Topographic sleep EEG changes in the acute and chronic stage of hemispheric stroke

After stroke, the injured brain undergoes extensive reorganization and reconnection. Sleep may play a role in synaptic plasticity underlying stroke recovery. To test this hypothesis, we investigated topographic sleep electroencephalographic characteristics, as a measure of brain reorganization, in the acute and chronic stages after hemispheric stroke. We studied eight patients with unilateral stroke in the supply territory of the middle cerebral artery and eight matched controls. All subjects underwent a detailed clinical examination including assessment of stroke severity, sleep habits and disturbances, anxiety and depression, and high‐density electroencephalogram examination with 128 electrodes during sleep. The recordings were performed within 10 days after stroke in all patients, and in six patients also 3 months later. During sleep, we found higher slow‐wave and theta activity over the affected hemisphere in the infarct area in the acute and chronic stage of stroke. Slow‐wave, theta activity and spindle frequency range power over the affected hemisphere were lower in comparison to the non‐affected side in a peri‐infarct area in the patients’ group, which persisted over time. Conversely, in wakefulness, only an increase of delta, theta activity and a slowing of alpha activity over the infarct area were found. Sleep slow‐wave activity correlated with stroke severity and outcome. Stroke might have differential effects on the generation of delta activity in wakefulness and sleep slow waves (1–8 Hz). Sleep electroencephalogram changes over both the affected and non‐affected hemispheres reflect the acute dysfunction caused by stroke and the plastic changes underlying its recovery. Moreover, these changes correlate with stroke severity and outcome.     

Unilateral thalamic stroke does not decrease ipsilateral sleep spindles

STUDY OBJECTIVES: To measure the sleep spindle characteristics in patients with unilateral thalamic stroke. DESIGN: A prospective study of patients with thalamic stroke and age-matched healthy controls. SETTING: Department of Neurology of a University Hospital. PARTICIPANTS: Thirteen patients (mean age: 67 years, SD: 13,44) with an isolated, unilateral acute thalamic stroke and 18 healthy age-matched volunteers. INTERVENTIONS: A polysomnogram recording from 14 scalp EEG electrodes performed during 2 consecutive nights, the second or third week after the stroke. Only the sleep of the second night was analyzed. MEASUREMENTS AND RESULTS: Sleep spindles were counted during two separate 10-minute epochs of stage II. Spindles appearing synchronously in both sides with similar amplitude were called "bilateral." Spindles with twice the amplitude in one side than the other were "right" or "left-side predominant". There were 8 patients with posterolateral, 3 with global and 2 with anterior lesions. Eight were right and 5 left-sided. The number of spindles was similar in patients (39.8 +/- 23.4 in 20 minutes) than controls (26.07 +/- 29.07; p=0.173). Spindles with a centroparietal (34%) and centroparieto-occipital localization (22%) were the most frequent. In controls approximately 66% of the spindles had a bilateral and symmetric distribution over the scalp, 23% of the spindles were predominantly left-sided and 5% were predominantly right-sided. In patients, bilateral spindles decreased (p<0.0001) but asymmetric spindles did not change. CONCLUSION: Unilateral acute thalamic stroke does not decrease sleep spindles ipsilaterally; rather, it seems to produce a bilateral diminution in their number.     

Interhemispheric asymmetry of human sleep EEG in response to selective slow-wave sleep deprivation

Recent evidence suggests that the human sleep electroencephalogram (EEG) shows regional differences over both the sagittal and coronal planes. In the present study, in a group of 10 right-handers, the authors investigated the presence of hemispheric asymmetries in the homeostatic regulation of human sleep EEG power during and after selective slow-wave sleep (SWS) deprivation. The SWS deprivation was slightly more effective over the right hemisphere, but the left hemisphere showed a markedly larger increase of EEG power in the 1.00-24.75 Hz range during recovery-night non-REM sleep, and a larger increase of EEG power during both deprivation-night and recovery-night REM sleep. These results support the greater need for sleep recuperative processes of the left hemisphere, suggesting that local sleep regulation processes may also act during REM sleep.     

