Number Of Sleep Stage Changes Research Articles

Nightmares and Sleep Disturbances in Children with PTSD: A Polysomnographic and Actigraphy Approach Evaluation.

Sleep disturbances (insomnia and nightmare symptoms) are the most sensitive and persistent symptoms of pediatric post-traumatic stress disorder (PTSD). Untreated, these sleep disturbances (SD) associated with PTSD are predictive of PTSD persistence and increased psychiatric complications. The aim of this study was to evaluate sleep and circadian rhythms in children with PTSD under both laboratory and ecological conditions in comparison with a control population and to test for the first time the hypothesis that SD and circadian rhythms are positively correlated with PTSD severity and its comorbidities. This prospective pilot study evaluated PTSD, SD (insomnia, nightmares), and sleep-wake rhythms in 11 children with PTSD (aged 3-18), compared with the age and sex-matched control groups. Assessment of PTSD and subjective and objective measures of sleep and sleep-wake rhythms (questionnaires, 24-h in-laboratory video-polysomnography, 15-day at-home actigraphy recording) were performed between 1 and 6 months after the traumatic event. Children with PTSD had higher sleep fragmentation (increased wake-after-sleep onset, increased number of sleep stage changes) compared to controls, with a change in sleep microarchitecture (micro-arousal index at 14.8 versus 8.2, p = 0.039). Sleep fragmentation parameters correlated with PTSD symptomatology, insomnia, and post-traumatic nightmare severity. The within-group comparison revealed a better sleep architecture in the controlled (sleep laboratory) than in the ecological condition (at home) (total sleep time 586 versus 464 min, p = 0.018). Sleep and rhythm disturbances are strongly associated with PTSD in children. The assessment of SD in children with PTSD should be carried out systematically and preferentially under ecological conditions, and management of SD should integrate the environment (environmental design, psycho-education for the children and their parents) more fully into therapy focused on sleep and trauma.

Swaddling: a traditional care method rediscovered

This study was undertaken to compare the sleep profiles of healthy infants in swaddling and sleeping bag conditions. Polysomnographs of 85 healthy infants (40 in the study group, 45 in the control group) with a mean age of 7.5 weeks were recorded in the sleeping laboratory. A positive decision from the local Ethics Committee and the written consent of the parents were obtained for the study. Swaddling significantly reduces the rate of spontaneous waking (events/h: 1.39 [0.85-2.77] vs. 2.81 [1.49-4.53], P=0.020) and the number of sleep stage changes (events/h: 3.82 [2.97-5.16] vs. 5.37 [3.58-6.67], P=0.015). Swaddling promotes quiet sleep (36.37% [29%-40.31%] vs. 30.2% [24.45%-36.78%], P=0.032), the time spent awake was decreased (8.98% [4.62%-14.25%] vs. 14.17% [9.2%-18.94%], P=0.001) and sleep efficiency was increased (91.02% [85.75%-95.38%] vs. 85.83% [81.06%-90.8%], P=0.001). Swaddling promotes a more quiet sleep in infants.

