Hypersynchronous delta waves and somnambulism: brain topography and effect of sleep deprivation

STUDY OBJECTIVES: Hypersynchronous delta activity (HSD) is usually described as several continuous high-voltage delta waves (> or = 150 microV) in the sleep electroencephalogram of somnambulistic patients. However, studies have yielded varied and contradictory results. The goal of the present study was to evaluate HSD over different electroencephalographic derivations during the non-rapid eye movement (NREM) sleep of somnambulistic patients and controls during normal sleep and following 38 hours of sleep deprivation, as well as prior to sleepwalking episodes. DESIGN: N/A. SETTING: Sleep disorders clinic. PATIENTS: Ten adult sleepwalkers and 10 sex- and age-matched control subjects were investigated polysomnographically during a baseline night and following 38 hours of sleep deprivation. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: During normal sleep, sleepwalkers had a significantly higher ratio of HSD over the time spent in stage 2, 3 and 4 on frontal and central derivations when compared with controls. Sleep deprivation resulted in a significant increase in the ratio of the time in HSD over the time in stage 4 on the frontal lead in both groups and on the central lead in controls. There was no evidence for a temporal accumulation of HSD prior to the episodes. CONCLUSIONS: HSD shows a clear frontocentral gradient across all subjects during both baseline and recovery sleep and has relatively low specificity for the diagnosis of NREM parasomnias. Increases in HSD after sleep deprivation may reflect an enhancement of the homeostatic process underlying sleep regulation.     

Sleep and sex: what can go wrong? A review of the literature on sleep related disorders and abnormal sexual behaviors and experiences

STUDY OBJECTIVES: To formulate the first classification of sleep related disorders and abnormal sexual behaviors and experiences. DESIGN: A computerized literature search was conducted, and other sources, such as textbooks, were searched. RESULTS: Many categories of sleep related disorders were represented in the classification: parasomnias (confusional arousals/sleepwalking, with or without obstructive sleep apnea; REM sleep behavior disorder); sleep related seizures; Kleine-Levin syndrome (KLS); severe chronic insomnia; restless legs syndrome; narcolepsy; sleep exacerbation of persistent sexual arousal syndrome; sleep related painful erections; sleep related dissociative disorders; nocturnal psychotic disorders; miscellaneous states. Kleine-Levin syndrome (78 cases) and parasomnias (31 cases) were most frequently reported. Parasomnias and sleep related seizures had overlapping and divergent clinical features. Thirty-one cases of parasomnias (25 males; mean age, 32 years) and 7 cases of sleep related seizures (4 males; mean age, 38 years) were identified. A full range of sleep related sexual behaviors with self and/or bed partners or others were reported, including masturbation, sexual vocalizations, fondling, sexual intercourse with climax, sexual assault/rape, ictal sexual hyperarousal, ictal orgasm, and ictal automatism. Adverse physical and/or psychosocial effects from the sleepsex were present in all parasomnia and sleep related seizure cases, but pleasurable effects were reported by 5 bed partners and by 3 patients with sleep related seizures. Forensic consequences were common, occurring in 35.5% (11/31) of parasomnia cases, with most (9/11) involving minors. All parasomnias cases reported amnesia for the sleep-sex, in contrast to 28.6% (2/7) of sleep related seizure cases. Polysomnography (without penile tumescence monitoring), performed in 26 of 31 parasomnia cases, documented sexual moaning from slow wave sleep in 3 cases and sexual intercourse during stage 1 sleep/wakefulness in one case (with sex provoked by the bed partner). Confusional arousals (CAs) were diagnosed as the cause of "sleepsex" ("sexsomnia") in 26 cases (with obstructive sleep apnea [OSA] comorbidity in 4 cases), and sleepwalking in 2 cases, totaling 90.3% (28/31) of cases being NREM sleep parasomnias. REM behavior disorder was the presumed cause in the other 3 cases. Bedtime clonazepam therapy was effective in 90% (9/10) of treated parasomnia cases; nasal continuous positive airway pressure therapy was effective in controlling comorbid OSA and CAs in both treated cases. All five treated patients with sleep related sexual seizures responded to anticonvulsant therapy. The hypersexuality in KLS, which was twice as common in males compared to females, had no reported effective therapy. CONCLUSIONS: A broad range of sleep related disorders associated with abnormal sexual behaviors and experiences exists, with major clinical and forensic consequences.     