Supine sleep and positional sleep apnea after acute ischemic stroke and intracerebral hemorrhage

OBJECTIVE:

Obstructive sleep apnea is frequent during the acute phase of stroke, and it is associated with poorer outcomes. A well-established relationship between supine sleep and obstructive sleep apnea severity exists in non-stroke patients. This study investigated the frequency of supine sleep and positional obstructive sleep apnea in patients with ischemic or hemorrhagic stroke.

METHODS:

Patients who suffered their first acute stroke, either ischemic or hemorrhagic, were subjected to a full polysomnography, including the continuous monitoring of sleep positions, during the first night after symptom onset. Obstructive sleep apnea severity was measured using the apnea-hypopnea index, and the NIHSS measured stroke severity.

RESULTS:

We prospectively studied 66 stroke patients. The mean age was 57.6±11.5 years, and the mean body mass index was 26.5±4.9. Obstructive sleep apnea (apnea-hypopnea index ≥5) was present in 78.8% of patients, and the mean apnea-hypopnea index was 29.7±26.6. The majority of subjects (66.7%) spent the entire sleep time in a supine position, and positional obstructive sleep apnea was clearly present in the other 23.1% of cases. A positive correlation was observed between the NIHSS and sleep time in the supine position (r_s = 0.5; p<0.001).

CONCLUSIONS:

Prolonged supine positioning during sleep was highly frequent after stroke, and it was related to stroke severity. Positional sleep apnea was observed in one quarter of stroke patients, which was likely underestimated during the acute phase of stroke. The adequate positioning of patients during sleep during the acute phase of stroke may decrease obstructive respiratory events, regardless of the stroke subtype.     

Effect of cognitive behavioural therapy for insomnia on sleep architecture and sleep EEG power spectra in psychophysiological insomnia

There is now an overwhelming preponderance of evidence that cognitive behavioural therapy for insomnia (CBT-I) is effective, as effective as sedative hypnotics during acute treatment (4-8 weeks), and is more effective in long term (following treatment). Although the efficacy of CBT-I in the treatment of chronic insomnia is well known, however there is little objective data on the effects of CBT-I on sleep architecture and sleep EEG power densities. The present study evaluated, first, subjective change in sleep quality and quantity, and secondly the modifications occurring in polysomnography and EEG power densities during sleep after 8 weeks of CBT-I. Nine free drug patients with psychophysiological insomnia, aged 33-62 years (mean age 47 +/- 9.7 years), seven female and two male participated in the study. Self-report questionnaires were administered 1 week before and 1 week after CBT-I, a sleep diary was completed each day 1 week before CBT-I, during CBT-I and 1 week after CBT-I. Subjects underwent two consecutive polysomnographic nights before and after CBT-I. Spectral analysis was performed the second night following 16 h of controlled wakefulness. After CBT-I, only scales assessing insomnia were significantly decreased, stages 2, REM sleep and SWS durations were significantly increased. Slow wave activity (SWA) was increased and the SWA decay shortened, beta and sigma activity were reduced. In conclusion CBT-I improves both subjective and objective sleep quality of sleep. CBT-I may enhance sleep pressure and improve homeostatic sleep regulation.     

Handedness leads to interhemispheric EEG asymmetry during sleep in the rat

Sleep electroencephalographic (EEG) slow-wave activity is increased after wakefulness and decreases during sleep. Regional sleep EEG differences are thought to be a consequence of activation of specific cortical neuronal circuits during waking. We investigated the relationship between handedness and interhemispheric brain asymmetry. Bilateral EEG recordings were obtained from the frontal and occipital cortex in rats with a clear paw preference in a food-reaching task (right, n = 5; left, n = 5). While still na?ve to the task, no waking or sleep EEG asymmetry was present. During the food-reaching task, the waking EEG showed significant, substantial power increases in the frontal hemisphere contralateral to the dominant paw in the low theta range (4.5-6.0 Hz). Moreover, the non-REM sleep EEG following feeding bouts was markedly asymmetric, with significantly higher power in the hemisphere contralateral to the preferred paw in frequencies >1.5 Hz. No asymmetry was evident in the occipital EEG. Correlation analyses revealed a positive association between the hemispheric asymmetry during sleep and the degree of preferred use of the contralateral paw during waking in frequencies <9.0 Hz. Our findings show that handedness is reflected in specific, regional EEG asymmetry during sleep. Neuronal activity induced by preferential use of a particular forelimb led to a local enhancement of EEG power in frequencies within the delta and sigma ranges, supporting the hypothesis of use-dependent local sleep regulation. We conclude that inherent laterality is manifested when animals are exposed to complex behavioral tasks, and sleep plays a role in consolidating the hemispheric dominance of the brain.     

