Percentage Of Total Sleep Time Research Articles

High prevalence of previously unknown subclinical hypothyroidism in obese patients referred to a sleep clinic for sleep disordered breathing

To evaluate the prevalence of previously unknown hypothyroidism in adult male and female patients with a wide range of body mass index (BMI) values, referred to a Sleep Clinic because of sleep disordered breathing (SDB). Serum concentrations of thyroid stimulating hormone (TSH) and free thyroxin (fT4), as well as forced vital capacity (FVC), PaO2, PaCO2, the Epworth sleepiness scale (ESS), respiratory disturbance index (RDI), loud snoring, and the percentage of total sleep time (TST) with <90% oxyhemoglobin saturation (TST(saO2<90%)) were measured in 78 overweight and obese adult subjects with no previous diagnosis of hypothyroidism (age: 18-72 years). The prevalence of previously undiagnosed subclinical hypothyroidism in the population as a whole was 11.5%. BMI, TSH and ESS were significantly higher in the hypothyroid than the euthyroid subjects, but there was no significant between-group difference in RDI, TST(saO2<90%) or the other investigated variables, including the prevalence of obstructive sleep apnea (OSA). Among the hypothyroid individuals, BMI, neck circumference, ESS, RDI and TST(Sao2<90%) were significantly higher in those with than in those without OSA. Furthermore, there was a clear trend towards a lower FVC% and higher snoring score in the OSA patients. Our results demonstrate a higher prevalence of hypothyroidism than that commonly reported in overweight and obese individuals referred to a Sleep Clinic for polysomnography because of SDB, thus suggesting that thyroid function should be evaluated in all obese patients suffering from SDB despite economic concerns.

Sleep pressure score: a new index of sleep disruption in snoring children.

Excessive daytime sleepiness (EDS), as measured by objective criteria, is infrequent in snoring children despite a high prevalence of EDS-related behavioral manifestations. We hypothesized that sleep architecture and arousal indexes may be altered relative to the severity of sleep-disordered breathing (SDB). Retrospective and prospective study. Questionnaires were distributed through sleep clinic or school program; polysomnograms were performed at Kosair Children's Hospital in Louisville, Kentucky. To examine this issue, 182 children with SDB, 163 children with primary snoring, and 214 control children with a mean age of 6.9 +/- 2.6 years underwent polysomnographic evaluation in the laboratory. Significant increases in slow-wave sleep (percentage of total sleep time) and decreases in rapid eye movement sleep (percentage of total sleep time) occurred in the SDB group (P < .0001). Spontaneous and respiratory arousal indexes and the apnea-hypopnea index (AHI) displayed negative and positive correlations, respectively, suggesting reciprocal interactions. Based on these observations, a sleep pressure score (SPS) was derived as a surrogate numeric measure for disrupted sleep homeostasis. The SPS exhibited linear increases relative to AHI, reaching a plateau at an AHI of 30 to 40 per hour of total sleep time. Furthermore, SPS values were significantly higher among African American and obese children (P < .0001). Sleep architecture is not preserved in children with SDB. An algorithm allowing for calculation of sleep propensity and disturbed sleep homeostasis in children who snore is proposed and may be of practical value in the assessment of sleepiness.

Diurnal PaCO2 tension in obese women: relationship with sleep disordered breathing.

Several obese subjects show a wide array of respiratory disturbances during sleep due to an increased upper-airway resistance. The aim of the present study was to evaluate diurnal PaCO(2) tension in nonsmoking obese women and the possible relationship of this parameter with the presence of sleep disordered breathing (SDB). Cross-sectional study of PaCO(2) tension in obese women. A total of 91 nonsmoking obese women (BMI > or =30 kg/m(2), aged 42.8+/-15.7 y) were recruited and evaluated for general and anthropometric parameters, respiratory function, sleep-related symptoms, and sleep disorders of breathing. A total of 10 subjects (10.9%) had diurnal hypercapnia (PaCO(2)> or =43 mmHg). Age, BMI, neck circumference, apnoea/hypopnoea index, and nocturnal desaturation (expressed as TST(SaO(2<90%)); TST(SaO(2<90%))=percentage of total sleep time with oxyhaemoglobin saturation <90%) were significantly higher in obese patients with diurnal hypercapnia, compared to normocapnic women. Moreover, hypercapnic patients had reduced forced expiratory volume in 1 s compared to normocapnic individuals. By using multiple regression analysis, the best fitting model (r=0.62, P<0.001) for predicting diurnal PaCO(2) tension in the study population showed that 24.23% of the variance may be explained by TST(SaO(2<90%)), according to the equation: PaCO(2)=0.09 age+0.07 TST(SaO(2<90%))+33.00. This study suggests that severity of SDB is the most important factor in determining diurnal PaCO(2) tension in apparently healthy nonsmoking obese women.

