Sleep breathing and periodic leg movement pattern in Angelman Syndrome: a polysomnographic study.

OBJECTIVE: The aim of this study was to evaluate the sleep breathing patterns and to detect the eventual presence of periodic leg movements (PLMs) in patients affected by Angelman syndrome (AS). METHODS: Ten children with AS were recruited to participate in the study; the clinical diagnosis was confirmed by the genetic analysis (maternal 15q deletion, uniparental paternal disomy, or mutation of the UBE3A gene). All patients but two had presented epileptic seizures. Two age-matched groups of patients with mental retardation (MR) associated (MRE+) or not (MRE-) to epilepsy were used as control groups. All subjects underwent one polysomnographic recording, after one adaptation night. Sleep stages were scored according to standard criteria slightly modified in order to take into account the specific EEG patterns of AS, also the apnea/hypopnea index (AHI) was quantified; PLMs were identified and the PLM index (PLMI) was computed. The statistical analysis was carried out by means of the one-way ANOVA, followed by the Fisher LSD post-hoc test, when appropriate, and by means of the linear correlation coefficient between AHI and PLMI. RESULTS: Sleep macrostructure showed only few significant differences between children with AS and the other two groups of subjects: AS patients showed higher percentage of wakefulness after sleep onset and sleep onset latency; moreover, the percentage of REM sleep was reduced in AS and in MRE+ subjects. A tendency for AS subjects to present a higher PLMI than the other two groups was also found. AHI >5 was found in 30% of AS subjects, in 30.8% of MRE+, and only in 20% of MRE- patients (chi(2) = 2.359, NS); 70% of AS patients, 38.5% of MRE+, and 46.7% of MRE- subjects had PLMI >5 (chi(2) = 3.088, NS). CONCLUSIONS: These results confirm our previous questionnaire-based findings of a high prevalence of sleep breathing disorder and important PLMs in AS and allow us to hypothesize that epilepsy, rather than mental retardation, might exacerbate these sleep disorders. SIGNIFICANCE: Sleep breathing disorder and PLMs might contribute to the cognitive impairment and to the worsening of life quality of subjects with AS and with MR (mostly those with epilepsy). Therefore, our findings suggest the need to explore these sleep disorders in children affected by MR and to set up a correct treatment.     

Sleep EEG of patients with obsessive-compulsive disorder

Summary Twenty-two patients suffering from an obsessive and compulsive disorder (OCD) according to DSM-III-R were investigated by polysomnographic sleep EEG recordings under drug-free conditions and compared to age- and sex-matched healthy controls. Sleep efficiency was significantly lower and wake % SPT was significantly increased in the patient group compared to healthy subjects. Sleep architecture did not differ among the two samples. Especially REM sleep measures, in particular, REM latency did not differ among the groups. No positive correlation was found between sleep variables and rating inventories for obsession and compulsions (Y-BOCS), depression (Hamilton) and anxiety (CAS). A secondary depression did not influence sleep EEG variables. The results of this study contradict the assumption that OCD patients show REM sleep and slow wave sleep abnormalities similar to those shown by patients with primary depression.     

NREM sleep alterations in narcolepsy/cataplexy.