Insomnia and Hypertension

We would like to respond to the 2 letters to the editor,1,2 which were published in SLEEP, August 2009, in regard to our study, “Insomnia with objective short sleep duration is associated with a high risk for hypertension.”3 The objective of our study was to assess the cross-sectional association of two prevalent conditions, i.e., insomnia and hypertension, in a general-population sample. Our study demonstrated a strong and significant association between insomnia with objective short sleep and hypertension. Given the high prevalence of hypertension in the general population, we did not intend to imply that the odds ratio is a reliable estimate of the relative risk for this condition in insomniacs with short sleep, versus the reference group. In less technical terms, our odds ratios indicate that the odds or the likelihood of having hypertension is 5-fold higher in the insomnia–short sleep-duration group versus the control group. Thus, we agree with Sainani et al., that the phrase “a risk for hypertension 500% or 350% higher,” although commonly used, is grammatically incorrect and may lead to misinterpretation. Dr. Krakow suggests that, in our study, we underestimated the severity of obstructive sleep apnea because we used only thermocouple technology. In our study, in contrast with many previous reports, subjects were evaluated for sleep apnea, the prevalence of which was the primary goal of our project, with technology very similar to other large epidemiology cohorts, i.e., Sleep Heart Health Study and Wisconsin cohort. In our analysis, for the association of insomnia with hypertension, we controlled even for mild forms of apnea, i.e., an apnea-hypopnea index of 5 or less, which usually are not treated in most clinical settings. Dr. Krakow also suggests that we did not assess for other forms of the apnea spectrum disorder, such as upper airway resistance syndrome. This syndrome is usually associated with sleep fragmentation but not with apneas or hypopneas based on standard definition. In our study, we controlled for indices of sleep fragmentation, i.e., number of awakenings, number of sleep-stage changes, and percentage of stage 1 sleep, and the results remained significant and strong (see results section, fourth paragraph). Further, the author states that upper airway resistance syndrome occurs more frequently in subjects with short sleep duration. We do not know of any evidence supporting such a claim. However, even if we accept such a claim, how can we explain that the adjusted odds ratio for subjects with short sleep duration, i.e., less than 5 hours, is lowest in those with no sleep complaint (1.13, 95% confidence interval 0.79-1.62), intermediate in those with “poor sleep” (a milder form of insomnia) (2.43, 95% confidence interval 1.36-4.35), and highest in those with chronic insomnia (5.12, 95% confidence interval 2.22-11.79)? This strong dose-response association between the joint effect of insomnia with short sleep duration and hypertension can only be explained by the difference in the severity or chronicity of the insomnia complaint and not by the “underestimation of the severity of sleep apnea” and the lack of detection of upper airway resistance syndrome that should be equally distributed, based on the author's argument, in these 3 groups. Notably, our new study on the same population showed a similar pattern on the association between insomnia–short sleep duration and diabetes.4 The difficulties in treating mild or moderate sleep apnea (apnea-hypopnea index < 30) are well recognized, whereas the effects of current standard treatment, i.e., continuous positive airway pressure, on hypertension in this population are very doubtful, albeit very costly.5,6 Effective treatment for a large group of insomniacs with short sleep duration may be crucial to protect them from the significant cardiometabolic problems associated with this very prevalent disorder.

Sleep stage dynamics differ between children with and without obstructive sleep apnea.

Analysis of sleep dynamics--distributions of contiguous sleep and sleep stage durations--reveal exponential distributions and potential clinical utility in adults. We sought to examine these polysomnographic variables for the first time in children, and in the context of childhood sleep disordered breathing (SDB). Analysis of polysomnographic data available from the Washtenaw County Adenotonsillectomy Cohort. Selected subjects were 48 children aged 5-12 years with SDB (pediatric apnea/hypopnea index > or = 1.5) who were scheduled for adenotonsillectomy and 20 control subjects of similar ages without SDB. Subjects were studied at enrollment and again one year later in almost all cases. Durations of sleep and specific sleep stage bouts generally followed exponential distributions. At baseline, the number of sleep stage changes, proportion of total sleep time occupied by stage 1 sleep, proportion stage 2 sleep, mean stage 2 duration, and mean stage REM duration each distinguished subjects with and without SDB (P < 0.05), but only mean stage 2 duration did so independently after accounting for the other variables (P = 0.03). At one-year follow-up, changes in total sleep time, mean stage 2 duration, and mean stage REM duration distinguished SDB from control subjects, but again only changes in mean stage 2 duration did so independently (P = 0.01). Durations of uninterrupted sleep and specific sleep stages appear to follow exponential distributions in children with or without SDB. Parameters that describe these distributions--particularly mean duration of stage 2 sleep periods--may provide useful additions to standard sleep stage analyses.

Diclofenac potassium restores objective and subjective measures of sleep quality in women with primary dysmenorrhea.

