Impaired Neurobehavioural Performance in Untreated Obstructive Sleep Apnea Patients Using a Novel Standardised Test Battery (original) (raw)
Related papers
2018
Objective/Background<p>Although polysomnography (PSG) is the gold-standard measure for assessing disease severity in obstructive sleep apnea (OSA), it has limited value in identifying individuals experiencing significant neurobehavioural dysfunction. This study used a brief and novel computerised test battery to examine neurobehavioural function in adults with and without OSA.</p>Patients/Methods<p>204 patients with untreated OSA [age 49.3 (12.5) years; body mass index, [BMI] 33.6 (8.0) kg/m<sup>2</sup>; Epworth sleepiness scale 12 (4.9)/24; apnea hypopnea index 33.6 (25.8)/h] and 50 non-OSA participants [age 39.2 (14.0) years; BMI 25.8 (4.2) kg/m<sup>2</sup>, ESS 3.6 (2.3)/24]. All participants completed a computerised neurobehavioural battery during the daytime in the sleep clinic. The OSA group subsequently underwent an overnight PSG. The 30 min test battery assessed cognitive domains of visual spatial scanning and selective attention (Le...
Sleep Medicine Reviews, 2017
Obstructive sleep apnea (OSA) results in significantly impaired cognitive functioning and increased daytime sleepiness in some patients leading to increased risk of motor vehicle and workplace accidents and reduced productivity. Clinicians often face difficulty in identifying which patients are at risk of neurobehavioural dysfunction due to wide inter-individual variability, and disparity between symptoms and conventional metrics of disease severity such as the apnea hypopnea index. Quantitative electroencephalogram (EEG) measures are determinants of awake neurobehavioural function in healthy subjects. However, the potential value of quantitative EEG (qEEG) measurements as biomarkers of neurobehavioural function in patients with OSA has not been examined. This review summarises the existing literature examining qEEG in OSA patients including changes in brain activity during wake and sleep states, in relation to daytime sleepiness, cognitive impairment and OSA treatment. It will speculate on the mechanisms which may underlie changes in EEG activity and discuss the potential utility of qEEG as a clinically useful predictor of neurobehavioural function in OSA.
Applied sciences (Basel, Switzerland), 2021
We aim to determine the sleep correlates of age-related brain loss in a sample of middle-aged to older males with obstructive sleep apnea (OSA). We recruited consecutive treatment naïve male patients with moderate to severe OSA from January to November of 2019. We excluded participants if they had dementia, stroke or heart disease. We collected demographic variables and vascular risk factors. We also obtained the insomnia severity index, the Epworth sleepiness scale and the Pittsburgh sleep quality index. We also obtained computerized neurocognitive testing with the go-no-go response inhibition test, Stroop interference test, catch game test, staged information processing speed test, verbal memory test and non-verbal memory test. We derived age and education adjusted domain-specific Z-scores for global cognition, memory, attention, processing speed and executive function. We used brain MRI T1-weighted images to derive total hippocampal and gray matter volumes. Partial correlations e...
Obstructive sleep apnea–hypopnea and neurocognitive functioning in the Sleep Heart Health Study
Sleep Medicine, 2006
Background and purpose: Obstructive sleep apnea-hypopnea (OSAH) is associated with sleep fragmentation and nocturnal hypoxemia. In clinical samples, patients with OSAH frequently are found to have deficits in neuropsychological function. However, the nature and severity of these abnormalities in non-clinical populations is less well defined. Patients and methods: One hundred and forty-one participants from the Tucson, AZ and New York, NY field centers of the Sleep Heart Health Study completed a battery of neuropsychological tests for 9-40 months (meanZ24 months, SDZ7 months) after an unattended home polysomnogram. Sixty-seven participants had OSAH (AHIO10) and 74 did not have OSAH (control (CTL), apnea-hypopnea index (AHI)!5). In addition to the individual tests, composite variables representing attention, executive function, MotorSpeed and processing speed were constructed from the neuropsychological test battery. Results: There were no significant differences in any individual neuropsychological test or composite variable between the OSAH and CTL groups. However, when time spent with O 2 saturations less than 85% was dichotomized into those participants in the top quartile of the distribution and those in the lower three quartiles, motor speed was significantly impaired in those who were more hypoxemic. In addition, poorer motor speed (model adjusted R 2 Z0.242, P!0.001) and processing speed performance (model adjusted R 2 Z0.122, P!0.001) were associated with more severe oxygen desaturation even after controlling for degree of daytime sleepiness, age, gender and educational level. Conclusions: Mild to moderate OSAH has little impact on the selected measures of attention, executive function, motor speed and processing speed. However, hypoxemia adversely affects both motor and processing speed. These results suggest that in middle-aged to elderly adults the neuropsychological effects of clinically unrecognized mild to moderate OSAH are neither global nor large. q
Impact of obstructive sleep apnea on cognitive performance
Arquivos de Neuro-Psiquiatria, 2011
OBJECTIVE: To evaluate the impact of obstructive sleep apnea (OSA) on cognition. METHOD: We compared the performance of 17 patients with polysomnographic diagnosis of OSA in brief cognitive tests to that of 20 healthy controls, matched for age and education. The testing battery included the Mini-Mental State Examination (MMSE), Brief Cognitive Screening Battery (BCSB), Digit-Symbol (DS) and Phonemic Verbal Fluency (FAS). Anthropometric measures and scores from the Epworth Sleepiness Scale were also recorded. RESULTS: OSA patients performed significantly worse than controls in the MMSE, in memory items from the BCSB, in DS and also in FAS. OSA patients also exhibited higher body mass index, increased neck circumference and higher scores in Epworth Sleepiness Scale than controls. CONCLUSION: OSA significantly impairs cognitive performance, especially within the domains of attention, memory and executive functioning. These deficits may be detected by brief and easy-to-administer cognit...