Respiratory paradox as an indicator of arousal from non-REM sleep

Increasing respiratory effort is the likely stimulus for arousal in patients with sleep-disordered breathing. Changes in the phase angle waveform (an indirect measure of respiratory effort) may provide a useful non-EEG indicator of respiratory-related arousal. The aim of this study was to investigate the relationship between phase angle change (using a continuous measurement technique) and EEG arousal. Polysomnographic sleep recordings (including: EEG, EOG, EMG, respiratory effort [ribcage and abdominal movement], respiratory paradox [continuous phase angle measurement], oral-nasal airflow, and oxygen saturation) were performed in a purpose built laboratory on 30 patients with sleep-disordered breathing (15 patients with obstructive sleep apnoea/hypopnoea syndrome [OSAHS]; 15 chronic heavy snorers without OSAHS) and 15 age and weight matched, non-snoring normal subjects. All data, including the temporal relationship between phase angle change and EEG arousal, were analyzed manually (4,545 phase angle changes and 6,473 EEG arousals). There was a highly significant correlation (p<0.001) between phase angle index (changes/hour of sleep) and EEG arousal index (arousals/hour of sleep). However, mean phase angle index allowed a much clearer differentiation between the three subject groups, with the mean phase angle index providing a six-fold difference between normal and OSAHS groups, while the EEG arousal index gave only a two-fold difference. In support of the suggestion that phase angle changes represent respiratory-related sleep disruption, more than twice as many EEG arousals were associated with a change in the phase angle waveform in patients with sleep-disordered breathing than in normal subjects. This study highlights the limitations of EEG arousal scoring in the assessment of patients with sleep-disordered breathing and provides further evidence to support phase angle change as an indicator of respiratory-related sleep disruption.     

Determinants of subjective sleepiness in suspected obstructive sleep apnoea

Although daytime sleepiness is commonly associated with obstructive sleep apnoea (OSA), the relationship between OSA severity and subjective sleepiness has been documented elusive. This study aimed to identify clinical and polysomnographic determinants of subjective sleepiness among patients suspected of having OSA. A sleep clinic-based sample of 915 patients was interviewed with a structured questionnaire and underwent diagnostic overnight polysomnography. Subjective sleepiness was quantified by Epworth Sleepiness Scale (ESS). Excessive daytime sleepiness (defined as ESS score > 10) was present in 38.8% of patients. In multiple linear regression analysis, respiratory disturbance index [RDI; used to define (whenever RDI was >5) and quantify OSA], depression and diabetes were the most important determinants of ESS score accounting for 17%, 11% and 6% of its variability respectively. Chronic obstructive pulmonary disease (COPD), stroke, heart disease, alcohol use and body mass index were less important determinants of ESS score explaining 1-3% of its variability. In conclusion, OSA should not be considered the sole potential cause of increased subjective sleepiness in patients suspected of having OSA. Primarily depression and diabetes, but also COPD, stroke, heart disease, alcohol use and increased body mass index may contribute to increased subjective sleepiness.     

