Hypercapnia-induced vasodilation in the cerebral circulation is reduced in older adults with sleep-disordered breathing.

The prevalence of sleep-disordered breathing (SDB) is higher in older adults compared with younger individuals. The increased propensity for ventilatory control instability in older adults may contribute to the increased prevalence of central apneas. Reductions in the cerebral vascular response to CO2 may exacerbate ventilatory overshoots and undershoots during sleep. Thus, we hypothesized that hypercapnia-induced cerebral vasodilation (HCVD) will be reduced in older compared with younger adults. In 11 older and 10 younger adults with SDB, blood flow velocity in the middle cerebral artery (MCAV) was measured using Doppler transcranial ultrasonography during multiple steady-state hyperoxic hypercapnic breathing trials while awake, interspersed with room air breathing. Changes in ventilation, MCAV, and mean arterial pressure (MAP) via finger plethysmography during the trials were compared with baseline eupneic values. For each hyperoxic hypercapnic trial, the change (Δ) in MCAV for a corresponding change in end-tidal CO2 and the HCVD or the change in cerebral vascular conductance (MCAV divided by MAP) for a corresponding change in end-tidal CO2 was determined. The hypercapnic ventilatory response was similar between the age groups, as was ΔMCAV/Δ[Formula: see text]. However, compared with young, older adults had a significantly smaller HCVD (1.3 ± 0.7 vs. 2.1 ± 0.6 units/mmHg, P = 0.004). Multivariable analyses demonstrated that age and nadir oxygen saturation during nocturnal polysomnography were significant predictors of HCVD. Thus, our data indicate that older age and SDB-related hypoxia are associated with diminished HCVD. We hypothesize that this impairment in vascular function may contribute to breathing instability during sleep in these individuals.NEW & NOTEWORTHY This study demonstrates, for the first time, in individuals with sleep-disordered breathing (SDB) that aging is associated with decreased hypercapnia-induced cerebral vasodilation (HCVD). In addition to advanced age, the magnitude of nocturnal oxygen desaturation due to SDB is an equal independent predictor of HCVD.

Can lifetime exposure to intimate partner violence predict suicidality in a sample of Egyptian pregnant women: a cross-sectional study?

Background and objectives: Research on suicidal behaviors during pregnancy in Egypt is limited; being apparently rationalized by pregnancy is a protective period. This study aimed to address the current suicide risk (CSR), and evaluate its correlates of among pregnant women in Egypt.MethodsIt is a cross-sectional study which included 835 of Egyptian pregnant women who were receiving their antenatal care at Zagazig University Obstetrics and Gynecology Outpatient clinics, during the period from 1 October 2017 to 30 September 2018. The sociodemographic and clinical data were collected by a simple semi-structured questionnaire. The psychometric assessment included Beck Suicidal Ideation Scale (BSS), Zagazig Depression Scale (ZDS), Hamilton Anxiety Rating Scale (HAM-A), and Structured Clinical Interview for DSM-IV-TR Axis II Personality Disorders (SCID-II) for assessment of CSR, and comorbid depression, anxiety and personality disorders, respectively.ResultsAmong pregnant women, 23.4% reported CSR. This included suicidal ideation of 21.6% and suicidal attempt of 1.8%. Predictors of CSR were history of intimate partner violence (IPV) exposure (OR 8.8, 95% CI: 2.8, 27.7), identification of their current pregnancy as a female baby (OR 6.9, 95% CI: 2.0, 23.5), previous history of fetal loss (OR 3.9, 95% CI: 1.5, 10.6), and moderate-to-severe depression (OR 3.0, 95% CI: 1.0, 8.7).ConclusionsOur findings suggest that CSR, including suicidal ideation and attempts, is not rare during pregnancy. Exposure to IPV is the most robust predictor of CSR. Pregnant women should be routinely screened for suicidal behaviors, violence exposure and depressive symptoms, as part of their antenatal assessments. (AU)

Amelioration of sleep-disordered breathing with supplemental oxygen in older adults.

