement (NREM) sleep stage 4 was increased, and waking after sleep onset was reduced in recovery relative to baseline sleep. Spectral power of the NREM sleep EEG was enhanced after sleep deprivation in the low-frequency range (1.6-3.6 Hz in Tanner 1/2; 0.8-6.0 Hz in Tanner 5) and reduced in the sigma range (11-15 Hz). Sleep deprivation resulted in a stronger increase of slow-wave activity (EEG power 0.6-4.6 Hz, marker for sleep homeostatic pressure) in Tanner 5 (39% above baseline) than in Tanner 1/2 adolescents (18% above baseline). Sleep homeostasis was modeled according to the two-process model of sleep regulation. The build-up of homeostatic sleep pressure during wakefulness was slower in Tanner 5 adolescents (time constant of exponential saturating function 15.4 +/- 2.5 hours) compared with Tanner 1/2 children (8.9 +/- 1.2 hours). In contrast, the decline of the homeostatic process was similar in both groups.
CONCLUSION:
Maturational changes of homeostatic sleep regulation are permissive of the sleep phase delay in the course of adolescence.
383 citations
TL;DR: The results suggest that playing an exciting computer game affects sleep latency and REM sleep but that a bright display does not affect sleep variables.
Abstract: Epidemiological studies have shown that playing a computer game at night delays bedtime and shortens sleeping hours, but the effects on sleep architecture and quality have remained unclear. In the present study, the effects of playing a computer game and using a bright display on nocturnal sleep were examined in a laboratory. Seven male adults (24.7+/-5.6 years old) played exciting computer games with a bright display (game-BD) and a dark display (game-DD) and performed simple tasks with low mental load as a control condition in front of a BD (control-BD) and DD (control-DD) between 23:00 and 1:45 hours in randomized order and then went to bed at 2:00 hours and slept until 8:00 hours. Rectal temperature, electroencephalogram (EEG), heart rate and subjective sleepiness were recorded before sleep and a polysomnogram was recorded during sleep. Heart rate was significantly higher after playing games than after the control conditions, and it was also significantly higher after using the BD than after using the DD. Subjective sleepiness and relative theta power of EEG were significantly lower after playing games than after the control conditions. Sleep latency was significantly longer after playing games than after the control conditions. REM sleep was significantly shorter after the playing games than after the control conditions. No significant effects of either computer games or BD were found on slow-wave sleep. These results suggest that playing an exciting computer game affects sleep latency and REM sleep but that a bright display does not affect sleep variables.
304 citations
TL;DR: The behavioral and neurobiological evidence suggests that in rodents and humans, the circadian clock actively promotes both wake and sleep, at different phases of the circadian cycle.
302 citations
TL;DR: This review provides brief tutorials on the elements of the innate immune system that detect infection, how sleep is characterized in the laboratory, issues regarding the interpretation of sleep effects on immune function, the interaction of sleep with circadian rhythms and stress, and some of the microbial products, cytokines, and neuropeptides associated with sleep regulation.
Abstract: Sleep is a fundamental physiologic process with unknown functions. It is divided into 2 distinct states: non-rapid-eye-movement sleep and rapid-eye-movement sleep. After acute infection with nonneurotropic agents, there are stereotypic changes in non-rapid-eye-movement sleep, particularly increased time spent in slow-wave sleep, and often a reduction of time spent in rapid-eye-movement sleep. It is now recognized that both infection-associated sleep and spontaneous sleep are regulated, in part, by immune mediators called cytokines. This review provides brief tutorials on the elements of the innate immune system that detect infection, how sleep is characterized in the laboratory, issues regarding the interpretation of sleep effects on immune function, the interaction of sleep with circadian rhythms and stress, and some of the microbial products, cytokines, and neuropeptides associated with sleep regulation. We also summarize our current understanding of the role of sleep in host defense and asthma exacerbation.
259 citations
TL;DR: It is shown in humans that a genetic variant of adenosine deaminase, which is associated with the reduced metabolism ofAdenosine to inosine, specifically enhances deep sleep and slow-wave activity during sleep and SWA during sleep.
