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At least 937 records · Page 52Linked to original sources
PubMed1995

Sleeping positions and dental arch dimensions in children with suspected obstructive sleep apnea syndrome.

The present paper analyzed the association between children's sleeping positions and dental arch morphology. The sleeping patterns of 27 children, aged 3 to 10 yr, suspected of having the obstructive sleep apnea syndrome (OSAS) were studied by polysomnography (PSG) and videotape recordings under laboratory conditions. The PSG recordings were used to calculate the apnea index (AI) and the relative time spent sleeping on the back, and the videotapes to categorize distinctly different sleep and head postures. Plaster casts were made for the assessment of dental arch morphology. Sleeping predominantly on one's back, was associated with a reduced maxillary intercanine width, while prolonged head extension during sleep correlated inversely with the overjet. The subjects with the highest AI scores (> 4) had larger dental arches. We suggest that sleeping on the back causes a more posterior tongue position, reducing its moulding effect on the anterior dental arch. As nasopharyngeal airway obstruction in OSAS-patients might trigger an anterior tongue position to secure a free airway passage, there will be increased lingual pressure on the dental arches, leading to their dimensional increase.

Child↗
PubMed2005

The effect of sleep onset on upper airway muscle activity in patients with sleep apnoea versus controls.

Pharyngeal dilator muscles are important in the pathophysiology of obstructive sleep apnoea syndrome (OSA). We have previously shown that during wakefulness, the activity of both the genioglossus (GGEMG) and tensor palatini (TPEMG) is greater in patients with OSA compared with controls. Further, EMG activity decreases at sleep onset, and the decrement is greater in apnoea patients than in healthy controls. In addition, it is known that the prevalence of OSA is greater in middle-aged compared with younger men. Thus, we had two goals in this study. First we compared upper airway muscle activity between young and middle-aged healthy men compared with men with OSA. We also explored the mechanisms responsible for the decrement in muscle activity at sleep onset in these groups. We investigated muscle activity, ventilation , and upper airway resistance (UAR) during wakefulness and sleep onset (transition from alpha to EEG activity) in all three groups. Measurements were obtained during basal breathing (BB) and nasal continuous positive airway pressure (CPAP) was applied to reduce negative pressure-mediated muscle activation). We found that during wakefulness there was a gradation of GGEMG and UAR (younger < older < OSA) and that muscle activity was reduced by the application of nasal CPAP (to a greater degree in the OSA patients). Although CPAP eliminated differences in UAR during wakefulness and sleep, GGEMG remained greater in the OSA patients. During sleep onset, a greater initial fall in GGEMG was seen in the OSA patients followed by subsequent muscle recruitment in the third to fifth breaths following the alpha to transition. On the CPAP night, and GGEMG still fell further in the OSA patients compared with control subjects. CPAP prevented the rise in UAR at sleep onset along with the associated recruitment in GGEMG. Differences in TPEMG among the groups were not significant. These data suggest that the middle-aged men had upper airway function midway between that of young normal men and the abnormal airway of those with OSA. Furthermore it suggests that the initial sleep onset reduction in upper airway muscle activity is due to loss of a 'wakefulness' stimulus, rather than to loss of responsiveness to negative pressure, and that this wakefulness stimulus may be greater in the OSA patient than in healthy controls.

Adolescent↗
PubMed2004

Posthypoxic ventilatory decline during NREM sleep: influence of sleep apnea.

