Rabec C, Laurent G, Baudouin N, Merati M, Massin F, Foucher P, Brondel L, Reybet-Degat O
Service de Pneumologie et Réanimation Respiratoire, Centre Hospitalier Universitaire de Dijon, France.
Eur Respir J. 1998 Dec;12(6):1482-5. doi: 10.1183/09031936.98.12061482.
We report on the case of two young patients with type I Arnold-Chiari malformation (ACM), as revealed by a central sleep apnoea (CSA) syndrome without any other neurological defect. Case 1 was a 14-yr-old male patient, who developed severe alveolar hypoventilation and needed long-term mechanical ventilation via a tracheostomy. Case 2 was a 39-yr-old male patient, who developed features suggestive of sleep apnoea and responded to nasal continuous positive airway pressure ventilation despite the central type of apnoeas. These two cases illustrate the different pathophysiological mechanisms involved in CSA, namely a blunted chemical drive (in hypercapnic patients) and an increased chemical drive, which destabilizes the breathing pattern during sleep (in normo/hypocapnic patients). Central sleep apnoea can be the initial manifestation of Arnold-Chiari malformation and can lead to a life-threatening condition.
我们报告了两例I型阿诺德-奇亚里畸形(ACM)的年轻患者,其表现为中枢性睡眠呼吸暂停(CSA)综合征,且无任何其他神经缺陷。病例1是一名14岁男性患者,出现严重的肺泡通气不足,需要通过气管造口进行长期机械通气。病例2是一名39岁男性患者,出现提示睡眠呼吸暂停的症状,尽管是中枢性呼吸暂停,但对经鼻持续气道正压通气有反应。这两个病例说明了CSA所涉及的不同病理生理机制,即化学驱动减弱(在高碳酸血症患者中)和化学驱动增加,这会破坏睡眠期间的呼吸模式(在正常/低碳酸血症患者中)。中枢性睡眠呼吸暂停可能是阿诺德-奇亚里畸形的初始表现,并可能导致危及生命的情况。