The role of mean inspiratory effort on daytime sleepiness.

This study has investigated the role of average maximum inspiratory effort in excessive daytime sleepiness in patients with obstructive sleep apnoea syndrome (OSAS) and upper airway resistance syndrome (UARS). Fifteen patients diagnosed with UARS and 32 patients with OSAS, with >5.5 h total sleep time (TST) during 8 h of nocturnal polygraphic recordings, were included in the study. Demographical data, polysomnographical data and data about daytime sleepiness, including Epworth sleepiness scale (ESS) and multiple sleep latency test (MSLT), were evaluated. In order to compute the average maximum inspiratory effort from oesophageal pressure (Poes) measurements, maximum Poes was obtained from 20 representative obstructive respiratory events (obstructive apnoeas, hypopnoeas or flow limitations) for each sleep stage in both supine and side positions. From Poes measurements during sleep, the increase in Poes (deltaPoes) during respiratory events was also calculated. The average maximum Poes, deltaPoes, respiratory disturbance index (RDI) and arousal index were significantly correlated with ESS in OSAS patients. In patients with UARS, the only significant correlation was obtained between average maximum Poes and ESS. The MSLT score did not show any significant correlation with arousal index, number of stage variations, RDI, average Poes, deltaPoes, minimum oxygen saturation (Sa,O2) and percentage of TST with an Sa,O2 <90% in both UARS and OSAS patients. The results of multiple regression analysis showed that average maximum Poes correlates best with the variance in ESS for OSAS patients. In conclusion, the data from this study indicate the possible important role of average inspiratory effort in determining subjective sleepiness in both obstructive sleep apnoea syndrome and upper airway resistance syndrome patients.

The Effects of Hormone Replacement Therapy on Sleep-Disordered Breathing in Postmenopausal Women: A Pilot Study

To evaluate the impact of estrogen and estrogen plus progesterone hormone-replacement therapy (HRT) on mild-to-moderate sleep-disordered breathing (SDB) in postmenopausal women. Within-subjects, progesterone placebo-controlled prospective HRT trial in a clinical laboratory. Six postmenopausal women, diagnosed with mild-moderate SDB. Transdermal estradiol and oral micronized progesterone. Subjects underwent polysomnography (PSG) on four occasions: a screening/adaptation night; a baseline night on no HRT; and two nights on HRT: one night after 7 to 12 days on estrogen plus placebo followed by a second night after 7-13 days on estrogen plus progesterone. The PSG was performed with a Sandman computerized PSG system using a standard clinical montage. Modified sleep diaries were used in the baseline week and throughout the study period. Mood was measured with the 20-item version of the Positive and Negalive Affect Schedule (PANAS). Estrogen monotherapy was associated with a significant reduction in the overall apnea-hypopnea index (AHI) (from a mean of 22.7 events per hour at baseline to a mean of 12.2 events per hour), but the AHI reduction on estradiol plus progesterone relative to baseline was not statistically significant (AHI=16.2 events per hour). Similar results were found for the percentages of total sleep time and of total non-rapid eye movement sleep time with oxygen saturation less than 90%. Estrogen, neither alone nor in combination with progesterone, significantly altered PSG- or diary-based measures of total sleep time, time to sleep onset, or time awake after sleep onset. While the data are preliminary and based on a small number of subjects, estrogen appeared to have a substantial beneficial effect on measures of SDB in postmenopausal women. Overall, no additional benefit was seen with the addition of progesterone. In fact, progesterone attenuated the beneficial effects of estrogen in 4 out of the 6 participants.

