SLEEP

Turek, Fred W.

doi: 10.1093/sleep/28.5.548pmid: 16171267

Fenik, Victor B.; Ogawa, Hiromasa; Davies, Richard O.; Kubin, Leszek

doi: 10.1093/sleep/28.5.551pmid: 16171268

AbstractStudy Objectives:Two pontine reticular regions are implicated in cholinergic triggering of rapid eye movement (REM) sleep: the dorsomedial tegmental region and the ventral nucleus pontis oralis. We previously determined that, in urethane-anesthetized rats, microinjections of a cholinergic agonist, carbachol, into the dorsal region produce REM sleep-like effects comprising cortical activation, hippocampal theta rhythm, suppression of hypoglossal (XII) nerve activity, and silencing of pontine noradrenergic neurons. Our goal was to determine whether carbachol injections into the ventral nucleus pontis oralis elicits comparable effects.Design:Recording of cortical electroencephalogram, hippocampal activity, XII nerve activity, and discharge of noradrenergic cells of the locus coeruleus.Setting:Basic neurophysiologic research laboratory.Participants and Interventions:Urethane-anesthetized, paralyzed, and artificially ventilated or nonparalyzed and spontaneously breathing rats with microinjections of carbachol (10 nL, 10 mM) into the ventral nucleus pontis oralis.Measurements and Results:In artificially ventilated rats, carbachol injections repeatedly elicited cortical activation and hippocampal theta rhythm. Concomitantly, the activity of locus coeruleus neurons increased from 2.0 per second ± 0.4 (SE) to 2.6 per second ± 0.4 (P < .05, n = 8), as did XII nerve activity (by 42.5% ± 8.8%; P < .01). In spontaneously breathing animals, carbachol similarly activated the cortical electroencephalogram and hippocampal activity, whereas XII nerve activity was reduced by 6.7% ± 2.5% (P < .05) together with increased ventilation, as indicated by reduced end-expiratory CO2.Conclusion:Carbachol injections into the ventral nucleus pontis oralis activate, rather than silence, noradrenergic locus coeruleus neurons. This is not compatible with the state of REM sleep.

Saponjic, Jasna; Cvorovic, Jovana; Radulovacki, Miodrag; Carley, David W.

doi: 10.1093/sleep/28.5.560pmid: 16171269

AbstractStudy Objectives:We hypothesized that 2 important neurotransmitters related to behavioral state control, serotonin and noradrenaline, could also be modulators of pedunculopontine tegmental nucleus (PPT)-induced respiratory dysrhythmia.Design:We examined the impact of serotonin and noradrenaline at respiratory control sites in the PPT functionally identified by immediate apnea of 2.5- to 10-second duration, followed by increased variability of breath time (CVTT) (P < .04) after locally injecting glutamate in anesthetized rats.Setting:Basic sleep and respiratory neurobiology laboratory.Participants:Sixteen adult, male Sprague-Dawley rats.Measurements and Results:Glutamate-induced respiratory responses, including increases of total apnea duration and CVTT, were not different between groups of rats in which we further tested monoaminergic modulatory effects (for CVTT, P = .98, and for total apnea duration, P = .80). Serotonin or noradrenaline injected at the same sites as glutamate had equal impact on CVTT (P = .34) and on mean total apnea duration (P = .80), but pretreatment of PPT sites with serotonin blocked (remained equal to preinjection; P = .11), whereas pretreatment with noradrenaline potentiated (P = .04) the increment of respiratory-timing variability induced by glutamate. The serotonergic-blocking effect on glutamate-induced respiratory dysrhythmia was specific to the PPT: the respiratory responses induced by glutamate injection outside the PPT were not modulated by serotonin (for CVTT , P = .46, and for mean apnea duration, P = .99).Conclusions:The opposed impact of serotonin and noradrenaline on PPT-induced respiratory dysrhythmia, in contrast to their convergent regulatory role in behavioral state control, suggests a functionally distinct role for the PPT in respiratory-pattern control independent of rapid eye movement sleep control.