Abstract: Slow, rhythmic oscillations (<5 Hz) in the sleep electroencephalogram may be a sign of synaptic plasticity occurring during sleep. The oscillations, referred to as slow-wave activity (SWA), reflect sleep need and sleep intensity. The amount of SWA is homeostatically regulated. It is enhanced after sleep loss and declines during sleep. Animal studies suggested that sleep need is genetically controlled, yet the physiological mechanisms remain unknown. Here we show in humans that a genetic variant of adenosine deaminase, which is associated with the reduced metabolism of adenosine to inosine, specifically enhances deep sleep and SWA during sleep. In contrast, a distinct polymorphism of the adenosine A(2A) receptor gene, which was associated with interindividual differences in anxiety symptoms after caffeine intake in healthy volunteers, affects the electroencephalogram during sleep and wakefulness in a non-state-specific manner. Our findings indicate a direct role of adenosine in human sleep homeostasis. Moreover, our data suggest that genetic variability in the adenosinergic system contributes to the interindividual variability in brain electrical activity during sleep and wakefulness.
256 citations
TL;DR: Interindividual differences in sleep timing, duration, and morning or evening preference are associated with changes of circadianor sleep homeostatic processes or both and molecular genetic correlates, including polymorphisms in clock genes, of some of these interindividual differences are emerging.
Abstract: Daily rhythms in sleep and waking performance are generated by the interplay of multiple external and internal oscillators. These include the light-dark and social cycles, a circadian hypothalamic oscillator oscillating virtually independently of behavior, and a homeostatic oscillator driven primarilyby sleep-wake behavior. Both internal oscillators contribute to variation in many aspects of sleep and wakefulness (e.g., sleep timing and duration, REM sleep, non-REM sleep, REM density, sleep spindles, slow-wave sleep, electroencephalographic oscillations during wakefulness and sleep, and performance parameters, including attention and memory). The relative contribution of the oscillators varies greatly between these variables. Sleep and performance cannot be predicted by either oscillator independently but critically depend on their phase relationship and amplitude. The homeostatic oscillator feeds back onto the central pacemaker or its outputs. Thus, the amplitude of observed circadian variation in sleep ...
TL;DR: Results from the sleep laboratory do not seem to support the subjective complaints of poor sleep in patients with obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD), and no significant differences were found in all sleep parameters between social phobia patients and controls.
Abstract: Many patients suffering from the majority of anxiety disorders complain about their sleep by reporting difficulties in initiating and maintaining it. Polysomnographic studies have shown that, in comparison to normal subjects, the sleep of patients with panic disorder is characterized by longer sleep latency, increased time awake and reduced sleep efficiency. Sleep architecture is normal and there are no significant changes in REM sleep measures. Nocturnal panic attacks are non-REM-related events and occur without an obvious trigger in 18-45% of panic disorder patients. Regarding generalized anxiety disorder, the patients complain of 'trouble sleeping' in 60-70%, while polysomnography has shown increased sleep latency and decreased sleep continuity measures. The findings in REM sleep and sleep architecture generally do not show any aberration to exist. In patients with obsessive-compulsive disorder (OCD) and post-traumatic stress disorder (PTSD), results from the sleep laboratory do not seem to support the subjective complaints of poor sleep. The early reports of shortened REM latency in OCD could not be replicated by recent studies. A dysregulation of the REM sleep control system has been reported for patients with PTSD. Finally, no significant differences were found in all sleep parameters between social phobia patients and controls.
TL;DR: The significance of a meta-analysis of a large dataset of positron emission tomography scans acquired during wakefulness, slow wave sleep and REM sleep to explain the alteration in executive processes, episodic memory retrieval and self representation during REM sleep dreaming as well as the incorporation of external stimuli into the dream narrative is discussed.
Abstract: In this chapter, we aimed at further characterizing the functional neuroanatomy of the human rapid eye movement (REM) sleep at the population level. We carried out a meta-analysis of a large dataset of positron emission tomography (PET) scans acquired during wakefulness, slow wave sleep and REM sleep, and focused especially on the brain areas in which the activity diminishes during REM sleep. Results show that quiescent regions are confined to the inferior and middle frontal cortex and to the inferior parietal lobule. Providing a plausible explanation for some of the features of dream reports, these findings may help in refining the concepts, which try to account for human cognition during REM sleep. In particular, we discuss the significance of these results to explain the alteration in executive processes, episodic memory retrieval and self representation during REM sleep dreaming as well as the incorporation of external stimuli into the dream narrative.
Journal Article•
TL;DR: A significant lengthening of the R-R interval during subsequent cycles of Stage 2 non-REM sleep was documented, which is probably related to the shift of sympathovagal balance to a prevailing parasympathetic influence in the course of sleep.