We wished to determine the severity of posthypoxic ventilatory decline in patients with sleep apnea relative to normal subjects during sleep. We studied 11 men with sleep apnea/hypopnea syndrome and 11 normal men during non-rapid eye movement sleep. We measured EEG, electrooculogram, arterial O(2) saturation, and end-tidal P(CO2). To maintain upper airway patency in patients with sleep apnea, nasal continuous positive pressure was applied at a level sufficient to eliminate apneas and hypopneas. We compared the prehypoxic control (C) with posthypoxic recovery breaths. Nadir minute ventilation in normal subjects was 6.3 +/- 0.5 l/min (83.8 +/- 5.7% of room air control) vs. 6.7 +/- 0.9 l/min, 69.1 +/- 8.5% of room air control in obstructive sleep apnea (OSA) patients; nadir minute ventilation (% of control) was lower in patients with OSA relative to normal subjects (P < 0.05). Nadir tidal volume was 0.55 +/- 0.05 liter (80.0 +/- 6.6% of room air control) in OSA patients vs. 0.42 +/- 0.03 liter, 86.5 +/- 5.2% of room air control in normal subjects. In addition, prolongation of expiratory time (Te) occurred in the recovery period. There was a significant difference in Te prolongation between normal subjects (2.61 +/- 0.3 s, 120 +/- 11.2% of C) and OSA patients (5.6 +/- 1.5 s, 292 +/- 127.6% of C) (P < 0.006). In conclusion, 1) posthypoxic ventilatory decline occurred after termination of hypocapnic hypoxia in normal subjects and patients with sleep apnea and manifested as decreased tidal volume and prolongation of Te; and 2) posthypoxic ventilatory prolongation of Te was more pronounced in patients with sleep apnea relative to normal subjects.

Analysis of Variance↗
PubMed2002

Tumor necrosis factor (TNF) ligand and TNF receptor deficiency affects sleep and the sleep EEG.

Tumor necrosis factor (TNF) and lymphotoxin-alpha (LT-alpha) are proinflammatory cytokines involved in host defense and pathogenesis of various diseases. In addition, there is evidence that TNF is involved in sleep. TNF and LT-alpha both bind to the tumor necrosis factor receptors (TNFR). Recently, it was shown that TNF receptor 1 (TNFR1) knockout mice (R1KO) sleep less during the light period than controls. We investigated the effect of a TNF and LT-alpha double deficiency on sleep in mice (Ligand KO) and compared their sleep with that of R1KO, TNFR2 knockout (R2KO) mice, and wild-type (WT) controls. All mice were adapted to a 12:12 h light:dark cycle and their electroencephalographs (EEG) and electromyographs (EMG) were continuously recorded during a baseline day, 6-h sleep deprivation (SD), and 18-h recovery. Ligand KO and R2KO had 15% less rapid eye movement (REM) sleep during the baseline light period due to a reduction in REM sleep episode frequency. After SD, all genotypes showed an initial increase in slow-wave activity (SWA) (EEG power density between 0.75 and 4.0 Hz) in non-REM sleep, which gradually declined in the following hours. In Ligand KO the increase was mainly caused by an increase in fast SWA (2.75-4.0 Hz), which was also increased in R2KO. In contrast, in R1KO mice the increase was limited to the slow portion of SWA (0.75-2.5 Hz). R2KO and WT mice showed increases in both frequency ranges. The sub-division into fast and slow SWA frequencies corresponds to previous electrophysiological data where the two types of slow-waves were induced by either excitatory or inhibitory stimuli. Our data suggest that in Ligand KO the SWA increase is caused by an increase in excitatory input to the cortex, whereas in R1KO this input seems to be almost absent.

Animals↗
PubMed1985

Evaluation of the effects of antiepileptic drugs on sleep-wakefulness patterns following 1 night total sleep deprivation in epileptic patients.

Sleep-wakefulness patterns recorded following 1 night total sleep deprivation were studied in 15 normal subjects and in 252 epileptic patients. The patients were taking various types and combinations of antiepileptic medication. Sleep deprivation caused a reduction in sleep latency and an increase in NREM stage 3 + 4 sleep. This effect persisted in patients treated with valproate sodium and/or carbamazepine. In patients treated with diphenylhydantoin light NREM 1 + 2 sleep increased. In those treated with antiepileptics + chlorazepate, both an increase in NREM 1 + 2 and NREM 3 + 4 sleep was seen. The former probably reflects a benzodiazepine effect, the latter is due to a sleep deprivation effect. In patients treated with antiepileptics + clonazepam, a benzodiazepine effect predominated.

Adolescent↗
PubMed1994

Acute effects of transdermal nicotine on sleep architecture, snoring, and sleep-disordered breathing in nonsmokers.