Primary dysmenorrhea is a common gynecological disorder that disrupts daytime functioning and nighttime sleep quality. We determined the effectiveness of diclofenac potassium, compared to placebo, in alleviating nighttime pain and restoring sleep architecture in women with primary dysmenorrhea. Randomized, double-blind, crossover study. Sleep laboratory. Ten healthy women (21 +/- 1 years) with a history of primary dysmenorrhea. Placebo or diclofenac potassium (150 mg per day) for menstrual pain. We assessed objective measures of sleep (polysomnography) and subjective measures of sleep quality, mood, and intensity of menstrual pain. Compared to a pain-free phase of the menstrual cycle (mid-follicular), women receiving placebo for their menstrual pain had a poorer mood (P < 0.01), decreased sleep efficiency (P < 0.05), less REM sleep (P < 0.05), more stage 1 sleep (P < 0.01), and more sleep stage changes per hour of sleep during the night. Administration of diclofenac potassium compared to placebo not only attenuated the women's menstrual pain (P < 0.05), but also increased sleep efficiency (P < 0.05) and percentage of REM sleep (P < 0.01), decreased percentage of stage 1 sleep (P < 0.05) and number of sleep stage changes per hour of sleep (P < 0.05), and improved subjective ratings of sleep quality and morning vigilance (P < 0.05). Diclofenac potassium effectively attenuates nighttime dysmenorrheic pain and restores subjective and objective measures of sleep quality to values recorded in a pain-free phase of the menstrual cycle.

Disturbed sleep in children with Tourette syndrome: A polysomnographic study

Objective: To evaluate objective data on sleep quantity/quality and motor activity during night sleep in children with Tourette syndrome (TS). Method: Polysomnography of 17 unmedicated TS children (ages: 7;11–15;5, mean: 11;10 years) without comorbid attention-deficit hyperactivity disorder (ADHD) was compared with 16 age-, sex- and IQ-matched healthy controls. Sleep analyses according to the procedure of Rechtschaffen and Kales were supplemented by counting epochs with short arousal-related movements (≤15 s), thus allowing to calculate correlations between motor activity and sleep parameters. Results: Children with TS demonstrated changes in sleep parameters, including longer sleep period time, longer sleep latency, reduced sleep efficiency, and prolonged wakefulness after sleep onset. Their sleep profiles showed significantly more time awake and less sleep stage II. However, REM sleep variables, slow-wave sleep, and number of sleep stage changes were unaffected. Movement time was similar in both groups, but epochs with short arousal-related movements were increased in TS. Further analyses showed no significant correlations between sleep parameters and nighttime nontic movements, level of psychopathology or tic severity during daytime. Periodic limb movements during sleep (PLMS) were only seen in one TS patient (low PLMS index of 7.8/h). Conclusions: Children with TS have disturbed sleep quality with increased arousal phenomena, which both may be intrinsic to the disorder and might trigger tics and other behavioral problems during daytime. This indicates the need for sleep evaluation in patients with TS.

The effect of combined therapy (ultrasound and interferential current) on pain and sleep in fibromyalgia

Multidisciplinary treatment has proven to be the best therapeutic option to fibromyalgia (FM) and physiotherapy has an important role in this approach. Considering the controversial results of electrotherapy in this condition, the aim of this study was to assess the effects of combined therapy with pulsed ultrasound and interferential current (CTPI) on pain and sleep in FM. Seventeen patients fulfilling FM criteria were divided into two groups, CTPI and SHAM, and submitted to pain and sleep evaluations. Pain was evaluated by body map (BM) of the painful areas; quantification of pain intensity by visual analog scale (VAS); tender point (TP) count and tenderness threshold (TT). Sleep was assessed by inventory and polysomnography (PSG). After 12 sessions of CTPI or SHAM procedure, patients were evaluated by the same initial protocol. After treatment, CTPI group showed, before and after sleep, subjective improvement of pain in terms of number (BM) and intensity (VAS) of painful areas ( P<0.001, both); as well as objective improvement, with decrease in TP count and increase in TT ( P<0.001, both). Subjective sleep improvements observed after CTPI treatment included decrease in morning fatigue and in non-refreshing sleep complaint ( P<0.001, both). Objectively, PSG in this group showed decrease in sleep latency ( P<0.001) and in the percentage of stage 1 ( P<0.001), increase in the percentage of slow wave sleep ( P<0.001) and in sleep cycle count ( P<0.001). Decrease in arousal index ( P<0.001), number of sleep stage changes ( P<0.05) and wake time after sleep onset ( P<0.05), were also observed and no difference regarding pain or sleep parameters were verified after SHAM procedure. This study shows that CTPI can be an effective therapeutic approach for pain and sleep manifestations in FM.