Elderly adults demonstrate increased propensity for breathing instability during sleep compared with younger adults, and this may contribute to increased prevalence of sleep-disordered breathing (SDB) in this population. Hence, in older adults with SDB, we examined whether addition of supplemental oxygen (O2) will stabilize breathing during sleep and alleviate SDB. We hypothesized that exposure to supplemental O2 during non-rapid eye movement (NREM) sleep will stabilize breathing and will alleviate SDB by reducing ventilatory chemoresponsiveness and by widening the carbon dioxide (CO2) reserve. We studied 10 older adults with mild-to-moderate SDB who were randomized to undergo noninvasive bilevel mechanical ventilation with exposure to room air or supplemental O2 (Oxy) to determine the CO2 reserve, apneic threshold (AT), and controller and plant gains. Supplemental O2 was introduced during sleep to achieve a steady-state O2 saturation ≥95% and fraction of inspired O2 at 40%-50%. The CO2 reserve increased significantly during Oxy versus room air (-4.2 ± 0.5 mmHg vs. -3.2 ± 0.5 mmHg, P = 0.03). Compared with room air, Oxy was associated with a significant decline in the controller gain (1.9 ± 0.4 L/min/mmHg vs. 2.5 ± 0.5 L/min/mmHg, P = 0.04), with reductions in the apnea-hypopnea index (11.8 ± 2.0/h vs. 24.4 ± 5.6/h, P = 0.006) and central apnea-hypopnea index (1.7 ± 0.6/h vs. 6.9 ± 3.9/h, P = 0.03). The AT and plant gain were unchanged. Thus, a reduced slope of CO2 response resulted in an increased CO2 reserve. In conclusion, supplemental O2 reduced SDB in older adults during NREM sleep via reduction in chemoresponsiveness and central respiratory events.NEW & NOTEWORTHY This study demonstrates for the first time in elderly adults without heart disease that intervention with supplemental oxygen in the clinical range will ameliorate central apneas and hypopneas by decreasing the propensity to central apnea through decreased chemoreflex sensitivity, even in the absence of a reduction in the plant gain. Thus, the study provides physiological evidence for use of supplemental oxygen as therapy for mild-to-moderate SDB in this vulnerable population.

Resveratrol ameliorates oxidative stress and organ dysfunction in Schistosoma mansoni infected mice.

Schistosoma mansoni causes a major chronic debilitating disease in more than 230 million people around the world. The pathognomonic granuloma is a major cause of the oxidative stress encountered as a consequence of infection not only in the liver, but also in other important organs as spleen, lung, brain and kidney. Resveratrol administration at a dose of 20 mg/kg once daily for two weeks to mice infected with Schistosoma mansoni resulted in improvement in serum cholesterol and triglyceride levels. Enzymatic antioxidant profile showed significant modulations in Superoxide dismutase, catalase activities and reduced glutathione levels. Specific biomarkers for homeostasis of brain and lung i.e. Tau and RAGE respectively, showed significant improvement after resveratrol administration.

LOOP-MEDIATED ISOTHERMAL AMPLIFICATION (LAMP): SENSITIVE AND RAPID DETECTION OF SCHISTOSOMA HAEMATOBIUM DNA IN URINE SAMPLES OF EGYPTIAN SUSPECTED CASES.

Schistosomiasis haemalobium is a major endemic parasitic disease in many tropical regions including Egypt. Typical infection results in haematuria, dysuria, anaemia, genital as well as urinary tract lesions, with prospect of kidney damage in complicated cases. In addition, deposited eggs in the tissue, eventually leads to squamous cell carcinoma of urinary bladder in chronically infected individuals. Microscopic detection of excreted ova in urine samples remains the gold standard diagnostic method, in spite of its inherited low sensitivity, inconsistent egg excretion and unreliable results in chronic phase of the disease. Moreover due to pre-requisite for skilled personals and pricey equipment, PCR-based technologies are of limited use especially in low-income endemic countries. So emergence of loop-mediated isothermal DNA amplification (LAMP) seemed a promising technique. Our study evaluated application of LAMP technique in detection of S. haematobium DNA in 69 urine samples of suspected patients for urogenital schistosomiasis, versus conventional urine filtration followed by microscopy ova detection method. Specificity of LAMP was tested using other parasites DNA samples that showed no cross reactivity. Furthermore our results of the calculated diagnostic parameters for sensitivity and specificity for LAMP assay were 100%, with 95% CI (88.78%-100%), and 63.16%, with 95% CI (45.99%-78.19%) respectively, moreover Positive likelihood ratio (LR+) 2.7, and Negative likelihood ratio (LR-) 0.0, which display that LAMP technique is an up-to-date simple, sensitive, diagnostic important tool that could be employed in clinical diagnosis in poorly equipped facilities, as well as in surveillance of infectious diseases. As authors knowledge, this is the first national report evaluation of LAMP technique as a promising diagnostic tool for urogenital schistosomiasis.