OBJECTIVE: NREM sleep patterns of narcoleptic patients with cataplexy were studied, focusing on their sleep 'microstructure', by analyzing the cyclic alternating pattern (CAP). METHODS: Forty-nine HLA DQB1*0602-positive patients with narcolepsy/cataplexy (32 men and 17 women, aged 18-46 years) were included together with 37 age-matched normal controls. Each subject underwent one polysomnographic night recording after an adaptation night. Sleep stages were scored following standard criteria and CAP A phases were detected and classified into 3 subtypes (A1, A2, and A3). Power spectra for frequencies between 0.5 and 25 Hz were obtained for each CAP condition, separately in sleep stage 2 and SWS. RESULTS: Narcoleptic patients displayed reduced total CAP rate. A selective reduction in the number of A1 subtypes/hour and a reduced A3 index were found in narcoleptics who had also a smaller average number of CAP sequences. Narcoleptic patients had higher power spectra for fast frequencies mostly during SWS, while REM sleep power spectra showed significantly higher power density for frequency bins 0.5-1.5, 8.5-9.5, and 17.5-25 Hz. Similarly, CAP A1 subtypes and NCAP epochs during SWS displayed significantly higher power density for fast frequency bins. CONCLUSIONS: The main finding of this study is that the occurrence of the A1 CAP subtypes is impaired during NREM sleep in narcoleptic patients. Thus, narcolepsy seems to be accompanied not only by alterations of REM but also NREM sleep which is subtly but significantly impaired, as reflected by CAP and the corresponding EEG spectral analysis. SIGNIFICANCE: Our findings might indicate that in narcolepsy very-slow oscillation processes less effective than normal might be present, with a subtly impaired capability of grouping the other sleep EEG activities; this aspect deserves further insight in order to obtain a better understanding of its functional meaning.     

Clinical significance of sleep EEG abnormalities in chronic schizophrenia

This study aimed to investigate the relationship between measures of clinical symptom severity and sleep EEG parameters in a relatively diagnostically homogeneous group of patients with schizophrenia. We obtained sleep EEG data in 15 drug-free inpatients who met DSM-IV-R criteria for schizophrenia, undifferentiated type, with 15 age- and sex-matched normal controls over two consecutive night polysomnographic recordings. Clinical symptoms were assessed by the Positive and Negative Symptom Scale (PANSS) and Hamilton Rating Scale for Depression. Characteristic features of sleep disturbance were seen in patients with schizophrenia: profound difficulties in sleep initiation and maintenance, poor sleep efficiency, a slow wave sleep (SWS) deficit, and an increased REM density. SWS was inversely correlated with cognitive symptoms. REM density was inversely correlated with positive, cognitive, and emotional discomfort symptoms as well as PANSS total score. Our data demonstrate that drug-free patients with chronic undifferentiated type schizophrenia suffer from profound disturbances in sleep continuity and sleep architecture. Both the SWS deficit and cognitive impairment found in schizophrenics in this study may relate to similar underlying structural brain abnormalities.     

Sleep instability and cognitive status in drug-resistant epilepsies

ObjectiveThe aims of this study were to evaluate the sleep habits of children with drug resistant epilepsy and to correlate sleep abnormalities with epilepsy and level of intelligence.Subjects and methodsTwenty five subjects with drug resistant epilepsy (14 males, age range 2–16.4 years) were recruited for this study. A control group was formed by 23 normal children. Two instruments to assess sleep habits were administered to the patients with epilepsy: a questionnaire on sleep habits (to preschool children) and a questionnaire on sleep behavior (for children aged more than seven years old); a cognitive test (Wechsler Intelligence Scale for Children-WISC) was also performed. Patients underwent a complete polysomnographic study and sleep parameters, including CAP, were analyzed and correlated according to cognitive-behavioral measures in children with epilepsy.ResultsChildren with drug-resistant epilepsy and severe mental retardation showed sleep abnormalities such as low sleep efficiency, high percentage of wakefulness after sleep onset, reduced slow wave sleep, and reduced REM sleep. Sleep microstructure evaluated by means of CAP analysis showed a decrease in A1 index during N3 in patients with more severe cognitive impairment. Children with epilepsy and cognitive impairment (n = 10) had higher Sleep Behavior Questionnaire for Children (SBQC) total scores (65.60 ± 18.56) compared to children with epilepsy and normal IQ (50.00 ± 10.40), p < 0.05.ConclusionsChildren with drug-resistant epilepsy have a greater incidence of sleep problems regarding qualitative aspects, macrostructure, and CAP. The decrease of CAP rate and of A1, mainly during slow wave sleep (associated to REM sleep reduction), might represent a sleep microstructural pattern of intellectual disability.     

