Mayer P, Dematteis M, Pépin J L, Wuyam B, Veale D, Vila A, Lévy P
Department of Respiratory Medicine and Sleep Laboratory, Department of Neurology, EMG Laboratory, and Physiologie Respiratoire Expérimental Théorique at Appliquée (PRETA)-TIMC Laboratory UMR-CNRS 5525, Grenoble Cedex, France.
Am J Respir Crit Care Med. 1999 Jan;159(1):213-9. doi: 10.1164/ajrccm.159.1.9709051.
Because chronic obstructive pulmonary disease (COPD) is well known to induce peripheral neuropathy and resistance to ischemic nerve conduction failure (RICF), we performed a case-control study examining peripheral nerve function during ischemia in 17 patients with severe obstructive sleep apnea (OSA) without daytime hypoxemia and 10 control subjects. Median nerve conduction was studied before, during, and after a 30-min period of ischemia. Preischemic sensory and mixed nerve potential amplitudes and sensory conduction velocity were lower in OSA patients than in control subjects despite higher supramaximal stimulation. During ischemia, seven OSA patients manifested RICF (OSA-RICF), whereas both the other 10 patients, who were nonresistant to ischemic conduction failure (OSA-NR), and control subjects did not. OSA-RICF patients had the lowest initial nerve-potential amplitude, whereas OSA-NR patients had a response intermediate between that of control subjects and OSA-RICF patients. OSA-RICF patients had a lower mean nocturnal SaO2 and a higher body mass index (BMI) and duration of SaO2 < 70% than did OSA-NR patients. Seven patients (four OSA-RICF and three OSA-NR) were reevaluated after at least 2 mo of treatment with nasal continuous positive airway pressure (nCPAP). RICF disappeared in all OSA-RICF patients, whereas preischemic nerve conduction parameters were unchanged in both OSA-RICF and OSA-NR patients. Thus OSA patients have peripheral nerve dysfunction whose severity is partly related to the level of nocturnal hypoxemia. Abnormal preischemic nerve conduction suggests axonal lesions, whereas RICF, which appears to be a sensitive but nonspecific tissue marker of the severity of hypoxemia, may result from adaptative mechanisms.
由于众所周知慢性阻塞性肺疾病（COPD）会诱发周围神经病变以及对缺血性神经传导衰竭（RICF）产生抵抗，我们进行了一项病例对照研究，以检查17例无日间低氧血症的重度阻塞性睡眠呼吸暂停（OSA）患者和10名对照者在缺血期间的周围神经功能。在30分钟的缺血期之前、期间和之后研究正中神经传导。尽管刺激强度超过最大刺激，但OSA患者缺血前的感觉和混合神经电位幅度以及感觉传导速度均低于对照者。在缺血期间，7例OSA患者出现RICF（OSA-RICF），而另外10例对缺血性传导衰竭无抵抗的患者（OSA-NR）和对照者均未出现。OSA-RICF患者的初始神经电位幅度最低，而OSA-NR患者的反应介于对照者和OSA-RICF患者之间。与OSA-NR患者相比，OSA-RICF患者的夜间平均血氧饱和度（SaO2）更低，体重指数（BMI）更高，SaO2<70%的持续时间更长。7例患者（4例OSA-RICF和3例OSA-NR）在接受鼻持续气道正压通气（nCPAP）治疗至少2个月后进行了重新评估。所有OSA-RICF患者的RICF均消失，而OSA-RICF和OSA-NR患者的缺血前神经传导参数均未改变。因此，OSA患者存在周围神经功能障碍，其严重程度部分与夜间低氧血症水平有关。缺血前神经传导异常提示轴索病变，而RICF似乎是低氧血症严重程度的敏感但非特异性组织标志物，可能由适应性机制导致。
