1 The Sleep Center, Children's Hospital of Philadelphia, University of Pennsylvania's Perelman School of Medicine, Philadelphia, Pennsylvania.
Am J Respir Crit Care Med. 2013 Oct 1;188(7):852-7. doi: 10.1164/rccm.201307-1257OC.
Children with obstructive sleep apnea syndrome (OSAS) have impaired cortical processing of respiratory afferent stimuli, manifested by blunted sleep respiratory-related evoked potentials (RREP). However, whether this impairment is limited to respiratory stimuli, or reversible after successful treatment, is unknown. We hypothesized that, during sleep, children with OSAS have (1) abnormal RREP, (2) normal cortical processing of nonrespiratory stimuli, and (3) persistence of abnormal RREP after treatment.
To measure sleep RREP and auditory evoked potentials in normal control subjects and children with OSAS before and after treatment.
Twenty-four children with OSAS and 24 control subjects were tested during N3 sleep. Thirteen children with OSAS repeated testing 4-6 months after adenotonsillectomy.
RREP were blunted in OSAS compared with control subjects (N350 at Cz -27 ± 15.5 vs. -47.4 ± 28.5 μV; P = 0.019), and did not improve after OSAS treatment (N350 at Cz pretreatment -25.1 ± 7.4 vs. -29.8 ± 8.1 post-treatment). Auditory evoked potentials were similar in OSAS and control subjects at baseline (N350 at Cz -58 ± 33.1 vs. -66 ± 31.1 μV), and did not change after treatment (N350 at Cz -67.5 ± 36.8 vs. -65.5 ± 20.3).
Children with OSAS have persistent primary or irreversible respiratory afferent cortical processing deficits during sleep that could put them at risk of OSAS recurrence. OSAS does not seem to affect the cortical processing of nonrespiratory (auditory) afferent stimuli during sleep.
患有阻塞性睡眠呼吸暂停综合征（OSAS）的儿童存在呼吸传入刺激的皮质处理受损，表现为睡眠呼吸相关诱发电位（RREP）迟钝。然而，这种损害是否仅限于呼吸刺激，或者在成功治疗后是否可以逆转，尚不清楚。我们假设，在睡眠期间，患有 OSAS 的儿童存在（1）RREP 异常，（2）非呼吸刺激的皮质处理正常，以及（3）治疗后 RREP 持续异常。
在治疗前后，测量正常对照组和 OSAS 患儿的睡眠 RREP 和听觉诱发电位。
24 例 OSAS 患儿和 24 例对照组受试者在 N3 睡眠期间进行测试。13 例 OSAS 患儿在腺样体扁桃体切除术后 4-6 个月重复测试。
与对照组相比，OSAS 患儿的 RREP 减弱（Cz 处 N350 为-27 ± 15.5 与-47.4 ± 28.5 μV；P = 0.019），并且在 OSAS 治疗后并未改善（Cz 处 N350 为治疗前-25.1 ± 7.4 与治疗后-29.8 ± 8.1）。在基线时，OSAS 患儿和对照组的听觉诱发电位相似（Cz 处 N350 为-58 ± 33.1 与-66 ± 31.1 μV），并且在治疗后没有变化（Cz 处 N350 为-67.5 ± 36.8 与-65.5 ± 20.3）。
患有 OSAS 的儿童在睡眠期间存在持续性或不可逆的呼吸传入皮质处理缺陷，这可能使他们面临 OSAS 复发的风险。OSAS 似乎不会影响睡眠期间非呼吸（听觉）传入刺激的皮质处理。