Previous research has suggested that nicotine may be therapeutically useful in the treatment of sleep-disordered breathing. The development of transdermal nicotine delivery systems has allowed us to test the overnight effectiveness of nicotine. Twenty nonsmoking subjects (10 men, 10 women) were recruited on the basis of a history of habitual snoring that was confirmed by overnight laboratory monitoring. Subjects were then randomized (double-blind crossover design) to receive either placebo or an active patch that delivers 11 mg of nicotine over a 24-h period. Patches were applied at 6 P.M. and removed at 6 A.M. the following morning, at which time venous blood was obtained for determination of serum nicotine concentrations. Polysomnography was performed using standard techniques to assess sleep architecture and sleep-disordered breathing. Snoring was monitored with a sound-level meter and quantitatively analyzed to determine the snoring index (SI) (number of snores per hour of sleep) and mean and maximum snoring intensities. The age of the subjects was 46.9 +/- 11.4 yr (mean +/- SD) and their mean body mass index (BMI) 33.3 +/- 4.6 kg/m2. A mean nicotine level was nondetectable with placebo and 7.8 +/- 2.3 ng/ml with wearing of an active patch. Nicotine decreased total sleep time (TST) by 33 min (p < or 0.01), sleep efficiency from 89.7 to 83.5% (p < or = 0.01), and percent rapid eye movement (REM) sleep from 18.8 to 15.1% (p < or = 0.01), and prolonged initial sleep latency (ISL) from 6.7 to 18.2 min (p < or = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗
PubMed1989

Abnormal breathing during sleep and chemical control of breathing during wakefulness in patients with sleep apnea syndrome.

The possible role of ventilatory control in relation to sleep apnea has not yet been clarified. We investigated the relationship between awake ventilatory drives to hypoxia and hypercapnia and sleep-disordered breathing in 21 subjects with sleep apnea syndrome. The awake hypoxic ventilatory drive, which was evaluated by occlusion pressure responses, was inversely correlated with the magnitude of maximal oxygen desaturation during sleep as well as the ratio of duration with more than 4 and 10% oxygen desaturation to total sleep time. On the other hand, the awake hypercapnic ventilatory drive was not correlated with these parameters of sleep desaturation. Apnea index and duration were not correlated with the degree of hypoxic or hypercapnic ventilatory drive, respectively. Our study concluded that sleep desaturation is better correlated with hypoxic ventilatory drive than with hypercapnic ventilatory drive in patients with sleep apnea syndrome. These results are different from the results obtained in the patients with COPD in our previous study.

Adult↗
PubMed1990

Estimation of the probability of disturbed breathing during sleep before a sleep study.

We have investigated the ability of a statistical model developed from clinical data and questionnaire responses to predict disturbance of breathing during sleep. Data from 100 consecutive patients referred for sleep study for suspected sleep apnea were used to develop the model using logistic regression analysis. For each subject, the model predicted the probability of having an apnea-hypopnea index (AHI) greater than 15; this probability was compared with the AHI measured from sleep study. A probability cutoff point (= 0.15) was decided on that minimized the number of subjects with false-negative predictions. Four terms--apneas observed by bed partner, hypertension, body mass index, and age--were found to contribute significantly to the model with observed apneas being by far the most predictive term of the four (adjusted odds ratio 19.7). When the model was tested to estimate the probability of an AHI greater than 15 for 105 patients from a second group of consecutive patients referred for sleep study, the model correctly classified 33 of 36 patients with a measured AHI greater than 15 (sensitivity = 92%) and 35 of 69 patients with a measured AHI less than or equal to 15(specificity = 51%). This study shows that analysis of clinical features of patients presenting with suspected sleep apnea may reduce the need for sleep studies by about one-third yet still lead to the identification of the great majority of patients with abnormal breathing during sleep.

Female↗
PubMed1993

Effects of one night without nasal CPAP treatment on sleep and sleepiness in patients with obstructive sleep apnea.