Identification and treatment of sleep-disordered breathing in chronic spinal cord injury.

STUDY DESIGN: A follow up on an ongoing prospective cohort study. OBJECTIVE: Spinal cord injury or disorder (SCI/D) patients have higher rates of sleep-disordered breathing (SDB) than the general population. The objectives of this study were to examine predictors of SDB diagnosis and to estimate rates of SDB treatment in SCI/D patients. SETTING: A SCI clinical sleep research laboratory. METHODS: Twenty-eight SCI/D patients (7 women, age 42.8 ± 15.8 years; 16 cervical and 12 thoracic level injuries) completed a battery of questionnaires (Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Berlin questionnaire (BQ) and fatigue severity scale (FSS)) and had one night of attended laboratory polysomnography (PSG). Participants were then notified of the results of their PSG and were interviewed approximately 1 year later to assess clinical outcomes. RESULTS: The majority of patients reported poor sleep quality on all questionnaires. On the basis of PSG, 22 (79%) patients had SDB (apnea-hypopnea index (AHI)⩾ 5 events per hour), and 17 (61%) had moderate/severe SDB (AHI⩾15 events per hour). Higher ESS scores were associated with a higher risk of AHI ⩾ 5; however, other questionnaires did not distinguish between those with and without SDB using either AHI cutoff. In follow-up interviews, only 50% of patients had spoken to a health-care provider about SDB and only six patients with SDB were prescribed treatment, four of whom were using the treatment at follow-up. CONCLUSION: SDB is common and severe among SCI/D patients. Screening questionnaires do not appear to differentiate between those with and without SDB. Even when SDB was recognized, many patients remained untreated. The increased prevalence of cardiovascular disease in SCI/D patients could represent a consequence of untreated SDB, and improving diagnosis and management of SDB has the potential to improve outcomes for these patients.

Ventilatory long-term facilitation in non-snoring subjects during NREM sleep.

We hypothesized that very brief episodes of hypoxia (<1 min) would evoke long-term facilitation (LTF) in individuals free of inspiratory flow limitation (IFL). We studied 12 healthy participants who were self-reported non-snorers and confirmed the absence of IFL. We induced 15 brief episodes of hypoxia during non-REM sleep, reducing arterial oxygen saturation to 84-85%, followed by 1 min of room air. Ventilatory variables and resistance were measured during the control period, hypoxic trials, room air controls, and for 20 min following the last hypoxic episode. There was a significant increase in minute ventilation (108+/-1.3% of control, P < 0.05) and tidal volume (105+/-1.7% of control, P < 0.05) and a significant decrease in upper airway resistance (88+/-9.8% control, P < 0.05) during the recovery period. However, there were no significant changes in any variable during sham studies. We have shown for the first time that LTF can be elicited in sleeping humans free of IFL.

Upper airway mechanics and post-hypoxic ventilatory decline during NREM sleep.

Termination of hypoxia results in a transient ventilatory decline referred to as post-hypoxic ventilatory decline (PHVD). We wished to determine whether PHVD is due to changes in ventilatory motor output or upper airway mechanics. We studied 19 healthy normal subjects (15 men, 4 women) during stable non-REM (NREM) sleep. Subjects were exposed to multiple episodes of brief (3 min) hypoxia that terminated with one breath of 100% FI(O2). Minute ventilation (V (I)), tidal volume (V (T)), timing, and upper airway resistance (R (ua)) were measured during the control, hypoxia, and for the first six breaths immediately after cessation of hypoxia. In addition, we measured diaphragmatic electromyograms (EMGdia) via surface electrodes in four subjects. V (I) and V (T) decreased during the recovery period to a nadir of 81 and 83% of room air control, respectively. However, there was no significant change in respiratory frequency or upper airway resistance during the post-hypoxic recovery period. Decreased V (I) was associated with a comparable decrease in EMGdia. We conclude that: (1) PHVD occurs in normal humans during NREM sleep, (2) there is no evidence of post-hypoxic frequency decline in humans during NREM sleep, and (3) PHVD is centrally mediated and not driven by upper airway mechanics.