Concurrent occurrence of rapid eye movement with spindle burst during nocturnal sleep in mentally retarded children

Concurrence of REM and sleep spindle in 45 mentally retarded children (from 4 months to 8 years of age) was studied throughout nocturnal sleep, and the following results were obtained. (1) Twenty-five cases showed a single or burst of REMs during stage NREM with sleep spindles. (2) Twenty-nine cases showed sleep spindles at the beginning or toward the end of stage REM sleep. (3) No significant difference in DQ was found between the subjects with and without REMs during stage NREM sleep. The former subjects, however, had more normal clinical EEGs than the latter. (4) No significant difference in DQ or clinical EEG classification was revealed between the subjects with REMs during stage NREM sleep and those with spindles during stage REM sleep. (5) It was concluded that the concurrence of REM and sleep spindle during stage NREM is a useful sign for early diagnosis of mental retardation.     

Sleep architecture, slow wave activity and sleep spindles in mild sleep disordered breathing.

OBJECTIVE: A high degree of sleep fragmentation by arousals related to respiratory events would result in an abnormal distribution of slow wave activity (SWA) and a decrease in sleep spindle density in sleep disordered breathing (SDB) patients when compared to controls. METHODS: Eighteen mild SDB subjects (6 females and 12 males), aged 18-56 years with (5相似文献   

NREM sleep instability in children with sleep terrors: the role of slow wave activity interruptions.

OBJECTIVE: To evaluate NREM sleep instability, as measured by the cyclic alternating pattern (CAP), in children with sleep terrors (ST) vs. normal controls. METHODS: Ten boys (mean age: 8.5 years, range 5-13) meeting the following inclusion criteria: (a) complaint of ST several times a month, (b) a history of ST confirmed by a third person, and (c) a diagnosis of ST according to the ICSD-2 criteria. Eleven age-matched control children with parental report of at least 8.5h of nightly sleep, absence of known daytime consequences of sleep disorders were recruited by advertisement from the community. Sleep was visually scored for sleep macrostructure and CAP using standard criteria. RESULTS: Sleep macrostructure showed only a significantly increased number of awakenings per hour and reduced sleep efficiency in ST subjects. CAP parameters analysis revealed several significant differences in ST vs. controls: an increase of total CAP rate in SWS, of A1 index in SWS and of the mean duration of A phases while B phases had a decreased duration, exclusively in SWS. The normalized CAP interval-distribution graphs showed significant differences in SWS with interval classes 10< or = i < 35s higher in children with ST and intervals classes above 50s higher in normal controls. CONCLUSIONS: Children with ST showed faster alternations of the amplitude of slow EEG bursts during SWS. This abnormally fast alternation of the EEG amplitude in SWS is linked to the frequent intrusion of CAP B phases interrupting the continuity of slow delta activity and could be considered as a neurophysiological marker of ST. SIGNIFICANCE: This abnormal alternation of the EEG amplitude in SWS is associated with the occurrence of parasomnias and might be considered as a neurophysiological marker of disorders of arousal.     

Pergolide restores sleep maintenance but impairs sleep EEG synchronization in patients with restless legs syndrome

BACKGROUND: The treatment with the long-acting dopamine D1/D2 receptor agonist pergolide has been proven as very effective in lowering the frequency of periodic leg movements (PLM) in patients with restless legs syndrome (RLS). To further investigate the influence of this potent dopaminergic drug on the microstructure of rapid eye movement (REM) and non-REM sleep EEG we established a quantitative analysis of the EEG data. METHODS: The study group consisted of 15 patients with primary RLS (mean age 57.1+/-10.1 years) who were a subgroup of patients within a double-blind randomized crossover treatment study with pergolide versus placebo. The polysomnographic recordings were analyzed visually and submitted to a quantitative EEG analysis (fast Fourier transformation). RESULTS: The pergolide treatment induced a significant reduction of the spectral power in the delta range (0.78-3.9 Hz; P<0.05; t-test) during SWS, as well as a significant reduction of PLMs. In addition, we observed a decrease in the sigma EEG activity (12.1-14.8 Hz; P<0.03) during non-REM sleep and stage 2 sleep. The visual sleep scoring revealed a significant increase in stage 2 sleep (P<0.005), whereas wakefulness was markedly diminished (P<0.001). The REM sleep parameters including the EEG power spectrum remained unchanged. CONCLUSIONS: The treatment with pergolide markedly improved the sleep quality in RLS patients but did not restore SWS including the spectral power in the lower frequencies. Our results suggest that the dopamine agonist pergolide interferes with the subcortical mechanisms regulating the process of EEG synchronization during non-REM sleep.     