Nasal continuous positive airway pressure (CPAP) has become the nonsurgical treatment of choice for obstructive sleep apnea syndrome (OSAS). Recent evidence suggests that intermittent use of CPAP by patients is more common than nightly compliance. To determine the consequences of intermittent CPAP use, in terms of a return of sleep-disordered breathing and daytime hypersomnolence, 15 OSAS subjects were evaluated at three times: (1) before CPAP treatment (pretreatment), (2) after 30 to 237 days posttreatment during a night of CPAP use (on CPAP), and (3) during a night without CPAP (off CPAP). Evaluations of sleep-disordered breathing and three domains of hypersomnolence, physiologic sleep tendency, subjective sleepiness, and performance, were accomplished with the respiratory disturbance index (RDI), multiple sleep latency test (MSLT), Stanford sleepiness scale (SSS), and psychomotor vigilance task (PVT), respectively. CPAP use was encouraged and monitored from pretreatment to post-treatment by daily diaries for most subjects and an electronic device for a subset of subjects. As expected, CPAP eliminated apneas and hypopneas, and following the on CPAP night, there were statistically significant improvements in objective measures of sleepiness (MSLT and PVT). Subjective measures of sleepiness and fatigue also showed improvement. Sleeping without CPAP for one night reversed virtually all of the sleep and daytime alertness gains derived from sleeping with CPAP. This occurred despite a statistically significant reduction in the RDI on the night off CPAP (M = 36.8, SD = 28.0 events/h) relative to the pretreatment night (M = 56.6, SD = 24.8 events/h), which may be due to a lessening of the edema of the upper airway following CPAP use.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Genioglossus activity in children with obstructive sleep apnea during wakefulness and sleep onset.

A prominent role for upper airway neuromuscular control mechanisms in the pathophysiology of pediatric obstructive sleep apnea syndrome (OSAS) is suggested by the observation that obstruction does not occur during wakefulness and is infrequently seen during non-REM sleep. Using a custom intraoral surface electrode to record genioglossal activity (genioglossal electromyography [EMGgg]), normalized with a maximal maneuver, we studied 10 children with OSAS and 6 normal control subjects to determine EMGgg activity during (1) wakefulness, (2) the sleep onset period, and (3) stable non-REM sleep. We observed that the EMGgg activity in patients with OSAS compared with control subjects was significantly greater during wakefulness (3.6 +/- 1.8 vs. 1.6 +/- 1.8% maximum, p < 0.05) and had a greater decline during the early and late sleep onset period (p < 0.05). During stable non-REM sleep, EMGgg remained below the wakeful baseline in all normal control subjects but increased above the baseline in four of the patients with OSAS. We speculate that the increased EMGgg activity during wakefulness represents a reflex-driven neuromuscular compensation for an anatomically compromised airway. Furthermore, the larger decline in EMGgg at sleep onset observed in patients with OSAS is consistent with the relative loss of this reflex. Finally, the return of EMGgg activity above baseline in patients with severe OSAS suggests that some chemical or mechanical compensatory mechanisms remain active during stable non-REM sleep in children.

Adolescent↗
PubMed2004

Genioglossus activity during sleep in normal control subjects and children with obstructive sleep apnea.

Children with obstructive sleep apnea syndrome (OSAS) have more collapsible airways compared with normal subjects, yet sustain stable breathing during wakefulness and part of sleep. This indicates successful neuromuscular compensation. Using a custom intraoral surface electrode to record pharyngeal dilator muscle activity (the genioglossus [EMGgg] normalized to the wakeful baseline), we performed overnight polysomnograms in three groups of children: (1) patients with OSAS without continuous positive airway pressure (CPAP) (n = 13); (2) patients with OSAS with CPAP (n = 5); and (3) control subjects without CPAP (n = 13). Our objective was to evaluate the EMGgg as a function of sleep state and during disordered breathing, compared with stable sleep and wakefulness. In control subjects, the EMGgg decreased from wakefulness to Stage 2 (mean +/- SD, 65 +/- 6%), and further during REM (51 +/- 9%) (p < 0.05). In patients with OSAS, the EMGgg for apneic breaths during REM (37 +/- 9%) was lower than during stable breathing (83 +/- 17%) (p < 0.05) and wakefulness (p < 0.05). CPAP lowered the EMGgg in patients with OSAS during all sleep states. These data indicate that (1) EMGgg compensatory mechanisms remain active during sleep in patients with severe OSAS; (2) EMGgg reductions are temporally associated with sleep apnea events; and (3) REM sleep is associated with the lowest and most variable EMGgg.

Adolescent↗
PubMedDate not supplied

Brighton sleep survey: a study of sleep in 20-45-year olds.

