Alteration of sleep homeostasis and cognitive impairment in apneic obese adolescents

Abstract

To evaluate specific features of sleep pattern and neurocognitive performance in OSA obese adolescents to correlate sleep macrostructural parameters and phasic events (K-complexes, KCs; and sleep spindles, SSs) with cognitive functioning in these individuals. Polysomnography was recorded from 25 male apneic obese patients (15–17 years), 20 age- and sex-matched non-apneic obese and 15 lean adolescents. KCs and SSs were identified during stage 2 non-rapid eye movement sleep (N2) and characteristics were evaluated. Furthermore, all participants underwent cognitive performance assessment using a battery of neurocognitive tests. Participant’s data, macro- and microstructural sleep variables and cognitive measures were compared. Finding data were analyzed using descriptive and regression analyses. Differences were reliable at p < 0.05. Compared to both controls, the OSA obese group had significantly reduced sleep onset latency (p = 0.061), slow-wave sleep (SWS) and rapid eye movement (REM) sleep (p < 0.01 for both), but increased N1–N2 stage duration (p < 0.01), the appearance of KCs during apnea and after apnea episodes (DE-KCs and AE-KCs, respectively), reduced spontaneous KCs (SN-KCs) number and periodicity, and lowered amplitude of apnea evoked KCs. SSs activity was an atypical increased in the OSA group. SWS, REM sleep, minimal SaO2, DE-KCs, AE-KCs, and SSs, as well as SN-KCs number, were predictors of cognitive functioning (attention, memory, thinking, speech) changes in OSA adolescents. Together, the above results provide some evidence for impairment in sleep homeostatic mechanisms, when OSA and obesity are comorbid, and provide novel insights into the relationship between sleep microstructure disruption and waking cognitive functioning in these adolescents.