Sleep organization is unaffected by caffeine in premature infants

We performed 10-hour polysomnographic recordings in 15 neurologically normal and clinically stable 33- to 34-week postmenstrual age (PMA) neonates, 10 of whom had been treated >3 days with once-per-day oral caffeine citrate (5 mg/kg) given at ~2 PM. We analyzed (a) the usual sleep-wake variables, including wakefulness, active sleep, quiet sleep, and indeterminate sleep expressed as the number of episodes, duration, and percentage of total sleep time; (b) the duration and order of variable modifications during transitions between the main active sleep and quiet sleep states; and (c) the characteristics of morning data (before caffeine) compared with evening data (after caffeine). We found no significant differences between the controls and the infants receiving maintenance caffeine. (J Pediatr 2002;140:766-71)

Night-to-night variability in sleep in cystic fibrosis

Objectives: The impact of night-to-night variability (NNV) on polysomnography (PSG) has been reported mainly in normal subjects, the elderly and patients with obstructive sleep apnea with focus on changes in the apnea/hypopnea index, rather than measures of nocturnal oxygenation. There is very limited data on NNV in patients with cystic fibrosis (CF). The goal of this study was to assess for first-night effect and reliability of PSG measurements on nocturnal oxygenation and respiratory disturbance in CF. Methods: A prospective observational study was performed in patients with CF who consented to PSG on two consecutive nights. Paired t-tests and intra-class correlation coefficients (ICCs) were calculated for repeated measures of sleep stage time, sleep efficiency, arousal indices, measures of nocturnal oxygenation, and respiratory events in all sleep stages. Results: Thirty-one patients with CF were studied, aged 27±8 (mean±1SD) years and forced expiratory volume in 1 s (FEV 1) of 37±11% of predicted. Relative to the first-night PSG, on the second PSG, we observed the following: shorter latency to rapid eye movement (REM) sleep ( P<0.001), increased sleep efficiency ( P<0.01), decreased wake after sleep onset (WASO) time ( P<0.01), decreased percentage of non-REM time with oxyhemoglobin saturation by pulse oximetry (SpO 2)≤90% ( P<0.05), decreased number of central apneas per hour ( P<0.05) and reduced respiratory rate in stage 2 sleep on night 2 ( P<0.05). Despite these changes, the ICCs between night 1 and night 2 showed good repeatability/reliability for measures of nocturnal oxygenation and indices of respiratory disturbance, including the percentage of total sleep time with SpO 2≤90% (ICC=0.85) and apnea-hypopnea index (ICC=0.75). Likewise, the ICCs were extremely high for respiratory rate in stage 2 (ICC=0.94), slow wave sleep (ICC=0.97), and REM sleep (ICC=0.96). Conclusion: Although a first-night effect is seen with sleep efficiency, REM latency, and WASO, a single-night PSG in patients with CF yields reliable information on nocturnal oxygenation and respiratory disturbance.

Sleep apnea syndrome: a possible contributing factor to resistant.

There is evidence supporting an association between sleep apnea and hypertension. However, it is not clear if sleep apnea interteres with the pharmacotherapy of hypertension. To investigate this question, we studied the relationship between the effectiveness of anti-hypertensive treatment in reducing blood pressure, and severity of sleep apnea in a large group of apneic patients referred to a sleep disorders centre at St. Michael's Hospital at the University of Toronto. N/A. N/A. 1,485 adult patients with sleep apnea, as defined by the apnea/hypopnea index (AHI) >10 events/hr, were analyzed. There were 393 who reported using anti-hypertensive medications on a regular basis for more than 6 months. One hundred and eighty-three patients were treated "effectively" (i.e. blood pressure lower than 140/90 mm Hg in the morning and in the evening). Seventy-four patients were treated "ineffectively," defined as blood pressure >140/90 mm Hg in the morning or in the evening. Both groups were compared with respect to clinical and demographic data using analysis of covariance with gender, age, body mass index (BMI), and neck circumference (NC) as covariates. N/A. Ineffectively and effectively treated patients were similar in age (57 +/- 9) vs. 57 +/- 10 years, respectively), and had similar body mass index (33.8 +/- 7.4 vs. 33.4 +/- 7.3 kg/m2, respectively). However, ineffectively treated patients had significantly higher apnea/hypopnea index (44 +/- 29 vs. 33 +/- 25 events/hr, p<.0005), despite having similar nocturnal oxygenation (percent of total sleep time spent with oxygen desaturation lower than 90% was 36 +/- 34 vs. 29 +/- 30% in the ineffective and effective groups, respectively). The difference in AHI persisted even after adjusting for age, gender, and body mass index. Our results demonstrate that hypertensive patients with sleep apnea whose blood pressure responds beneficially to treatment have less severe sleep apnea than those patients whose blood pressure remains elevated despite anti-hypertensive therapy. Since neither obesity nor nocturnal hypoxemia appear to be important determinants of ineffective treatment, we suggest that resistant hypertension may be caused by frequent intermittent sympathetic stimulation.

