The behavioral morbidity of obstructive sleep apnea

Day, Ryan; Gerhardstein, Rebecca; Lumley, Alicia; Roth, Thomas; Rosenthal, León

doi:10.1053/pcad.1999.0410341

Cited by 66 publications

(49 citation statements)

References 50 publications

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“…In non-PWS adults, OSAS severity is associated with increased anxiety, distractibility, confusion, irritability, physical and general complaints, depressed mood, higher emotional reactivity, and reduced energy (D'Ambrosio, Bowman, & Mohsenin, 1999;Day, Gerhardstein, Lumley, Roth, & Rosenthal, 1999;Kales et al, 1985;Sanner et al, 2000). In non-PWS children, OSAS is further associated with reduced academic performance and increased problematic behavior (Spahis, 1994;Urschitz et al, 2003).…”

Section: Psychosocial Functioning In Prader-willi Syndrome and Non-prmentioning

confidence: 99%

Obstructive Sleep Apnea Syndrome in Prader-Willi Syndrome: An Unrecognized and Untreated Cause of Cognitive and Behavioral Deficits?

et al. 2006

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Prader-Willi Syndrome (PWS) is a rare genetic disorder characterized by a range of physical, psychological, and physiological abnormalities. It is also distinguished by the high prevalence of obstructive sleep apnea syndrome (OSAS), i.e., repetitive upper airway collapse during sleep resulting in hypoxia and sleep fragmentation. In non-PWS populations, OSAS is associated with a range of neurocognitive and psychosocial deficits. Importantly, these deficits are at least partly reversible following treatment. Given the findings in non-PWS populations, it is possible that OSAS may contribute to neurocognitive and psychosocial deficits in PWS. The present review examines this possibility. While acknowledging a primary contribution from the primary genetic abnormality to central neural dysfunction in PWS, we conclude that OSAS may be an important secondary contributing factor to reduced neurocognitive and psychosocial performance. Treatment of OSAS may have potential benefits in improving neurocognitive performance and behavior in PWS, but this awaits confirmatory investigation.

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Section: Psychosocial Functioning In Prader-willi Syndrome and Non-prmentioning

confidence: 99%

Obstructive Sleep Apnea Syndrome in Prader-Willi Syndrome: An Unrecognized and Untreated Cause of Cognitive and Behavioral Deficits?

et al. 2006

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“…The prevalence of OSA is estimated at 1 -5% of adult men in western countries (Young et al 2002). This disease is associated with excessive daytime sleepiness (EDS), neurocognitive deficits, and psychological problems (Day et al 1999). Furthermore, this disease is a risk factor for traffic accidents (Findley et al 1995, Barbé et al 1998 and cardiovascular disease morbidity and mortality (Peter et al 1995, Leung andBradley 2001).…”

Section: Introductionmentioning

confidence: 99%

Nonlinear characteristics of blood oxygen saturation from nocturnal oximetry for obstructive sleep apnoea detection

Álvarez¹,

Hornero²,

Abásolo³

et al. 2006

Physiol. Meas.

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Nocturnal oximetry is an attractive option for the diagnosis of obstructive sleep apnoea (OSA) syndrome because of its simplicity and low cost compared to polysomnography (PSG). The present study assesses non-linear analysis of blood oxygen saturation (SaO 2 ) from nocturnal oximetry as a diagnostic test to discriminate between OSA positive and OSA negative patients. A sample of 187 referred outpatients, clinically suspected of having OSA, were studied using nocturnal oximetry performed simultaneously with complete PSG. A positive OSA diagnosis was found for 111 cases, while the remaining 76 cases were classified as OSA negative. The following oximetric indexes were obtained: cumulative time spent below a saturation of 90% (CT90), oxygen desaturation indexes of 4% (ODI4), 3% (ODI3) and 2% (ODI2), and the delta index (∆ index). SaO 2 records were subsequently processed applying two non-linear methods: central tendency measure (CTM) and Lempel-Ziv (LZ) complexity. Significant differences (p < 0.01) were found between OSA positive and OSA negative patients. Using CTM we obtained a sensitivity of 90.1% and a specificity of 82.9%, while with LZ the sensitivity was 86.5% and the specificity was 77.6%. CTM and LZ accuracy was higher than that provided by ODI4, ODI3, ODI2 and CT90. The results suggest that non-linear analysis of SaO 2 signals from nocturnal oximetry could yield useful information in OSA diagnosis.