Toth, Linda A.; Hughes, Larry F.; Rehg, Jerold E.

doi: 10.1093/sleep/28.5.571pmid: 16171270

AbstractStudy objectives:To assess the suitability of concanavalin-A-induced hepatitis as a model for investigating the relationships between hepatic disease and alterations in somnolence.Design:We characterized the sleep patterns of various strains of inbred mice undergoing ConA-induced inflammation.Setting:Southern Illinois University School of Medicine, Springfield, IL.Intervention:Intravenous or intraperitoneal administration of concanavalin-A.Participants:Inbred mice.Measurements and Results:Intravenous and intraperitoneal administration of concanavalin-A both elicited strain-dependent changes in slow-wave sleep. ConA treatment also reduced spontaneous locomotor activity. ConA-induced changes in slow-wave sleep varied with dose, route of administration, and circadian period of administration. As compared with the other strains, C57BL/6J mice had lower serum concentrations of interferon-γ at 8 hours after ConA administration.Conclusions:These data provide the first demonstration that sleep enhancement and reduced locomotor activity accompany hepatic inflammation in mice.

Nguyen, Anh Tu Duy; Jobin, Vincent; Payne, Richard; Beauregard, Josée; Naor, Naftaly; Kimoff, R. John

doi: 10.1093/sleep/28.5.585pmid: 16171271

AbstractStudy Objective:To determine whether mucosal sensory dysfunction is present at multiple upper-airway sites in patients with obstructive sleep apnea (OSA).Design:Physiologic testing of consecutive patients with OSA and nonsnoring controls.Setting:University hospital sleep center.Participants:Thirty-nine subjects with OSA and 17 controls.Interventions:Endoscopic testing was used to determine sensory detection thresholds for air-pressure pulses delivered to the oropharynx, velopharynx, hypopharynx, and larynx (aryepiglottic eminence). The air-pulse stimulus intensity required to elicit the protective laryngeal adductor reflex was also determined.Measurements and Results:There was a significant impairment in sensory detection threshold for OSA versus control subjects in the oropharynx, as previously described by ourselves using other techniques, as well as at the velopharynx (median 11 mm Hg [confidence interval 9–11] for subjects with OSA vs 8 mm Hg [confidence interval 4–11] for controls, P = .03) and, at the larynx, 4 mm Hg [confidence interval 2–9] for subjects with OSA vs 2 mm Hg [confidence interval 2–3] for controls, P < .001). The threshold stimulus intensity for the laryngeal adductor reflex was also significantly higher for OSA subjects. For OSA patients with abnormal laryngeal sensation (61% of OSA subjects), there were significant correlations between laryngeal sensory values and measures of apnea severity, including apnea-hypopnea index (r = 0.82, P < .001) and nadir SaO2 (r = −0.48, P < .05).Conclusion:Mucosal sensory function is impaired at multiple upper-airway sites in OSA.