A total of 2714 people, aged 20-45 years from the Brighton area who completed a questionnaire were interviewed on their sleep patterns and complaints, medication, behavioural aids, and consumption of caffeine and alcohol. Analysis showed that 24% had delayed sleep onset, 23% awakened frequently, 19% awakened early, 21% were dissatisfied with sleep, and 8% took medication to aid sleep. Of those on night shifts, 29% awakened frequently and 25% awakened early. There were 648 responses describing behavioural sleeping aids. The moderate consumption of caffeine and alcohol had no significant effect on sleep. The main differences between this survey and other published data relate to the comparison of sleep reports from men with those from women, the sleep of nightshift and dayshift workers and the effects of caffeine and alcohol. These differences may arise from sampling characteristics and the form of the questionnaire.

Adult↗
PubMed2001

Importance of sleep stage- and body position-dependence of sleep apnoea in determining benefits to auto-CPAP therapy.

The influence of sleep stage- and body position-dependence of sleep apnoea on treatment efficacy and compliance between conventional continuous positive airway pressure (CPAP) and auto CPAP therapy was evaluated. Thirty-three newly treated sleep apnoea hypopnoea syndrome (SAHS) patients were randomly allocated to conventional or auto-CPAP therapy. Six patients of each treatment group were classified as having sleep stage- and body position-dependent obstructive breathing abnormalities according to the results of the baseline sleep study. After 3 weeks of treatment, the Epworth sleepiness score tended to be higher (p = 0.08) and the ability to stay awake lower (p = 0.02) in patients with dependent breathing abnormalities treated with fixed CPAP, than in the other patients. The effective pressure/time index was significantly lower in sleep stage- and body position-dependent patients treated with fixed CPAP, than in the other patients (p = 0.02). The number of hours the machine was turned on and a positive pressure applied, tended to be smaller in dependent patients treated with fixed CPAP than in independent patients of this treatment group and in patients treated with auto-CPAP. A night-to-night variability index (VI) of positive pressure changes was obtained in the auto-CPAP group. This index significantly decreased with time in the dependent patients while it remained unchanged in the independent group. It is concluded that auto-continuous positive airway pressure may have specific indications in a subset of obstructive sleep apnoea patients with sleep stage- and body position dependent nocturnal breathing abnormalities.

Adult↗
PubMed1996

Overnight growth hormone secretion in achondroplasia: deconvolution analysis, correlation with sleep state, and changes after treatment of obstructive sleep apnea.

The normal profile for overnight GH secretion in achondroplasia has not been previously studied. Factors that have been shown to influence GH secretion include age, obesity, sleep state, and the presence of obstructive sleep apnea (OSA). We assessed GH levels in a group of subjects with achondroplasia, during overnight polysomnography. Nineteen subjects with achondroplasia were studied at 11.3 y of age (median 6.7, range 1.8-30.9). Levels of GH were measured using time-resolved immunofluorometric assay (DELFIA, Pharmacia Biotech Inc.) and analyzed by a deconvolution method. Five subjects were restudied after treatment for OSA. Secretion rates of GH were greater in slow wave (SWS) and rapid eye movement (REM) sleep than in stage one and two (SI-II = light non-REM) sleep (p < 0.01). Total overnight GH secretion decreased with increasing age (r2 = 0.22 p < 0.04). Neither the frequency of arousals, frequency of sleep state transitions nor the severity of OSA correlated with measures of GH secretion. Levels of IGF-I correlated independently with age, body weight (percent ideal), and GH secretion rate (r2 = 0.76, p < 0.001). In a group of five subjects treated for OSA, improved respiratory distress index and reduced sleep state transitions were not associated with significant changes in GH secretion rate by sleep stage; SWS [from 0.62 +/- 0.28 mIU/L/min to 1.02 +/- 0.25 mIU/L/min (NS)] and SI-II sleep [from 0.26 +/- 0.07 mIU/L/min to 0.60 +/- 0.16 mIU/L/min (NS)]. However, in those five subjects, a GH secretion peak during the first 2 h of SWS was initially absent, appearing only after treatment of OSA (1.09 +/- 0.38 mIU/L/min) compared with (2.40 +/- 0.59 mIU/L/min (p = 0.01). A profile of overnight GH secretion is presented for subjects with achondroplasia.