Nocturnal plasma melatonin levels after flunitrazepam administration in healthy subjects

Polysomnographic sleep patterns and melatonin secretion were investigated in 5 young (age 25.6±1.1 years) and 5 middle-aged (age 49.4±5.4 years) healthy male subjects after intravenous administration of 1 mg flunitrazepam and placebo in a randomized, double-blind and cross-over setting. The area under the curve (AUC) of total nocturnal melatonin plasma concentration decreased 23.3±11.5% in young subjects ( P≤0.05) and 39.3±5.2% in middle-aged subjects ( P≤0.05) after flunitrazepam infusion compared with placebo infusion. Differences in nocturnal peak values of melatonin were 5.4±22.0%> in young subjects (not significant) and 34.0±14.7% in middle-aged subjects ( P≤0.05). Flunitrazepam significantly ( P≤0.05) improved sleep latency and the number of sleep stage changes in the group of all subjects. These results show that, although the benzodiazepine flunitrazepam improves sleep, it reduces the nocturnal secretion of melatonin, and therefore alters the circadian rhythm of a hormone which is supposed to play a special role in circadian sleep-wake rhythmicity.

Environmental Noise and Sleep—A Study of Arousals, Cardiac Arrhythmia and Urinary Catecholamines

Nine adult subjects with documented cardiac arrhythmia were studied during 4 nights of sleep in a laboratory. A sleep polygraph and single-channel electrocardiogram were recorded continuously throughout each night. After the 1st night's familiarization, the subjects were presented with 1 night each of 50 calibrated aircraft or truck noise events. One other night was noise-free. Intervals containing noise and paired quiet intervals were examined for sleep stage at interval onset, number of sleep stage changes and ventricular premature contractions (VPCs). Overnight urinary catecholamines were also assayed. It was found that noise increased the likelihood of arousal responses to the same extent in all sleep stages (p < 0.05). Four subjects showed frequent VPCs during the experiment. These VPCs were significantly related to sleep stage (p < 0.05) but not to noise events. Excretion of urinary catecholamines did not differ between noise and quiet nights.

Relative and Combined Effects of Heat and Noise Exposure on Sleep in Humans

In a counter-balanced design, the effects of daytime and/or nighttime exposure to heat and/or traffic noise on night sleep were studied in eight healthy young men. During the day, the subjects were exposed to baseline condition (ambient temperature = 20 degrees C; no noise) or to both heat (35 degrees C) and noise. The duration of the daytime exposure was 8 h ending 5 h before sleep onset. The following nights, the subjects slept either in undisturbed (20 degrees C; no noise) or in noise, heat, or noise plus heat-disturbed environments. During the day, the various types of traffic noise were distributed at a rate of 48/h with peak intensities ranging between 79 and 86 dB(A). The background noise level was at 45 dB(A). At night, the peak intensities were reduced by 15 dB(A), the rate was diminished to 9/h, and the background noise was at 30 dB(A). Electrophysiological measures of sleep and esophageal and mean skin temperatures were continuously recorded. The results showed that both objective and subjective measures of sleep were more disturbed by heat than by noise. The thermal load had a larger impact on sleep quality than on sleep architecture. In the nocturnal hot condition, total sleep time decreased while duration of wakefulness, number of sleep stage changes, stage 1 episodes, number of awakenings, and transitions toward waking increased. An increase in the frequency of transient activation phases was also found in slow-wave sleep and in stage 2. In the nocturnal noise condition, only total number of sleep stage changes, changes to waking, and number of stage 1 episodes increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiration and Abnormal Sleep in Patients with Congestive Heart Failure