Biological rhythm disturbance in depression: temporal coherence of ultradian sleep EEG rhythms

BACKGROUND: Recent studies have suggested that major depressive disorders are associated with a breakdown in the organization of ultradian rhythm in sleep EEG. The present study used cross-spectral analysis of sleep EEG to confirm this finding, in a larger-scale study, evaluating the influence of gender and age on ultradian rhythms in depression. METHODS: Temporal coherence of ultradian (80-120 min) rhythms in beta, theta and delta, recorded from central and parietal sites, were compared in 120 symptomatic, unmedicated, depressed outpatients and 59 healthy normal controls. RESULTS: Few macro-architectural differences were noted between patients and controls. However, interhemispheric beta and theta coherence and intrahemispheric coherence between beta and delta rhythms were significantly lower in depressed patients. Coherence measures were lowest in women with depression and highest in men in the control group, but were not strongly influenced by age. Over 65% of depressed patients were > or = 2 standard deviations below normal on at least one coherence measure, in sharp contrast to less than 10% of patients on macro-architectural variables. CONCLUSIONS: It was concluded that dysregulation of ultradian rhythms characterizes the majority of depressed out-patients, primarily women, even when macro-architecture did not differentiate groups. The outcome of this study supports the view that the pathophysiology of depression is strongly influenced by gender. It was suggested that low temporal coherence in depression reflects a breakdown in the organization of sleep EEG rhythms within and between the two hemispheres.     

Interhemispheric sleep EEG asymmetry in the rat is enhanced by sleep deprivation

Vigilance state-related topographic variations of electroencephalographic (EEG) activity have been reported in humans and animals. To investigate their possible functional significance, the cortical EEG of the rat was recorded from frontal and parietal derivations in both hemispheres. Records were obtained for a 24-h baseline day, 6-h sleep deprivation (SD), and subsequent 18-h recovery. During the baseline 12-h light period, the main sleep period of the rat, low-frequency (<7.0 Hz) power in the non-rapid eye-movement (NREM) sleep EEG declined progressively. Left-hemispheric predominance of low-frequency power at the parietal derivations was observed at the beginning of the light period when sleep pressure is high due to preceding spontaneous waking. The left-hemispheric dominance changed to a right-hemispheric dominance in the course of the 12-h rest-phase when sleep pressure dissipated. During recovery from SD, both low-frequency power and parietal left-hemispheric predominance were enhanced. The increase in low-frequency power in NREM sleep observed after SD at the frontal site was larger than at the parietal site. However, frontally no interhemispheric differences were present. In REM sleep, power in the theta band (5.25-8.0 Hz) exhibited a right-hemispheric predominance. In contrast to NREM sleep, the hemispheric asymmetry showed no trend during baseline and was not affected by SD. Use-dependent local changes may underlie the regional differences in the low-frequency NREM sleep EEG within and between hemispheres. The different interhemispheric asymmetries in NREM and REM sleep suggest that the two sleep states may subserve different functions in the brain.     

Reported chronic insomnia is independent of poor sleep as measured by electroencephalography

OBJECTIVE: Several behavioral, physiological, and subjective variables were examined in subjects reporting chronic insomnia (IN group) and subjects with no complaint of insomnia (NC group) to determine factors predictive of poor sleep as measured by electroencephalography (EEG sleep). METHODS: A total of 177 subjects (121 in the IN group and 56 in the NC group) were evaluated on the basis of EEG sleep, subjective sleep, sleepiness, performance, mood, personality, and metabolic parameters during a 36-hour laboratory stay. RESULTS: Equal percentages of subjects in each group had 0, 1, or 2 nights of poor EEG sleep, indicating that the IN group was not more likely to have impaired sleep in the laboratory. Results of the Minnesota Multiphasic Personality Inventory showed that subjects in the IN group had more pathological personality profiles, and results of laboratory studies showed that these subjects had worse mood ratings, less subjective sleepiness, poorer memory performance, and longer midafternoon sleep latencies. Subjects in the IN group also rated their laboratory sleep as poorer in quality with more time awake after sleep onset and longer sleep latencies, but no differences in EEG sleep were observed. Poor nights of EEG sleep were associated with being male, increasing age, and a history of more time awake after sleep onset; among the laboratory tests, poor EEG sleep was associated with worse mood ratings, poorer memory performance, longer sleep latencies (as indicated by higher scores on the Multiple Sleep Latency Test), higher sleep/wake ratios for metabolic parameters, lower ratings of sleep quality, and longer perceived sleep latencies. CONCLUSIONS: A history of chronic insomnia does not predict poor EEG sleep. Both chronic insomnia and poor EEG sleep are associated independently with dysphoria, hyperarousal, diminished waking function, and negative subjective sleep quality. Separate arousal and sleep systems are posited to account for these results.     

