Non-rapid Eye Movement Sleep Stages Research Articles

Heart rate variability during sleep and subsequent sleepiness in patients with chronic fatigue syndrome.

We determined whether alterations in heart rate dynamics during sleep in patients with chronic fatigue syndrome (CFS) differed from controls and/or correlated with changes of sleepiness before and after a night in the sleep laboratory. We compared beat-to-beat RR intervals (RRI) during nocturnal sleep, sleep structure, and subjective scores on visual analog scale for sleepiness in 18 CFS patients with 19 healthy controls aged 25-55 after excluding subjects with sleep disorders. A short-term fractal scaling exponent (α1) of RRI dynamics, analyzed by the detrended fluctuation analysis (DFA) method, was assessed after stratifying patients into those who reported more or less sleepiness after the night's sleep (a.m. sleepier or a.m. less sleepy, respectively). Patients in the a.m. sleepier group showed significantly (p<0.05) higher fractal scaling index α1 during non-rapid eye movement (non-REM) sleep (Stages 1, 2, and 3 sleep) than healthy controls, although standard polysomnographic measures did not differ between the groups. The fractal scaling index α1 during non-REM sleep was significantly (p<0.05) higher than that during awake periods after sleep onset for healthy controls and patients in the a.m. less sleepy group, but did not differ between sleep stages for patients in the a.m. sleepier group. For patients, changes in self-reported sleepiness before and after the night correlated positively with the fractal scaling index α1 during non-REM sleep (p<0.05). These results suggest that RRI dynamics or autonomic nervous system activity during non-REM sleep might be associated with disrupted sleep in patients with CFS.

Neural respiratory drive and nocturnal hypoventilation in patients with chronic obstructive pulmonary disease

To explore the effects of neural respiratory drive on ventilation in patients with chronic obstructive pulmonary disease (COPD) during sleep. Diaphragm electromyogram (EMG) from a multipair esophageal electrodes and airflow derived from pneumotachography were recorded during overnight polysomnography in 13 patients with stable COPD recruited from outpatient clinic of First Affiliated Hospital of Guangzhou Medical College from May 2010 to May 2011. Changes in diaphragm EMG and ventilation during wakefulness and different sleep stages were observed. Diaphragm EMG decreased by 26% in non-rapid eye movement sleep (NREM) stage and 39% in rapid eye movement (REM) as compared with wakefulness. Coinciding with change in diaphragm EMG, ventilation (VE) (ml×min(-1)×kg(-1)) significantly decreased from wakefulness (156 ± 53) ml×min(-1)×kg(-1) to steady NREM stage (112 ± 35) ml×min(-1)×kg(-1) (P < 0.05) and further decreased from NREM stage to REM stage (95 ± 27) ml×min(-1)×kg(-1) (P < 0.05). Oxygen saturation also decreased significantly from 97.1% ± 1.8% in wakefulness to REM stage (94.0% ± 3.9%) (P < 0.01). Reduced neural respiratory drive contributes to nocturnal hypoventilation in COPD patients.

Hypnic Headache Responsive to Sodium Ferulate in 2 New Cases

Hypnic headache is a rare disorder characterized by frequent nocturnal attacks of a generalized headache in the elderly. This is the first report identifying 2 Chinese hypnic headache cases according to its diagnostic criteria. Both of the patients received sodium ferulate (100 or 50 mg, 3 times/d) for 2 or 3 months. The results of polysomnography in our cases indicated the onset of headache attacks in non-rapid eye movement sleep stage 2. Their symptoms were completely relieved for 1 year after the treatment. Our results suggest that sodium ferulate could be a potential treatment for hypnic headache.

