Polysomnography and maintenance of wakefulness test as predictors of CPAP effectiveness in obstructive sleep apnea

Excessive daytime sleepiness (EDS) is a frequent symptom of patients with obstructive sleep apnoea (OSA). EDS is a high-risk factor for accidents at work and on the road. Thirty untreated patients with different levels of severity of OSA were studied concerning night sleep and EDS. The criterion for severity was the respiratory disturbance index (RDI): 15 patients were classified as 'moderately' apnoeic (RDI < 40), 15 as 'severely' apnoeic (RDI > 40). Following night-time polysomnography, objective and subjective aspects of EDS were studied. To assess objective EDS the Maintenance of Wakefulness Test (MWT) and a computer-based vigilance performance test were used. Subjective EDS was determined using the Stanford Sleepiness Scale (SSS), the Epworth Sleepiness Scale (ESS) and the Visual Analogue Scales for Performance (VAS-P) and Tiredness (VAS-T). Well-being was assessed using the Scale of Well-Being by von Zerssen (Bf-S/Bf-S'). Severe apnoea patients spent more time in stage 1 and less in slow-wave sleep. MWT latencies tended to be shorter in the severe apnoea group. Vigilance testing revealed no group differences. Patients with moderate apnoea described themselves as more impaired in all subjective scales, but only SSS scores reached statistical significance. Our results suggest that there is no simple correlation between polysomnographic and respiratory sleep variables at night on the one hand, and the extent of EDS on the other hand. Furthermore, subjective and objective evaluation of EDS does not yield the same results. New approaches which allow a more detailed analysis of night sleep and daytime function are required to identify high-risked patients.

show abstract

“…1992 ; Meurice et al . 1996 ; Tihonen and Partinen 1998), but not in patients with mild OSA, treated with CPAP ( Engleman et al . 1999 ).…”

Section: Discussionmentioning

confidence: 99%

Excessive daytime sleepiness in patients suffering from different levels of obstructive sleep apnoea syndrome

Sauter

Asenbaum

Popovic

et al. 2000

Journal of Sleep Research

View full text Add to dashboard Cite

show abstract

“…When treated for obstructive sleep apnea, patients typically report less somnolence, but therapy does not fully reverse wake impairments in individuals with severe sleepiness at presentation (Bedard et al, 1991;Engleman et al, 1994;Meurice et al, 1997;Tiihonen and Partinen, 1998;Kingshott et al, 2000;Patel et al, 2003;Marshall et al, 2006). In support of irreversible wake impairments, neuroimaging studies of humans with sleep apnea have identified gray matter lesions (Macey et al, 2002;Morrell et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Selective Loss of Catecholaminergic Wake–Active Neurons in a Murine Sleep Apnea Model

Zhu¹,

Fenik²,

Zhan³

et al. 2007

J. Neurosci.

163

117

View full text Add to dashboard Cite

The presence of refractory wake impairments in many individuals with severe sleep apnea led us to hypothesize that the hypoxia/ reoxygenation events in sleep apnea permanently damage wake-active neurons. We now confirm that long-term exposure to hypoxia/ reoxygenation in adult mice results in irreversible wake impairments. Functionality and injury were next assessed in major wake-active neural groups. Hypoxia/reoxygenation exposure for 8 weeks resulted in vacuolization in the perikarya and dendrites and markedly impaired c-fos activation response to enforced wakefulness in both noradrenergic locus ceruleus and dopaminergic ventral periaqueductal gray wake neurons. In contrast, cholinergic, histaminergic, orexinergic, and serotonergic wake neurons appeared unperturbed. Six month exposure to hypoxia/reoxygenation resulted in a 40% loss of catecholaminergic wake neurons. Having previously identified NADPH oxidase as a major contributor to wake impairments in hypoxia/reoxygenation, the role of NADPH oxidase in catecholaminergic vulnerability was next addressed. NADPH oxidase catalytic and cytosolic subunits were evident in catecholaminergic wake neurons, where hypoxia/reoxygenation resulted in translocation of p67 phox to mitochondria, endoplasmic reticulum, and membranes. Treatment with a NADPH oxidase inhibitor, apocynin, throughout hypoxia/reoxygenation exposures conferred protection of catecholaminergic neurons. Collectively, these data show that select wake neurons, specifically the two catecholaminergic groups, can be rendered persistently impaired after long-term exposure to hypoxia/reoxygenation, modeling sleep apnea; wake impairments are irreversible; catecholaminergic neurons are lost; and neuronal NADPH oxidase contributes to this injury. It is anticipated that severe obstructive sleep apnea in humans destroys catecholaminergic wake neurons.