Cerebrovascular response to arousal from NREM and REM sleep

STUDY OBJECTIVE: To determine the effect of arousal from sleep on cerebral blood flow velocity (CBFV) in relation to associated ventilatory and systemic hemodynamic changes. PARTICIPANTS: Eleven healthy individuals (6 men, 5 women). MEASUREMENTS: Pulsed Doppler ultrasonography was used to measure CBFV in the middle cerebral artery with simultaneous measurements of sleep state (EEG, EOG, and EMG), ventilation (inductance plethysmography), heart rate (ECG), and arterial pressure (finger plethysmography). Arousals were induced by auditory tones (range: 40-80 dB; duration: 0.5 sec). Cardiovascular responses were examined beat-by-beat for 30 sec before and 30 sec after auditory tones. RESULTS: During NREM sleep, CBFV declined following arousals (-15% +/- 2%; group mean +/- SEM) with a nadir at 9 sec after the auditory tone, followed by a gradual return to baseline. Mean arterial pressure (MAP; +20% +/- 1%) and heart rate (HR; +17% +/- 2%) increased with peaks at 5 and 3 sec after the auditory tone, respectively. Minute ventilation (VE) was increased (+35% +/- 10%) for 2 breaths after the auditory tone. In contrast, during REM sleep, CBFV increased following arousals (+15% +/- 3%) with a peak at 3 sec. MAP (+17% +/- 2%) and HR (+15% +/- 2%) increased during arousals from REM sleep with peaks at 5 and 3 sec post tone. VE increased (+16% +/- 7%) in a smaller, more sustained manner during arousals from REM sleep. CONCLUSIONS: Arousals from NREM sleep transiently reduce CBFV, whereas arousals from REM sleep transiently increase CBFV, despite qualitatively and quantitatively similar increases in MAP, HR, and VE in the two sleep states.     

Video polysomnographic findings in non‐rapid eye movement parasomnia

Although video polysomnography (vPSG) is not routinely recommended for the evaluation of typical cases of non‐rapid eye movement (NREM) parasomnias, it can aid diagnosis of unusual cases, other sleep disorders and complicated cases with REM behaviour disorder (RBD), and in differentiating parasomnias from epilepsy. In this study, we aimed to assess vPSG findings in consecutive patients with a clinical diagnosis of NREM‐parasomnia covering the whole phenotypic spectrum. Five hundred and twelve patients with a final diagnosis of NREM parasomnia who had undergone vPSG were retrospectively identified. vPSGs were analysed for features of NREM parasomnia and for the presence of other sleep disorders. Two hundred and six (40.0%) patients were clinically diagnosed with sleepwalking, 72 (14.1%) with sleep terrors, 39 (7.6%) with confusional arousals, 15 (2.9%) with sexsomnia, seven (1.4%) with sleep‐related eating disorder, 122 (23.8%) with mixed phenotype, and 51 (10.0%) with parasomnia overlap disorder (POD). The vPSG supported the diagnosis of NREM parasomnia in 64.4% of the patients and of POD in 98%. In 28.9% of the patients, obstructive sleep apnea (OSA) or/and periodic limb movements during sleep (PLMS) were identified, most commonly in older, male, sleepy and obese patients. vPSG has a high diagnostic yield in patients with NREM parasomnia and should be routinely performed when there is diagnostic doubt, or in patients where there is a suspicion of OSA and PLMS.     