Association Between Epileptiform Discharges and the Sleep Cycle in 200 Epileptic Patients

ABSTRACTObjective: The poor sleep quality of epileptic patients may be partly due to the occurrence epileptiform discharges (EDs). We observed the number of interictal discharges in each sleep stage and explored the associations between EDs and sleep phases in epileptic patients. Methods: Two hundred epileptic patients and 182 healthy volunteers were enrolled in the current study. For all subjects, video electroencephalography (EEG) monitoring and 24-hr night polysomnography were conducted to detect EDs and analyze the sleep structures. Results: EDs were detected in 91% of epileptic patients with the most frequent cases from the temporal lobe. The EDs detected during waking, sleeping, or both waking and nonrapid eye movement (NREM) sleep stages 1–2 accounted for 7.1%, 19.2%, and 25.3% of the total patients, respectively. EDs were rare during NREM stages 3–4 with 1.1% of total patients mainly in the central–temporal lobe. The total sleep time and time spent in REM were similar between the epileptic patients and healthy volunteers. However, epileptic patients spent a significantly longer mean sleep time in NREM stages 1–2 (293.91 ±27.57 min vs. 223.17 ±15.28; p = .000) and less in NREM stages 3–4 (50.11 ± 12.12 min vs. 133.96 ±10.77; p = .000) than healthy volunteers. Furthermore, asymmetric sleep spindles and fragmentary sleep structure as well as high inversion frequency were found in 26.7% and 43.3% of epileptic patients, respectively. Conclusion: Combination of long-term video EEG with polysomnography is a useful method to analyze associations between EDs and the sleep–wake cycle. This strategy can also help identify the nature of sleep disorders in epileptic patients, which may improve the treatment efficacy.

Sleep quality of mechanically ventilated patients sedated with dexmedetomidine

Dexmedetomidine is thought to activate an endogenous pathway that naturally promotes non-rapid eye movement (NREM) sleep. Dexmedetomidine may induce restorative sleep, that is, NREM stage 3 and 4 (slow wave sleep; SWS) or sleep continuity in mechanically ventilated patients. Few data have been published, however, on the sleep characteristics of mechanically ventilated patients during dexmedetomidine infusion. We recorded polysomnography (PSG) for 24 h in mechanically ventilated patients sedated with dexmedetomidine. Dexmedetomidine (0.2-0.7 μg/kg/h) was administered intravenously to maintain the Richmond Agitation-Sedation Scale between -1 and -4 only during the nighttime (9:00 p.m. to 6:00 a.m.). During the daytime, we interrupted the sedatives and analgesics unless the patient complained of discomfort. When this occurred midazolam or opioids were administered intermittently. Sleep stages and the frequency of arousal/awakening during the nighttime were analyzed using Rechtschaffen and Kales criteria. For the ten mechanically ventilated adult patients recruited into the study, the median total sleep time (TST) during the night was 4.7 h (IQR, 4.2-8.1 h), and 78 % of sleep occurred during the night (median 78 %, IQR: 69-88 %). Sleep architecture was exclusively NREM sleep stage 1 (median 28.9 % of TST) and stage 2 (median 71.2 % of TST). Neither SWS (median 0 % of TST) nor rapid eye movement (REM) sleep (median 0 % of TST) was observed. Median frequency of arousals/awakenings was 9.3/h (IQR, 3-19.5/h). In mechanically ventilated patients, nighttime infusion of dexmedetomidine preserved the day-night cycle of sleep but induced severely disturbed sleep architecture without evidence of SWS or REM sleep.

Sleep stage II contributes to the consolidation of declarative memories

Various studies suggest that non-rapid eye movement (NREM) sleep, especially slow-wave sleep (SWS), is vital to the consolidation of declarative memories. However, sleep stage 2 (S2), which is the other NREM sleep stage besides SWS, has gained only little attention. The current study investigated whether S2 during an afternoon nap contributes to the consolidation of declarative memories. Participants learned associations between faces and cities prior to a brief nap. A cued recall test was administered before and following the nap. Spindle, delta and slow oscillation activity was recorded during S2 in the nap following learning and in a control nap. Increases in spindle activity, delta activity, and slow oscillation activity in S2 in the nap following learning compared to the control nap were associated with enhanced retention of face-city associations. Furthermore, spindles tended to occur more frequently during up-states than down-states within slow oscillations during S2 following learning versus S2 of the control nap. These findings suggest that spindles, delta waves, and slow oscillations might promote memory consolidation not only during SWS, as shown earlier, but also during S2.