High frequency repetitive transcranial magnetic stimulation (rTMS) of the left dorsolateral cortex: EEG topography during waking and subsequent sleep

Repetitive transcranial magnetic stimulation (rTMS) is a novel research tool in neurology and psychiatry. It is currently being evaluated as a conceivable alternative to electroconvulsive therapy for the treatment of mood disorders. Eight healthy young (age range 21–25 years) right-handed men without sleep complaints participated in the study. Two sessions at a 1-week interval, each consisting of an adaptation night (sham stimulation) and an experimental night (rTMS in the left dorsolateral prefrontal cortex or sham stimulation; crossover design), were scheduled. In each subject, 40 trains of 2-s duration of rTMS (inter-train interval 28 s) were applied at a frequency of 20 Hz (i.e. 1600 pulses per session) and at an intensity of 90% of the motor threshold. Stimulations were scheduled 80 min before lights off. The waking EEG was recorded for 10-min intervals ∼30 min prior to and after the 20-min stimulations, and polysomnographic recordings were obtained during the subsequent sleep episode (23.00–07.00 h). The power spectra of two referential derivations, as well as of bipolar derivations along the antero-posterior axis over the left and right hemispheres, were analyzed. rTMS induced a small reduction of sleep stage 1 (in min and percentage of total sleep time) over the whole night and a small enhancement of sleep stage 4 during the first non-REM sleep episode. Other sleep variables were not affected. rTMS of the left dorsolateral cortex did not alter the topography of EEG power spectra in waking following stimulation, in the all-night sleep EEG, or during the first non-REM sleep episode. Our results indicate that a single session of rTMS using parameters like those used in depression treatment protocols has no detectable side effects with respect to sleep in young healthy males.

Nocturnal oximetry in infants with cystic fibrosis

AIMTo investigate whether children with cystic fibrosis under 3 years of age have disordered breathing and episodes of oxygen desaturation during sleep.METHODSWe studied 19 infants (9 boys and 10 girls)...

Does obstructive sleep apnea confound sleep architecture findings in subjects with depressive symptoms?

Background: Compared with normal subjects, depressed patients have shorter rapid eye movement sleep latency (REML), increased REM and decreased slow wave sleep as a percentage of total sleep time (REM%, SWS%), and longer sleep latency (SL). Obstructive sleep apnea (OSA) patients experience longer REML, decreased REM% and SWS%, and shorter SL. We examined the interplay of depressive symptoms, OSA, and sleep architecture. Methods: Subjects ( n = 106) were studied with polysomnography. OSA was defined as a Respiratory Disturbance Index ≥15. Subjects were divided into Hi/Lo groups using a Center for Epidemiological Studies—Depression (CES-D) score of 16. Results: OSA patients had shorter SL than non-OSA patients (14.5 vs. 26.8 min, p < .001); Hi CES-D subjects showed a trend toward longer SL than Lo CES-D subjects (23.7 vs. 17.5 min, p = .079). Significant OSA × CES-D interactions emerged, however, for REM% ( p = .040) and SL ( p = .002): OSA/Hi CES-D subjects had higher REM% than OSA/Lo CES-D subjects (19.3% vs. 14.3%, p = .021); non–OSA/Hi CES-D subjects had SL (35.3 min) 2–3 times as long as other subjects ( p = .002–.012). Conclusions: Because of the high prevalence of OSA and depression, findings suggest that OSA must be considered in studies of mood and sleep architecture. Conversely, depressive symptoms must be considered in studies of OSA and sleep architecture.