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

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

Effect of partial sleep deprivation on sleep stages and EEG power spectra: evidence for non-REM and REM sleep homeostasis.

The effect of repeated partial sleep deprivation on sleep stages and sleep EEG parameters was investigated in young subjects. After 2 baseline nights (B1, B2) of 7.5 h, sleep was restricted for 2 nights (D1, D2) to the first 4 h of the habitual bedtime period. Two recovery nights (R1, R2) with 7.5 h sleep followed. During the deprivation nights, stages 1 and 2 and REM sleep were reduced, while slow wave sleep (SWS; stages 3 and 4) was not significantly affected. However, the time integral of EEG power density in the range of 0.75-4.5 Hz (slow wave energy) was reduced. In the recovery period, SWS showed an enhancement in R1, and REM sleep showed a rebound in R1 and R2. An increase of REM sleep in the early part of the sleep period was evident in R1. Sleep latency was reduced in D2, R1 and R2. In accordance with the 2-process model of sleep regulation, EEG power density in non-REM sleep in the range of 0.75-4.5 Hz (slow wave activity) was only slightly higher in D2 and R1 than in baseline. An enhancement of slow wave activity in REM sleep was present in D2. Power density in the frequency range of 13-16 Hz was reduced in non-REM sleep (R1), SWS (R2) and stage 2 (R1). The results show (1) that the moderate reduction of slow wave energy in the deprivation nights induces only a minor enhancement of slow wave activity during recovery sleep; and (2) that a REM sleep deficit gives rise to an immediate rebound when 'slow wave pressure' is low.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sleep phenotypes of intellectual disability: a polysomnographic evaluation in subjects with Down syndrome and Fragile-X syndrome.

OBJECTIVE: To analyze sleep architecture and NREM sleep alterations by means of the Cyclic Alternating Pattern (CAP) in children with Down syndrome (DS) and Fragile-X syndrome (fraX), the two most common causes of inherited mental retardation, in order to find out eventual alterations of their sleep microstructure related to their mental retardation phenotypes. METHODS: Fourteen patients affected by fraX (mean age 13.1 years) and 9 affected by Down syndrome (mean age 13.8 years) and 26 age-matched normal controls were included. All subjects underwent overnight polysomnography in the sleep laboratory, after one adaptation night and their sleep architecture and CAP were visually scored. RESULTS: FraX subjects showed a reduced time in bed compared to DS subjects, whereas DS subjects showed a lower sleep efficiency, a higher percentage of wakefulness after sleep onset, and a reduced percentage of stage 2 NREM compared to the other groups. Furthermore, DS and fraX subjects, compared to normal controls, showed a higher percentage of stage 1 NREM and a lower percentage of REM sleep. FraX subjects showed the most disrupted sleep microstructure with low total CAP rate and CAP rate in S2 NREM. Both patient groups showed a lower percentage of A1 and higher percentage of A2 and A3 compared to normal controls. CONCLUSIONS: The analysis of CAP might be able to disclose new important findings in the sleep architecture of children with mental retardation and might characterize sleep microstructural patterns of the different phenotypes of intellectual disability. SIGNIFICANCE: The NREM sleep microstructure alterations found in our subjects, associated with the reduction in REM sleep percentage, seem to be distinctive features of intellectual disability.     