Cardiac autonomic dynamics during sleep are lost in patients with TIA and stroke

Ischaemic stroke is accompanied by important alterations of cardiac autonomic control, which have an impact on stroke outcome. In sleep, cardiac autonomic control oscillates with a predominant sympathetic modulation during REM sleep. We aimed to assess cardiac autonomic control in different sleep stages in patients with ischaemic stroke. Forty‐five patients enrolled in the prospective, multicentre SAS‐CARE study but without significant sleep‐disordered breathing (apnea–hypopnea index < 15/hr) and without atrial fibrillation were included in this analysis. The mean age was 56 years, 68% were male, 76% had a stroke (n = 34, mean National Institutes of Health Stroke Scale [NIHSS] score of 5, 11 involving the insula) and 24% (n = 11) had a transitory ischaemic attack. Cardiac autonomic control was evaluated using three different tools (spectral, symbolic and entropy analysis) according to sleep stages on short segments of 250 beats in all patients. Polysomnographic studies were performed within 7 days and 3 months after the ischaemic event. No significant differences in cardiac autonomic control between sleep stages were observed in the acute phase and after 3 months. Predominant vagal modulation and decreased sympathetic modulation were observed across all sleep stages in ischaemic stroke involving the insula. Patients with ischaemic stroke and transitory ischaemic attack present a loss of cardiac autonomic dynamics during sleep in the first 3 months after the ischaemic event. This change could represent an adaptive phenomenon, protecting the cardiovascular system from the instabilities of autonomic control, or a risk factor for stroke, which precedes the ischaemic event.     

Insufficient non-REM sleep intensity in narcolepsy-cataplexy

STUDY OBJECTIVES: To compare electroencephalogram (EEG) dynamics during nocturnal sleep in patients with narcolepsy-cataplexy and healthy controls. Fragmented nocturnal sleep is a prominent feature and contributes to excessive daytime sleepiness in narcolepsy-cataplexy. Only 3 studies have addressed changes in homeostatic sleep regulation as a possible mechanism underlying nocturnal sleep fragmentation in narcolepsy-cataplexy. DESIGN, SETTING AND PARTICIPANTS: Baseline sleep of 11 drug-naive patients with narcolepsy-cataplexy (19-37 years) and 11 matched controls (18-41 years) was polysomnographically recorded. The EEG was subjected to spectral analysis. INTERVENTIONS: None, baseline condition. MEASUREMENTS AND RESULTS: All patients with narcolepsy-cataplexy but no control subjects showed a sleep-onset rapid eye movement (REM) episode. Non-REM (NREM)-REM sleep cycles were longer in patients with narcolepsy-cataplexy than in controls (P = 0.04). Mean slow-wave activity declined in both groups across the first 3 NREM sleep episodes (P<0.001). The rate of decline, however, appeared to be steeper in patients with narcolepsy-cataplexy (time constant: narcolepsy-cataplexy 51.1 +/- 23.8 minutes [mean +/- SEM], 95% confidence interval [CI]: 33.4-108.8 minutes) than in controls (169.4 +/- 81.5 minutes, 95% CI: 110.9-357.6 minutes) as concluded from nonoverlapping 95% confidence interval of the time constants. The steeper decline of SWA in narcolepsy-cataplexy compared to controls was related to an impaired build-up of slow-wave activity in the second cycle. Sleep in the second cycle was interrupted in patients with narcolepsy-cataplexy, when compared with controls, by an increased number (P = 0.01) and longer duration (P = 0.01) of short wake episodes. CONCLUSIONS: Insufficient NREM sleep intensity is associated with nonconsolidated nocturnal sleep in narcolepsy-cataplexy. The inability to consolidate sleep manifests itself when NREM sleep intensity has decayed below a certain level and is reflected in an altered time course of slow-wave activity across NREM sleep episodes.     

Homeostatic sleep regulation in adolescents

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.     