Achondroplasia↗
PubMed1991

Breathing during sleep in patients treated for obstructive sleep apnea. Nasal CPAP for only part of the night.

To determine whether long-term NCPAP therapy influences severity of sleep disordered breathing during the second part of a night when NCPAP is applied for only the first four hours of sleep, we studied 21 patients with OSA receiving NCPAP therapy for 253 +/- 41.6 days. Results from polysomnography for the period after withdrawal from NCPAP (night B) were compared to the corresponding period of sleep prior to initiation of NCPAP therapy (night A). There was no significant change in RDI from night A (53.9 +/- 8.6) to night B (28.7 +/- 3.3), but maximal apnea length diminished from 55 +/- 2.9 s to 40 +/- 2.9 s (p less than 0.05). Whereas daytime Po2 and the amplitude of desaturations during sleep remained equal, overall oxygenation during sleep improved slightly (mean SaO2 night A = 90.6 +/- 0.9 percent; night B = 92.8 +/- 0.5 percent; p less than 0.05). Differences between nights A and B were more prominent the more severe sleep apnea had been prior to treatment and could not be explained by weight loss. There was strong correlation between improvements in oxygenation measurements and the daily time of NCPAP use. In conclusion, we found a subgroup of OSA patients receiving long-term NCPAP therapy with less disturbed ventilation during sleep following use of NCPAP for only the first part of the night, but in the majority of patients, sleep disordered breathing off NCPAP remained unchanged.

Female↗
PubMed2005

Effects of valerian extract on the sleep-wake cycle in sleep-disturbed rats.

The present study was performed to investigate the effects of valerian extract on the sleep-wake cycle using sleep-disturbed model rats. A significant shortening in sleep latency was observed with valerian extract at doses of 1000 and 3000 mg/kg. On the other hand, valerian extract had no significant effects on total times of wakefulness, non-rapid eye movement (non-REM) sleep, or REM sleep, even at a dose of 3000 mg/kg. Valerian extract at doses of 1000 and 3000 mg/kg showed a significant increase in the delta activity during non-REM sleep. In conclusion, valerian extract may be useful as an herbal medicine having not only sleep-inducing effects but also sleep quality-enhancement effects.

Animals↗
PubMed1985

Recovery of performance during sleep following sleep deprivation in older normal and insomniac adult males.

Groups of 12 normal and insomniac male subjects aged 55 to 71 yr. were sleep deprived for 64 hr. In both groups, the sleep loss was preceded by four baseline sleep nights and followed by four recovery nights. Reaction time, immediate recall, sleepiness, and body temperature were measured at approximately 2300, 0115, 0330, 0530, and 0800 during baseline, deprivation and recovery nights. Significant performance or mood differences were not found between the normal and insomniac males on any measure or at any testing period throughout the study. Performance of both groups declined characteristically during sleep loss while subjective sleepiness increased. As in young adults, degraded performance was restored by 8 hr. of recovery sleep. However, subjective sleepiness did not return to baseline levels until early in the second recovery night. It was concluded that chronic insomnia does not result in group performance deficits similar to those seen after chronic sleep loss; and the restorative function of sleep operates as efficiently in older insomniac subjects (who apparently have reduced need to sleep) as in older normal subjects.

Aged↗
PubMed1999

[Methods of sleep induction for EEG recordings: comparison between three hypnotics and natural sleep].

We compared the effects of three oral hypnotics, monosodium trichloroethyl phosphate (MTP), chloral hydrate (CH), and pentobarbital calcium (PTB), to those of non-medication on wake-sleep states and sleep activation of epileptic seizure discharges. The subjects consisted of 410 epileptics and 171 non-epileptic outpatients (mean age: 12.5 years) of the Department of Pediatrics, Nagoya City University Hospital. Complete EEG records including awake and sleep states were obtained in 230/241 (95%) of patients with MTP, 20/22 (91%) of those with CH, 72/85 (85%) of those with PTB, and 225/233 (97%) of those without any hypnotics. There were no statistically significant differences in the effect of sleep induction among the four groups. Sleep activation effects were observed in 25% of patients with natural sleep and 35% of those with induced sleep. There was no statistical difference (p > 0.05). These results suggested MTP, CH, and PTB are useful hypnotics for sleep EEG recordings.

Adolescent↗