Arousals and sleep stages in patients with obstructive sleep apnoea syndrome: changes under nCPAP treatment

Nocturnal arousals are the essential cause of disturbed sleep structure in patients with obstructive sleep apnoea syndrome (OSAS). The aim of this study was to analyse the relationship between sleep stages, respiratory (type-R) and movement (type-M) related EEG arousals. Furthermore, the value of these arousals as a criterion for the efficiency of nCPAP treatment was estimated. We examined 38 male patients aged between 30 and 71 (49.1±20.9 SD) y. All patients suffered from OSAS. The mean respiratory disturbance index (RDI) was 47.3±27.8 per h. Polysomnographic monitoring was carried out on 4 subsequent nights: baseline night, 2 nights of nCPAP titration and nCPAP control night. Sleep was visually scored and EEG arousals were classified into type R and M, depending on whether changes of respiration or movement caused the arousal. The RDI, the R index (type-R/h), the M index (type-M/h) and the R and M indices in different sleep stages were calculated. During the baseline night a deficit of slow wave sleep (SWS) and REM sleep was found. Furthermore there were more type-R than type-M arousals registered (17.4 h^?1[3.6–43.6] vs. 5.9 h^?1[1.6–11.8]) ( P <0.01). They occurred during stages NREM 1, NREM 2 and REM ( P <0.01). An SWS sleep rebound and a reduction of the SWS and REM latencies were already found during the first CPAP night. The R index was reduced during the first CPAP night in all sleep stages ( P <0.01) and remained approximately the same in the following 2 nights (3. CPAP night: 1.1 h^?1[0.3–5.0]). Type M arousals occurred more in stages 1 and 2 ( P <0.01), and remained unchanged under nCPAP. We concluded that differentiation of nocturnal arousals may provide more detailed information regarding the influence of breathing disturbances on sleep. Respiratory related, not movement related, arousals may be a useful additional tool in judging the efficiency of OSAS.     

EEG arousals in normal sleep: variations induced by total and selective slow-wave sleep deprivation

STUDY OBJECTIVES: Aim of the present study was to assess changes in arousal rates after selective slow-wave (SWS) and total sleep deprivations. DESIGN: Two-way mixed design comparing the arousal index (Al), as expressed by the number of EEG arousals divided by sleep duration, in totally or selectively sleep deprived subjects. SETTING: Sleep laboratory. PATIENTS OR PARTICIPANTS: Nineteen normal male subjects [mean age=23.3 years (S.E.M.=0.55)]. INTERVENTIONS: Al was measured in baseline nights and after selective SWS (N=10) and total sleep deprivation (N=9). MEASUREMENTS AND RESULTS: During the baseline nights AI values changed across sleep stages as follows: stage 1 > stage 2 and REM > SWS, but did not present any significant variations as a function of time elapsed from sleep onset. The recovery after deprivation showed a reduction in EEG arousals, more pronounced after total sleep deprivation; this decrease affected NREM but not REM sleep. During the baseline nights Al showed a close-to-significance negative correlation with REM duration, while during the recovery nights a significant positive relation with stage 1 duration was found. CONCLUSIONS: The present results suggest that recuperative processes after sleep deprivation are also associated with a higher sleep continuity as defined by the reduction of EEG arousals.     

Relationship of slow and rapid EEG components of CAP to ASDA arousals in normal sleep.

STUDY OBJECTIVES: Besides arousals (according to the ASDA definition), sleep contains also K-complexes and delta bursts which, in spite of their sleep-like features, are endowed with activating effects on autonomic functions. The link between phasic delta activities and enhancement of vegetative functions indicates the possibility of physiological activation without sleep disruption (i.e., arousal without awakening). A functional connection seems to include slow (K-complexes and delta bursts) and rapid (arousals) EEG events within the comprehensive term of activating complexes. CAP (cyclic alternating pattern) is the spontaneous EEG rhythm that ties both slow and rapid activating complexes together during NREM sleep. The present study aims at exploring the relationship between arousals and CAP components in a selected sample of healthy sleepers. DESIGN: Polysomnographic analysis according to the scoring rules for sleep stages and arousals. CAP analysis included also tabulation of subtypes A1 (slow EEG activating complexes), A2 and A3 (activating complexes with fast EEG components). SETTING: 40 sleep-lab accomplished recordings. PARTICIPANTS: Healthy subjects belonging to a wide age range (38 +/- 20 yrs.). INTERVENTIONS: N/A. MEASUREMENT AND RESULTS: Of all the arousals occurring in NREM sleep, 87% were inserted within CAP. Subtypes A2 and A3 of CAP corresponded strikingly with arousals (r=0.843; p<0.0001), while no statistical relationship emerged when arousals were matched with subtypes A1 of CAP. Subtypes A1 instead correlated positively with the percentages of deep sleep (r=0.366; p<0.02). CONCLUSIONS: The CAP subtype classification encompasses both the process of sleep maintenance (subtypes A1) and sleep fragmentation (subtypes A2 and A3), and provides a periodicity dimension to the activating events of NREM sleep.     

