Department of Clinical Neurophysiology and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Department of Clinical Neurophysiology and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Chest. 2020 May;157(5):1296-1303. doi: 10.1016/j.chest.2020.01.032. Epub 2020 Feb 12.
Signs of both motor and sensory nervous lesions have previously been shown in the upper airway of patients with OSA and habitual snorers. Snoring per se may damage all upper airway neurons over time, thereby causing progression to manifest sleep apnea. To test this hypothesis, nonsnoring subjects, untreated snorers, and CPAP-treated patients underwent repeated sensory testing of the soft palate in a prospective long-term study.
Cold detection threshold (CDT) testing at the soft palate and lip with a thermode and nocturnal respiratory recordings were performed in 2008 to 2009 with retesting 6 to 7 years later.
In 25 untreated snorers, palatal CDT worsened from a median (25th-75th percentile range) 4.2°C (3.2-5.9) to 11.0°C (7.0-17.4) (P < .001). The apnea-hypopnea index increased from a median 7.0 to 14.0 events/h (P < .05). There was no significant correlation between changes in CDT and the apnea-hypopnea index. In 21 nonsnoring control subjects, palatal CDT increased from a median 3.2°C to 5.6°C (P < .005). In 19 CPAP-treated patients, palatal CDT did not significantly change; eight patients had improved values. CDTs worsened significantly more in the snorers group than in the control subjects (P < .05) and the CPAP-treated patients (P < .001). There was no significant difference between control subjects and CPAP-treated patients.
CDT worsened considerably over time in untreated snorers, significantly more than in nonsnoring control subjects and CPAP-treated patients. Untreated snorers therefore risk developing poor sensitivity in the upper airway. In contrast, efficient treatment of OSA seems to protect the sensory innervation, as the CPAP-treated group maintained their sensitivity to cold and, in some cases, the sensitivity even improved.
先前的研究表明,OSA 患者和习惯性打鼾者的上气道存在运动和感觉神经病变的迹象。随着时间的推移,打鼾本身可能会损害所有上气道神经元,从而导致睡眠呼吸暂停的进展。为了验证这一假设,我们对非打鼾者、未经治疗的打鼾者和接受 CPAP 治疗的患者进行了前瞻性长期研究,重复测试了软腭的感觉功能。
2008 年至 2009 年,使用 Thermode 对软腭和唇部进行冷觉检测阈值(CDT)测试,并进行夜间呼吸记录,6 至 7 年后进行复测。
在 25 例未经治疗的打鼾者中,软腭 CDT 从中位数(25 百分位数-75 百分位数范围)4.2°C(3.2-5.9)恶化至 11.0°C(7.0-17.4)(P<.001)。呼吸暂停低通气指数从中位数 7.0 增加至 14.0 次/小时(P<.05)。CDT 的变化与呼吸暂停低通气指数之间无显著相关性。在 21 例非打鼾对照者中,软腭 CDT 从中位数 3.2°C 增加至 5.6°C(P<.005)。在 19 例接受 CPAP 治疗的患者中,软腭 CDT 无显著变化;8 例患者的 CDT 值改善。与对照组相比,打鼾组的 CDT 恶化更为显著(P<.05),与 CPAP 治疗组相比恶化更为显著(P<.001)。对照组和 CPAP 治疗组之间无显著差异。
未经治疗的打鼾者的 CDT 随时间推移显著恶化,明显甚于非打鼾对照组和 CPAP 治疗组。未经治疗的打鼾者因此有发生上气道敏感性降低的风险。相比之下,OSA 的有效治疗似乎能保护感觉神经支配,因为 CPAP 治疗组保持了对冷的敏感性,在某些情况下甚至有所改善。