Auditory event-related potentials in obstructive sleep apnea: effects of treatment with nasal continuous positive airway pressure

doi:10.1016/0168-5597(91)90094-E

Electroencephalography and Clinical Neurophysiology/Evoked Potentials Section

Volume 80, Issue 5, September–October 1991, Pages 454-457

https://doi.org/10.1016/0168-5597(91)90094-E Get rights and content

Abstract

Event-related potentials (ERPs) were recorded in 47 patients with obstructive sleep apnea (OSA) syndrome prior to and after 6 weeks of treatment with continuous positive airway pressure (CPAP). Compared with a control group, the OSA patients showed ERP abnormalities: lengthened P3 latencies and decreased N2-P3 amplitudes. After 6 weeks of CPAP treatment, there was a highly significant improvement in the abnormal ERPs: the P3 and N2 latencies were shortened, but remained longer than in controls, and the N2-P3 and N1-P2 amplitudes were increased. No correlations could be established with various sleep variables. ERPs may be used as an electrophysiological marker of brain dysfunction; treatment of OSA with CPAP is probably responsible for functional brain modifications. On the other hand, possible relationships between the ERP abnormalities and the neuropsychological disorders observed in OSA remain to be established.

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Citation Excerpt :
Some of the cognitive effects are similar to sleep deprivation or fragmentation (Fulda and Schulz, 2003); however, sleep apnea is also associated with hypoxemia and cortical arousals (Zeitzer et al., 2009; Leng et al., 2017). One hypothesis is that hypoxemic neural damage contributes to deficits (Naëgelé et al., 1995; Engleman et al., 2000), with some research documenting persistent neurophysiologic changes months after treatment with positive airway pressure (Rumbach et al., 1991; Sangal and Sangal, 1997). It is unclear to what extent changes related to sleep apnea are reversible and concern has been raised about the nonreversibility of changes to executive functioning (Durmer and Dinges, 2005).
Acute trauma to the brain can lead to chronic changes in an individual's neurologic functioning, with some of the most debilitating and far-reaching consequences leading to compromised goal-directed functioning. Underlying sources of dysfunction can be dynamic, complex, and challenging to effectively address. This chapter delineates key principles that can be valuable for improving goal-directed functioning. The chapter is grounded in neuroscience and theoretical underpinnings while emphasizing practical approaches to maximizing functional improvements in an individual's personal life. Rehabilitation efforts can be maximized by taking into account multiple levels and facets of goal-directed functioning in cohesive, individualized treatments. Core functions subserved by prefrontal cortical networks may be targeted and strengthened through specific approaches to training. Optimization of functioning may require unraveling and addressing some of the many factors that can modulate brain processes. We dedicate special emphasis to considering the regulation of cognitive–emotional functioning during goal pursuit, especially pertinent to treatment of combined physical and experiential trauma that is a hallmark of military service injuries. These foundations point to frontiers for innovation in strengthening goal-directed functioning after brain injury.
The multi-level impact of chronic intermittent hypoxia on central auditory processing
2017, NeuroImage
During hypoxia, the tissues do not obtain adequate oxygen. Chronic hypoxia can lead to many health problems. A relatively common cause of chronic hypoxia is sleep apnea. Sleep apnea is a sleep breathing disorder that affects 3–7% of the population. During sleep, the patient's breathing starts and stops. This can lead to hypertension, attention deficits, and hearing disorders. In this study, we apply an established chronic intermittent hypoxemia (CIH) model of sleep apnea to study its impact on auditory processing. Adult rats were reared for seven days during sleeping hours in a gas chamber with oxygen level cycled between 10% and 21% (normal atmosphere) every 90 s. During awake hours, the subjects were housed in standard conditions with normal atmosphere. CIH treatment significantly reduces arterial oxygen partial pressure and oxygen saturation during sleeping hours (relative to controls). After treatment, subjects underwent functional magnetic resonance imaging (fMRI) with broadband sound stimulation. Responses are observed in major auditory centers in all subjects, including the auditory cortex (AC) and auditory midbrain. fMRI signals from the AC are statistically significantly increased after CIH by 0.13% in the contralateral hemisphere and 0.10% in the ipsilateral hemisphere. In contrast, signals from the lateral lemniscus of the midbrain are significantly reduced by 0.39%. Signals from the neighboring inferior colliculus of the midbrain are relatively unaffected. Chronic hypoxia affects multiple levels of the auditory system and these changes are likely related to hearing disorders associated with sleep apnea.
Obstructive sleep apnea syndrome and cognition: A review
2016, Neurophysiologie Clinique
Le syndrome d’apnée obstructive du sommeil (SAOS) est un trouble du sommeil au cours duquel le dormeur souffre de pause (apnée) ou de diminution du débit respiratoire (hypopnée) pendant quelques secondes, qui provoquent des micro-éveils et une hypoxémie/hypoxie intermittente. Bien que les résultats soient divergents, le SAOS semble affecter les fonctions cognitives, principalement l’attention/vigilance, la mémoire et les fonctions exécutives. Les facteurs à l’origine de ces déficits sont multiples, l’hypoxie et la fragmentation apparaissant comme les deux principaux contributeurs. Les études de neuro-imagerie suggèrent que le SAOS pourrait provoquer des dommages cérébraux, notamment dans les régions hippocampiques et le lobe frontal. Des données récentes laissent supposer que le traitement par pression positive continue ou CPAP pourrait corriger les anomalies cérébrales et les déficits neurocognitifs. Néanmoins, ces données sont difficiles à interpréter dans un contexte où les comorbidités très fréquentes dans le SAOS pourraient elles-mêmes être à l’origine de ces troubles. L’objectif de cet article est de présenter une revue des données de la littérature sur les fonctions cognitives et la neuro-imagerie chez des patients SAOS avant et après traitement par CPAP. Les différents mécanismes potentiels à l’origine de ces déficits cognitifs et cérébraux sont également discutés.