Interrater reliability between scorers from eight European sleep laboratories in subjects with different sleep disorders

Interrater variability of sleep stage scorings is a well-known phenomenon. The SIESTA project offered the opportunity to analyse interrater reliability (IRR) between experienced scorers from eight European sleep laboratories within a large sample of patients with different (sleep) disorders: depression, general anxiety disorder with and without non-organic insomnia, Parkinson's disease, period limb movements in sleep and sleep apnoea. The results were based on 196 recordings from 98 patients (73 males: 52.3 +/- 12.1 years and 25 females: 49.5 +/- 11.9 years) for which two independent expert scorings from two different laboratories were available. Cohen's kappa was used to evaluate the IRR on the basis of epochs and intraclass correlation was used to analyse the agreement on quantitative sleep parameters. The overall level of agreement when five different stages were distinguished was kappa = 0.6816 (76.8%), which in terms of kappa reflects a 'substantial' agreement (Landis and Koch, 1977). For different groups of patients kappa values varied from 0.6138 (Parkinson's disease) to 0.8176 (generalized anxiety disorder). With regard to (sleep) stages, the IRR was highest for rapid eye movement (REM), followed by Wake, slow-wave sleep (SWS), non-rapid eye movement 2 (NREM2) and NREM1. The results of regression analysis showed that age and sex only had a statistically significant effect on kappa when the (sleep) stages are considered separately. For NREM2 and SWS a statistically significant decrease of IRR with age has been observed and the IRR for SWS was lower for males than for females. These variations of IRR most probably reflect changes of the sleep electroencephalography (EEG) with age and gender.     

Disorders of arousal from sleep and violent behavior: the role of physical contact and proximity

STUDY OBJECTIVES: To review medical and legal case reports to determine how many appear to support the belief that violence against other individuals that occurs during Disorders of Arousal - sleepwalking, confusional arousal, and sleep terrors - is triggered by direct physical contact or close proximity to that individual and does not occur randomly or spontaneously. DESIGN: Historical review of case reports in the medical and legal literature. MEASUREMENTS AND RESULTS: A total of 32 cases drawn from medical and legal literature were reviewed. Each case contained a record of violence associated with Disorders of Arousal; in each, details of the violent behavior were available. Violent behaviors associated with provocations and/or close proximity were found to be present in 100% of confusional arousal patients and 81% of sleep terror patients. Violent behaviors were associated with provocation or close proximity in 40%-90% of sleepwalking cases, depending on whether the legal verdict and other factors were taken into account. Often the provocation was quite minor and the response greatly exaggerated. The specific manner in which the violence was triggered differed among sleepwalking, confusional arousals, and sleep terrors. CONCLUSIONS: In the cases reviewed, violent behavior directed against other individuals associated with Disorders of Arousal most frequently appeared to follow direct provocation by, or close proximity to, another individual. Sleepwalkers most often did not seek out victims, but rather the victims sought out or encountered the sleepwalker. These conclusions are tempered by several limitations: the selection of cases was not random and may not represent an accurate sample of violent behaviors associated with Disorders of Arousal. Also, final verdicts by juries in reported legal cases should not be confused with scientific proof of the presence or absence of sleepwalking. The pathophysiology of Disorders of Arousal with and without violent behavior could be associated with normally occurring deactivation of the frontal lobes during slow wave sleep (SWS) connected via atypically active thalamocortical pathways to the limbic areas. It is not known if the violent sleepwalker, confusional arousal patient, or sleep terror patient differs from other patients with these disorders. The conclusions of this case series await confirmation by the results of future sleep laboratory based studies.     