Abstract: Spectral analysis of heart rate variability (HRV) during overnight polygraphic recording was performed in 11 healthy subjects. The total spectrum power, power of the VLF, LF and HF spectral bands and the mean R-R were evaluated. Compared to Stage 2 and Stage 4 non-REM sleep, the total spectrum power was significantly higher in REM sleep and its value gradually increased in the course of each REM cycle. The value of the VLF component (reflects slow regulatory mechanisms, e.g. the renin-angiotensin system, thermoregulation) was significantly higher in REM sleep than in Stage 2 and Stage 4 of non-REM sleep. The LF spectral component (linked to the sympathetic modulation) was significantly higher in REM sleep than in Stage 2 and Stage 4 non-REM sleep. On the contrary, a power of the HF spectral band (related to parasympathetic activity) was significantly higher in Stage 2 and Stage 4 non-REM than in REM sleep. The LF/HF ratio, which reflects the sympathovagal balance, had its maximal value during REM sleep and a minimal value in synchronous sleep. The LF/HF ratio significantly increased during 5-min segments of Stage 2 non-REM sleep immediately preceding REM sleep compared to 5-min segments of Stage 2 non-REM sleep preceding the slow-wave sleep. This expresses the sympathovagal shift to sympathetic predominance occurring before the onset of REM sleep. A significant lengthening of the R-R interval during subsequent cycles of Stage 2 non-REM sleep was documented, which is probably related to the shift of sympathovagal balance to a prevailing parasympathetic influence in the course of sleep. This finding corresponds to a trend of a gradual decrease of the LF/HF ratio in subsequent cycles of Stage 2 non-REM sleep.
TL;DR: A strong association was observed between rCBF in the ventromedial prefrontal regions and delta power, in agreement with electrophysiological studies, supporting the notion that delta activity is a valuable prominent feature of NREM sleep.
TL;DR: The majority of studies indicate that stage 4 sleep and rapid eye movement (REM) latency are reduced in schizophrenia, whereas REM sleep duration tends to remain unchanged, and the characterization of the neurotransmitter systems involved remains a challenging dilemma.
Abstract: Insomnia is a common symptom in schizophrenia, although it is seldom the predominant complaint Sleep-onset and maintenance insomnia is a characteristic feature of schizophrenic patients regardless of either their medication status (drug-naive or previously treated) or the phase of the clinical course (acute or chronic) Regarding sleep architecture, the majority of studies indicate that stage 4 sleep and rapid eye movement (REM) latency are reduced in schizophrenia, whereas REM sleep duration tends to remain unchanged Insomnia in schizophrenic patients could be partly related to the presumed over-activity of the dopaminergic system However, there is a possibility that the GABAergic system is also involved in sleep disturbance in schizophrenia Since many signal transmission systems within the CNS can be implicated in the reduction of REM latency in schizophrenia, the characterization of the neurotransmitter systems involved remains a challenging dilemma
TL;DR: At an early or middle stage of the disease, non‐obese PD patients frequently have AHI values suggesting SAS, however, without the oxygen desaturation profile of SAS, and longitudinal studies of patients with such “abortive” SAS are warranted to establish if this finding reflects benign nocturnal respiratory muscle dyskinesia or constitutes a precursor sign of dysautonomia in PD.
Abstract: In PD, the impact of nocturnal respiration on sleep continuity and architecture has not been systematically investigated by polysomnography (PSG). We performed a case-control study with retrospective analysis of PSG data of 49 PD patients. After classifying the PD patients according to their apnea/hypopnea index (AHI), they were matched with 49 controls in terms of age, gender, and AHI. There were 21 PD patients (43%) who had sleep apnea syndrome (SAS), classified as mild (AHI, 5-15) in 10 patients, moderate (AHI, >15-30) in 4 patients, and severe (AHI, > 30) in 7 patients. PD patients had more deep sleep (P = 0.02) and more nocturnal awakenings (P 15. PD patients had less obstructive sleep apneas (P = 0.035), independently from the factor AHI. Only the respiratory changes of 4 PD patients with BMI > 27 and AHI > 15 (8%) approximated those seen in the controls. At an early or middle stage of the disease, non-obese PD patients frequently have AHI values suggesting SAS, however, without the oxygen desaturation profile of SAS. Longitudinal studies of patients with such "abortive" SAS are warranted to establish if this finding reflects benign nocturnal respiratory muscle dyskinesia or constitutes a precursor sign of dysautonomia in PD.
TL;DR: If many factors, including pain, disease process per se, as well as medication, could disturb sleep, sleep disturbances may also adversely affect the natural course of the painful disease.
