Donzel-Raynaud Christine, Redolfi Stefania, Arnulf Isabelle, Similowski Thomas, Straus Christian
AP-HP, Groupe Hospitalier Pitié-Salpêtrière, Laboratoire de Physiopathologie Respiratoire, Paris, France.
Clin Physiol Funct Imaging. 2009 Jan;29(1):10-7. doi: 10.1111/j.1475-097X.2008.00830.x. Epub 2008 Sep 16.
Obstructive sleep apnoeas generate an intense afferent traffic leading to arousal and apnoea termination. Yet a decrease in the sensitivity of the afferents has been described in patients with obstructive sleep apnoea, and could be a determinant of disease severity. How mechanical changes within the respiratory system are processed in the brain can be studied through the analysis of airway occlusion-related respiratory-related evoked potentials. Respiratory-related evoked potentials have been found altered during sleep in mild and moderate obstructive sleep apnoea syndrome, with contradictory results during wake. We hypothesized that respiratory-related evoked potentials' alterations during wake, if indeed a feature of the obstructive sleep apnoea syndrome, should be present in untreated severe patients.
Ten untreated patients with severe obstructive sleep apnoea syndrome and eight matched controls were studied. Respiratory-related evoked potentials were recorded in Cz-C3 and Cz-C4, and described in terms of the amplitudes and latencies of their components P1, N1, P2 and N2.
Components amplitudes were similar in both groups. There was no significant difference in P1 latencies. This was also the case for N1 in Cz-C3. In contrast, N1 latencies in Cz-C4 were significantly longer in patients with obstructive sleep apnoea syndrome [median 98 ms (interquartile range 16.00) versus 79.5 ms (5.98), P = 0.015]. P2 and N2 were also significantly delayed, on both sides.
The cortical processing of airway occlusion-related afferents seems abnormal in untreated patients with severe obstructive sleep apnoea syndrome. This could be either a severity marker and/or an aggravating factor.
阻塞性睡眠呼吸暂停会产生强烈的传入神经冲动，导致觉醒和呼吸暂停终止。然而，已有研究描述阻塞性睡眠呼吸暂停患者的传入神经敏感性降低，这可能是疾病严重程度的一个决定因素。通过分析与气道阻塞相关的呼吸相关诱发电位，可以研究呼吸系统内的机械变化在大脑中是如何被处理的。在轻度和中度阻塞性睡眠呼吸暂停综合征患者中，睡眠期间呼吸相关诱发电位已被发现发生改变，而清醒时结果相互矛盾。我们假设，如果清醒时呼吸相关诱发电位的改变确实是阻塞性睡眠呼吸暂停综合征的一个特征，那么未经治疗的重症患者也应该存在这种改变。
研究了10例未经治疗的重度阻塞性睡眠呼吸暂停综合征患者和8例匹配的对照组。在Cz-C3和Cz-C4记录呼吸相关诱发电位，并根据其成分P1、N1、P2和N2的振幅和潜伏期进行描述。
两组的成分振幅相似。P1潜伏期无显著差异。Cz-C3导联的N1潜伏期也是如此。相比之下，阻塞性睡眠呼吸暂停综合征患者Cz-C4导联的N1潜伏期明显更长[中位数98毫秒（四分位间距16.00）对79.5毫秒（5.98），P = 0.015]。两侧的P2和N2也明显延迟。
未经治疗的重度阻塞性睡眠呼吸暂停综合征患者，与气道阻塞相关的传入神经在皮质的处理似乎异常。这可能是一个严重程度标志物和/或加重因素。