Pulmonary arterial hypertension in patients with sleep apnoea syndrome

BACKGROUNDPulmonary arterial hypertension (PAH) in patients with sleep apnoea syndrome (SAS) is classically ascribed to associated chronic obstructive pulmonary disease (COPD). The aim of this retrospective study was to evaluate...

Sleep architecture, slow wave activity, and sleep spindles in adult patients with sleepwalking and sleep terrors

Objectives: A very strong SWS intensity reflected by both an increased level of SWA and an abnormal sleep spindles distribution would be responsible for the major difficulty of parasomniac subjects in waking up from SWS, leading to episodes of parasomnia.Methods: Eleven adult parasomniac subjects, 6 females and 5 males, with sleepwalking (SW) and/or sleep terrors (ST) and 11 age- and sex-matched control subjects underwent polysomnography (PSG) during 2 consecutive nights. After an habituation and selection night followed by a 16 h period of controlled wakefulness, the sleep EEGs of the parasomniac and control subjects were analyzed on the second night by computer-aided visual scoring (integrated digital filtering analysis, IDFA) and spectral analysis (fast Fourier transform, FFT). Throughout the night subject behaviour was controlled and recorded by means of a video infra-red camera and videotape recorder.Results: Fifteen episodes of parasomnia were recorded during the second night in the 11 subjects. Sleep analysis showed significantly (P<0.05) decreased sleep efficiency and stage 2 sleep (absolute values and percentage of total sleep time) and increased (P<0.05) slow wave sleep (absolute values and percentage of total sleep time). Arousal index and wake-time after sleep onset were significantly higher in parasomniac subjects. Sleep fragmentation was mainly concentrated in stages 3 and 4. The slow wave activity (SWA) absolute values averaged during the 2 min immediately preceding an episode of parasomnia were significantly higher than the SWA averaged during 2 min in the same stage 10 min before an episode of parasomnia. Moreover, SWA was higher in the slow wave sleep (SWS) episodes preceding the episode of parasomnia than in the episodes preceding an awakening without an episode of parasomnia. The temporal course of SWA showed a slower exponential decay in both groups, but the time constant of the curve was larger in parasomniacs than in controls. Finally, in control subjects the sleep spindle index increased from the beginning to the end of the night while it was equally distributed in parasomniacs.Conclusions: An abnormal deep sleep associated with a high SWS fragmentation might be responsible for the occurrence of SW or ST episodes.

Effects of continuous positive airway pressure on sleep apnea and ventricular irritability in patients with heart failure.

Patients with heart failure and systolic dysfunction may develop disordered breathing during sleep. Repeated episodes of apnea and hypopnea may result in desaturation and arousals, which could adversely affect left ventricular function. The purpose of this study was to determine the short-term effects of continuous positive airway pressure (CPAP) on sleep-disordered breathing and its consequences in heart failure patients. The author prospectively studied 29 male patients whose initial polysomnograms showed 15 or more episodes of apnea and hypopnea per hour (apnea-hypopnea index, AHI). Twenty-one patients had predominately central and 8 patients obstructive sleep apnea. All were treated with CPAP during the subsequent night. In 16 patients, CPAP resulted in virtual elimination of disordered breathing. In these patients, the mean AHI (36+/-12 [SD] versus 4+/-3 per hour, P=0.0001), arousal index due to disordered breathing (16+/-9 versus 2+/-2 per hour, P=0.0001), and percent of total sleep time below saturation of 90% (20+/-23% to 0.3+/-0.7%, P=0.0001) decreased, and lowest saturation (76+/-8% versus 90+/-3%, P=0.0001) increased with CPAP. In 13 patients who did not respond to CPAP, these values did not change significantly. In patients whose sleep apnea responded to CPAP, the number of hourly episodes of nocturnal premature ventricular contractions (66+/-117 versus 18+/-20, P=0.055) and couplets (3.2+/-6 versus 0.2+/-0.21, P=0.031) decreased. In contrast, in patients whose sleep apnea did not respond to CPAP, ventricular arrhythmias did not change significantly. In 55% of patients with heart failure and sleep apnea, first-night nasal CPAP eliminates disordered breathing and reduces ventricular irritability.