Ontogeny of Feline Temporal Lobe Epilepsy. III: Spontaneous Sleep and Arousal Disorders in Amygdala-Kindled Kittens

Summary: We report the ontogeny and persistence of sleep and arousal disorders in amygdala-kindled kittens. We also identify procedural differences that may explain discrepancies in the literature on postkindling sleep disorders. The study population consisted of 12 preadolescent kittens kindled between 2.5 and 6.5 months of age, 8 of which were followed to adulthood (≥1 year), and 8 unkindled implanted control animals. Sleep and seizure patterns were monitored on 12-24-h polygraphic or split-screen video recordings of EEG and behavioral activity. Kindled kittens displayed spontaneous seizure and interictal sleep anomalies that persisted to adulthood, as follows. As compared with neurosurgical controls, kindled kittens exhibited slow-wave sleep (SWS) and REM sleep insomnia at least 1 year after kindling and 1–5 months after convulsions, regardless of postictal recording delay. Sleep and arousal defects in kindled kittens were similar to but more pronounced than those in kindled adult cats, possibly because kittens spontaneously became epileptic. Detection of postkindling SWS insomnia could be masked by brief scoring epochs (less than the preferred 1-min epoch for cats); recurrent behavioral arousals after kindling frequently aborted 1-min SWS epochs but often did not interrupt 30-s SWS epochs (based on 1-min vs. 30-s minimum duration scoring criteria). Detection of postkindling REM sleep insomnia could be masked in kittens with alternating patterns of REM loss and REM rebound; all these kittens showed periodic bouts of REM onset from waking after kindling. Different data collection and analysis procedures influence detection of sleep and arousal disorders in amygdala-kindled cats when replication of findings is attempted. We conclude that these differences explain some controversies regarding the nature and prevalence of sleep disturbances in the kindling literature in temporal lobe epilepsy (TLE).     

Correlation between sleep and cognitive functions after hemispheric ischaemic stroke

Background:  The aim of this study was to test the hypothesis of a link between sleep and cognitive functions, particularly memory and attention, after stroke.
Methods:  We studied 11 consecutive patients with first-ever hemispheric ischaemic stroke within eight days after symptoms onset and nine of them at least three months after stroke. Sleep EEG was recorded with a portable system. Cognitive functions were assessed using a standardized battery of tests allowing the estimation of the most relevant domains of cognition. Five age-matched healthy subjects served as controls.
Results:  The patients were aged 43 ± 12 years (18–59). In five patients stroke was right-sided and in six patients left-sided. In the acute stroke phase a correlation between attention and amounts of slow wave sleep (SWS), Rapid eye movement (REM) sleep and sleep efficiency was found. In the recovery phase verbal/figural memory and attention significantly improved in most patients. Furthermore, an association between (i) verbal/figural (non-verbal) memory and amounts of SWS, REM sleep and sleep efficiency, and between (ii) attention and sleep efficiency was observed.
Conclusions:  The results point to a link between sleep and cognitive functions and their recovery after hemispheric stroke. Further studies are needed to determine the specific nature of this link.     

Children with major depression show reduced rapid eye movement latencies

A substantial body of research in adults has established that certain sleep polysomnographic abnormalities are commonly found in depressed patients, including sleep continuity disturbances, reduced slow-wave sleep, shortened rapid eye movement (REM) latency, and increased REM density. To date, these abnormalities have not been documented in depressed children compared with age-matched controls. Three consecutive nights of polysomnographic recordings were obtained in 25 hospitalized depressed children and 20 age-matched healthy controls. The depressed patients had reduced REM latencies. The shortest single-night REM latency of each individual was the most sensitive discriminating value between depressed subjects and controls. The influence of different scoring criteria in distinguishing depressed children from healthy children is discussed. In addition, depressed children had an increased sleep latency and increased REM time but did not have stage 4 differences.     

