Showing papers on "Slow-wave sleep published in 1995"

Contribution of the circadian pacemaker and the sleep homeostat to sleep propensity, sleep structure, electroencephalographic slow waves, and sleep spindle activity in humans

Abstract: The role of the endogenous circadian pacemaker in the timing of the sleep-wake cycle and the regulation of the internal structure of sleep, including REM sleep, EEG slow-wave (0.75-4.5 Hz) and sleep spindle activity (12.75-15.0 Hz) was investigated. Eight men lived in an environment free of time cues for 33-36 d and were scheduled to a 28 hr rest-activity cycle so that sleep episodes (9.33 hr each) occurred at all phases of the endogenous circadian cycle and variations in wakefulness preceding sleep were minimized. The crest of the robust circadian rhythm of REM sleep, which was observed throughout the sleep episode, was positioned shortly after the minimum of the core body temperature rhythm. Furthermore, a sleep-dependent increase of REM sleep was present, which, interacting with the circadian modulation, resulted in highest values of REM sleep when the end of scheduled sleep episodes coincided with habitual wake-time. Slow-wave activity decreased and sleep spindle activity increased in the course of all sleep episodes. Slow-wave activity in non-REM sleep exhibited a low amplitude circadian modulation which did not parallel the circadian rhythm of sleep propensity. Sleep spindle activity showed a marked endogenous circadian rhythm; its crest coincident with the beginning of the habitual sleep episode. Analyses of the (nonadditive) interaction of the circadian and sleep-dependent components of sleep propensity and sleep structure revealed that the phase relation between the sleep-wake cycle and the circadian pacemaker during entrainment promotes the consolidation of sleep and wakefulness and facilitates the transitions between these vigilance states.

Sleep and sleep disorders in older adults.

Abstract: Complaints of sleep disturbance increase with age. Objective sleep assessments using polysomnography reveal sleep impairments (increased wakefulness and arousal from sleep; decreased slow wave sleep) even in healthy seniors. Both polysomnographic sleep and subjective sleep worsen in the presence of health impairments related to drug use, pain, cardiovascular disease, diabetes, depression, or other emotional disorders. In addition to normal aging and chronic disease, sleep complaints can also result from poor sleep habits, specific occult disorders during sleep, or some combination of these factors. Occult disorders include sleep apnea syndrome, periodic leg movements, and restless legs syndrome during sleep. Diagnosis and treatment of these and other sleep disorders is discussed. Both pharmacological and nonpharmacological treatments are considered, with an emphasis on behavioral and educative treatment approaches.

First-night effect in normal subjects and psychiatric inpatients.

Abstract: The goal of the present study was to evaluate the first-night effect in psychiatric inpatients using large subject samples (n > 30) in order to obtain a good statistical evaluation. Thirty-two normal subjects and 94 psychiatric inpatients (38 depressives and 56 insomniacs) were studied for three consecutive nights in the hospital sleep laboratory. Our results showed clearly that there was a first-night effect in normal subjects, similar to that reported in previously published data, characterized by a longer rapid eye movement (REM) sleep latency (p < 0.05), increased wakefulness (p < 0.01) and total sleep time (p < 0.02) and a decreased sleep efficiency (p < 0.01). REM sleep latency and stage REM in the first third of the night were still altered in the second night. Both clinical groups had a less marked first-night effect than normal subjects, showing alterations only observed in REM sleep (p < 0.01) (decreased REM sleep, longer REM sleep latency, increased REM sleep gravity center). However, the first-night effect was more pronounced in insomniacs than in depressed patients. No statistical differences between the second and third nights' recordings were found in sleep parameters. It is suggested that first-night data should not be simply discarded but could be used in subsequent analyses.

Regional cerebral glucose metabolism in children with deterioration of one or more cognitive functions and continuous spike-and-wave discharges during sleep.