We investigated the interaction between respiration and sleep in ten male outpatients with severe, stable, maximally treated congestive heart failure (CHF). Cheyne-Stokes respiration (CSR), defined as periodic breathing with apnea or hypopnea, was found in all patients with a mean duration of 120 +/- 87 minutes [50.2 +/- 34.4 percent total sleep time (TST)]. The CSR was found predominantly during stage 1 (20.6 +/- 6.7 percent TST) and stage 2 (25.8 +/- 6 percent TST) NREM sleep and occurred rarely during slow wave sleep (SWS) (1.6 +/- 1 percent TST) and REM sleep (1.6 +/- 0.5 percent TST). All apneas and hypopneas were central. Despite normal awake arterial oxygenation (SaO2) (96.1 +/- 1.6 percent), significant, severe hypoxemia was found during sleep in seven patients with SaO2 less than 90 percent for 9 to 59 percent TST (mean +/- SD, 23 +/- 23 percent TST), and this was significantly related to the duration of CSR (r = 0.66, p less than 0.05). The mean minimum SaO2 for sleep stage was lowest during stage 1 (82.1 percent +/- 2.6 percent) and stage 2 (78.9 percent +/- 2.8 percent) NREM sleep, intermediate during REM sleep (84.5 percent +/- 1.8 percent) and highest during SWS (87.6 percent +/- 2.7 percent). Sleep was disrupted to a variable extent in all patients with a short mean TST (287 +/- 106 minutes), a high proportion of stage 1 sleep (26 +/- 19 percent TST), virtual absence of SWS (5 +/- 7 percent TST) which was found in only four patients, and a high number of sleep stage changes (30 +/- 27/hour) and arousals (28 +/- 25/hour). Arousals occurred predominantly during stage 1 (17 +/- 20/hour) and stage 2 (10 +/- 7/hour) NREM sleep and the majority immediately followed the hyperpneic phase of CSR. The amount of CSR (percent TST) was inversely related to the length of TST (r = -0.73, p less than 0.05), and directly related to the number of sleep stage changes (r = 0.79, p less than 0.01) and the number of arousals (r = 0.66, p less than 0.05). We conclude that in severe, stable CHF, CSR occurs predominantly during light sleep, that despite normal awake arterial oxygen saturation, significant hypoxemia may develop during sleep due to CSR, and that sleep is unstable and disrupted due to frequent arousals caused by the hyperpneic phase of CSR. These sequelae of CSR may be important determinants of the clinical status and outcome of patients with severe CHF.

Effects of evening activity on early night sleep.

ABSTRACTThis study was designed to determine the effects of presleep activity on a variety of physiological variables during 3½ hrs of subsequent sleep. Three presleep conditions were investigated for each of 15 Ss:6 hrs of strenuous physical exercise, 6 hrs of concentrated studying, and 6 hrs of relaxation, i.e. watching TV, listening to records, and reading magazines. The following variables were recorded during a 3½ hr sleep period: EEG, EOG, body movements, heart rate, respiratory rate, peripheral pulse voltime, phasic vasoconstrictions, rectal temperature, and rapid variations in skin potential.None of the experimental presleep activities influenced the EEG cycle during the 3½ hrs of sleep. In particular, there were no significant differences in the following measurements as a result of presleep condition: amount of REMP time, time to first REMP, amount of delta sleep, time to first delta sleep, amount of stage 2 sleep, or number of sleep stage changes. These findings indicate a surprising stability of the sleep stage cycle vis a vis the markedly different evening activities.Physiological arousal after exercise decreased rapidly until it was no longer distinguishable from the base levels following studying or relaxation. A tendency to approach these base levels was observed even in heart rate, a variable which remained elevated after exercise throughout the 3½ hrs of sleep. For none of the physiological variables was the level of physiological arousal during sleep inversely related to the level of physiological arousal during wakefulness.Relating EEG sleep stages to the other variables of this study, it was observed that on nights when respiratory rate was high there was more delta sleep and less stage 2 sleep. Also, respiratory minima were most often found during stage 2 sleep immediately following a REMP, and respiratory maxima during NREM sleep were significantly associated with delta sleep. These results support Bülow's (1963) proposal that a close coupling exists between respiratory centers and those neural structures that regulate EEG arousal.