Distinctive polysomnographic traits in nocturnal frontal lobe epilepsy

Purpose: To describe the polysomnographic features and distribution of epileptic motor events, in relation to conventional sleep measures and cyclic alternating pattern (CAP) parameters, in 40 untreated patients with nocturnal frontal lobe epilepsy (NFLE). Methods: We analyzed the basal polysomnographic recordings of 40 patients (20 male and 20 female; mean age: 31 ± 10 years) with a diagnosis of nocturnal frontal lobe epilepsy. Conventional sleep measures and CAP parameters were assessed. Polysomnographic recordings were subdivided in sleep cycles. The distribution of the epileptic motor events (including minor motor events, paroxysmal arousals, tonic‐dystonic, or hyperkinetic seizures and epileptic nocturnal wandering) was analyzed throughout: total sleep time, non–rapid eye movement (NREM) and REM sleep, light sleep (S1 + S2), slow wave sleep (SWS), each sleep cycle, CAP or non‐CAP sleep, phase A and phase B of CAP. Only clear epileptic motor events supported by video–polysomnographic evidence were taken into consideration. Polysomnographic findings of patients with NFLE were compared with those of 24 age‐ and gender‐balanced healthy subjects without sleep complaints. Key Findings: Compared to controls, patients with NFLE showed a significant increase in wake after sleep onset, SWS duration, and REM latency, whereas REM sleep duration was significantly lower in NFLE patients. The patients with NFLE showed a significant increase of CAP time, CAP rate (72% vs. 32% in control group), CAP cycles, and mean duration of a CAP sequence. These findings were associated with a significant enhancement of all subtypes of the A phases of CAP (mainly subtype A1). A total of 139 epileptic motor events supported by video‐polysomnographic evidence were counted: 98% of all seizures occurred in NREM sleep and 72% of NREM seizures emerged from SWS, the latter being particularly collected in the first sleep cycles and decreasing in frequency together with the progressive decline of deep sleep. Ninety percent of total NREM seizures occurred during a CAP sequence, and CAP‐related seizures occurred in association with a phase A. Significance: Significant polysomnographic alterations seem to emerge in patients with NFLE (increased REM latency, epileptic fragmentation of SWS, and increase of CAP rate). The analysis of seizure distribution showed that most epileptic events occurred in SWS, with predominance in the first sleep cycle and decreasing in frequency together with the homeostatic decline of SWS across the night. Within the NREM sleep, CAP is a manifestation of unstable sleep and represents a powerful predisposing condition for the occurrence of nocturnal motor seizures, which arise in concomitance with a phase A.     

Sleep effects following intrathecal administration of the 5-HT1A agonist 8-OH-DPAT and the NMDA antagonist AP-5 in rats

The modulating effect of an intrathecally (i.t.) administered 5-HT_1A agonist and an NMDA antagonist on sleep, waking and EEG power spectra was investigated in rats. The 5-HT_1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) (38 nmol) increased total slow wave sleep (TSWS) and decreased waking over the 8 h recording period. The TSWS increase was mostly due to an increase in SWS1. Sleep latency to SWS1 was also reduced. The NMDA antagonist dl-2-amino 5-phosphonovaleric acid (AP-5) (31.5 nmol) reduced waking. SWS1 was increased, but TSWS was not changed. An increase in REM sleep was seen during the last part of the recording. Combined treatment with 8-OH-DPAT and AP-5 reduced waking and increasd TSWSS. No change in REM sleep was seen. There were no systematic changes in either waking, TSWS or REM fronto-frontal or fronto-parietal EEG power spectrum after any of the treatments. The results suggest that in the spinal cord stimulation of 5-HT_1A receptors have a dampening effect on transmission of sensory information, leading to deactivation and thereby increased possibilities for sleep induction. Blockade of the NMDA receptors may also lead to a small dampening of sensory transmission with similar consequences.     