Abstract: The Landau-Kleffner syndrome (LKS) and the syndrome of continuous spike-and-wave discharges during slow sleep (CSWS) were originally described, and are still considered, separately. The former combines an acquired aphasia with spike-and-wave discharges that are activated by slow wave sleep, behavioural disturbances, and sometimes epileptic seizures. The latter is characterized by continuous spike-and-wave discharges during slow wave sleep, usually combined with global intellectual deterioration and epileptic seizures. These two syndromes share many common features: (i) onset during childhood; (ii) deterioration of cognitive functions that were previously normally acquired; (iii) seizure type; (iv) EEG pattern; (v) pharmacological reactivity; (vi) regression of the neuropsychological symptoms, of the EEG abnormalities and of the seizures before the end of adolescence; (vii) absence of obvious structural lesion detected by CT or MRI scan. Therefore, we postulated that these patients might, in fact, be presenting several facets of a single process associating the deterioration of cognitive functions and continuous spike-and-wave discharges during slow wave sleep. The pathogenesis of this syndrome remains unknown. Seven patients, presenting CSWS associated with neuropsychological deterioration (isolated aphasia, three cases; language disturbances with more widespread cognitive deterioration, three cases; isolated apraxia, one case) were studied using PET with [18F]fluorodeoxyglucose (FDG). We hoped to find metabolic arguments in favour of a unifying hypothesis, and to reveal clues as to pathogenesis. We present the retrospective analysis of 21 studies performed between 1986 and 1993, 12 of which were done during sleep. For three of these patients, follow-up studies were obtained until recovery. The metabolic patterns were very variable from one patient to another and in the same patient over time. Among the six patients studied during the active phase of the affection, our results showed unilateral, focal or regional increase in glucose metabolism of the cortex in five patients. This hypermetabolism was observed during sleep with continuous spike-and-wave discharges, but also persisted during wakefulness. In the last patient, the metabolic pattern was different: decreased regional glucose metabolism was observed during wakefulness, whereas during sleep, the metabolic pattern in the temporal areas varied during the course of the affection. After recovery, the metabolic pattern in four children (including the seventh patient) was either normal or showed focal or regional, uni- or bilateral decrease in cortical glucose metabolism. Despite this apparent disparity, four basic metabolic characteristics formed a common pattern in all patients, in line with our unifying postulate: (i) the metabolism of the cortical mantle was higher than in the subcortical structures, especially in the thalamic nuclei. This metabolic pattern is characteristic of an immature brain. (ii) The metabolic abnormalities involved focal or regional areas of the cortex. This finding is in good agreement with recent neurophysiological data suggesting a focal origin of the spike-and-wave discharges. (iii) The metabolic disturbances predominantly involved associative cortices. The pattern of neuropsychological deterioration is in good agreement with the topography of the disturbances of cortical glucose metabolism. (iv) The thalamic nuclei remained symmetrical despite significant cortical asymmetries, suggesting either that cortico-thalamic neurons do not participate in the generation of spike-and-wave discharges or that they are inhibited by the pathologic mechanisms. We hypothesize that the acquired deterioration of cognitive function with CSWS is caused by an alteration of the maturation of one or several associative cortices, primarily involving local interneurons and cortico-cortical associative neurons.

Physiology of REM sleep, cataplexy, and sleep paralysis.