Abstract: Objective Clinical experiences as well as specific investigations show that pain and sleep disturbances are closely correlated. The aims of this review are first to describe sleep disturbances related to painful medical diseases and analgesics and secondly to propose management possibilities for these sleep disturbances. Method The viewpoints presented were based mainly on objective rest activity and sleep studies using actigraphy and polysomnography. Results Polysomnographic and actigraphic studies have described significant sleep disturbances in patients suffering from different pain disorders. These disturbances are: reduced sleep efficiency and altered sleep architecture characterized by increased wakefulness and stage 1 non-rapid eye movement sleep, associated with diminished slow wave sleep and rapid eye movement sleep. Sleep disturbances may be related to pain and to the analgesic or sedative medications administered. Conclusion If many factors, including pain, disease process per se, as well as medication, could disturb sleep, sleep disturbances may also adversely affect the natural course of the painful disease. Improving sleep quantity and quality in patients with painful disorders may break this vicious circle and as consequence enhance the patients' overall health and quality of life.
TL;DR: The data indicate that age-related changes in sleep propensity are clearly related to a reduced circadian signal opposing the homeostatic drive for sleep.
TL;DR: The data indicate that in a task that allows separating the contribution of explicit and implicit memory, sleep particularly supports explicit memory formation and the mechanism of this effect appears to be linked to SWS.
Abstract: Recognition memory is considered to be supported by two different memory processes, i.e., the explicit recollection of information about a previous event and an implicit process of recognition based on an acontextual sense of familiarity. Both types of memory supposedly rely on distinct memory systems. Sleep is known to enhance the consolidation of memories, with the different sleep stages affecting different types of memory. In the present study, we used the process-dissociation procedure to compare the effects of sleep on estimates of explicit (recollection) and implicit (familiarity) memory formation on a word-list discrimination task. Subjects studied two lists of words before a 3-h retention interval of sleep or wakefulness, and recognition was tested afterward. The retention intervals were positioned either in the early night when sleep is dominated by slow-wave sleep (SWS), or in the late night, when sleep is dominated by REM sleep. Sleep enhanced explicit recognition memory, as compared with wakefulness (P < 0.05), whereas familiarity was not affected by sleep. Moreover, explicit recognition was particularly enhanced after sleep in the early-night retention interval, and especially when the words were presented with the same contextual features as during learning, i.e., in the same font (P < 0.05). The data indicate that in a task that allows separating the contribution of explicit and implicit memory, sleep particularly supports explicit memory formation. The mechanism of this effect appears to be linked to SWS.
TL;DR: The results suggest that excessive daytime sleepiness in Japanese is associated with several sleep problems, and these findings may be useful in attempts to prevent excessive daytimeSleepiness in the general population of Japan.
TL;DR: In PD nocturnal sleep 'destructuring' is linked to disease duration and evolves independently from other major disease parameters.
TL;DR: The recognition of RBD has shed additional scientific light on the "bumps in the night"; expanded knowledge of states of being and state dissociation; opened up new areas of research on brain and mind dysfunction during sleep; and reaffirmed the vital link between basic research and clinical medicine.
TL;DR: Investigating in a population of patients with an early thalamic injury the presence of an activation of paroxysmal activities during sleep, their characteristics, and possible relations to neuroimaging and neuropsychological features found nothing untoward.
Abstract: Summary: Purpose: Mechanisms inducing continuous spike–wave during slow sleep (CSWS) in encephalopathy with electrical status epilepticus during sleep are still unclear. Recently, some sporadic cases with early thalamic injury associated with CSWS have been reported. The aim of the study was to investigate in a population of patients with an early thalamic injury the presence of an activation of paroxysmal activities during sleep, their characteristics, and possible relations to neuroimaging and neuropsychological features.
Methods: Thirty-two patients with prenatal or perinatal thalamic injuries, mostly due to a vascular mechanisms, were fully examined, including neuroimaging, EEG monitoring, and cognitive follow-up.
Results and Conclusions: Twenty-nine of 32 patients showed major sleep EEG activation. Among these 29 patients, two different groups were distinguished: the first included the more or less typical CSWS (12 cases), generally with symmetry of spike and waves (SWs) and often with no spindle at all. The other cases had an usual asymmetry of SWs and presence or reduction of spindles, plus other atypical features concerning synchronism and morphology of SWs. Behavioral disorders were significantly more present in patients with a true CSWS; their improvement (and in one case of the three thoroughly followed the improvement of cognitive competence) paralleled the disappearance of CSWS. The generally predominant injury of the lateral aspect of the thalamus included reticular nucleus and ventral nuclei. An imbalance of γ-aminobutyric acid (GABA)B- versus GABAA -mediated receptors may be evoked as a cofactor predisposing to CSWS.
TL;DR: It is demonstrated in the mouse that the gene encoding the retinoic acid receptor beta determines the contribution of delta oscillations to the sleep EEG and regulates cortical synchrony in the adult.
