The association between obstructive sleep apnea and neurocognitive performance–the Apnea Positive Pressure Long-term Efficacy Study (APPLES)

Arizona Respiratory Center, University of Arizona, Tucson, AZ, USA.
Sleep (Impact Factor: 4.59). 03/2011; 34(3):303-314B.
Source: PubMed


To determine associations between obstructive sleep apnea (OSA) and neurocognitive performance in a large cohort of adults.
Cross-sectional analyses of polysomnographic and neurocognitive data from 1204 adult participants with a clinical diagnosis of obstructive sleep apnea (OSA) in the Apnea Positive Pressure Long-term Efficacy Study (APPLES), assessed at baseline before randomization to either continuous positive airway pressure (CPAP) or sham CPAP.
Sleep and respiratory indices obtained by laboratory polysomnography and several measures of neurocognitive performance.
Weak correlations were found for both the apnea hypopnea index (AHI) and several indices of oxygen desaturation and neurocognitive performance in unadjusted analyses. After adjustment for level of education, ethnicity, and gender, there was no association between the AHI and neurocognitive performance. However, severity of oxygen desaturation was weakly associated with worse neurocognitive performance on some measures of intelligence, attention, and processing speed.
The impact of OSA on neurocognitive performance is small for many individuals with this condition and is most related to the severity of hypoxemia.

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    • "Neuroimaging studies have showed structural changes in the brains of individuals with OSA [5] [6] [7] [8] [9] [10] [11]. Diffusion-weighted Imaging (DWI) enables valuable information in certain pathologies of the brain. "
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    ABSTRACT: Purpose: We investigated diffusion alterations in specific regions of the brain in morbid obese, obese, and nonobese OSA patients and searched whether there is a correlation between BMI and ADC values. Materials and methods: DWIs of 65 patients with OSA were evaluated. The patients were classified according to BMI as morbid obese (n = 16), obese (n = 27), and nonobese (control, n = 22) groups. ADC measurements were performed from 24 different regions of the brain in each patient. The relationship of BMI with ADC values was searched. Results: The ADC values in hypothalamus, insular cortex, parietal cortex, caudate nucleus, frontal white matter, and posterior limb of internal capsule were all increased in obese patients (n = 43) compared to control group. The ADC values of midbrain, hypothalamus, orbitofrontal cortex, and parietal cortex were significantly increased in morbid obese compared to obese patients. In obese patients, the degree of BMI was positively correlated with ADC values of orbitofrontal cortex, parietal cortex, and hypothalamus. Conclusion: We observed increasing brain vasogenic edema with increasing BMI, suggesting that the main reason of brain diffusion alteration in patients with OSA could be obesity related.
    The Scientific World Journal 03/2014; 2014:768415. DOI:10.1155/2014/768415 · 1.73 Impact Factor
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    • "Clinicians often face difficulty in identifying which patients are at risk of accidents because of the disparity between daytime symptoms and conventional metrics of disease severity [e.g. apnea hypopnea index (AHI)] (Beebe, 2005; Al-Shawwa et al., 2008; Quan et al., 2011). Moreover, the heterogeneity of impairment in the patient population adds to this problem -one patient may be relatively asymptomatic whereas another may be greatly compromised even though both have the same degree of disease measured by sleep study (Beebe, 2005). "
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    ABSTRACT: OBJECTIVE: To explore the use of detrended fluctuation analysis (DFA) scaling exponent of the awake electroencephalogram (EEG) as a new alternative biomarker of neurobehavioural impairment and sleepiness in obstructive sleep apnea (OSA). METHODS: Eight patients with moderate-severe OSA and nine non-OSA controls underwent a 40-h extended wakefulness challenge with resting awake EEG, neurobehavioural performance (driving simulator and psychomotor vigilance task) and subjective sleepiness recorded every 2-h. The DFA scaling exponent and power spectra of the EEG were calculated at each time point and their correlation with sleepiness and performance were quantified. RESULTS: DFA scaling exponent and power spectra biomarkers significantly correlated with simultaneously tested performance and self-rated sleepiness across the testing period in OSA patients and controls. Baseline (8am) DFA scaling exponent but not power spectra were markers of impaired simulated driving after 24-h extended wakefulness in OSA (r=0.738, p=0.037). OSA patients had a higher scaling exponent and delta power during wakefulness than controls. CONCLUSIONS: The DFA scaling exponent of the awake EEG performed as well as conventional power spectra as a marker of impaired performance and sleepiness resulting from sleep loss. SIGNIFICANCE: DFA may potentially identify patients at risk of neurobehavioural impairment and assess treatment effectiveness.
    Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology 04/2013; 124(8). DOI:10.1016/j.clinph.2013.02.022 · 3.10 Impact Factor
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    • "Our findings of opposite response in deactivation of the temporal brain regions after 2 months of active and sham-CPAP treatment support our initial hypothesis: that OSAS has a negative impact particularly on the temporal lobe part of the DMN, possibly via the effects of nocturnal hypoxemia. Our results are corroborated by the findings of the recent multicentric APPLES study showing hypoxemia as the major OSAS-related factor to correlate with behavioral cognitive deficit in OSAS patients [26] and by the fact that overall, the most consistent findings in structural neuroimaging studies of OSAS patients are signs of hippocampal injury (atrophy or metabolic anomaly) [27], [28], [29], [30]. Similarly, in a recent study, O'Donghue et al have found metabolic abnormalities in the hippocampus of OSAS patients comparable in magnitude to changes found in Alzheimer's disease [31]. "
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    ABSTRACT: Functional magnetic resonance imaging studies enable the investigation of neural correlates underlying behavioral performance. We investigate the effect of active and sham Continuous Positive Airway Pressure (CPAP) treatment on working memory function of patients with Obstructive Sleep Apnea Syndrome (OSAS) considering Task Positive and Default Mode networks (TPN and DMN). An experiment with 4 levels of visuospatial n-back task was used to investigate the pattern of cortical activation in 17 men with moderate or severe OSAS before and after 2 months of therapeutic (active) or sub-therapeutic (sham) CPAP treatment. Patients with untreated OSAS had significantly less deactivation in the temporal regions of the DMN as compared to healthy controls, but activation within TPN regions was comparatively relatively preserved. After 2 months of treatment, active and sham CPAP groups exhibited opposite trends of cerebral activation and deactivation. After treatment, the active CPAP group demonstrated an increase of cerebral activation in the TPN at all task levels and of task-related cerebral deactivation in the anterior midline and medial temporal regions of the DMN at the 3-back level, associated with a significant improvement of behavioral performance, whereas the sham CPAP group exhibited less deactivation in the temporal regions of Default Mode Network and less Task Positive Network activation associated to longer response times at the 3-back. OSAS has a significant negative impact primarily on task-related DMN deactivation, particularly in the medial temporal regions, possibly due to nocturnal hypoxemia, as well as TPN activation, particularly in the right ventral fronto-parietal network. After 2 months of active nasal CPAP treatment a positive response was noted in both TPN and DMN but without compete recovery of existing behavioral and neuronal deficits. Initiation of CPAP treatment early in the course of the disease may prevent or slow down the occurrence of irreversible impairment.
    PLoS ONE 12/2012; 7(12):e47433. DOI:10.1371/journal.pone.0047433 · 3.23 Impact Factor
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