Sleep EEG changes after middle cerebral artery infarcts in mice: different effects of striatal and cortical lesions

STUDY OBJECTIVES: Hemispheric stroke in humans is associated with sleep-wake disturbances and sleep electroencephalogram (EEG) changes. The correlation between these changes and stroke extent remains unclear. In the absence of experimental data, we assessed sleep EEG changes after focal cerebral ischemia of different extensions in mice. DESIGN: Following electrode implantation and baseline sleep-wake EEG recordings, mice were submitted to sham surgery (control group), 30 minutes of intraluminal middle cerebral artery (MCA) occlusion (striatal stroke), or distal MCA electrocoagulation (cortical stroke). One and 12 days after stroke, sleep-wake EEG recordings were repeated. The EEG recorded from the healthy hemisphere was analyzed visually and automatically (fast Fourier analysis) according to established criteria. MEASUREMENTS AND RESULTS: Striatal stroke induced an increase in non-rapid eye movement (NREM) sleep and a reduction of rapid eye movement sleep. These changes were detectable both during the light and the dark phase at day 1 and persisted until day 12 after stroke. Cortical stroke induced a less-marked increase in NREM sleep, which was present only at day 1 and during the dark phase. In cortical stroke, the increase in NREM sleep was associated in the wake EEG power spectra, with an increase in the theta and a reduction in the beta activity. CONCLUSION: Cortical and striatal stroke lead to different sleep-wake EEG changes in mice, which probably reflect variable effects on sleep-promoting and wakefulness-maintaining neuronal networks.     

Evening administration of melatonin and bright light: Interactions on the EEG during sleep and wakefulness

Both the pineal hormone melatonin and light exposure are considered to play a major role in the circadian regulation of sleep. In a placebo- controlled balanced cross-over design, we investigated the acute effects of exogenous melatonin (5 mg p.o. at 20.40 hours) with or without a 3-h bright light exposure (5000 lux from 21.00 hours–24.00 hours) on subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in healthy young men. The acute effects of melatonin, bright light and their interaction were measured on the first day (treatment day), possible circadian phase shifts were assessed on the post-treatment day. On the treatment day, the evening rise in subjective sleepiness was accelerated after melatonin and protracted during bright light exposure. These effects were also reflected in specific changes of EEG power density in the theta/alpha range during wakefulness. Melatonin shortened and bright light increased sleep latency. REMS latency was reduced after melatonin administration but bright light had no effect. Slow-wave sleep and slow-wave activity during the first non-rapid eye movement (NREMS) episode were suppressed after melatonin administration and rebounded in the second NREMS episode, independent of whether light was co-administered or not. Self rated sleep quality was better after melatonin administration whereas the awakening process was rated as more difficult after bright light. On the post-treatment day after evening bright light, the rise in sleepiness and the onset of sleep were delayed, independent of whether melatonin was co-administered or not. Thus, although acute bright light and melatonin administration affected subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in a additive manner, the phase shifting effect of a single evening bright light exposure could not be blocked by exogenous melatonin     

Poor compensatory function for sleep loss as a pathogenic factor in patients with delayed sleep phase syndrome

OBJECTIVE: Delayed sleep phase syndrome (DSPS) is a condition in which the patient is unable to reset or phase-advance his/her sleep timing properly after transient sleep delay and consequently shows persistent sleep phase delay. Prior studies suggested that DSPS is associated with a phase delay in the circadian pacemaker, but there was no evidence to explain the patient's inability to reset sleep phase. SUBJECTS AND METHODS: We used an ultra-short sleep-wake schedule together with simultaneous measurement of dim light melatonin rhythm after 24-hour sleep deprivation to allow the differential observation of diurnal sleep propensity fluctuation both from circadian and homeostatic aspects in 11 patients with DSPS (17-37 years; 8 men, 3 women) and 15 healthy controls (19-32 years; 8 men, 7 women). SETTING: NA. PATIENTS OR PARTICIPANTS: NA. INTERVENTIONS: NA. RESULTS: DSPS patients showed less ability to compensate for previous sleep loss during their circadian day and first hours of their circadian nighttime determined by dim light melatonin onset compared with controls, while controls compensated for previous sleep loss at most circadian times. Though shapes of dim light melatonin rhythm did not differ between the groups, phase angle between melatonin and sleep propensity rhythms was wider in DSPS patients than in controls. CONCLUSIONS: These findings suggest that poor compensatory function for sleep loss predisposes DSPS patients to failure to reset their sleep phase. Our results provide implications for understanding not only the pathophysiology of DSPS but also the biological basis for why some people can change their sleep schedule easily according to personal or social demands while others cannot.     