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“…Obstructive sleep apnea (OSA) affects 2-4% of the general population (Young et al, 1993), and is characterized by apneic moments during sleep, which are terminated by brief arousals and a reestablishment of the upper airway patency. Thus, sleep fragmentation is a primary physiological disturbance, and may be responsible for some of the symptoms/signs associated with OSA, including excessive daytime sleepiness, which is a principal presenting complaint of patients (Roth et al, 1995;Roth et al, 1995;Roth and Roehrs, 1996;Day et al, 1999). Furthermore, patients suffering from a variety of psychiatric, medical, and sleep/respiratory disorders may also experience sleep fragmentation leading to excessive daytime somnolence and impairments of both attention and memory (for review, see Hoyt, 1995;Kryger et al, 2000;Sateia et al, 2000;Soldatos and Paparrigopoulos, 2005).…”

mentioning

confidence: 99%

Sleep fragmentation elevates behavioral, electrographic and neurochemical measures of sleepiness

et al. 2007

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Sleep fragmentation, a feature of sleep apnea as well as other sleep and medical/psychiatric disorders, is thought to lead to excessive daytime sleepiness. A rodent model of sleep fragmentation was developed (termed sleep interruption, SI), where rats were awakened every 2 min by the movement of an automated treadmill for either 6 or 24 h of exposure. The sleep pattern of rats exposed to 24h of SI resembled sleep of the apneic patient in the following ways: sleep was fragmented (up to 30 awakening/h), total REM sleep time was greatly reduced, NREM sleep episode duration was reduced (from 2 min, 5 s baseline to 58 s during SI), whereas the total amount of NREM sleep time per 24h approached basal levels. Both 6 and 24 h of SI made rats more sleepy, as indicated by a reduced latency to fall asleep upon SI termination. Electrographic measures in the recovery sleep period following either 6 or 24 h of SI also indicated an elevation of homeostatic sleep drive; specifically, the average NREM episode duration increased (e.g., for 24 h SI, from 2 min, 5 s baseline to 3 min, 19 s following SI), as did the NREM delta power during recovery sleep. Basal forebrain (BF) levels of extracellular adenosine (AD) were also measured with microdialysis sample collection and HPLC detection, as previous work suggests that increasing concentrations of BF AD are related to sleepiness. BF AD levels were significantly elevated during SI, peaking at 220% of baseline during 30 h of SI exposure. These combined findings imply an elevation of the homeostatic sleep drive following either 6 or 24 h of SI, and BF AD levels appear to correlate more with sleepiness than with the cumulative amount of prior wakefulness, since total NREM sleep time declined only slightly. SI may be partially responsible for the symptom of daytime sleepiness observed in a number of clinical disorders, and this may be mediated by mechanisms involving BF AD. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2007 December 27. Published in final edited form as:Neuroscience. Obstructive sleep apnea (OSA) affects 2-4% of the general population (Young et al., 1993), and is characterized by apneic moments during sleep, which are terminated by brief arousals and a reestablishment of the upper airway patency. Thus, sleep fragmentation is a primary physiological disturbance, and may be responsible for some of the symptoms/signs associated with OSA, including excessive daytime sleepiness, which is a principal presenting complaint of patients (Roth et a...

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The behavioral morbidity of obstructive sleep apnea

Cited by 66 publications

References 50 publications

Obstructive Sleep Apnea Syndrome in Prader-Willi Syndrome: An Unrecognized and Untreated Cause of Cognitive and Behavioral Deficits?

Obstructive Sleep Apnea Syndrome in Prader-Willi Syndrome: An Unrecognized and Untreated Cause of Cognitive and Behavioral Deficits?

Nonlinear characteristics of blood oxygen saturation from nocturnal oximetry for obstructive sleep apnoea detection

Sleep fragmentation elevates behavioral, electrographic and neurochemical measures of sleepiness

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