Abstract: The main neural structures generating muscle atonia and other phenomena characteristic of REM sleep are present in dorsolateral portions of the pons in the brainstem. Occurrence of REM sleep and the NREM-REM sleep cycle are probably determined by a balance or interaction between the cholinergic and cholinoceptive REM sleep-on neuronal populations and the monoaminergic REM sleep-off neuronal population. Neural activities producing generalized muscle atonia in REM sleep originate mainly in dorsolateral portions of the pontine reticular formation, descend through the medulla and spinal cord, and inhibit the motoneurons in the brainstem and spinal cord, bringing about postural atonia. Cataplexy and sleep paralysis are pathological, dissociated manifestations of the generalized muscle atonia characteristic REM sleep. Cataplexy is triggered by emotional stimuli, probably through activation of the neural structure generating the muscle atonia of REM sleep. During long-lasting cataplectic attacks, narcoleptic humans often experience sleep paralysis and vivid hypnagogic hallucinations in the latter sleep state. Sleep paralysis is caused by the marked dissociation between level of alertness and muscle atonia that often occurs in SOREM sleep episodes. Frequent SOREM sleep episodes in narcoleptic humans and dogs may occur when some of the neural mechanisms producing wakefulness and/or NREM sleep that normally inhibit the occurrence of REM sleep are abnormally weak, or when neural mechanisms facilitating the occurrence of REM sleep are hypersensitive or hyperactive, or both. Both abnormalities may contribute to the occurrence of SOREM sleep episodes and sleep paralysis, and also to the emotional triggering of cataplexy. Frequent occurrence of SOREM sleep episodes seems to be prerequisite but not sufficient for the occurrence of cataplexy. Some additional neural activities induced by emotion also contribute by inhibiting and/or activating the disturbed neural mechanisms related to SOREM sleep episodes. These abnormalities in neural mechanisms probably involve hypersensitivity or hyperactivity of muscarinic cholinergic and/or cholinoceptive neuronal populations in the pontine and suprapontine structures, and/or abnormally decreased activity of noradrenergic or serotonergic neuronal populations in the pons and/or other brainstem structures. This last monoaminergic neuronal population probably has a gating or inhibiting effect upon the cholinergic and cholinoceptive neuronal populations related to the generation of generalized muscle atonia and REM sleep. In spite of many studies and published reports on REM sleep, as well as on cataplexy and sleep paralysis, we are still far from a complete understanding of the physiological mechanisms producing muscle atonia in REM sleep and of the pathophysiological mechanisms of cataplexy and sleep paralysis--though it is apparent that these mechanisms are closely related.

In quest of identifying vulnerability markers for psychiatric disorders by all-night polysomnography.

Abstract: Background: The persistence of a depressionlike sleep pattern in fully remitted depressed patients suggests that the pattern is a trait characteristic of sleep measurements. However, in the past, subjects have undergone investigation only after the onset of the disorder, and, therefore, the altered sleep pattern may merely represent a biological scar. Methods: We polysomnographically investigated 54 healthy subjects who had no lifetime or current diagnosis of a psychiatric disorder but had at least one first-degree relative with major depression or a bipolar disorder and at least one further close relative with major depression, a bipolar disorder, or a schizophrenic disorder. Twenty unrelated control probands without a personal and family history of psychiatric disorders and 18 unrelated inpatients with major depression served as reference groups. Prior to investigation, all healthy subjects had been free of any prescription and nonprescription drug for at least 3 months. The depressed patients were free of drugs for at least 1 week. All subjects slept for 2 nights in the sleep research unit. The sleep of the second night was recorded and visually scored. Results: Analysis of the individual sleep cycles in these subjects revealed both a reduced amount of slow wave sleep and increased rapid eye movement density in the first sleep cycle. Discriminant analysis showed that 10 subjects (18%) had sleep patterns similar to those of depressed patients. Conclusions: According to our observations, one fifth of the healthy subjects with a high genetic load for psychiatric disorders showed a conspicuous (depression-like) sleep pattern. The follow-up will determine whether this sleep pattern indeed represents a trait marker indicating vulnerability.

Neuronal discharge of preoptic/anterior hypothalamic thermosensitive neurons: relation to NREM sleep

Abstract: Thermosensitive neurons of the preoptic/anterior hypothalamic area (POAH) have been implicated in the regulation of non-rapid eye movement (NREM) sleep. We attempted to identify those medial POAH thermosensitive neurons that may be involved in NREM sleep regulation. The thermosensitivity of medial POAH neurons was studied in five freely moving adult cats by local cooling or warming of the medial POAH with a water-perfused thermode. Of 308 neurons, 65 (21%) were classified as thermosensitive, including 31 (10%) warm-sensitive and 34 (11%) cold-sensitive neurons. The spontaneous discharge rates of 28 warm-sensitive, 34 cold-sensitive, and 115 randomly selected thermoinsensitive neurons were recorded through one to three sleep-waking cycles. Patterns of spontaneous activity for warm- and cold-sensitive neurons were different. Of 28 warm-sensitive neurons, 18 (64%) exhibited increased discharge rate during NREM sleep compared with waking (NREM/wake, > or = 1.2). This subpopulation of warm-sensitive neurons also exhibited significantly increased thermosensitivity when tested during NREM sleep. Of 34 cold-sensitive neurons, 25 (74%) discharged more slowly during NREM sleep compared with waking (NREM/wake, < or = 0.8). This subpopulation of cold-sensitive neurons exhibited decreased thermosensitivity during NREM sleep. These results are consistent with a hypothesis that the activation of sleep-related warm-sensitive neurons and the deactivation of wake-related cold-sensitive neurons may play a key role in the onset and regulation of NREM sleep.