Itzhaki, Sarah; Lavie, Lena; Pillar, Giora; Tal, Galit; Lavie, Peretz

doi: 10.1093/sleep/28.5.594pmid: 16171272

AbstractStudy Objective:The aim of this study was to investigate endothelial functioning in sleep apnea patients using a novel plethysmographic device that monitors peripheral arterial tone response in the finger to reactive hyperemia induced by forearm ischemia.Participants:Forty-six sleep apnea patients, 74.0% men, mean age 46.8 ± 9.3 years, and 17 control subjects without sleep apnea, 64.7% men, mean age 47.1 ± 6.7 years.Setting:Eight-bed Technion Sleep Medicine Center in Haifa, Israel0.Design:Endothelial functioning assessed by the reactive hyperemia peripheral arterial tone index was measured twice, before sleep and after waking from sleep monitored by polysomnography in the laboratory. The reactive hyperemia peripheral arterial tone index was calculated as the average amplitude of the peripheral arterial tone signal after the cuff deflation divided by the average amplitude before the cuff inflation.Results:Morning index of endothelial functioning was significantly lower in patients with moderate to severe sleep apnea (apnea-hypopnea index ≥ 30) than in patients with mild sleep apnea (30 < apnea-hypopnea index ≤10) and in the control group without sleep apnea (apnea-hypopnea index <10). The morning index was significantly inversely correlated with apnea-hypopnea index. Patients with a history of hypertension or cardiovascular disease had significantly lower morning and evening indexes of endothelial functioning than patients without such a history. Multivariate analysis revealed that apnea-hypopnea index and sleep efficiency were significant predictors of the morning index.Conclusion:Measurements of the response of the peripheral arterial tone in the finger to reactive hyperemia can be used as a substitute for the brachial artery ultrasound technique to measure endothelial functioning in patients with sleep apnea.

Czupryniak, Leszek; Loba, Jerzy; Pawlowski, Maciej; Nowak, Dariusz; Bialasiewicz, Piotr

doi: 10.1093/sleep/28.5.601pmid: 16171273

AbstractStudy Objectives:Obstructive sleep apnea syndrome (OSAS) is often associated with impaired glucose metabolism. Data on the effects of OSAS treatment with continuous positive airway pressure (CPAP) on blood glucose and insulin resistance are conflicting. The study aimed at assessing the immediate effect of CPAP on glucose control measured with a continuous glucose monitoring system (CGMS).Participants and Measurements:Nine non-diabetes subjects with OSAS (mean age 53.0 ± 8.0 years; body mass index 34.8 ± 5.3 kg/m2) underwent 2 overnight polysomnographic examinations: a diagnostic study and one with CPAP treatment. Continuous glucose monitoring system (CGMS) was applied overnight on both occasions. Glucose metabolism was assessed with a 75-g oral glucose tolerance test, plasma insulin and homeostatic model assessment of insulin resistance (HOMA-IR) index.Results:The mean (± SD) apnoea-hypopnea index (AHI) at diagnostic polysomnography was 54.3 ± 29.3 (range 16–81). Fasting plasma insulin levels in patients with OSAS was 84.3 ± 43.4 pM at baseline, and the HOMA-IR was 3.6 ± 2.2. CPAP treatment in the subjects with OSAS resulted in a significant reduction in the AHI to 4.5 ± 7.1. All of the major saturation parameters improved significantly on CPAP. CGMS showed mean glucose values significantly higher during the CPAP night than during the diagnostic night: 80 ± 11 mg/dL versus 63 ± 7 mg/dL (P < .01). Fasting insulin and HOMA-IR measured after the CPAP night tended to be higher than at baseline (98.4 ± 51.0 pmol vs 84.3 ± 43.4 pmol and 3.9 pmol ± 2.6 vs 3.6 ± 2.2 pmol, respectively, P > .05).Conclusion:CPAP treatment in nondiabetic obese patients with OSAS may have an immediate elevating effect on blood glucose.