Analysis of postarousal EEG activity during somnambulistic episodes

Early studies found that electroencephalographic (EEG) recordings during somnambulistic episodes were characterized by a combination of alpha, theta, and delta frequencies, without evidence of clear wakefulness. Three postarousal EEG patterns associated with slow-wave sleep (SWS) arousals were recently identified in adults with sleepwalking and sleep terrors. The goal of the present study was to evaluate the distribution of these postarousal EEG patterns in 10 somnambulistic patients (three males, seven females, mean age: 25.1, SD: 4.1) evaluated at baseline and following 38 h of sleep deprivation. A total of 44 behavioral arousals were recorded in the laboratory; seven episodes at baseline (five from SWS, two from stage 2 sleep) and 37 episodes during recovery sleep (30 from SWS, seven from stage 2 sleep). There was no significant difference in the distribution of postarousal EEG patterns identified during baseline and recovery sleep. One pattern, comprised of diffuse rhythmic and synchronous delta activity, was preferentially associated with relatively simple behavioral episodes but did not occur during episodes from stage 2 sleep. Overall, delta activity was detected in 48% of the behavioral episodes from SWS and in 22% of those from stage 2. There was no evidence of complete awakening during any of the episodes. The results support the view of somnambulism as a disorder of arousal and suggest that sleepwalkers' atypical arousal reactions can manifest themselves in stage 2 sleep in addition to SWS.     

Is there a common motor dysregulation in sleepwalking and REM sleep behaviour disorder?

This study sought to determine if there is any overlap between the two major non‐rapid eye movement and rapid eye movement parasomnias, i.e. sleepwalking/sleep terrors and rapid eye movement sleep behaviour disorder. We assessed adult patients with sleepwalking/sleep terrors using rapid eye movement sleep behaviour disorder screening questionnaires and determined if they had enhanced muscle tone during rapid eye movement sleep. Conversely, we assessed rapid eye movement sleep behaviour disorder patients using the Paris Arousal Disorders Severity Scale and determined if they had more N3 awakenings. The 251 participants included 64 patients with rapid eye movement sleep behaviour disorder (29 with idiopathic rapid eye movement sleep behaviour disorder and 35 with rapid eye movement sleep behaviour disorder associated with Parkinson's disease), 62 patients with sleepwalking/sleep terrors, 66 old healthy controls (age‐matched with the rapid eye movement sleep behaviour disorder group) and 59 young healthy controls (age‐matched with the sleepwalking/sleep terrors group). They completed the rapid eye movement sleep behaviour disorder screening questionnaire, rapid eye movement sleep behaviour disorder single question and Paris Arousal Disorders Severity Scale. In addition, all the participants underwent a video‐polysomnography. The sleepwalking/sleep terrors patients scored positive on rapid eye movement sleep behaviour disorder scales and had a higher percentage of ‘any’ phasic rapid eye movement sleep without atonia when compared with controls; however, these patients did not have higher tonic rapid eye movement sleep without atonia or complex behaviours during rapid eye movement sleep. Patients with rapid eye movement sleep behaviour disorder had moderately elevated scores on the Paris Arousal Disorders Severity Scale but did not exhibit more N3 arousals (suggestive of non‐rapid eye movement parasomnia) than the control group. These results indicate that dream‐enacting behaviours (assessed by rapid eye movement sleep behaviour disorder screening questionnaires) are commonly reported by sleepwalking/sleep terrors patients, thus decreasing the questionnaire's specificity. Furthermore, sleepwalking/sleep terrors patients have excessive twitching during rapid eye movement sleep, which may result either from a higher dreaming activity in rapid eye movement sleep or from a more generalised non‐rapid eye movement/rapid eye movement motor dyscontrol during sleep.     

Arousal reactions in sleepwalking and night terrors in adults: the role of respiratory events

STUDY OBJECTIVES: The aim of the study was to determine the role of respiratory events, assessed by means of esophageal pressure monitoring, during arousals from slow wave sleep in adult patients with parasomnias. DESIGN: N/A. SETTING: N/A. PATIENTS: Ten patients with parasomnias (sleepwalking, night terrors, or both) and 10 control subjects matched for gender and age underwent 3 consecutive nights of polysomnography. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: By increasing sleep fragmentation, esophageal pressure monitoring has a deleterious effect on sleep architecture in patients with parasomnias and in control subjects. Respiratory events occur more frequently in parasomniacs than in controls. Respiratory effort seems to be responsible for the occurrence of a great number of arousal reactions in parasomniacs and is involved in triggering the parasomnia episodes. CONCLUSION: Sleep-disordered breathing seems to be frequently associated with parasomnias during slow wave sleep, emphasizing the utility of performing esophageal pressure monitoring in cases of sleep walking or night terrors.     