Obstructive sleep apnea syndrome (OSAS) is a sleep-related breathing disorder characterized by repetitive episodes of airflow cessation, resulting in brief arousals and intermittent hypoxemia. OSAS is associated with a number of adverse health consequences, and cognitive difficulties. The overall pattern of cognitive impairment in OSAS is complex, and research in this field is mixed. On balance, OSAS have negative effects on cognition, most likely in the domain of attention/vigilance, verbal and visual delayed long-term memory, and executive functions. A still unanswered question is whether these deficits are primarily a consequence of sleep fragmentation and/or hypoxemia, or whether they coexist independently from OSAS. Continuous positive airway pressure (CPAP) is the most effective and widely used treatment of OSAS. No consistent effect of CPAP use on cognitive performance was evident. This may be due, in part, to variability in study design and sampling methodology across studies. Structural changes have been reported in different brain regions, particularly in hippocampus and frontal cortex. Recent evidence suggests that the OSAS-related structural changes may improve with CPAP treatment. However, one of the challenges is to interpret the findings in light of comorbid conditions that also cause neural lesions. Animal models will be specifically useful to disentangle the different potential contributors to cognitive impairment in OSAS. The purpose of this article is to provide a review of the literature on cognition and neuroimaging in OSAS patients before and after CPAP treatment. We also discuss the mechanisms that have been proposed to explain cognitive deficits in OSAS patients.
Cognitive impairment in obstructive sleep apnea
2014, Pathologie Biologie
Obstructive sleep apnea (OSA) is characterised by repetitive cessation or reduction of airflow due to upper airway obstructions. These respiratory events lead to chronic sleep fragmentation and intermittent hypoxemia. Several studies have shown that OSA is associated with daytime sleepiness and cognitive dysfunctions, characterized by impairments of attention, episodic memory, working memory, and executive functions. This paper reviews the cognitive profile of adults with OSA and discusses the relative role of altered sleep and hypoxemia in the aetiology of these cognitive deficits. Markers of cognitive dysfunctions such as those measured with waking electroencephalography and neuroimaging are also presented. The effects of continuous positive airway pressure (CPAP) on cognitive functioning and the possibility of permanent brain damage associated with OSA are also discussed. Finally, this paper reviews the evidence suggesting that OSA is a risk factor for developing mild cognitive impairment and dementia in the aging population and stresses the importance of its early diagnosis and treatment.
L’apnée obstructive du sommeil est caractérisée par des pauses respiratoires ou des réductions du débit aérien répétées qui sont dues à une obstruction des voies aériennes supérieures. Ces évènements respiratoires entraînent une fragmentation chronique du sommeil et une hypoxémie intermittente. Plusieurs études ont montré que l’apnée obstructive du sommeil est associée à la somnolence diurne ainsi qu’aux dysfonctions cognitives incluant des déficits au niveau de l’attention, de la mémoire épisodique, de la mémoire de travail et des fonctions exécutives. Cet article examine le profil cognitif observé chez les adultes présentant l’apnée obstructive du sommeil. Les rôles spécifiques de l’altération du sommeil et de l’hypoxémie dans l’étiologie des dysfonctions cognitive seront également abordés. Les marqueurs de dysfonctions cérébrales tels que ceux mesurés en électroencéphalographie et en neuroimagerie seront aussi présentés. Les études examinant l’efficacité du traitement par pression positive continue afin d’améliorer les déficits cognitifs dans cette population seront discutées ainsi que la possibilité que l’apnée obstructive du sommeil puisse causer des dommages permanents au cerveau. Enfin, cet article présente les récents résultats concernant la relation entre l’apnée obstructive du sommeil et le risque de développer un trouble cognitif léger et une démence dans la population âgée et souligne l’importance d’un diagnostic précoce en vue d’initier un traitement de l’apnée obstructive du sommeil.
Auditory evoked potentials remain abnormal after CPAP treatment in patients with severe obstructive sleep apnoea
2012, Clinical Neurophysiology
Citation Excerpt :
These early components have been found to be sensitive to an individual’s state of arousal (Naatanen and Picton, 1987) and sleep deprivation (Lee et al., 2004), and abnormalities have been reported in untreated OSA (Sforza and Haba-Rubio, 2006; Wong et al., 2006). However, only two early studies (Walsleben et al., 1989; Rumbach et al., 1991) have examined the effects of OSA treatment on early ERP components and the adequacy of control data remains unclear in both. Thus, this study aimed to assess the effects of ∼3 months of optimal CPAP treatment on the N1, P2, N2 and P3 components of auditory ERP (AERP) waveforms in severe OSA patients compared to age and gender matched controls.
To assess the effects of 3 months of optimal CPAP treatment on auditory event related potentials (AERP) in patients with severe obstructive sleep apnoea (OSA) compared with healthy controls.
Auditory odd-ball related N1, P2, N2 and P3 AERP components were assessed in 9 severe OSA subjects and 9 healthy controls at baseline evaluation and at ∼3 months follow-up in both groups, with OSA subjects treated with continuous positive air-way pressure (CPAP) during this period.
Severe OSA subjects showed significantly delayed, P2, N2 and P3 latencies, and significantly different P2 and P3 amplitudes compared to controls at baseline (group effect, all p < 0.05). At follow-up evaluation P3 latency shortened in treated OSA patients but remained prolonged compared to controls (group by treatment interaction, p < 0.05) despite high CPAP compliance (6 h/night). The earlier AERP (P2 and N2) components did not change in either controls or OSA patients at follow-up and remained different in patients versus controls.
This study demonstrates that in severe OSA patients AERP responses show minimal or no improvement and remain abnormal following 3 months of optimal CPAP treatment.
Persistent cortical sensory processing abnormalities despite treatment in severe OSA may have implications for daytime neurobehavioral performance and safety in OSA patients. AERP responses may help identify residual performance deficits and risks.
Altered cortical excitability in patients with untreated obstructive sleep apnea syndrome
2010, Sleep Medicine
To investigate cortical excitability in patients with obstructive sleep apnea syndrome (OSAS) during wakefulness.
The authors recruited 45 untreated severe OSAS (all males, mean age 47.2 years, mean apnea–hypopnea index = 44.6 h⁻¹) patients and 44 age-matched healthy male volunteers (mean apnea–hypopnea index = 3.4 h⁻¹). The TMS parameters measured were resting motor threshold (RMT), motor evoked potential (MEP) amplitude, cortical silent period (CSP), and short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF). These parameters were measured in the morning (9–10 am) more than 2 h after arising and the parameters of patients and controls were compared. The Epworth Sleepiness Scale (ESS) and the Stanford Sleepiness Scale (SSS) were also measured before the TMS study.
OSAS patients had a significantly higher RMT and a longer CSP duration (t-test, p < 0.001) compared to healthy volunteers. No significant difference was observed between MEP amplitudes at any stimulus intensity or between the SICI (2, 3, 5 ms) and ICF (10, 15, 20 ms) values of OSAS patients and healthy volunteers (p > 0.05).
This TMS-based study suggests that untreated severe OSAS patients have imbalanced cortical excitabilities that enhanced inhibition or decreased brain excitability when awake during the day.