Effect of testosterone on the apneic threshold in women during NREM sleep.

The hypocapnic apneic threshold (AT) is lower in women relative to men. To test the hypothesis that the gender difference in AT was due to testosterone, we determined the AT during non-rapid eye movement sleep in eight healthy, nonsnoring, premenopausal women before and after 10-12 days of transdermal testosterone. Hypocapnia was induced via nasal mechanical ventilation (MV) for 3 min with tidal volumes ranging from 175 to 215% above eupneic tidal volume and respiratory frequency matched to eupneic frequency. Cessation of MV resulted in hypocapnic central apnea or hypopnea depending on the magnitude of hypocapnia. Nadir minute ventilation as a percentage of control (%Ve) was plotted against the change in end-tidal CO(2) (Pet(CO(2))); %Ve was given a value of zero during central apnea. The AT was defined as the Pet(CO(2)) at which the apnea closest to the last hypopnea occurred; hypocapnic ventilatory response (HPVR) was defined as the slope of the linear regression Ve vs. Pet(CO(2)). Both the AT (39.5 +/- 2.9 vs. 42.1 +/- 3.0 Torr; P = 0.002) and HPVR (0.20 +/- 0.05 vs. 0.33 +/- 0.11%Ve/Torr; P = 0.016) increased with testosterone administration. We conclude that testosterone administration increases AT in premenopausal women, suggesting that the increased breathing instability during sleep in men is related to the presence of testosterone.

Long-term facilitation in obstructive sleep apnea patients during NREM sleep.

Repetitive hypoxia followed by persistently increased ventilatory motor output is referred to as long-term facilitation (LTF). LTF is activated during sleep after repetitive hypoxia in snorers. We hypothesized that LTF is activated in obstructive sleep apnea (OSA) patients. Eleven subjects with OSA (apnea/hypopnea index = 43.6 +/- 18.7/h) were included. Every subject had a baseline polysomnographic study on the appropriate continuous positive airway pressure (CPAP). CPAP was retitrated to eliminate apnea/hypopnea but to maintain inspiratory flow limitation (sham night). Each subject was studied on 2 separate nights. These two studies are separated by 1 mo of optimal nasal CPAP treatment for a minimum of 4-6 h/night. The device was capable of covert pressure monitoring. During night 1 (N1), study subjects used nasal CPAP at suboptimal pressure to have significant air flow limitation (>60% breaths) without apneas/hypopneas. After stable sleep was reached, we induced brief isocapnic hypoxia [inspired O(2) fraction (FI(O(2))) = 8%] (3 min) followed by 5 min of room air. This sequence was repeated 10 times. Measurements were obtained during control, hypoxia, and at 5, 20, and 40 min of recovery for ventilation, timing (n = 11), and supraglottic pressure (n = 6). Upper airway resistance (Rua) was calculated at peak inspiratory flow. During the recovery period, there was no change in minute ventilation (99 +/- 8% of control), despite decreased Rua to 58 +/- 24% of control (P < 0.05). There was a reduction in the ratio of inspiratory time to total time for a breath (duty cycle) (0.5 to 0.45, P < 0.05) but no effect on inspiratory time. During night 2 (N2), the protocol of N1 was repeated. N2 revealed no changes compared with N1 during the recovery period. In conclusion, 1) reduced Rua in the recovery period indicates LTF of upper airway dilators; 2) lack of hyperpnea in the recovery period suggests that thoracic pump muscles do not demonstrate LTF; 3) we speculate that LTF may temporarily stabilize respiration in OSA patients after repeated apneas/hypopneas; and 4) nasal CPAP did not alter the ability of OSA patients to elicit LTF at the thoracic pump muscle.

Influence of gender on upper airway mechanics: upper airway resistance and Pcrit.