Visual and spectral analysis of sleep EEG in acute hemispheric stroke

BACKGROUND: Reports on the effects of focal hemispheric damage on sleep EEG are rare and contradictory. PATIENTS AND METHODS: Twenty patients (mean age +/- SD 53 +/- 14 years) with a first acute hemispheric stroke and no sleep apnea were studied. Stroke severity [National Institute of Health Stroke Scale (NIHSS)], volume (diffusion-weighted brain MRI), and short-term outcome (Rankin score) were assessed. Within the first 8 days after stroke onset, 1-3 sleep EEG recordings per patient were performed. Sleep scoring and spectral analysis were based on the central derivation of the healthy hemisphere. Data were compared with those of 10 age-matched and gender-matched hospitalized controls with no brain damage and no sleep apnea. RESULTS: Stroke patients had higher amounts of wakefulness after sleep onset (112 +/- 53 min vs. 60 +/- 38 min, p < 0.05) and a lower sleep efficiency (76 +/- 10% vs. 86 +/- 8%, p < 0.05) than controls. Time spent in slow-wave sleep (SWS) and rapid eye movement (REM) sleep and total sleep time were lower in stroke patients, but differences were not significant. A positive correlation was found between the amount of SWS and stroke volume (r = 0.79). The slow-wave activity (SWA) ratio NREM sleep/wakefulness was lower in patients than in controls (p < 0.05), and correlated with NIHSS (r = -0.47). CONCLUSION: Acute hemispheric stroke is accompanied by alterations of sleep EEG over the healthy hemisphere that correlate with stroke volume and outcome. The increased SWA during wakefulness and SWS over the healthy hemisphere contralaterally to large strokes may reflect neuronal hypometabolism induced transhemispherically (diaschisis).     

Intraindividual long-term stability of sleep electroencephalography in school-aged children

ObjectiveTo examine the long-term stability of sleep duration, sleep continuity, and sleep architecture assessed via unattended home sleep electroencephalography (EEG) during middle childhood.MethodsA total of 69 healthy children (18 girls and 51 boys) aged 8.2 years (standard deviation = 1.3 years) at T1 underwent unattended home sleep EEG on two nights separated by 18.5 months (standard deviation = 3.9 months). Of the children, 34 (49.3%) children were born prematurely (<32 gestational weeks; mean birth weight = 1367 g) and 35 (50.7%) children were born at term (mean birth weight = 3275 g).ResultsWe found moderate to substantial stability (all p <0.001) for total sleep time (TST; intraclass correlation coefficient [ICC] = 0.65), slow wave sleep (SWS; min, %: ICC = 0.49), and stage 2 sleep (min; ICC = 0.47), and found fair stability (all p <0.013) for sleep efficiency (ICC = 0.28), nocturnal awakenings (ICC = 0.33), stage 2 sleep (%; ICC = 0.32), and rapid eye movement (REM) sleep (min: ICC = 0.33; %: ICC = 0.27). Prematurity status was not associated with stability of sleep EEG indices over time.ConclusionsLong-term follow-up of one night of unattended home sleep EEG during middle childhood reveals that TST, stage 2 sleep, and SWS are relatively stable, trait-like characteristics. This applies less strongly for sleep efficiency, nocturnal awakenings, and REM sleep. Stage 1 sleep and REM latency showed no stability.     

Increased delta power and discrepancies in objective and subjective sleep measurements in borderline personality disorder

BACKGROUND: Previous studies have shown depression-like sleep abnormalities in borderline personality disorder (BPD). However, findings in BPD are not unequivocal for REM dysregulation, as well as for a decrement of slow wave sleep and sleep continuity disturbances. Earlier findings in sleep EEG abnormalities in BPD may have been confounded by concomitant depressive symptoms. METHODS: Twenty unmedicated female BPD patients without current comorbid major depression and 20 sex- and age-matched control subjects entered the study. Conventional polysomnographic parameters and for the first time sleep EEG spectral power analysis was performed on two sleep laboratory nights. Subjective sleep parameters were collected by sleep questionnaires in order to assess the relationship between objective and subjective sleep measurements. RESULTS: BPD patients showed a tendency for shortened REM latency and significantly decreased NonREM sleep (stage 2). Spectral EEG analysis showed increased delta power in total NREM sleep as well as in REM sleep in BPD patients. Subjective ratings documented drastically impaired sleep quality in BPD patients for the two weeks before the study and during the two laboratory nights. CONCLUSION: Not-depressed BPD patients only showed tendencies for depression-like REM sleep abnormalities. Surprisingly, BPD patients displayed higher levels of delta power in the sleep EEG in NREM sleep than healthy control subjects. There was a marked discrepancy between objective and subjective sleep measurements, which indicates an altered perception of sleep in BPD. The underlying psychological and neurobiological mechanisms of these alterations are still unclear and need to be clarified in future studies including interventions on a pharmacological and cognitive-behavioral level.