Influence of sleep onset on upper-airway muscle activity in apnea patients versus normal controls
Influence of sleep onset on upper-airway muscle activity in apnea patients versus normal controls
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DOI：
10.1164/ajrccm.153.6.8665050
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发表时间：
1996-06-01
影响因子：
24.7
通讯作者：
White, DP
中科院分区：
文献类型：
--
作者：
Mezzanotte, WS;Tangel, DJ;White, DP
目前的证据表明，阻塞性睡眠呼吸暂停（OSA）患者可能在清醒时增强咽扩张肌活动，以弥补解剖缺陷。然而，睡眠对这些肌肉活动的单独影响（将OSA患者与对照组进行比较）尚未得到研究。因此，我们确定了10名OSA患者和8名对照者的颏舌肌（GG）和腭张肌（TP）的清醒水平（最大肌电活动的百分比），然后评估了一段时间稳定清醒后睡眠的前两次呼吸（θ脑电图[EEG]活动）的影响。在清醒状态下，呼吸暂停患者的颏舌肌（27.4 +/- 4.0比10.7 +/- 2.1%）和palatini张量（31.9 +/- 6.5比10.6 +/- 1.9%）肌电图活动高于对照组。这种增强的肌肉活动在呼吸暂停患者可以减少到接近控制水平，在清醒期间应用持续气道正压通气（CPAP）上气道。在睡眠开始时，对照组受试者的前颞肌和前颞肌的活动都出现了小幅但持续的下降。另一方面，与对照组相比，呼吸暂停患者在睡眠开始时表现出更大、更显著的颞叶肌电图下降。睡眠对呼吸暂停患者GG肌电图的影响是不一致的，大多数（n = 7）显示大（显著大于对照组）的颏舌活动下降。然而;3例OSA患者在睡眠时GG肌电信号小幅增加，尽管TP肌电信号下降，阻塞性呼吸暂停或低通气。我们的结论是，与对照组相比，睡眠发作与阻塞性睡眠呼吸暂停患者的颞肌肌电图活动明显减少有关，这可能代表了清醒期间存在的神经肌肉代偿的丧失。然而，我们关于GG肌的结果变化更大，并不总是支持这一假设。
Current evidence suggests that patients with obstructive sleep apnea (OSA) may have augmented pharyngeal dilator muscle activity during wakefulness, to compensate for deficient anatomy. However, the isolated effect of sleep on the activity of these muscles (comparing OSA patients with controls) has not been studied. We therefore determined waking levels of genioglossus (GG) and tensor palatini (TP) muscle activity (% of maximum electromyographic [EMG] activity) in 10 OSA patients and eight controls, and then assessed the impact of the first two breaths of sleep (theta electroencephalographic [EEG] activity) following a period of stable wakefulness. Apnea patients demonstrated greater genioglossal (27.4 +/- 4.0 versus 10.7 +/- 2.1%) and tensor palatini (31.9 +/- 6.5 versus 10.6 +/- 1.9%) EMG activity than did controls during wakefulness. This augmented muscle activity in apnea patients could be reduced to near control levels during wakefulness with the application of continuous positive airway pressure (CPAP) to the upper airway. At sleep onset, control subjects demonstrated small but consistent decrements in the activity of both the TP and GG muscles. On the other hand, apnea patients demonstrated large, significantly greater decrements in TP EMG at sleep onset than did the control subjects. The effect of sleep on GG EMG in apnea patients was inconsistent, with most (n = 7) demonstrating large (significantly larger than controls) decrements in genioglossal activity. However; three OSA patients demonstrated small increments in GG EMG at sleep onset despite falling TP EMG and obstructive apnea or hypopnea. We conclude that sleep onset is associated with significantly larger decrements in TP muscle EMG activity in OSA patients than in controls, which may represent a loss of neuromuscular compensation that is present during wakefulness. However, our results for the GG muscle were more variable, and did not always support this hypothesis.