It has been proposed that the difference in sleep apnea prevalence is related to gender differences in upper airway anatomy and physiology. To explain the prevalence difference, we hypothesized that men would have an increased upper airway resistance and increased critical closing pressure (Pcrit) compared with women. In protocol 1, resistance at two points, fixed flow of 0.2 l/s (RL) and peak flow (Rpk), was measured in 33 men and 27 women without significant sleep-disordered breathing. We found no difference in either RL (-6.9 +/- 5.9 vs. -8.6 +/- 8.2 cmH2O) or Rpk (-9.3 +/- 6.8 vs. -10.0 +/- 11.9 cmH2O) between the men and women. A multiple linear regression to correct for the effects of age and body mass index confirmed that gender had no effect on resistance. In protocol 2, Pcrit was measured in eight men and eight women without sleep-disordered breathing. We found no difference in Pcrit (-10.4 +/- 3.1 vs. -8.8 +/- 2.7 cmH2O) between men and women. We conclude that there are no significant differences in collapsibility between men and women. We present an unifying hypothesis to explain the divergent findings of gender differences in upper airway physiology.

Effect of REM sleep on retroglossal cross-sectional area and compliance in normal subjects.

It has been proposed that the upper airway compliance should be highest during rapid eye movement (REM) sleep. Evidence suggests that the increased compliance is secondary to an increased retroglossal compliance. To test this hypothesis, we examined the effect of sleep stage on the relationship of retroglossal cross-sectional area (CSA; visualized with a fiber-optic scope) to pharyngeal pressure measured at the level of the oropharynx during eupneic breathing in subjects without significant sleep-disordered breathing. Breaths during REM sleep were divided into phasic (associated with eye movement, PREM) and tonic (not associated with eye movements, TREM). Retroglossal CSA decreased with non-REM (NREM) sleep and decreased further in PREM [wake 156.8 +/- 48.6 mm(2), NREM 104.6 +/- 65.0 mm(2) (P < 0.05 wake vs. NREM), TREM 83.1 +/- 46.4 mm(2) (P = not significant NREM vs. TREM), PREM 73.9 + 39.2 mm(2) (P < 0.05 TREM vs. PREM)]. Retroglossal compliance, defined as the slope of the regression CSA vs. pharyngeal pressure, was the same between all four conditions (wake -0.7 + 2.1 mm(2)/cmH(2)O, NREM 0.6 +/- 3.0 mm(2)/cmH(2)O, TREM -0.2 +/- 3.3 mm(2)/cmH(2)O, PREM -0.6 +/- 5.1 mm(2)/cmH(2)O, P = not significant). We conclude that the intrinsic properties of the airway wall determine retroglossal compliance independent of changes in the neuromuscular activity associated with changes in sleep state.

Sleep fragmentation, awake blood pressure, and sleep-disordered breathing in a population-based study.

Arousal from sleep produces transient increases in systemic blood pressure, leading to the suggestion that repeated arousals are associated with a sustained increase in daytime blood pressure. Using data from the Wisconsin Sleep Cohort Study, a population-based study, we tested the hypothesis that sleep fragmentation is associated with elevated awake blood pressure. Sleep, breathing, and seated blood pressure measurements from 1,021 participants (age 42 +/- 8 yr; 590 males) were analyzed. Sleep fragmentation was defined as the total number of awakenings and shifts to Stage 1 sleep divided by the total sleep time (sleep fragmentation index: SFI). To reduce the confounding influence of sleep-disordered breathing, which is related to both increased daytime blood pressure and sleep fragmentation, all participants with an apnea-hypopnea index (AHI) > or = 1 were analyzed separately. Accounting for the influences of sex, age, body mass index, and antihypertensive medication use, the SFI was significantly associated with higher levels of awake systolic blood pressure in people with an AHI < 1; a 2 standard deviation increase in the SFI was associated with a 3.1 mm Hg rise in awake systolic blood pressure. In participants with an AHI > or = 1, there was no independent association between the SFI and awake blood pressure after controlling for the influence of the AHI.

The use of clinical prediction formulas in the evaluation of obstructive sleep apnea.