Influence of Exercise on Human Sleep

Abstract: Several research paradigms have been used to examine the influence of exercise on sleep. Epidemiological studies show that exercise is perceived as helpful in promoting sleep and suggest that regular physical activity may be useful in improving sleep quality and reducing daytime sleepiness. Additional epidemiological inquiry is clearly warranted based on the available evidence. Acute exercise experiments that have measured sleep physiology directly from subjects who either performed, or refrained from, daytime exercise indicate that exercise is associated with a small, but reliable increase in Stage 2 and slow wave sleep. The mechanism(s) that underlie exercise-associated increases in SWS is unknown. However, there is evidence that links elevations in daytime core body temperature to increases in SWS. Acute exercise experiments were found to be associated with a reduction in REM sleep and a delay in REM onset latency that were larger in magnitude than the effects observed for Stage 2 and SWS. These REM sleep observations highlight the need for continued study of the consequences of exercise on both circadian and homeostatic aspects of sleep. The delay in REM onset latency observed in the naturalistic acute exercise studies was consistent with the results of experiments in which environmental factors were more rigorously controlled and showed that physical exercise, or a concomitant, can induce a phase delay in markers of the human circadian pacemaker. It is worth pointing out that the most sophisticated and rigorous experiments from a standpoint of understanding sleep, such as those involving constant routines, bed rest, and temporal isolation, have for the most part used exercise in a crude manner. Because exercise is a stressor with diverse psychophysiological consequences that depends in part upon the interaction of multiple factors (e.g., the setting; degree of environmental heat stress; the activity history and fitness of the subject; the duration, intensity, and timing of the exercise bout; body position, etc.), understanding the influence of exercise on sleep will be stymied until carefully designed sleep studies also use exercise in an equally sophisticated and systematic way. Exercise is widely believed to have large effects on sleep. However, the scientific evidence does not strongly support this common belief. This incongruity may well be explained in part by considering the paradigms that have been used to study exercise and sleep.(ABSTRACT TRUNCATED AT 400 WORDS)

A reconceptualization of EEG alpha activity as an index of arousal during sleep: all alpha activity is not equal.

Abstract: SUMMARY Alpha activity occurring during sleep is generally considered to reflect arousal processes and a shift toward wakefulness. This long-standing interpretation is based on physiological and behavioural arousal correlates of alpha activity presumed to have an occipital focus. In addition to the application of this interpretation to sleep/wake state determinations, there have been reports of nonrefreshing or nonrestorative sleep in clinical populations exhibiting dramatic amounts of alpha intrusion during sleep in the absence of awakening. Reports of the presence of alpha activity during sleep in normal subjects without sleep disruption or complaints of daytime sleepiness call into question the interpretation that this activity is associated with arousal. A re-examination of this literature, incorporating the results from recent investigations employing multi-site EEG recordings, electronic processing and source diple analyses of this activity, suggests the existence of alpha activity which differs in generation site (thalamus), scalp distribution (frontal-central), and behavioural correlates (e.g. enhancement to stimulation during wakefulness, concentration in the first-half of the night during sleep, and absence of sleep disturbance) from occipital alpha activity. Such marked differences in defining characteristics imply different functional correlates for these activities. In this context, it is proposed that this fronto-central alpha activity is associated with sleep-maintaining processes which may be enhanced in response to sleep-disturbing events.