Watch peripheral arterial tonometry in the diagnosis of obstructive sleep apnea: Influence of aging

To investigate the consequences of aging and associated peripheral vascular tone impairment on peripheral arterial tonometry (Watch PAT)-based sleep and respiratory disturbance analysis in obstructive sleep apnea (OSA) diagnosis. Prospective, nonrandomized, clinical trial. A total of 56 subjects with age ranges of 20 to 35 years (group I, n = 27) and 50 to 65 years (group II, n = 29) referred to the sleep laboratory for overnight polysomnography (PSG) with suspected OSA were enrolled. All patients underwent simultaneous overnight PSG and Watch PAT monitoring. The data derived from PSG and Watch PAT records, including apnea-hypopnea index (AHI), rapid eye movement (REM) AHI, non-rapid eye movement (NREM) AHI, oxygen desaturation index (ODI), mean O(2) saturation (mean O(2) sat), minimum O(2) saturation (min O(2) sat), sleep duration, and the percentages of NREM sleep stages 1-2 and 3 and of REM sleep were used for comparisons. The calculated ΔPSG-Watch PAT of the two groups were compared statistically. The correlations between the PSG-Watch PAT measurements in each group were assessed. The comparison of AHI, REM AHI, NREM AHI, ODI, mean O(2) sat, min O(2) sat, NREM sleep stage 1-2, and REM sleep ΔPSG-Watch PAT between the two groups did not reveal statistical significance. The difference between the two groups in terms of ΔPSG-Watch PAT of sleep duration and sleep stage 3 was statistically significant. In addition to the good agreement confirmed between PSG and Watch PAT data in each group, aging did not negatively impact Watch PAT recorded data in terms of included parameters, except the difference in ΔPSG-Watch PAT of sleep stage 3, which may be attributable to aging and impaired vascular tone.

Noninvasive Ventilation in COPD: Impact of Inspiratory Pressure Levels on Sleep Quality

Although high-intensity noninvasive positive pressure ventilation (HI-NPPV) is superior to low-intensity noninvasive positive pressure ventilation (LI-NPPV) in controlling nocturnal hypoventilation in stable hypercapnic patients with COPD, it produces higher amounts of air leakage, which, in turn, could impair sleep quality. Therefore, the present study assessed the difference in sleep quality during HI-NPPV and LI-NPPV. A randomized, controlled, crossover trial comparing sleep quality during HI-NPPV (mean inspiratory positive airway pressure 29 ± 4 mbar) and LI-NPPV (mean inspiratory positive airway pressure 14 mbar) was performed in 17 stable hypercapnic patients with COPD who were already familiar with HI-NPPV. Thirteen patients (mean FEV(1) 27% ± 11% predicted) completed the trial; four patients refused to sleep under LI-NPPV. There was no significant difference in sleep quality between the treatment groups (all P > .05), with a mean difference of -3.0% (95% CI, -10.0 to 3.9; P = .36) in the primary outcome, namely non-rapid eye movement sleep stages 3 and 4. However, nocturnal Paco(2) was lower during HI-NPPV compared with LI-NPPV, with a mean difference of -6.4 mm Hg (95% CI, -10.9 to -1.8; P = .01). In patients with COPD, high inspiratory pressures used with long-term HI-NPPV produce acceptable sleep quality that is no worse than that produced by lower inspiratory pressures, which are more traditionally applied in conjunction with LI-NPPV. In addition, higher pressures are more successful in maintaining sufficient alveolar ventilation compared with low pressures. Thus, HI-NPPV is a very promising new approach, but still requires large, longer-term trials to determine the impact on outcomes such as exacerbation rates and longevity. German Clinical Trials Register (DRKS); No.: DRKS00000520; URL: www.drks.de.

