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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intermittent snoring and cyclic oscillations of heart rate and oxyhaemoglobin saturation (Sao2) are characteristic features of the obstructive sleep apnoea syndrome (OSAS). Thus, overnight recordings of laryngeal sounds and heart rate by a portable device (MESAM) and of Sao2 by oximetry are applicable to screen outpatients for the presence of OSAS. Computerized analysis for time intervals of constant heart rate and intervals between snoring sounds is used by MESAM to quantify respiratory disturbances during sleep. Rapid increases in Sao2 during the postapnoeic hyperventilation period together with the number of desaturations are used by a new software for quantitative analysis of oximetry. To elucidate reliability of results from automatically scored MESAM and oximetry recordings, we compared the four computer calculated respiratory disturbance indices from heart rate (RDIH), snoring (RDIS), resaturations (RDIR) and desaturations (RDID) with the apnoea plus hypopnoea index (AHI) from simultaneously performed polysomnography. The study population consisted of 53 snorers with an AHI of 19.0 +/- 2.6 (median +/- SEM; range 0.7-87.8). Whereas both RDI's from MESAM correlated rather weakly with the AHI from polysomnography (RDIH: r = 0.32, p less than 0.05; RDIS: r = 0.33, p less than 0.05), this correlation was much better for the RDI's from oximetry (RDIR: r = 0.951, RDID: r = 0.93; p much less than 0.0001). Accepting a plus/minus 30 percent difference from the AHI, the RDIR classified 77% of patients correctly, the RDID 62%, the RDIS 32% and the RDIH 23%. In conclusion, results from computerized analysis of oximetry for desaturations and rapid resaturations correlate more closely with polysomnography than those from automatic scoring of MESAM recordings.
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PMID:Quantification of sleep disordered breathing by computerized analysis of oximetry, heart rate and snoring. 188 91

Posture has a major effect on breathing during sleep. Snoring, hypopneas, and apneas are all more common lying than sitting and more common supine than in a lateral lying position. Because the effect of the lateral lying position on upper airway caliber has not previously been studied, we examined this in 20 normal awake subjects and also determined the effect of neck position. The acoustic reflection technique was used. Pharyngeal cross-sectional areas (CSA) fell significantly from the sitting to supine position (oropharyngeal junction, from 1.65 +/- [SEM] 0.6 cm to 1.31 +/- 0.07 cm), but there was no difference in CSA between the supine and lateral positions for oropharyngeal junction (1.36 +/- 0.06 cm), mean pharyngeal area, maximal pharyngeal area, or pharyngeal volume. Neck hyper-extension significantly increased pharyngeal CSA (e.g., oropharyngeal junction null position 1.51 +/- 0.08, hyper-extension 1.94 +/- 0.11 cm), but there was no significant effect of neck flexion on airway CSA. These results confirm that in normal awake subjects, pharyngeal areas are smaller lying than sitting but also showed no significant difference between CSA in the supine and lateral lying positions. The study also demonstrates that the upper airway caliber increases with neck extension in conscious adults.
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PMID:Effect of posture on upper airway dimensions in normal human. 811 73

We evaluated the effects of protriptyline on snoring characteristics in 14 nonapneic snorers (age range, 23 to 54 years; body mass index, 27.4 +/- 0.9 kg/m2, mean +/- SEM). The study design was a double-blind placebo-controlled crossover trial. Patients were evaluated during a polysomnographic study after each 2 weeks of treatment. Breathing sounds were recorded with two microphones symmetrically placed on each side of the bed, the signal being preamplified, equalized, and analyzed by using a real time analyzer. A snoring event was defined as a breathing sound with a sound pressure level (SPL) greater than 60 dB SPL. The snoring index (number/sleep hour) and the sound intensity of each event were automatically determined. Mild side effects were observed in ten subjects, but no subject interrupted the study because of them. The REM sleep time decreased with protriptyline with a parallel increase in stages 1 to 2. There was no difference in body position during sleep between the placebo and protriptyline trials. The snoring index decreased from 335 +/- 40 with placebo to 238 +/- 41 with protriptyline (p < 0.05) with important individual differences. Among the different sleep stages, the highest values of the snoring index were observed in slow-wave sleep with placebo. The snoring index decreased in each sleep stage with protriptyline, the highest decrease occurring in slow-wave sleep. The percentage of total sleep time (TST) spent above 60 dB SPL was significantly lower with protriptyline (6.1 +/- 1.2 percent TST) than with placebo (8.6 +/- 1.2 percent TST). Changes in snoring characteristics were not correlated with snoring severity, the drug blood level, the body mass index, or the drug-induced modifications in sleep architecture. We conclude that protriptyline can improve both snoring frequency and loudness in some nonapneic snorers, and that this improvement occurs mostly in the sleep stages where snoring is worst.
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PMID:Effects of protriptyline on snoring characteristics. 832 70