STUDY OBJECTIVES: To prospectively study the utility of four clinical prediction models for either predicting the presence of obstructive sleep apnea (OSA, apnea-hypopnea index [AHI] > or = 10/hour), or prioritizing patients for a split-night protocol (AHI(3)20/hour). DESIGN: All patients presenting for OSA evaluation completed a research questionnaire that included questions from previously developed clinical prediction models. The probability of sleep apnea for each patient for each model was calculated based upon the equation used in the model. Based upon two cutoffs of apnea-hypopnea index, 10 and 20, the sensitivity, specificity, and positive predictive value were calculated. For the cutoffs AHI > or =10 and > or =20, receiver operating characteristic curves were generated and the areas under the curves calculated. Comparisons of demographic information and symptom response were compared between patients with and without OSA, and men vs. women. SETTING: Urban, accredited sleep disorders center. PATIENTS OR PARTICIPANTS: All patients referred for evaluation of OSA who underwent polysomnography. INTERVENTIONS: N/A. RESULTS: 370 patients (191 men, 179 women) completed the study. 248 of the 370 (67%) patients had an AHI(3)10; 180 of the 370 (49%) had an AHI> or =20. For AHI > or =10, the sensitivities ranged from 76 to 96%, specificities from 13%-54%, positive predictive values from 69%-77% using the probability cutoff of the original investigators; the areas under the curve from 0.669 to 0.736. For AHI(3)20, the areas under the ROC curves ranged from 0.700 to 0.757; using cutoffs to maximized specificity, the sensitivities ranged from 33%-39%, specificities from 87%-93%, and positive predictive values from 72%-85%. All the models performed better for men. CONCLUSIONS: The clinical prediction models tested are not be sufficiently accurate to discriminate between patients with or without OSA but could be useful in prioritizing patients for split-night polysomnography.

Effect of gender on the development of hypocapnic apnea/hypopnea during NREM sleep.

We hypothesized that a decreased susceptibility to the development of hypocapnic central apnea during non-rapid eye movement (NREM) sleep in women compared with men could be an explanation for the gender difference in the sleep apnea/hypopnea syndrome. We studied eight men (age 25-35 yr) and eight women in the midluteal phase of the menstrual cycle (age 21-43 yr); we repeated studies in six women during the midfollicular phase. Hypocapnia was induced via nasal mechanical ventilation for 3 min, with respiratory frequency matched to eupneic frequency. Tidal volume (VT) was increased between 110 and 200% of eupneic control. Cessation of mechanical ventilation resulted in hypocapnic central apnea or hypopnea, depending on the magnitude of hypocapnia. Nadir minute ventilation in the recovery period was plotted against the change in end-tidal PCO(2) (PET(CO(2))) per trial; minute ventilation was given a value of 0 during central apnea. The apneic threshold was defined as the x-intercept of the linear regression line. In women, induction of a central apnea required an increase in VT to 155 +/- 29% (mean +/- SD) and a reduction of PET(CO(2)) by -4.72 +/- 0.57 Torr. In men, induction of a central apnea required an increase in VT to 142 +/- 13% and a reduction of PET(CO(2)) by -3.54 +/- 0.31 Torr (P = 0.002). There was no difference in the apneic threshold between the follicular and the luteal phase in women. Premenopausal women are less susceptible to hypocapnic disfacilitation during NREM sleep than men. This effect was not explained by progesterone. Preservation of ventilatory motor output during hypocapnia may explain the gender difference in sleep apnea.

Sleep apnea and quality of life.

OBJECTIVE: To investigate the effects of sleep apnea (SA) on the quality of life (QOL). DESIGN: A prospective study of QOL in patients with and without SA as defined by an apnea-hypopnea index (AHI) >5. SETTING: University-based outpatient clinics. PATIENTS: Primary care patients followed in a general internal medicine clinic as well as those referred to a sleep disorders clinic at the University of Wisconsin Hospital and Clinics were consecutively recruited and classified into 3 groups of subjects: (1) patients without SA (AHI<5) (n=46), (2) patients with mild SA (AHI 5-15) (n=16), and (3) patients with moderate to severe SA (AHI>15) (n=21). INTERVENTIONS: NA. MEASUREMENTS: QOL was assessed with the Medical Outcomes Study SF-36 Health Survey. Health history and demographic data were obtained via structured interview and medical record review. All subjects underwent overnight polysomnography for diagnosis of SA. RESULTS: After controlling for age, gender, body mass index, and number of comorbid conditions, the association between sleep apnea and QOL was significant in the domains of physical functioning and role limitation due to physical health problems (p<0.05) and was borderline in vitality (p<0.1). Patients with both mild and moderately severe SA scored significantly lower (worse) than did patients without SA in physical functioning and in role limitations due to physical-health (82 and 83 vs. 92, respectively). Moderate to severe SA subjects scored significantly lower in vitality than did subjects without SA (51 vs. 64, p<0.05). Subscales analysis revealed that subjects with moderate to severe SA had significantly lower scores that did those without SA in positive affect (69 vs. 79), current health perceptions (71 vs. 80) and vitality (50 vs. 70), p<0.05 for all comparisons. A large percentage of patients without SA had perfect scores of 100 (ceiling effect) on the physical, social, and role functioning scales. CONCLUSIONS: SA has an independent impact on several QOL domains after adjusting for differences in age, gender, body mass index, and comorbidity. QOL outcomes were likely attenuated by ceiling effects. Disentangling the scales that measure multidimensional QOL (positive and negative aspects) enhanced the ability of the SF-36 to detect important consequences of sleep apnea on QOL.