Sleep Characteristics in Children with Growth Hormone Deficiency

Background/Aims: Growth hormone (GH) is preferentially secreted during slow wave sleep and the interactions between human sleep and the somatotropic system are well documented, although only few studies have investigated the sleep EEG in children with GH deficiency (GHD). The aim of this study was to evaluate the sleep structure of children with dysregulation of the GH/insulin-like growth factor axis. Methods: Laboratory polysomnographic sleep recordings were obtained from 10 GHD children and 20 normal healthy age-matched children. The classical sleep parameters were evaluated together with sleep microstructure, by means of the cyclic alternating pattern (CAP), in GHD patients and compared to the control group. Results: GHD children showed a significant decrease in total sleep time, sleep efficiency, movement time and in non-rapid eye movement sleep stage 2. Although some indicators of sleep fragmentation were increased in GHD children, we found a general decrease in EEG arousability represented by a significant global decrease in the CAP rate, involving all CAP A phase subtypes. Conclusions: The analysis of sleep microstructure by means of CAP, in children with GHD, showed a reduction of transient EEG amplitude oscillations. Further studies are needed in order to better clarify whether GH therapy is able to modify sleep microstructure in GHD children, and the relationships between sleep microstructure, hormonal secretion and neurocognitive function in these patients.

Mutations of the orexin system, a regulator of sleep arousal, are not a common cause of ADNFLE

Gain-of-function mutations in genes coding for subunits of the neuronal nicotinic acetylcholine receptor have been identified in 15% of families with autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE),1 and in the promoter of the corticotropin-releasing hormone (CRH) gene.1 In remaining families, the responsible genes are unknown. Patients with ADNFLE typically present many seizures per night involving intense motor agitation (frenetic movements of the trunk and limbs or sequence of various dystonic postures) lasting less than 1 minute. There are no clinical differences between families with and without identified mutations. The seizures seem to occur at the time of arousal from nonrapid eye movement (non-REM) sleep stage 2.2 Clinical and EEG observations and the identification by in vivo nuclear imaging in patients with ADNFLE carrying nicotinic receptor mutations of an increased nicotinic receptor density in the brainstem, suggesting a hyperactivity of the brainstem-thalamic cholinergic ascending arousal pathway, led to ADNFLE being considered as an arousal disorder.3 In parallel to the cholinergic system, the orexin/hypocretin system is also involved in inducing arousal from sleep. Orexin neurons, like cholinergic neurons, discharge …

Development of the Brain's Default Mode Network from Wakefulness to Slow Wave Sleep

Falling asleep is paralleled by a loss of conscious awareness and reduced capacity to process external stimuli. Little is known on sleep-associated changes of spontaneously synchronized anatomical networks as detected by resting-state functional magnetic resonance imaging (rs-fMRI). We employed functional connectivity analysis of rs-fMRI series obtained from 25 healthy participants, covering all non-rapid eye movement (NREM) sleep stages. We focused on the default mode network (DMN) and its anticorrelated network (ACN) that are involved in internal and external awareness during wakefulness. Using independent component analysis, cross-correlation analysis (CCA), and intraindividual dynamic network tracking, we found significant changes in DMN/ACN integrity throughout the NREM sleep. With increasing sleep depth, contributions of the posterior cingulate cortex (PCC)/retrosplenial cortex (RspC), parahippocampal gyrus, and medial prefrontal cortex to the DMN decreased. CCA revealed a breakdown of corticocortical functional connectivity, particularly between the posterior and anterior midline node of the DMN and the DMN and the ACN. Dynamic tracking of the DMN from wakefulness into slow wave sleep in a single subject added insights into intraindividual network fluctuations. Results resonate with a role of the PCC/RspC for the regulation of consciousness. We further submit that preserved corticocortical synchronization could represent a prerequisite for maintaining internal and external awareness.

Sleep disorders in Wilson’s disease

Wilson's disease (WD) is an autosomal recessive inherited disease with copper accumulation; neurodegeneration is associated with dopaminergic deficit. The aim of the study is to verify sleep co-morbidity by questionnaire and objective sleep examinations (polysomnography, multiple sleep latency test). fifty-five patients with WD (22 hepatic, 28 neurological, five asymptomatic form) and 55 age- and sex-matched control subjects completed a questionnaire concerning their sleep habits, sleep co-morbidity, Epworth sleepiness scale (ESS), and answered screening questions for rapid eye movement (REM) behaviour disorder (RBD-SQ). Twenty-four patients with WD and control subjects underwent polysomnographic examination. unlike the controls, patients with WD were more prone to daytime napping accompanied by tiredness and excessive daytime sleepiness, cataplexy-like episodes and poor nocturnal sleep. Their mean ESS as well as RBD-SQ was higher than that of the controls. Total sleep time was lower, accompanied by decreased sleep efficiency and increased wakefulness. Patients with WD had lower latency of stage 1 and stage 2 of non-rapid eye movement (NREM) sleep and less amount of NREM sleep stage 2. One-third of the patients with WD were found to have short or borderline multiple sleep latency test (MSLT) values independent of nocturnal pathology (sleep apnoea, periodic leg movements and/or restless leg syndrome). patients with WD often suffer from sleep disturbances (regardless of the clinical form). The spectrum of sleep/wake symptoms raises the suspicion that altered REM sleep function may also be involved.