Snoring characteristics depend on several factors (sleep position, sleep architecture, breathing route) that can be influenced by changes in sleep habits and by the presence of the different probes and electrodes during polysomnographic studies. Our objective in this study was to compare the characteristics of snoring in the home environment with those of the sleep laboratory where most conventional studies are carried out. Fourteen nonapneic snorers were subjected to three night recording sessions within a two-week period, two at home and one in the sleep laboratory. To eliminate any sleep interference by the apparatus, breathing sounds were recorded with two microphones symmetrically placed on either side of the bed, the signal being preamplified and stored on a VHS hi-fi video recorder. The recorded signal was analyzed by using a spectrum analyzer (real time analyzer) and an equalizer to correct for acoustic resonances of the bedrooms. A snoring event was defined as a breathing sound with a sound pressure level (SPL) greater than 60 dB SPL. The snoring index (number/sleep hour) and the sound intensity of each event were automatically determined. The total sleep time (TST) was similar for the two home recordings (6.8 +/- 0.2 and 7.0 +/- 0.2 h, respectively, mean +/- SEM), but it was significantly shorter during the hospital study (6.0 +/- 0.3 h). The snoring indices obtained at home were 141.4 +/- 33.3 and 144.1 +/- 41.2/h and not statistically different from those obtained during the hospital recording (209.1 +/- 41.5/h). The percentage of TST spent above 60 dB SPL was significantly greater during the polysomnographic study (4.3 +/- 1.2 percent) than during the home recordings (2.5 +/- 0.7 and 2.9 +/- 1.0 percent, respectively). We conclude that the severity of snoring may be overestimated during polysomnographic recordings.
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PMID:Comparison of snoring measured at home and during polysomnographic studies. 840 99

Snoring worsens with high alcohol consumption. It is unclear whether moderate alcohol intake worsens sleep and breathing in subjects with obstructive sleep apnoea syndrome (OSAS), and whether alcohol increases the pressure requirement for nasal continuous positive airway pressure (CPAP). Fourteen adult males with untreated OSAS but without heart or lung disease were studied (age 53+/-9 yrs, body mass index (BMI) 33+/-5 kg x m(-2) (mean+/-SD). The subjects underwent overnight polysomnography on four occasions: control, alcohol, CPAP, and alcohol + CPAP. On the alcohol nights, the subjects drank 1.5 mL x kg(-1) body weight (BW) vodka (40% alcohol by volume) (blood alcohol with and without CPAP 0.45+/-0.1 and 0.47+/-0.2 mg x mL(-1) (mean+/-SD)). On the CPAP nights, the pressure required to prevent apnoea, snoring, and silent inspiratory airflow limitation was determined using an autotitrating nasal CPAP system (ResCare AutoSet). Alcohol and control nights were performed in random order. Without CPAP, alcohol produced a small non-significant decrease in the percentage of rapid eye movement (REM) sleep (control 11+/-2 vs alcohol 8+/-1% (mean+/-SEM)), but with CPAP there was no such effect (control 15+/-2 vs 17+/-2%; CPA x alcohol interaction p=0.015). With CPAP, slow-wave sleep in the first 2 h increased slightly with alcohol (control 39+/-6 vs alcohol 51+/-4%; p=0.004). Arousal index without CPAP increased slightly with alcohol (control 43+/-5 vs alcohol 49+/-6 events x h(-1); p=0.02). There was little or no effect of alcohol on other sleep stages, arousal index, apnoea index, apnoea/hypopnoea index, mean or longest event duration, mean or worst arterial oxygen saturation, with or without CPAP, either for the full night or for the first 2 h. There was no change in the pressure requirement for CPAP (full night: control 11.9+/-0.9 vs alcohol 12.5+/-0.9 cm H2O; first 2 h: 10.9+/-0.6 vs 11.1+/-0.8 cm H2O). Moderate alcohol intake (in the form of vodka) has little effect on breathing or saturation during sleep in subjects with mild-to-severe obstructive sleep apnoea, and no effect on the pressure required for continuous positive airway pressure in order to prevent apnoea, snoring, and flow limitation. These results cannot be extrapolated to other doses or forms of alcohol, or to subjects with concurrent heart or lung disease.
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PMID:Influence of moderate alcohol consumption on obstructive sleep apnoea with and without AutoSet nasal CPAP therapy. 894 88