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^∗: Present address: Service de Neurologie, Hôpital J. Minjoz, F-25030 Besançon Cedex, France.

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Short communicationAuditory event-related potentials in obstructive sleep apnea: effects of treatment with nasal continuous positive airway pressure

Abstract

Electroenceph. clin. Neurophysiol.

Biol. Psychol.

Chest

Electroenceph. clin. Neurophysiol.

J. Chron. Dis.

Electroenceph. clin. Neurophysiol.

Electroenceph. clin. Neurophysiol.

Neuropsychologia

Lancet

Rev. EEG Neurophysiol.

Electroenceph. clin. Neurophysiol.

Physiol. Behav.

Cognitive and psychological dysfunction in sleep apnea before and after treatment with CPAP

Sleep Res.

Cerebrospinal fluid adenosine 3′,5′-monophosphate, 5-hydroxyindolacetic acid and homovanillic acid in patients with sleep apnoea syndrome

J. Neurol. Neurosurg. Psychiat.

Unilateral temporal lobe lesions alter P300 scalp topography

Int. J. Neurosci.

Neuropsychologic symptoms in obstructive sleep apnea improve after treatment with nasal continuous positive airway pressure

Chest

Surprise!…surprise?

Psychophysiology

Is the P300 component a manifestation of context updating?

Behav. Brain Sci.

Short communication
Auditory event-related potentials in obstructive sleep apnea: effects of treatment with nasal continuous positive airway pressure