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.

为了评估OSA肥胖青少年的睡眠模式和神经认知表现的特定特征，以将这些个体的认知功能与睡眠宏观结构参数和阶段性事件（K-复合物，KC；和睡眠纺锤体，SS）相关联。多导睡眠图记录了25例男性呼吸暂停肥胖患者（15-17岁），20例年龄和性别匹配的非呼吸性肥胖患者和15例青少年瘦身。在第2阶段非快速眼动睡眠（N2）期间确定了KC和SS，并评估了特征。此外，所有参与者都使用一系列神经认知测试进行了认知表现评估。比较参与者的数据，宏观和微观结构的睡眠变量以及认知指标。使用描述性和回归分析对发现的数据进行了分析。差异在p处是可靠的 <0.05。与两个对照组相比，OSA肥胖组的睡眠发作潜伏期（p  = 0.061），慢波睡眠（SWS）和快速眼球运动（REM）睡眠（ 两者p均<0.01 ）显着降低，但N1-N2期增加持续时间（p  <0.01），呼吸暂停期间和呼吸暂停发作后KC的出现（分别为DE-KC和AE-KC），自发性KC（SN-KC）数量和周期性降低，以及呼吸暂停诱发的KC幅度降低。在OSA组中，SS的活动是非典型的增加。速帝世界总冠军大赛，REM睡眠，最少的SaO ₂，DE-KC，AE-KC和SS以及SN-KC数量是OSA青少年认知功能（注意力，记忆力，思维，言语）变化的预测指标。综上，以上结果为OSA和肥胖合并症时睡眠稳态机制的损害提供了一些证据，并为这些青少年的睡眠微结构破坏与醒来的认知功能之间的关系提供了新颖的见解。