Alcohol-induced sleepwalking or confusional arousal as a defense to criminal behavior: a review of scientific evidence, methods and forensic considerations

An increasing number of criminal cases have claimed the defendant to be in a state of sleepwalking or related disorders induced by high quantities of alcohol. Sleepwalkers who commit violent acts, sexual assaults and other criminal acts are thought to be in a state of automatism, lacking conscious awareness and criminal intent. They may be acquitted in criminal trials. On the other hand, criminal acts performed as the result of voluntary alcohol intoxication alone cannot be used as a complete defense. The alcohol-induced sleepwalking criminal defense is most often based on past clinical or legal reports that ingestion of alcohol directly 'triggers' sleepwalking or increased the risk of sleepwalking by increasing the quantity of slow wave sleep (SWS). A review of the sleep medicine literature found no sleep laboratory studies of the effects of alcohol on the sleep of clinically diagnosed sleepwalkers. However, 19 sleep laboratory studies of the effects of alcohol on the sleep of healthy non-drinkers or social drinkers were identified with none reporting a change in SWS as a percentage of total sleep time. However, in six of 19 studies, a modest but statistically significant increase in SWS was found in the first 2-4 h. Among studies of sleep in alcohol abusers and abstinent abusers, the quantity and percentage of SWS was most often reduced and sometimes absent. Claims that direct alcohol provocation tests can assist in the forensic assessment of these cases found no support of any kind in the medical literature with not a single report of testing in normative or patient groups and no reports of validation testing of any sort. There is no direct experimental evidence that alcohol predisposes or triggers sleepwalking or related disorders. A legal defense of sleepwalking resulting from voluntarily ingested alcohol should be consistent with the current state of art sleep science and meet generally accepted requirements for the diagnosis of sleepwalking and other parasomnias.     

Effects of sleep on endotoxin-induced host responses in healthy men

OBJECTIVE: To examine whether increased sleep during viral or bacterial infections supports host defense mechanisms. METHODS: To test this assumption in humans, healthy male subjects were assigned either to sleep from 2300 to 0700 hours (n = 10) or to stay awake through the night (n = 10). In the sleeping subjects Salmonella abortus equi endotoxin (0.4 ng/kg) or placebo were intravenously injected in balanced order during the first SWS episode. The age-matched, sleep-deprived subjects were injected at the same time point. RESULTS: As expected, endotoxin significantly increased rectal temperature, the plasma levels of cortisol, tumor necrosis factor-alpha (TNF-alpha), the soluble TNF receptors p55 and p75, Interleukin (IL)-6, the IL-1 receptor antagonist (RA), leukocyte, and granulocyte counts in both sleeping and sleep-deprived subjects, whereas lymphocyte and monocyte counts were transiently reduced. Time courses of endotoxin-induced host responses did not differ between the sleep and sleep deprivation groups. Endotoxin did not affect the amount of nocturnal wakefulness, nonrapid-eye-movement (NREM) sleep, or rapid-eye-movement (REM) sleep across the total night compared with placebo, but significantly increased electroencephalogram-arousals (EEG-arousals) in stage 2 and decreased arousals in SWS. In addition, the amount of SWS, spectral EEG-delta and -theta power was increased at the beginning and at the end of the sleep period, respectively, when the degree of immune activation was relatively low. CONCLUSION: The present results support the notion that short-term sleep deprivation is unlikely to harm the immune system as far as unspecific acute responses are concerned. The effects of endotoxin on sleep in this case support prior observations that in humans, enhanced SWS and intensified NREM sleep occur when host defense activation is subtle.     