Dissociation Between Neurovegetative Signs and Subjective Symptoms in a Case of Idiopathic Pilomotor Seizures

Pilomotor seizure (PS) is a rare subtype of simple and complex partial seizures, often related to temporal lobe epilepsy and occasionally linked to alterations of amygdala. The physiologic role played by this latter region in the coordination of autonomic responses to fear-induced emotional changes raises the question as to whether the involvement of amygdala in PS might elicit a disconnection between subjective symptoms and neurovegetative signs. We report a case of idiopathic bilateral PS studied with video electroencephalogram, polygraphic 24-hour Holter electroencephalogram, and magnetic resonance imaging, plus spectral functional magnetic resonance imaging, in which the seizures were associated with abrupt tachycardia occurring in a state of emotional neutrality, without either clouding or loss of consciousness. Electroencephalogram documented PS episodes occurring during waking, rapid eyes movements, and nonrapid eye movement sleep stages. Although no morphologic alteration was detected, spectral magnetic resonance imaging visualized alterations of the metabolic ratios of N-acetylaspartate and creatine-phosphocreatine in hippocampus and amygdala, whereas no apparent involvement of the temporal lobe was found. These findings suggest that the limited involvement of amygdala and hippocampus in PS triggers the repertoire of fear-related sympathetic responses uncoupled from alterations in emotional status. This phenomenon supports the possibility that autonomic responses involved in fear or extreme alertness follow a kind of "ethological" modularity.

Plasma adiponectin level and sleep structures in children with Prader-Willi syndrome

Adiponectin, an adipose tissue-derived hormone, has been negatively related to obstructive sleep apnea syndrome. Besides sleep apnea, children with Prader-Willi syndrome (PWS) may have excessive daytime sleepiness and rapid eye movement (REM) sleep abnormality. The aim of this study is to determine whether changes in sleep structures are related to plasma adiponectin levels in PWS. Correlations between adiponectin level and sleep variables were analyzed in 28 children with PWS and 18 controls. Overnight polysomnography was performed. The fasting plasma adiponectin levels were higher in the children with PWS than in the controls (P = 0.0006). In the PWS, Epworth sleepiness scale was significantly higher (P = 0.002); sleep latency (P = 0.003) and REM latency (P = 0.001) were significantly shortened; the apnea-hypopnea index (AHI) was significantly increased (P = 0.0001); and the duration of non-rapid eye movement (NREM) sleep stages 3 and 4 was decreased (P = 0.005). Multiple regression analysis revealed correlations between the adiponectin level and the total sleep time (beta = 0.688, P = 0.009), AHI (beta = 1.274, P = 0.010), REM latency (beta = -0.637, P = 0.021) and the percentage of NREM sleep (beta = -7.648, P = 0.002) in PWS. In children with PWS, higher plasma adiponectin levels were independently associated with several sleep variables, which was not observed in the control group. These results suggest a potential influence of elevated adiponectin level on the sleep structures in PWS.

