重度阻塞性睡眠呼吸暂停患者不同睡眠期脑电能量密度分布及变化规律

Distribution of electroencephalograph power density in patients with severe obstructive sleep apnea during different sleep stages

目的分析重度阻塞性睡眠呼吸暂停患者（OSA）不同睡眠时期的脑电能量密度分布及其变化规律。方法前瞻性纳入天津医科大学总医院呼吸与危重症医学科收治的重度OSA患者15例为OSA组，其中男9例，女6例，年龄27-60岁，平均（45±15）岁；同期健康体检者12名为对照组，其中男7名，女5名，年龄26-61岁，平均（44±16）岁。计算和比较两组在清醒期、睡眠一期、睡眠二期、睡眠三期和快速眼动期16通道脑电网δ, θ, α, σ, β 及 γ频段的能量密度，观察差异显著的特征睡眠期、特征频段和特征脑区，并与睡眠监测指标进行相关性分析。结果两组患者清醒期脑电能量密度分别为（0．82±0．13）和（0．66±0．02）μV^2／Hz，睡眠一期分别为（1．28±0．07）和（0．92±0．04）μV^2／Hz，睡眠三期分别为（2．74±0．22）和（2．04±0．07）μV^2／Hz，组间比较差异均有统计学意义（t=4．309，-3．369，-2．669，均P〈0．05）。OSA组δ频段能量密度较对照组显著增强，进一步分析发现两组δ频段的脑电能量密度差异主要集中在清醒期的额区[（0．90±0．02），（0．66±0．02）μV^2／Hz，t=8．539，P〈0．01]和中央区[（1．15±0．06），（0．72±0．02）μV^2／Hz，t=6．669，P〈0．01]，睡眠一期的额区[（1．23±0．03），（0．99±0．03）μV^2／Hz，t=5．983，P〈0．01]和中央区[（1．52±0．05），（1．14±0．04）μV^2／Hz，t=5．714，P〈0．01]以及睡眠三期的中央区[（3．2±0．17），（2．71±0．08）μV^2／Hz，t=2．707，P〈0．05]。脑电能量密度分布与主要睡眠监测指标的相关性分析结果显示，重度OSA患者在睡眠一期和三期8频段中央区的脑电能量密度与微觉醒指数呈正相关（r值分别为0．877、0．656），提示OSA患者的睡眠片段化与其夜间睡眠脑电的能量变化密切相关。结论重度OSA患者的睡眠特征期为清醒期、睡眠一期和三期，其脑电δ频段能量密度显著增强，主要发生在清醒期、睡眠一期的额区和中央区以及睡眠三期期的中央区，表明重度OSA患者脑电在额区和中央区为主的脑区呈现慢波化现象，提示阻塞性睡眠呼吸暂停可能导致OSA患者的额区和中央区脑区神经功能受损。

Objective To investigate the variation of electroencephalograph （EEG） power density during different sleep stages in OSA for understanding of the mechanisms underlying the brain dysfunction in OSA as well as its earlier diagnosis and treatment. Methods Sixteen-channel EEGs from OSA patients and normal controls in stage wake, sleep stage 1, sleep stage 2, sleep stage 3 and rapid eye movement stage were analyzed by time-frequency analysis method. The EEG power density in different frequency bands （ including δ, θ, α, σ, β and γ） was respectively compared between the 2 groups. The correlation between the variation in the EEG power and primary indices of polysomnography was further analyzed. Results The EEG power density in δ band in stage wake [OSA： （0. 82 ± 0. 13） μV^2/Hz, Control： （0.66 ±0. 02） μV^2/Hz, t = 4. 309, P 〈 0. 05 ], stage 1 [ OSA： （ 1.28 ± 0. 07 ） μV^2/nz, Control： （ 0. 92 ± 0. 04）μV^2/Hz, t = - 3.369, P 〈 0. 05 ] and stage 3 [ OSA ： （2. 74 ± 0. 22 ） μV^2/Hz, Control： （2. 04 ± 0. 07） μV^2/Hz, t = - 2. 669, P 〈 0. 05 ] was significantly higher in OSA, compared with that in the control. Statistical analysis showed that the EEG power density was significantly higher in frontal and central regions in stage wake [ frontal： OSA： （0. 90 ± 0. 02） μV^2/Hz, Control： （0. 66 ± 0. 02） μV^2/Hz, t = 8. 539, P 〈 0. 01 ; central： OSA ： （ 1.15 ± 0. 06） μV^2/Hz, Control ： （0. 72 ± 0. 02） μV^2/Hz, t = 6. 669, P〈0.01] and stage 1 [frontal： OSA： （1.23±0.03） μV^2/Hz, Control： （0.99±0.03） μV^2/Hz, t= 5.983, P〈0.01; central： OSA： （1.52±0.05） μV^2/Hz, Control： （1.14±0.04） μV^2/Hz, t =5.714, P〈0. 01], as well as central region in stage 3 [OSA： （3.24 ±0. 17） μV^2/Hz, Control： （2.71 ± 0.08） μV^2/Hz, t = 2. 707, P 〈 0.05 ]. The correlation analysis showed that the power density in central region in stage 1 and stage 3 was positively correlated with arousal index （ r =0. 877 in stage 1, 0. 656 in stage 3 ）, implying that sleep fragmentation was closely related to the variation of EEG power density during nocturnal sleep in OSA. Conclusions The feature stages for OSA are stage wake, stage 1 and stage 3. The EEG power density in OSA （ δ band） was significantly higher than that in the control. The EEG power density in OSA and the control shows differences in frontal and central regions in stage wake and stage 1, as well as in central region in stage 3. The results indicate that low-frequency EEG power density giving priority to frontal area and central area has improved in severe OSA, which may be related to the neurologic deficits in corresponding brain areas.