Moderate-to-large quantities of alcohol are known to aggravate severe obstructive sleep apnoea (OSA), however, the reported effects of moderate alcohol consumption upon mild-to-moderate OSA are inconsistent. Given the reported benefits of moderate alcohol consumption on cardiovascular mortality, recommendations regarding the management of patients with OSA are difficult to formulate. The aim of this study was to evaluate the effects of moderate alcohol on sleep and breathing in subjects with mild-to-moderate OSA. Twenty-one male volunteers, who snored habitually, underwent polysomnography with and without 0.5 g alcohol x kg body weight (BW)(-1) consumed 90 min prior to sleep time, in random order. The mean blood alcohol concentration (BAC) following alcohol at the time of lights out was 0.07 g x dL(-1). The distribution amongst the various sleep stages was not significantly altered by alcohol. The mean apnoea/hypopnoea index rose from 7.1+/-1.9 to 9.7+/-2.1 events x h(-1) (mean+/-SEM, p=0.017); however, there was no significant change in the minimum arterial oxygen saturation measured by pulse oximetry Sp,O2, apnoea length or snoring intensity. Mean sleep cardiac frequency rose significantly from 53.9+/-1.4 to 59.9+/-1.9 beats x min(-1) (P<0.001) and overnight urinary noradrenalin increased from 14.9+/-2.3 to 18.8+/-2.3 nmol x mmol creatinine(-1) (p=0.061) on the alcohol night compared to the nonalcohol night. To conclude, modest alcohol consumption, giving a mean blood alcohol concentration of 0.07 g x dL(-1), significantly increases both obstructive sleep apnoea frequency and mean sleep cardiac frequency.
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PMID:Effect of moderate alcohol upon obstructive sleep apnoea. 1115 91

The aim of this case-control study was to test the hypothesis that maxillary morphology differs between obstructive sleep apnoea (OSA) patients and non-snoring, non-apnoeic subjects. Forty randomly selected patients [36 M, 4 F; mean age 49 +/- 2 (SEM) years] with varying degrees of OSA (mean Apnoea/Hypopnoea Index 32 +/- 4/hour) were compared with 21 non-snoring, non-apnoeic control subjects (18 M, 3 F; mean age 40 +/- 2 years). An intra-oral assessment of the occlusion was carried out, particularly for the presence or absence of posterior transverse discrepancies. Maxillary dental arch width was assessed by standardized lateral inter-tooth measurements (inter-canine, inter-premolar, and inter-molar) from dental models. Palatal height and maxillary depth were also measured. The maxillary dental arch was described by a 4th order polynomial equation. The ratios of maxillary to mandibular width (max/mand) and maxillary to facial width (max/facial) were determined from standardized postero-anterior cephalometric radiographs in a subgroup of patients (n = 29) and all controls. Twenty patients (50 per cent) had evidence of posterior transverse discrepancies compared with one control subject (5 per cent; P < 0.01). All patients had significantly reduced inter-canine, inter-premolar, and inter-molar distances (P < 0.05). The maxillary depth was also shorter (P < 0.05), but palatal height was not different. The quadratic coefficient of the polynomial equation was greater in the patients than in the controls (P < 0.05), indicative of greater arch tapering. Patients had smaller maxillary to mandibular and maxillary to facial width ratios (P < 0.01). These results suggest that OSA patients have narrower, more tapered, and shorter maxillary arches than non-snoring, non-apnoeic controls. Further work is required to determine the relevance of these findings in the pathophysiology of OSA.
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PMID:Maxillary morphology in obstructive sleep apnoea syndrome. 1189 66