Phillips, Craig; Hedner, Jan; Berend, Norbert; Grunstein, Ronald

doi: 10.1093/sleep/28.5.604pmid: 16171274

AbstractStudy Objectives:Nocturnal and early morning elevation of blood pressure are common acute manifestations of obstructive sleep apnea (OSA) that do not always carry over into a sustained daytime hypertension. Using pulse wave analysis, we examined the effect of OSA on arterial stiffness and central aortic blood pressure to assess whether each would be elevated independent of diurnal changes in peripheral blood pressure.Design:Cross-sectional sleep laboratory cohort study.Setting:Two university teaching hospitals.Patients:57 male nonsmokers referred for suspected OSA and free of known cardiovascular disease or blood-pressure and lipid-lowering medications.Measurements and Results:The augmentation index, a quantification of augmentation of central aortic pressure due to the reflected component of the pulse pressure waveform, and brachial and aortic blood pressure were determined in the evening and early morning. The augmentation index consistently increased from evening to morning (P < .001) and was accompanied by an increase in central systolic blood pressure (P = .007) and a decrease in pulse pressure amplification (P < .001). However, these changes were unaccompanied by any changes in peripheral blood pressure. Overnight changes in mean blood pressure and heart rate were the only predictors of this effect, but they only accounted for a third of the variance (r2= 0.339, P = .002). After adjustment for known confounders, the respiratory disturbance index was positively correlated with augmentation index at both time points (PM: P = .008,aM: P = .016). The respiratory disturbance index did not correlate with any indexes of peripheral or central blood pressure.Conclusions:Systemic arterial stiffness is positively correlated with OSA severity and, in addition, is increased in magnitude in the early morning independent of OSA severity.

Jefferson, Catherine D.; Drake, Christopher L.; Scofield, Holly M.; Myers, Eric; McClure, Tara; Roehrs, Timothy; Roth, Thomas

doi: 10.1093/sleep/28.5.611pmid: 16171275

AbstractStudy Objectives:The present study was designed to assess selected aspects of sleep hygiene from a population-based sample of individuals with insomnia compared to age- and sex-matched controls.Design:A random-sample phone survey of 258 individuals meeting Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-based criteria for insomnia was compared to age- and sex-matched normal sleepers on specific measures of sleep hygiene. Sleep hygiene practices measured included cigarette smoking, smoking near bedtime, alcohol use, caffeine use, napping, time in bed, and reported likelihood of sleeping in on weekends.Setting:Detroit tricounty population.Participants:258 individuals 18 to 65 years old with insomnia and 258 age- and sex-matched controls.Interventions:N/A.Measurements and Results:Insomniacs reported poorer sleep hygiene, as evidenced by an increase in prevalence of smoking close to bedtime and increased use of alcohol. They also reported more naps per week and sleeping in on days not worked. Caffeine use did not differ between groups. Time in bed was also comparable between insomniacs and controls.Conclusion:Insomniacs do engage in specific poor sleep hygiene practices, such as smoking and drinking alcohol just before bedtime. These particular aspects of sleep hygiene may be important components that exacerbate or perpetuate insomnia.

Lack, Leon; Wright, Helen; Kemp, Kristyn; Gibbon, Samantha

doi: 10.1093/sleep/28.5.616pmid: 16171276

AbstractStudy Objective:To assess the effectiveness of brief bright-light therapy for the treatment of early-morning awakening insomnia.Participants:Twenty-four healthy adults with early-morning awakening insomnia were assigned to either the bright-light condition (2,500-lux white light) or the control (dim red light) condition.Measurements and Results:The circadian phase of rectal temperature and urinary melatonin rhythms were assessed with 26-hour constant routines before and after 2 evenings of light therapy. Sleep and daytime functioning were monitored using sleep diaries, activity monitors, and mood scales before light therapy and for 4 weeks during the follow-up period. While there were no significant circadian phase changes in the dim-light control group, the bright-light group had significant 2-hour phase delays of circadian temperature and melatonin rhythm. Compared to pretreatment measures, over the 4-week follow-up period, the bright-light group had a greater reduction of time awake after sleep onset, showed a trend toward waking later, and had a greater increase of total sleep time. Participants in the bright-light condition also tended to report greater reductions of negative daytime symptoms, including significantly fewer days of feeling depressed at the 4-week follow-up, as compared with the control group.Conclusion:Two evenings of bright-light exposure phase delayed the circadian rhythms of early-morning awakening insomniacs. It also improved diary and actigraphy sleep measures and improved some indexes of daytime functioning for up to 1 month after light exposure. The study suggests that a brief course of evening bright-light therapy can be an effective treatment for early-morning awakening insomniacs who have relatively phase advanced circadian rhythms.