Light Treatment for Sleep Disorders: Consensus Report II. Basic Properties of Circadian Physiology and Sleep Regulation

Abstract: The rationale for the treatment of sleep disorders by scheduled exposure to bright light in seasonal affective disorder, jet lag, shift work, delayed sleep phase syndrome, and the elderly is, in pa...

Sleep features in Tourette's syndrome, neuroacanthocytosis and Huntington's chorea.

Abstract: Summary Twenty-one patients affected by extrapyramidal disorders were polygraphically recorded during spontaneous nocturnal sleep for two consecutive nights to assess their sleep and movement patterns. The patients (pts) sample included: Gilles de La Tourette syndrome (TS, nine pts), neuroacanthocytosis (NA, six pts) and Huntington's chorea (HC, six pts). Sleep recording included C3/A2, 01/A2, ROC/LOC, submental EMG, EKG, nasal airflow thoracoabdominal respirogram, bilateral anterior tibialis and other EMGs, in relation to the individual distribution of the abnormal movements. According to our observations, abnormal movements always decreased but never ceased completely during sleep. Sleep efficiency (SE) was nearly always poor with a high percentage of wakefulness after sleep onset (WASO) and increased number of arousals. REM sleep was often reduced and in some cases (3 TS pts) incompletely defined as far as its microstructural aspects. Slow wave sleep (SWS) was reduced in HC, normal in NA, and increased in all TS patients with the exception of the two adult subjects more severely affected, while the percentage of stage 2 was not affected. Spindling was increased in NA, HC and in the two most severely affected adult TS patients.

The distribution of EEG frequencies in REM and NREM sleep stages in healthy young adults.

Abstract: Period-analyzed electroencephalographic (EEG) activity was evaluated in 11 men and 11 women to explore the distribution of EEG frequencies during sleep and potential gender differences. Significant stage-of-sleep main effects were noted for both incidence and amplitude measures. Power measures seemed to best differentiate between non-rapid eye movement (NREM) stages, although incidence measures showed roughly the same distributions across sleep stages. Beta incidence and amplitude was highest in stage 1 sleep followed in descending order by rapid eye movement (REM), stage 2, and slow-wave sleep (SWS). Delta incidence and amplitude were highest in SWS, with slightly lower values in stage 2. Interestingly, REM was characterized by higher incidence and amplitude delta than those found in stage 1 sleep. EEG variables did not show striking sex differences in any sleep stage, although a global measure of delta power in NREM sleep was higher among women. Hemispheric asymmetries were small throughout REM and NREM stages. These findings suggest that period analysis provides a detailed description of EEG frequency characteristics during sleep but does not reveal dramatic gender differences.

Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. II. Effects on two nights of recovery sleep.

Abstract: SUMMARY Polysomnograms were obtained from 37 volunteers, before (baseline) and after (two consecutive recovery nights) a 64-h sleep deprivation, with (d-amphetamine or modafinil) or without (placebo) alerting substances. The drugs were administered at 23.00 hours during the first sleep deprivation night (after 17.5 h of wakefulness), to determine whether decrements in cognitive performance would be prevented; at 05.30 hours during the second night of sleep deprivation (after 47.5 h of wakefulness), to see whether performance would be restored; and at 15.30 hours during the third day of continuous work, to study effects on recovery sleep. The second recovery night served to verify whether drug-induced sleep disturbances on the first recovery night would carry over to a second night of sleep. Recovery sleep for the placebo group was as expected: the debt in slow-wave sleep (SWS) and REM sleep was paid back during the first recovery night, the rebound in SWS occurring mainly during the first half of the night, and that of REM sleep being distributed evenly across REM sleep episodes. Recovery sleep for the amphetamine group was also consistent with previously published work: increased sleep latency and intrasleep wakefulness, decreased total sleep time and sleep efficiency, alterations in stage shifts, Stage 1, Stage 2 and SWS, and decreased REM sleep with a longer REM sleep latency. For this group, REM sleep rebound was observed only during the second recovery night. Results for the modafinil group exhibited decreased time in bed and sleep period time, suggesting a reduced requirement for recovery sleep than for the other two groups. This group showed fewer disturbances during the first recovery night than the amphetamine group. In particular, there was no REM sleep deficit, with longer REM sleep episodes and a shorter REM latency, and the REM sleep rebound was limited to the first REM sleep episode. The difference with the amphetamine group was also marked by less NREM sleep and Stage 2 and more SWS episodes. No REM sleep rebound occurred during the second recovery night, which barely differed from placebo. Hence, modafinil allowed for sleep to occur, displayed sleep patterns close to that of the placebo group, and decreased the need for a long recovery sleep usually taken to compensate for the lost sleep due to total sleep deprivation.