Electroencephalographic and eye movement patterns during sleep in chronic schizophrenic patients

Continuous all night sleep EEG recordings were obtained from a group of 25 chronic, hospitalized schizophrenic patients and ten normal control subjects for 5 consecutive nights. Analyses are presented for the second night of sleep. Results for mean percentage of stages I, II, III, IV and I-REM for control subjects were found to be similar to values reported for comparable control populations using similar scoring techniques. In contrast, 40% ( N = 10) of the schizophrenic patients failed to manifest any scorable stage IV and were significantly reduced in amount of stage III. For all patients, a reduction in amplitude of the delta wave component of stages III and IV was apparent relative to control subject records. Schizophrenic patients were found to have a more disturbed sleep compared to controls, although no distinction was apparent between patients with or without stage IV present. Differences in time of onset, duration, and number of sleep stage changes were noted between schizophrenic and control subjects. Possible implications arising from the observed disturbance of “slow wave” patterns in the sleep EEGs of schizophrenic patients are discussed in light of research on the loci of this activity in the brain, as well as recent reports linking amino acid levels and EEG sleep patterns.

Sleep patterns in young adults: an EEG study

1. 1. EEG sleep stages do not appear in any consistent temporal sequence from night to night in a given subject nor in a group of subjects. 2. 2. The typical young adult in our study spent an individually characteristics relative amount of time in each sleep stage each night. 3. 3. The length of stages was short, usually less than 10 min, with the exception of stage 1-REM which ranged up to 39 min in length. Our subjects characteristically changed stages fewer times on successive nights. The number of sleep stage changes differed among subjects. 4. 4. The stage change was usually smooth, moving from one stage to the next when sleep was deepening, but less smooth, often “jumping”.

Studies in congestive heart failure. XXII. A method for obtaining “mixed” venous blood by arterial puncture: Friedman, Ben, Clark, Gurney, and Harrison, T. R.: J. Clin. Investigation 13: 533, 1934

We investigated the interaction between respiration and sleep in ten male outpatients with severe, stable, maximally treated congestive heart failure (CHF). Cheyne-Stokes respiration (CSR), defined as periodic breathing with apnea or hypopnea, was found in all patients with a mean duration of 120±87 minutes [50.2±34.4 percent total sleep time (TST)]. The CSR was found predominantly during stage 1 (20.6±6.7 percent TST) and stage 2 (25.8±6 percent TST) NREM sleep and occurred rarely during slow wave sleep (SWS) (1.6±1 percent TST) and REM sleep (1.6±0.5 percent TST). All apneas and hypopneas were central. Despite normal awake arterial oxygenation (SaO2) (96.1±1.6 percent), significant, severe hypoxemia was found during sleep in seven patients with SaO2 less than 90 percent for 9 to 59 percent TST (mean ± SD, 23 ± 23 percent TST), and this was significantly related to the duration of CSR (r = 0.66, p<0.05). The mean minimum SaO2 for sleep stage was lowest during stage 1 (82.1 percent ±2.6 percent) and stage 2 (78.9 percent ±2.8 percent) NREM sleep, intermediate during REM sleep (84.5 percent ±1.8 percent) and highest during SWS (87.6 percent ±2.7 percent). Sleep was disrupted to a variable extent in all patients with a short mean TST (287±106 minutes), a high proportion of stage 1 sleep (26±19 percent TST), virtual absence of SWS (5±7 percent TST) which was found in only four patients, and a high number of sleep stage changes (30±27/hour) and arousals (28±25/hour). Arousals occurred predominantly during stage 1 (17±20/hour) and stage 2 (10±7/hour) NREM sleep and the majority immediately followed the hyperpneic phase of CSR. The amount of CSR (percent TST) was inversely related to the length of TST (r = –0.73, p<0.05), and directly related to the number of sleep stage changes (r = 0.79, p<0.01) and the number of arousals (r = 0.66, p<0.05). We conclude that in severe, stable CHF, CSR occurs predominantly during light sleep, that despite normal awake arterial oxygen saturation, significant hypoxemia may develop during sleep due to CSR, and that sleep is unstable and disrupted due to frequent arousals caused by the hyperpneic phase of CSR. These sequelae of CSR may be important determinants of the clinical status and outcome of patients with severe CHF.