Sleep Polygraphic Study of Children and Adolescents With Narcolepsy/Cataplexy

The alterations of the Cyclic Alternating Pattern (CAP) recently found in narcoleptic adult patients suggest the presence of an impaired modulation of the fluctuations of the arousal level during their non-rapid eye movement (NREM) sleep, possibly because of the persistence of neurophysiological mechanisms typical of rapid eye movement (REM) sleep. The same mechanism might play a role in the occurrence of leg movement (LM) activity during sleep characterized by low levels of periodicity. The aim of this study was to evaluate CAP and sleep LM activity in a group of children and adolescents with narcolepsy, to interpret the results under a developmental point of view and integrate this new information with data already available for adults. Thirteen young patients with narcolepsy/cataplexy were consecutively recruited for this study, together with 13 age- and sex-matched normal controls. Nocturnal polysomnography was carried out after a night of adaptation in a sleep laboratory room; sleep stages, CAP, and LMs were scored and evaluated following standard criteria. Narcoleptic patients showed shorter sleep onset and REM sleep latency, higher number of stage shifts and awakenings per hour of sleep, and higher percentage of wakefulness after sleep onset; CAP rate was found to be decreased in all NREM sleep stages (in particular CAP A1 subtypes) in narcoleptic patients who also showed significant higher values of all types of LMs (periodic or isolated), during both REM and NREM sleep; however, the most evident differences were found during REM sleep. The results of this study confirm that the sleep microstructure and LM activity changes observed in adulthood are already present and detectable in childhood and might have a role in the already known impaired prefrontal functioning of these subjects. The well-established orexin deficiency might be the unifying factor playing a major role in the modulation of CAP and LMs during sleep in children and adolescents with narcolepsy/cataplexy.

Multiple sleep latency measures in narcolepsy and behaviourally induced insufficient sleep syndrome

Background Short mean latencies to the first epoch of non-rapid eye movement sleep stage 1 (NREM1) and the presence of ⩾2 sleep onset REM (SOREM) periods on multiple sleep latency test (MSLT) occur in both narcolepsy–cataplexy (NC) and behaviourally induced insufficient sleep syndrome (BIISS). It is not known whether specific MSLT findings help differentiate the two disorders. Methods We analyzed MSLT data including sleep latencies to and between different sleep stages of 60 age-, gender- and body mass index (BMI)-matched subjects (hypocretin-deficient NC, actigraphy-confirmed BIISS, healthy controls: each 20). Results Mean latency (in minutes) to NREM1 sleep was significantly shorter in NC (1.8 ± 1.5) than in BIISS (4.7 ± 2.1, p < 0.001) and controls (11.4 ± 3.3, p < 0.001). Mean latency to NREM2 sleep was similar in NC (8.6 ± 4.7) and BIISS (8.1 ± 2.7, p = 0.64); latency to either NREM2 or rapid eye movement (REM) sleep (i.e., the sum of the sleep latency to NREM1 and the duration of the first NREM1 sleep sequence), however, was shorter in NC (4.4 ± 2.9) than in BIISS (7.9 ± 3.5, p < 0.001). Referring to all naps with SOREM periods, the sequence NREM1–REM–NREM2 was more common (71%) in NC than in BIISS (15%, p < 0.001), reflecting the shorter latency from NREM1 to NREM2 in BIISS (3.7 ± 2.5) than in NC (6.1 ± 5.9, p < 0.001). Conclusions Our findings show that both sleepiness (as measured by NREM1 sleep latency) and REM sleep propensity are higher in NC than in BIISS. Furthermore, our finding of frequent REM sleep prior to NREM2 sleep in NC is in line with the recent assumption of an insufficient NREM sleep intensity in NC. Together with detailed clinical interviews, sleep logs, actigraphy, and nocturnal polysomnography, mean sleep latencies to NREM1 ⩽2.5 min, the presence of multiple SOREM periods, and the sequence NREM1–REM–NREM2 may be the best MSLT measures to discriminate NC from BIISS.

Successful treatment with levothyroxine for idiopathic hypersomnia patients with subclinical hypothyroidism