Clustering of sleep electroencephalographic patterns in patients with the fibromyalgia syndrome

Abstract: Several electroencephalographic (EEG) abnormalities have been observed during sleep in patients suffering from the fibromyalgia syndrome (FMS). In this study, 12 patients with fibromyalgia and 14 control subjects had two polysomnographic recordings obtained at home. Data from the second night were subjected to blinded manual scoring as well as signal processing using linked or 'step-wise clustering for pattern recognition. In this procedure, a common learning set was generated using the spectral information in three 2 min EEG samples from each of the sleep stages selected from five patients with FMS and five controls. In this way, 17 characteristic EEG classes were defined. All 2 s EEG segments from the whole night from all subjects were then assigned to one of these classes. Five of the classes (dominated by 0.5-4.5 Hz activity) were more frequent in the control group, whereas three other classes (dominated by 8-11 Hz activity) were prevalent in the patient group. This trend was consistent in all sleep stages, although most striking in non-rapid eye movement (NREM) sleep. The predominance of these classes in the patient group may correspond to the alpha-EEG sleep anomaly previously reported in subjects with FMS. More importantly, as the EEG power in the lowest frequency range (prevalent in controls) probably is a marker for restorative sleep, the findings may reflect important aspects of sleep disturbances n subjects suffering from FMS, thereby contributing to some of the daytime symptoms in these patients.

Sleep disorders in tuberous sclerosis: a polysomnographic study

Abstract: Overnight polysomnography was performed in 10 subjects with tuberous sclerosis (TS) and partial epilepsy in order to investigate the relationships between sleep organization, sleep disorders and epilepsy Sleep architecture abnormalities were observed in 9 cases Compared with ten healthy age-matched controls, the TS group showed a shorter total sleep time, a reduced sleep efficiency, a higher number of awakenings and stage transitions, an increased wake after sleep onset and stage 1 and a decreased REM sleep Children with seizures showed a more disrupted sleep architecture compared with seizure-free children Sleep disorders in TS were mainly due to sleep-related epileptic events and were more evident in children who showed large bifrontal or temporal tubers on MRI

K-complexes: are they signs of arousal or sleep protective?

Abstract: The number of K-complexes recorded at the central-temporal EEG derivation (C3-T3) during 5 min periods for both the ascending and descending phase of Stage 2 of NREM sleep for cycles 1, 2 etc were counted in 10 subjects for each of the following five groups: normal persons, patients with a primary generalized form of epilepsy, narcolepsy, insomnia and obstructive sleep apnoea The differences in time spent in different stages of sleep were as expected for these types of patients A 2-within, 1-between factors, repeated measure ANOVA was applied to the data on K-complexes Overall, there was no significant difference between the number of K-complexes observed during the ascending and descending phases of the different sleep cycles Patients with a sleep disorder had significantly less well-defined K-complexes than the normals and the patients with a primary form of generalized epilepsy: for insomnia (P = 0035), for apnoea (P = 0011) and for narcolepsy (P = 0001) There was a significant, but very low correlation coefficient between the number of K-complexes observed during Stage 2 of NREM sleep and the time spent during that stage for all groups combined (Rho 027, P = 0002) and for the narcoleptic patients (Rho 044, P = 0017) In all, the findings lend support to the hypothesis that a K-complex can be seen as a 'defensive response', or has a sleep protective function