Effects of intravenous catheter on sleep in healthy men and in depressed patients

The effects of intravenous catheter and nocturnal blood samplings at frequent intervals on sleep electroencephalogram (EEG) variables were investigated in 8 male healthy controls and 12 depressed patients, who were studied in the same experimental conditions. After one night of habituation, sleep was recorded during 4 consecutive nights in the sleep laboratory. A catheter was inserted around noon the day before the fourth night, and blood was sampled every 15 min for 25 h. The night-to-night comparison of sleep EEG variables did not show significant sleep continuity modifications in the control subjects, other than a weak trend toward an increase in nocturnal awakenings during the night with the catheter. A lengthening of sleep onset latency during the fourth night was found in the depressed patients. No significant changes were detected in percentage of rapid eye movement (REM) sleep in the two groups. However, a gradual increase in Stage 3 was observed across the 4 nights in the control subjects. These results indicate that intravenous blood sampling via a catheter can be performed without inducing significant disruption of sleep length and structure.     

Stroke etiology is associated with symptom onset during sleep

BACKGROUND AND OBJECTIVES: Almost every fifth stroke occurs during sleep. Data about characteristics and etiology of stroke during sleep are conflicting. We investigated the association of the activity at stroke onset (onset during night sleep vs. onset while awake) with stroke subtypes of different etiology. METHODS: A total of 1448 patients with first-ever stroke with known time of symptom presentation were prospectively evaluated. Statistical comparisons were performed between patients with stroke during sleep and stroke while awake in terms of demographic features, known risk factors, vascular comorbidities, and stroke subtypes. Multiple variable logistic regression analyses were performed to identify predictor variables (including stroke risk factors and stroke subtypes) for stroke during sleep. RESULTS: Stroke during sleep was documented in 264 cases (18.2%). In subjects with stroke during sleep, lacunar infarction was the most prevalent stroke subtype (39%), while in patients with stroke while awake, small-vessel disease was the underlying mechanism significantly (P < .001) less often (13.8%). In contrast, patients with stroke while awake suffered significantly (P < .001) more frequently from intracerebral hemorrhage (18.2%) and cardioembolic stroke (34.9%) when compared with subjects with stroke during sleep (6.4% and 18.9%, respectively). The multiple variable logistic regression model identified the following factors as independent predictors of stroke during sleep: atrial fibrillation (odds ratio: 0.346, 95% confidence interval: 0.237-0.505, P < .001) and intracerebral hemorrhage versus ischemic stroke (odds ratio: 0.238, 95% confidence interval: 0.138-0.410, P < .001). Lacunar infarction was the only ischemic stroke subgroup that was positively associated with stroke during sleep (odds ratio: 2.568, 95% confidence interval: 1.447-4.560, P < .001). CONCLUSIONS: There are significant differences between stroke during sleep and stroke while awake concerning vascular risk profile and stroke etiologic subtypes.     

EEG sleep in adolescents with major depression: the role of suicidality and inpatient status

All night sleep EEG recordings were performed for three consecutive nights in 27 adolescents with a diagnosis of major depressive disorder (MDD) and 30 normal adolescent controls. Group comparisons between the entire MDD group and the normal controls revealed no significant diagnostic group differences for any of the major sleep variables. Analyses within subgroups of MDD adolescents, however, revealed heterogeneity of EEG sleep findings in association with suicidality and inpatient status. The findings of this study suggest that the discrepancies among the EEG sleep studies in adolescent MDD may be accounted for by the relative proportions of inpatients, suicidality, or bipolarity within the MDD sample being studied.