Objective Our objective was to discuss the effect of levothyroxine on excessive daytime sleepiness (EDS) and a prolonged nocturnal sleep at patients with idiopathic hypersomnia who presented with subclinical hypothyroidism. Methods We present two patients with hypersomnia who complained of EDS and a prolonged nocturnal sleep time. Sleep architecture and subjective daytime sleepiness were estimated by polysomnography (PSG) and Epworth Sleepiness Scale (ESS), respectively. Diagnoses were made using the International Classification of Sleep Disorders, 2nd Edition criteria for idiopathic hypersomnia with long sleep time. Results PSG demonstrated a short sleep latency, a prolonged total sleep time and normal proportions of all non-rapid eye movement (REM) and REM sleep stages. Nocturnal PSG excluded other causes of EDS. No medical, neurological and mental disorders were present. Their laboratory data indicated mildly elevated thyrotropin, despite free thyroxine (T4) and triiodothyronine (T3) estimates within their reference ranges, which is a characteristic of latent hypothyroidism. Levothyroxine (25 μg/day) was administrated orally. After treatment with levothyroxine for 8 weeks, the mean daily sleep times decreased. EDS was also improved, and a significant decrease in the ESS score was observed. Levothyroxine was effective for their hypersomnia and well tolerated. Conclusions It should be noted that hypersomnia may be associated with subclinical hypothyroidism, although few abnormalities in physical and neurological examinations are present.

Sleep and recovery from critical illness and injury: A review of theory, current practice, and future directions*

The objectives of this article were to describe the deleterious effects of sleep deprivation, characterize sleep in patients cared for in an intensive care unit (ICU) environment, and propose an integrated strategy to improve sleep in critical care units. Clinical trials and review articles assessing sleep deprivation, sleep in a critical care setting, and interventions to improve sleep in the critical care environment were identified through an in depth PubMed search. Sleep deprivation and disruption are particularly prevalent in patients cared for in the critical care environment. Although numerous observational studies during the past several decades have demonstrated that sleep in patients cared for in ICUs is highly abnormal, little is known about the effects of poor sleep quality on outcomes from critical illness or injury. Reasons for sleep deprivation during recovery from illness and injury in the ICU are multifactorial. Major contributing factors in this patient population are type and severity of underlying illness, the pathophysiology of acute illness/injury, pain from surgical procedures, and perhaps most importantly, the ICU environment itself. Sleep in ICU patients is characterized by prolonged sleep latencies, sleep fragmentation, decreased sleep efficiency, frequent arousals, a predominance of stage 1 and 2 nonrapid eye movement sleep, decreased or absent stage 3 and 4 nonrapid eye movement sleep, and decreased or absent rapid eye movement sleep. Optimizing patient comfort and ensuring that patients achieve adequate restorative sleep while cared for in the ICU is an arduous task. However, environmental alterations in the ICU may reliably improve sleep quality and subsequently alter outcomes during recovery from critical illness and injury.

Somnambulism Induced by Quetiapine: Two Case Reports and a Review of the Literature

Somnambulism, a previously unreported side effect of quetiapine, is described in two cases. Both cases involved individuals who had no prior or family history of somnambulism and had attention-deficit/hyperactivity disorder. The possible significance of this will also be discussed. Somnambulism is a common parasomnia that reflects an impairment in the normal mechanisms of arousal from sleep in which motor behaviors are activated without full consciousness. Motor behaviors are initiated during deep non-rapid eye movement or slow-wave sleep (stages 3-4), and may be limited to relatively simple manifestations, such as sitting up, fumbling with objects or bedclothes, or mumbling.

Iron deficiency anemia in infancy is associated with altered temporal organization of sleep states in childhood.

The highest prevalence of iron deficiency anemia (IDA) in infancy coincides with a time of rapid changes in sleep organization. Since IDA in infancy is associated with long-lasting neurofunctional effects despite iron treatment, the normal development of sleep patterns might be affected. Night polysomnographic recordings were performed in 55 healthy 4-y-old children (former IDA = 27, nonanemic controls = 28). Both groups were followed from infancy and were similar in background characteristics. The duration of each waking episode was measured, as was the duration of each episode of nonrapid eye movement (NREM) sleep stages 1 (NREM1), 2 (NREM2), and 3-4 (SWS), and rapid eye movement (REM) sleep. The data were analyzed according to the successive thirds of the total sleep time (TST). Relative to controls, former IDA children showed: a) longer duration of REM sleep episodes in the first third and shorter in the last third; b) more REM sleep episodes in the first third and fewer in the second third; and c) shorter latency to the first REM sleep episode and shorter NREM stage 2 and SWS episodes within the first sleep cycle. The results show that early IDA is associated with long-lasting alterations in the temporal organization of sleep patterns.