Effects of Nasal O2 on Sleep-Related Disordered Breathing in Ambulatory Patients with Stable Heart Failure

The purpose of this study was 1) to determine the effects of nasal O2 on periodic breathing, arterial oxyhemoglobin desaturation and nocturnal ventricular arrhythmias in patients with heart failure and 2) determine the characteristics of patients whose periodic breathing will be reversed by O2 administration; our hypothesis was that patients with more severe periodic breathing and desaturation, will respond more favorably to oxygen. Prospective study. Referral sleep laboratory of a Department of Veterans Affairs Medical Center. 36 ambulatory male patients with heart failure whose initial polysomnograms showed periodic breathing with fifteen or more episodes of apnea (A) and hypopnea (H) per hour (AH index, AHI) were treated with nasal O2 during the subsequent full night polysomnography. Oxygen. Arterial blood gases and hydrogen ion concentrations were measured, and cardiac radionuclide ventriculography, Holter monitoring, and polysomnography were done. The studies were scored blindly. Treatment with O2 resulted in a significant reduction in AHI (49+/-19 vs 29+/-29, means+/-SD), central apnea index (28+/-23 vs 13+/-18 per hour), and the percent of total sleep time below an arterial oxyhemoglobin saturation of 90% (23+/-21% vs 0.8+/-2.3%). In spite of virtual normalization of saturation with O2 therapy, the number of ventricular arrhythmias during sleep did not change significantly. In 39% of the patients (14 out of 36), O2 therapy resulted in reversal of central sleep apnea (defined by a reduction in AHI to less than 15/hr). In this group, the AHI decreased by 78% which was significantly (p=0.0001) more than improved (22%) in AHI of the remaining patients (n=22). The main differences between baseline characteristics of the two groups was a significantly higher mean PaCO2 in patients who did respond fully to O2 (39.3+/-5.4 vs 36.1+/-4.2 mm Hg, p=0.03). In both groups, however, O2 administration resulted in significant and similar improvement in arterial oxyhemoglobin saturation (saturation <90%, percent total sleep time 0.1+/-0.3% vs 1+/-3%). In patients with stable heart failure, administration of nasal O2 significantly improves periodic breathing and virtually eliminates clinically significant arterial oxyhemoglobin desaturation. The beneficial effects of O2, however, may be modulated by the level of arterial PCO2. Acute O2 therapy has important benefits on sleep apnea and nocturnal arterial oxyhemoglobin desaturation in heart failure patients. Long term benefits of O2 therapy in heart failure and sleep apnea need to be determined.

Upper Airway Resistance Syndrome: Effect of Nasal Dilation, Sleep Stage, and Sleep Position

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. We evaluated the effect of external nasal dilation and sleep position on sleep in UARS. 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. 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. 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.

Mandibular posture during sleep in patients with obstructive sleep apnoea

Vertical mandibular posture is thought to be related to narrowing of the upper airway, because mouth opening is associated with an inferior–posterior movement of the mandible and the tongue which influences pharyngeal airway patency. To test whether the mandibular posture is related to the occurrence and/or termination of obstructive sleep apnoea (OSA), the vertical mandibular position was recorded intraorally using a magnet sensor during a standard sleep study in seven patients with OSA. Measurements were recorded during sleep both in the supine and lateral recumbent positions. The percentage of total sleep time spent with mandibular opening greater than 5 mm was significantly larger ( p<0.001) in patients with OSA (69.3±23.3%) compared with our previous results obtained from healthy adults without OSA (11.1±11.6%). The stage of sleep affected the vertical mandibular posture during sleep in the supine position, but not in the lateral recumbent position in patients with OSA. In non-rapid eye-movement sleep, mandibular opening increased progressively during apnoeic episodes and decreased at the termination of apnoeic episodes. In contrast, no significant change in mandibular posture occurred in apnoeic episodes during rapid eye-movement sleep. It was concluded that the vertical mandibular posture is more open during sleep in patients with OSA than in healthy adults and that mandibular opening increases progressively during apnoeic episodes and decreases at the termination of those episodes.

SIDS, abnormal nighttime REM sleep and CNS immaturity.