American Journal of Respiratory and Critical Care Medicine, 2011
Rationale: Obstructive sleep apnea (OSA) is commonly associated with neurocognitive impairments that have not been consistently related to specific brain structure abnormalities. Knowledge of the brain structures involved in OSA and the corresponding functional implications could provide clues to the pathogenesis of cognitive impairment and its reversibility in this disorder. Objectives: To investigate the cognitive deficits and the corresponding brain morphology changes in OSA, and the modifications after treatment, using combined neuropsychologic testing and voxelbased morphometry. Methods: A total of 17 patients treatment-naive to sleep apnea and 15 age-matched healthy control subjects underwent a sleep study, cognitive tests, and magnetic resonance imaging. After 3 months of treatment, cognitive and imaging data were collected to assess therapy efficacy. Measurements and Main Results: Neuropsychologic results in pretreatment OSA showed impairments in most cognitive areas, and in mood and sleepiness. These impairments were associated with focal reductions of gray-matter volume in the left hippocampus (entorhinal cortex), left posterior parietal cortex, and right superior frontal gyrus. After treatment, we observed significant improvements involving memory, attention, and executive-functioning that paralleled gray-matter volume increases in hippocampal and frontal structures. Conclusions: The cognitive and structural deficits in OSA may be secondary to sleep deprivation and repetitive nocturnal intermittent hypoxemia. These negative effects may be recovered by consistent and thorough treatment. Our findings highlight the importance of early diagnosis and successful treatment of this disorder.
Sleep Medicine, 2018
Background: Executive dysfunction (ED) is often observed in subjects diagnosed with obstructive sleep apnea (OSA), but their assessment requires facilities that are not always available. We aim to evaluate the extent to which Frontal Assessment Battery (FAB) discriminates ED in newly diagnosed, untreated, and without-comorbidity OSA patients. Methods: Sixty subjects participated in the study. Of these, 40 (31 males and 9 females) were newly diagnosed for OSA through full-night polysomnography (apnea/hypopnea index; M ¼ 39.01, SD ¼ 27.16), untreated, with a mean age of 54.50 years (SD ¼ 8.90), while the remaining 20 (15 males and 5 females) had no symptoms of OSA (M ¼ 51.60 years, SD ¼ 10.70). The instruments used were the following: Questionnaire for Sleep Apnea Risk, Epworth Sleepiness Scale, Mini-Mental State Examination, and FAB. Results: The group with OSA exhibited significantly lower values in the FAB global score (p ¼ 0.003) and in Conceptualization (p ¼ 0.001) and Mental Flexibility (p ¼ 0.009) subtests. ROC analysis showed adequate discriminative capacity for the FAB global score (AUC ¼ 0.74) and for Conceptualization (AUC ¼ 0.75) and Mental Flexibility (AUC ¼ 0.70) scores. Conclusions: The FAB is a short and no-time-consuming tool that can be used to investigate the presence of ED in untreated OSA patients with no comorbidities, providing clinicians with a simple and effective way of detecting the presence of this dysfunction and allowing a more informed decision for the need of a full neuropsychological assessment.
Sleep, 2021
Study Objectives: Extended wakefulness (EW) and obstructive sleep apnea (OSA) impair working memory (WM), but their combined effects are unclear. This study examined the impact of EW on WM function in OSA patients and identified clinical predictors of WM impairment. Methods: Following polysomnography (PSG), 56 OSA patients (mean ± SD, age 49.5 ± 8.9, apnea hypopnea index 38.1 ± 25.0) completed WM 2-back performance tasks 10 times over 24 h of wakefulness to assess average accuracy and completion times measured after 6-12 h awake (baseline) compared to 18-24 h awake (EW). Hierarchical cluster analysis classified participants with poorer versus better WM performance at baseline and during EW. Clinical predictors of performance were examined via regression and receiver operator characteristic (ROC) analyses. Results: WM performance decreased following EW and showed consistent correlations with age, Epworth Sleepiness Score (ESS), total sleep time, and hypoxemia (O 2 nadir and mean O 2 desaturation) at baseline and with EW (all p < .01). O 2 nadir and age were significant independent predictors of performance at baseline (adjusted R 2 = 0.30, p < .01), while O 2 nadir and ESS were predictors of WM following EW (adjusted R 2 = 0.38, p < .001). ROC analysis demonstrated high sensitivity and specificity of models to predict poorer versus better performing participants at baseline (83% and 69%) and during EW (84% and 74%). Conclusions: O 2 nadir, age, and sleepiness show prognostic value for predicting WM impairment in both rested and sleep-deprived OSA patients and may guide clinicians in identifying patients most at risk of impaired WM under both rested and heightened sleep pressure conditions. Clinical Trial Registration: This manuscript presents data collected as part of a larger trial-ANZCTR: Novel brain biomarkers of performance impairment in sleep apnea-https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=363830, No. ACTRN12613001171707.
Neurocognitive Decline in Obstructive Sleep Apnea: An Ignored Entity
Indian Journal of Sleep Medicine, 2019
Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder causing cognitive dysfunction. Unfortunately, both the disease itself and this disastrous complication go unnoticed due to poor perception for the same. This review attempts to explain the pathophysiology, consequences, and treatment options for the same. The keypoint is early diagnosis and treatment of OSA so as to prevent the cognitive decline.