show abstract

“…Despite therapy to alleviate OSA events, many individuals with OSA have residual sleepiness (3,4). Mechanisms of the residual hypersomnolence in persons with OSA are not understood, but severity of hypoxemia in OSA predicts, in part, the severity of hypersomnolence (5,6).…”

mentioning

confidence: 99%

NADPH Oxidase Mediates Hypersomnolence and Brain Oxidative Injury in a Murine Model of Sleep Apnea

Zhan

Serrano²,

Fenik³

et al. 2005

Am J Respir Crit Care Med

232

188

View full text Add to dashboard Cite

Rationale:Persons with obstructive sleep apnea may have significant residual hypersomnolence, despite therapy. Long-term hypoxia/ reoxygenation events in adult mice, simulating oxygenation patterns of moderate-severe sleep apnea, result in lasting hypersomnolence, oxidative injury, and proinflammatory responses in wakeactive brain regions. We hypothesized that long-term intermittent hypoxia activates brain NADPH oxidase and that this enzyme serves as a critical source of superoxide in the oxidation injury and in hypersomnolence. Objectives: We sought to determine whether long-term hypoxia/ reoxygenation events in mice result in NADPH oxidase activation and whether NADPH oxidase is essential for the proinflammatory response and hypersomnolence. Methods: NADPH oxidase gene and protein responses were measured in wake-active brain regions in wild-type mice exposed to long-term hypoxia/reoxygenation. Sleep and oxidative and proinflammatory responses were measured in adult mice either devoid of NADPH oxidase activity (gp91 phox -null mice) or in which NADPH oxidase activity was systemically inhibited with apocynin osmotic pumps throughout hypoxia/reoxygenation. Main Results: Long-term intermittent hypoxia increased NADPH oxidase gene and protein responses in wake-active brain regions. Both transgenic absence and pharmacologic inhibition of NADPH oxidase activity throughout long-term hypoxia/reoxygenation conferred resistance to not only long-term hypoxia/reoxygenation hypersomnolence but also to carbonylation, lipid peroxidation injury, and the proinflammatory response, including inducible nitric oxide synthase activity in wake-active brain regions. Conclusions: Collectively, these findings strongly support a critical role for NADPH oxidase in the lasting hypersomnolence and oxidative and proinflammatory responses after hypoxia/reoxygenation patterns simulating severe obstructive sleep apnea oxygenation, highlighting the potential of inhibiting NADPH oxidase to prevent oxidation-mediated morbidities in obstructive sleep apnea.Keywords: intermittent hypoxia; non-REM sleep; oxidation; peroxynitrite Obstructive sleep apnea (OSA) with daytime hypersomnolence is present in at least 2 to 4% of adults in developed countries (1). This disorder manifests as repeated events of sleep statedependent reductions in upper airway dilator motoneuronal activity, with consequent upper airway occlusions and oxyhemoglobin desaturations, each terminating with abrupt arousal and reoxygenation (2). The hypoxia and reoxygenation events may occur as frequently as once every minute of sleep. Despite therapy to alleviate OSA events, many individuals with OSA have residual sleepiness (3, 4). Mechanisms of the residual hypersomnolence in persons with OSA are not understood, but severity of hypoxemia in OSA predicts, in part, the severity of hypersomnolence (5, 6).Long-term intermittent hypoxia (LTIH) in mice, modeling the patterns of hypoxia/reoxygenation observed in moderate to severe sleep apnea, results in protracted hypersomnolence (7,8) and h...

show abstract

Polysomnography and maintenance of wakefulness test as predictors of CPAP effectiveness in obstructive sleep apnea

Cited by 13 publications

References 11 publications

Excessive daytime sleepiness in patients suffering from different levels of obstructive sleep apnoea syndrome

Excessive daytime sleepiness in patients suffering from different levels of obstructive sleep apnoea syndrome

Selective Loss of Catecholaminergic Wake–Active Neurons in a Murine Sleep Apnea Model

NADPH Oxidase Mediates Hypersomnolence and Brain Oxidative Injury in a Murine Model of Sleep Apnea

Contact Info

Product

Resources

About