Abstract: Delta oscillations, characteristic of the electroencephalogram (EEG) of slow wave sleep, estimate sleep depth and need and are thought to be closely linked to the recovery function of sleep. The cellular mechanisms underlying the generation of delta waves at the cortical and thalamic levels are well documented, but the molecular regulatory mechanisms remain elusive. Here we demonstrate in the mouse that the gene encoding the retinoic acid receptor beta determines the contribution of delta oscillations to the sleep EEG. Thus, retinoic acid signaling, which is involved in the patterning of the brain and dopaminergic pathways, regulates cortical synchrony in the adult.
01 Jan 2005
TL;DR: The data suggest that in JME patients CAP may be a neurophysiologic oscillator organizing expression of the epileptiform discharges independent of the tendency of the individual patient to produce epileptic EEG discharges.
Abstract: Clinical and EEG manifestations of juvenile myoclonic epilepsy (JME) occur in a strict relationship to the sleepwake cycle, particularly to transition phases (awakening, falling asleep, afternoon relaxation after work). JME manifestations are deactivated during sleep. Because arousal fluctuations during NREM sleep may be controlled by the same neurophysiologic mechanisms regulating awakening, we studied the relationship between the cyclic alternating pattern (CAP) and JME manifestations. All-night polysomnographic recordings of 10 JME patients were analyzed for variations of epileptiform EEG abnormalities in relation to sleep stages and to different microstructural variables (NCAP, CAP, phases A and B). CAP rates (ratio between total CAP duration and total NREM sleep duration) were also calculated. Average CAP rate was 46.70%, significantly higher than that (23%) of an age-matched control group. Macrostructural analysis showed only a trend toward a slight predominance of EEG epileptiform activity during slow wave sleep but no significant correlation between spiking rates and sleep stages. Microstructural analysis confirmed the CAP modulation of EEG epileptiform activity, with maximum appearance of epileptiform abnormalities during phase A CAP (normalized spiking rate = 4.00 ? 0.98) and strong inhibition during phase B (0.06 +00.6). Intermediate values were noted during NCAP (0.54 ? 0.27). N o correlation was noted between spiking rates during NREM sleep and CAP rates, possibly indicating that in JME patients the increased CAP rate may be partially independent of epileptiform EEG activity. Our data suggest that in JME patients CAP may be a neurophysiologic oscillator organizing expression of the epileptiform discharges independent of the tendency of the individual patient to produce epileptiform EEG discharges.
TL;DR: The frequency domain analysis of HRV appears to be an easy tool to estimate the autonomic changes related to PLMS and PLMS- arousals and to differentiate their occurrence during stage 2 and deep sleep.
TL;DR: Chronic sleepwalkers have instability of non-rapid eye movement (NREM) sleep detectable only by the calculation of CAP rate, which is probably related to the presence of the associated sleep disorders.
TL;DR: Fatal Familial Insomnia represents a model disease for the study of sleep-wake regulation and the profound thalamic hypometabolism/atrophy associated with lack of sleep spindles and delta sleep implicate the thalamus in the origin of slow wave sleep (SWS).
TL;DR: It is suggested that the inflammatory marker IL-6 is associated with sleep quality and that certain individual characteristics such as race, gender, age, and age modify that relationship.
Abstract: We examined the relationship between the pro-inflammatory cytokine IL-6 and sleep architecture in 70 healthy men and women. Blood was drawn in the early morning for assessment of IL-6 followed by nocturnal sleep monitoring with polysomnography. Sleep records were scored for sleep stages using standard criteria. Morning IL-6 levels were positively correlated with REM latency after sleep onset [rho = .31, p = .01], percent (%) stage 1 sleep [rho = .23, p = .053], % wake after sleep onset (WASO) [rho = .29, p<.05]. IL-6 levels were negatively correlated with sleep efficiency [rho = -.36, p<.01] and slow wave sleep (SWS) [rho = -.26, p<.05]. After controlling for demographic variables including race, gender, age, and BMI, multiple hierarchical regression analyses revealed that morning IL-6 levels accounted for a significant portion of the variance of REM latency (p<.01), sleep efficiency (p<.01), and % WASO (p = .01). IL-6 was no longer associated with % stage 1 sleep, SWS, and total sleep time after controlling for the demographic characteristics. These findings suggest that the inflammatory marker IL-6 is associated with sleep quality and that certain individual characteristics such as race, gender, and age modify that relationship. Higher IL-6 levels were associated with lower quality of sleep among healthy asymptomatic men and women.