title: Peripheral neuropathy in sleep apnea. A tissue marker of the severity of nocturnal desaturation.
abstract: 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.
authors.affiliation: 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.
authors.forename: P
authors.initials: P
authors.lastname: Mayer
authors.forename: M
authors.initials: M
authors.lastname: Dematteis
authors.forename: J L
authors.initials: JL
authors.lastname: Pépin
authors.forename: B
authors.initials: B
authors.lastname: Wuyam
authors.forename: D
authors.initials: D
authors.lastname: Veale
authors.forename: A
authors.initials: A
authors.lastname: Vila
authors.forename: P
authors.initials: P
authors.lastname: Lévy
mesh_terms: D000328:Adult; D000368:Aged; D015992:Body Mass Index; D016022:Case-Control Studies; D002940:Circadian Rhythm / Q000502:physiology; D004594:Electrophysiology; D005260:Female; D006801:Humans; D007511:Ischemia / Q000503:physiopathology; D008297:Male; D008475:Median Nerve / Q000098:blood supply / Q000503:physiopathology; D008875:Middle Aged; D009431:Neural Conduction / Q000502:physiology; D010100:Oxygen / Q000097:blood*; D010523:Peripheral Nervous System Diseases / Q000209:etiology*; D011175:Positive-Pressure Respiration; D012016:Reference Values; D012677:Sensation / Q000502:physiology; D012891:Sleep Apnea Syndromes / Q000150:complications* / Q000503:physiopathology
chemical_list: D010100:Oxygen