Pathogenesis of obstructive sleep apnea.

Obstructive sleep apnea is a fairly common disorder with significant adverse health consequences. However, the pathogenetic mechanisms remain incompletely understood. Upper airway (UA) patency is determined by several neuromuscular and nonneuromuscular factors including (1) UA dilating muscle activity, (2) the collapsing transmural pressure generated during inspiration, (3) changes in caudal traction, (4) vasomotor tone, and (5) mucosal adhesive forces. This review addresses the effect of sleep on UA function and how these factors conspire to cause UA obstruction.

Progressive retropalatal narrowing preceding obstructive apnea.

Pharyngeal occlusion during obstructive apnea is thought to be an inspiratory-related event; however, occlusion also occurs in the absence of negative intrathoracic pressure. We hypothesized that inspiratory-related pharyngeal occlusion would be preceded by significant expiratory narrowing. Eight sleeping patients with obstructive apnea were studied. Pharyngeal caliber, airflow, and esophageal pressure (Pes) were simultaneously monitored during three to four consecutive breaths preceding occlusion (between 3 and 22 events were studied per subject). Relative changes in retropalatal airway cross-sectional area (CSA) were determined from fiberoptic images (five frames per second) normalized to the maximum CSA. During inspiration, CSA was significantly reduced only during the breath immediately preceding the apnea (Group mean CSA +/- SEM: 51 +/- 8% at the start of inspiration compared with 37 +/- 8% at midinspiration). During expiration, for all breaths there was an initial significant increase in CSA compared with the nadir CSA during the preceding inspiration (CSA: breath-3, 57 +/- 10% to 79 +/- 3%; breath-2, 59 +/- 8% to 76 +/- 4%; breath-1, 37 +/- 8% to 64 +/- 8%), followed by a significant narrowing at end-expiration compared with the peak CSA during that expiration (CSA: breath-3, 79 +/- 3% to 62 +/- 6%; breath-2, 76 +/- 4% to 50 +/- 10%; breath-1, 64 +/- 8% to 36 +/- 10%). Occlusion occurred at a pressure significantly less than that generated during the previous unoccluded breath (Pes: breath-1, -10.8 +/- 2.9 cm H2O; occlusion, -8.2 +/- 1.9 cm H2O). These results show that expiratory narrowing produced a significant reduction of CSA at end-expiration prior to obstructive apnea.

The effect of rapid eye movement (REM) sleep on upper airway mechanics in normal human subjects.

1. It has been proposed that the upper airway is more compliant during rapid eye movement (REM) sleep than during non-rapid eye movement (NREM) sleep. The purpose of this study was to test this hypothesis in a group of subjects without sleep-disordered breathing. 2. On the first night, the effect of sleep stage on the relationship of retropalatal cross-sectional area (CSA; visualized with a fibre-optic scope) to pharyngeal pressure (PPH) measured at the soft palate during eupnoeic breathing was studied. Breaths during REM sleep were divided into phasic (associated with eye movements) and tonic (not associated with eye movements). There was a significant decrease in pharyngeal CSA during NREM sleep compared with wakefulness. There was no further decrease observed during either tonic or phasic REM sleep. Pharyngeal compliance, defined as the slope of the regression CSA versus PPH, was significantly increased during NREM sleep compared with wakefulness and REM sleep, with the compliance during both tonic and phasic REM sleep being similar to that observed in wakefulness. 3. On the second night, the effect of sleep stage on pressure-flow relationships of the upper airway was investigated. There was a trend towards the upper airway resistance being highest in NREM sleep compared with wakefulness and REM sleep. 4. We conclude that the upper airway is stiffer and less compliant during REM sleep than during NREM sleep. We postulate that this difference is secondary to differences in upper airway vascular perfusion between REM and NREM sleep.