Sleep extension in humans: sleep stages, EEG power spectra and body temperature

In eight male subjects the electroencephalogram (EEG) and core body temperature (Tcore) were recorded during long sleep episodes from 0000 to 1,500 hr. EEGs were visually scored and subjected to spectral analysis by fast Fourier transform. Slow-wave sleep [SWS, i.e. stages 3 + 4 of non-rapid eye movement (NREM) sleep and slow wave activity (SWA, mean EEG power density in the range of 0.75-4.5 Hz)] in NREM sleep attained highest values in the first 3 hr of sleep and lowest values in the morning hours when rapid eye movement (REM) sleep was at its maximum. Wakefulness was significantly enhanced in the last 3 hr of the recording period. Occasional NREM episodes containing SWS were observed in the late morning and early afternoon. However, no significant increase in SWS or SWA in the last 3 hr of the sleep episode over any of the preceding 3-hr intervals was present and SWA in this interval was significantly below the values observed at the beginning of sleep. The duration of NREM episodes varied significantly over the sleep episode. Analysis of the dynamics of SWA within NREM episodes revealed that SWA gradually rose during the episode. Consequently, SWA averaged per episode was positively correlated with episode duration. Tcore dropped in the initial part of sleep, rose during the morning hours and reached values in the afternoon that were higher than at the beginning of sleep. Thus the time course of Tcore dissociated from the time course of SWA. This indicates that SWA in NREM sleep is not directly related to the variation in core body temperature.     

Upper airway resistance syndrome: effect of nasal dilation, sleep stage, and sleep position.

BACKGROUND: The upper airway resistance syndrome (UARS) is one of the mild variants of obstructive sleep disordered breathing. Nasal obstruction is proposed as one of the mechanisms that lowers intrapharyngeal pressure and hence increases airway collapsibility. OBJECTIVE: We evaluated the effect of external nasal dilation and sleep position on sleep in UARS. METHOD: A double blind, randomized, controlled study with a crossover design (using therapeutic and placebo dilators) was conducted in 18 consecutive patients with UARS. Each patient had two overnight sleep studies one to two weeks apart. Cardiorespiratory parameters (AHI, percentage of time that SaO2 was more than 2% below awake [desaturation time] and mean overnight heart rate), sleep architecture (sleep stages, sleep efficiency, and arousal index), and body position were determined. RESULTS: Application of the external nasal dilator resulted in a significant increase in the nasal cross-sectional area (p < 0.001). Treatment reduced stage 1 sleep (as a percent of total sleep time) from 8.6 +/- 0.8% to 7.1 +/- 0.7 (SEM), p = 0.034). Desaturation time was significantly lower with treatment (12.2 +/- 2.2% on placebo versus 9.1 +/- 1.3 on treatment, p = 0.04). There were no additional significant effects on the cardiorespiratory parameters, sleep architecture, or MSLT when the entire night was examined. Controlling for interactions of sleep stage and position and treatment we found that treatment reduced desaturation time (p = 0.03) but not AHI or arousal index. AHI was significantly lower in the lateral position compared to the supine (p = 0.0001) and in NREM sleep compared to REM (p = 0.001). Desaturation time was significantly lower on the lateral compared to the supine position (p = 0.002) and in NREM sleep compared to REM (p = 0.006). Arousal index was highly dependent on sleep stage (p = 0.0001): the index was higher in stage 2 compared to slow wave sleep and REM. Sleep position and treatment had no significant effect on arousals. CONCLUSIONS: External nasal dilation reduced stage 1 sleep, an indirect marker of disrupted sleep, and desaturation time. There were no additional effects on sleep architecture or sleep disordered breathing. Both sleep position and sleep stage had a significant effect on sleep disordered breathing in UARS.     

Performance and sleepiness following moderate sleep disruption and slow wave sleep deprivation

Recent studies have shown that periodically disrupted sleep resulted in significant daytime sleepiness and performance loss in normal young adults. One study suggested that the periodicity of disturbance rather than the total number of sleep disturbances was the primary factor in causing degraded function. However, in that study, increased performance levels could have been associated with increased levels of slow wave sleep. The present study was designed to determine whether the amount of SWS rather than the periodic disruption of sleep accounts for decreased performance of Ss with disrupted sleep. Twelve normal young adults spent two 4-night periods in the laboratory. During one 4-night series, Ss were briefly aroused either following each 10 min of sleep or whenever they entered stage 3 sleep (No SWS condition). During the second series of nights, Ss were briefly aroused after each 10 min of sleep (SWS condition). In the second series, additional arousals were performed after 5-min periods (but not when Ss were in SWS) to equalize the total number of arousals in the SWS conditions with those in the No SWS condition. Total experimental arousals were equal in the disruption conditions, and the experimental manipulation was successful in reducing total SWS to infrequent epochs of stage 3 in the No SWS condition while allowing significantly more SWS in the SWS condition. In terms of sleep stages, this difference was balanced by increased stage 2 in the No SWS condition. Despite the differential occurrence of SWS, no performance, mood, or nap latency measure was different in the SWS vs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impairment of the production of delta sleep in anorectic adolescents