SIDS (Sudden Infant Death Syndrome) is the major cause of death in young, apparently healthy, infants, yet its etiology and pathogenesis remain unknown. SIDS peaks at 2-4 months, is more prevalent in the winter months and typically occurs in the early morning hours when most babies are asleep, suggesting that sleep may be part of the pathophysiological mechanism of SIDS. The sleep patterns of infants at high risk for SIDS were analyzed to test the hypothesis that there are abnormalities specific to nighttime sleep which may be indicative of a central nervous system (CNS) deficit that contributes to a high frequency of SIDS during the night. Electrophysiological sleep variables were recorded at monthly intervals in 1-6 months-old infants during the peak age of SIDS. The risk group (R) was resuscitated from a potentially life-threatening Sudden A-Ventilatory Event (S.A.V.E.) and compared to a group of control infants (C) with no family history of SIDS. The data representing four equal time intervals from 11 p.m.-11 a.m. show an abrupt, statistically significant increase in REM sleep from 2-5 a.m. in R infants. In C infants, time spent in REM sleep after 2 a.m. becomes progressively shorter while NREM sleep is proportionately longer. From 11 p.m.-2 a.m., however, R and C infants do not differ either in the duration or in the percent of total sleep time (TST) of REM sleep. We hypothesize that these REM sleep abnormalities in vulnerable infants are indicative of a pervasive CNS immaturity. The higher prevalence of SIDS in the cold winter months and in the early morning hours, when darkness is prolonged, is discussed in relation to the possible involvement of the circadian rhythm of melatonin.

Effects of chondroitin sulfate on snoring characteristics: a pilots study

The efficacy of bedtime nasal instillation of chondroitin sulfate solution was tested in a double-masked, crossover, placebo-controlled trial of seven nonapneic subjects who snored. Subjects were assessed for reduction in snoring using conventional polysomnographic studies. The analysis of snoring was performed using the recordings obtained by a multidirectional microphone placed above the subject's head. Snoring was defined as an inspiratory, raspy, snort-like sound. The percentage of total sleep time (TST) spent snoring and the equal energy level related to sleep were calculated for each nocturnal sleep recording. Results of the sleep studies were similar with placebo and chondroitin sulfate. However, the mean percentage of TST spent snoring decreased from 46.5% with placebo to 31.3% with chondroitin sulfate, with important interindividual differences. Differences in the equivalent noise level related to TST decrease in the five subjects who were adequately recorded (74.1 ± 5.6 dB vs 70.0 ± 4.9 dB) did not reach statistical significance. Results of this study suggest that chondroitin sulfate, a long-acting tissue-coating agent, has the potential to reduce snoring.

Afternoon Exercise Improves the Quality of Night Sleep: A Case Study Observed by EEG and Self‐Rating Scale

Afternoon Exercise Improves the Quality of Night Sleep: A Case Study Observed by EEG and Self‐Rating Scale: Sasazawa Yosiaki, et al. Department of Public Health, Gunma University School of Medicine—This study was designed to assess the effects of morning (10:00‐12:00) and afternoon (15:00‐17:00) exercise on the objective and subjective quality of sleep. The subject was a 24‐year‐old man in the habit of performing soccer exercises. Exercise duration was 2 hr a day with an average exercise load of 70% V02max, and the energy expenditure was approximately 1,300 kcal. The polygraphic parameters of sleep were sleep stages expressed as percentages of total sleep time (%S1, %S2, %S (3 + 4), %SREM, %MT)r time in bed, sleep time, total sleep time, sleep onset latency (SOL), waking from sleep (WAKE), sleep efficiency (SEFI), number of awakenings (NOAW), number of stage shifts, number of spindles and percentages of alpha and delta waves, all of which were assessed by an automatic computer analyzing system. The OSA questionnaire was used to assess the quality of subjective sleep. The five scales of the OSA are sleepiness, sleep maintenance, worry about sleep, integrated sleep feeling and sleep initiation. Comparisons were made between sleep parameters when the subject performed morning exercise and afternoon exercise, and in the non‐exercise days by Dunnett's multiple comparison test. Sleep EEGs after afternoon exercise days showed higher %MT (p&lt;0.05), shorter SOL (p&lt;0.05), less WAKE (p&lt;0.05), higher SEFI (p&lt;0.05) and decreased NOAW (p&lt;0.05) than those of non‐exercise days. There were no significant differences between any of the sleep EEG parameters on non‐exercise and morning exercise days. Only the falling asleep score of the self‐rated sleep should be significantly improved by the afternoon exercise. The results suggest that afternoon exercise has a better effect on sleep than morning exercise.