OBJECTIVE: Total sleep time and slow-wave sleep (SWS) are frequently reported to be reduced in anorectics. A preliminary study showed that slow-wave activity (SWA, 0.5-4.5 Hz) is decreased in anorectic adolescents. The present study investigates whether this reduction is the result of the increased sleep fragmentation or is dependent on an intrinsic weakness of SWA-producing mechanisms. DESIGN: Statistical analysis of spectral electroencephalogram data recorded during sleep from a group of anorectics and a control group. SETTING: Polysomnographic data were recorded in single rooms in the hospital for 1 night following an adaptation night. PARTICIPANTS: 20 adolescent anorectic girls (13.9 +/- 2.0 years) and 12 age-matched control subjects. INTERVENTIONS: Refeeding and psychotherapy. MEASUREMENTS AND RESULTS: Anorectics had an increase of wakefulness after sleep onset, a higher number of arousals, and a reduction of SWS and SWA during total sleep time. No relationship between the reduction of SWA and duration of illness was found, while a relationship between SWA decrease and the level of emaciation (body mass index) was present. The analysis limited to the first non-rapid eye movement sleep cycle did not show any difference between the 2 groups in the number of awakenings and arousals. Nevertheless, anorectics showed a reduction of SWS and SWA. CONCLUSIONS: Sleep of anorectic patients seems to be characterized by an impairment of SWA-producing mechanisms independent of the increased sleep fragmentation. This is probably related to the primary pathophysiologic characteristics of the illness but could also reflect secondary functional and anatomic alterations of the brain.     

NREM Arousal Parasomnias and Their Distinction from Nocturnal Frontal Lobe Epilepsy: A Video EEG Analysis

Study Objectives.

To describe the semiological features of NREM arousal parasomnias in detail and identify features that can be used to reliably distinguish parasomnias from nocturnal frontal lobe epilepsy (NFLE).

Design.

Systematic semiologial evaluation of parasomnias and NFLE seizures recorded on video-EEG monitoring.

Patients.

120 events (57 parasomnias, 63 NFLE seizures) from 44 subjects (14 males).

Interventions.

The presence or absence of 68 elemental clinical features was determined in parasomnias and NFLE seizures. Qualitative analysis of behavior patterns and ictal EEG was undertaken. Statistical analysis was undertaken using established techniques.

Results.

Elemental clinical features strongly favoring parasomnias included: interactive behavior, failure to wake after event, and indistinct offset (all P < 0.001). Cluster analysis confirmed differences in both the frequency and combination of elemental features in parasomnias and NFLE. A diagnostic decision tree generated from these data correctly classified 94% of events. While sleep stage at onset was discriminatory (82% of seizures occurred during stage 1 or 2 sleep, with 100% of parasomnias occurring from stage 3 or 4 sleep), ictal EEG features were less useful. Video analysis of parasomnias identified three principal behavioral patterns: arousal behavior (92% of events); non-agitated motor behavior (72%); distressed emotional behavior (51%).

Conclusions

Our results broadly support the concept of confusion arousals, somnambulism and night terrors as prototypical behavior patterns of NREM parasomnias, but as a hierarchical continuum rather than distinct entities. Our observations provide an evidence base to assist in the clinical diagnosis of NREM parasomnias, and their distinction from NFLE seizures, on semiological grounds.

Citation:

Derry CP; Harvey AS; Walker MC; Duncan JS; Berkovic SF. NREM arousal parasomnias and their distinction from nocturnal frontal lobe epilepsy: a video EEG analysis. SLEEP 2009;32(12):1637-1644.