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Titolo:
Peripheral neuropathy in sleep apnea - A tissue marker of the severity of nocturnal desaturation
Autore:
Mayer, P; Dematteis, M; Pepin, JL; Wuyam, B; Veale, D; Vila, A; Levy, P;
Indirizzi:
Univ Hosp Grenoble, Dept Resp Med, Grenoble, France Univ Hosp Grenoble Grenoble France ble, Dept Resp Med, Grenoble, France Univ Hosp Grenoble, Dept Neurol, Sleep Lab, Grenoble, France Univ Hosp Grenoble Grenoble France Neurol, Sleep Lab, Grenoble, France Univ Hosp Grenoble, EMG Lab, Grenoble, France Univ Hosp Grenoble Grenoble France Grenoble, EMG Lab, Grenoble, France Univ,Hosp Grenoble, Physiol Resp Expt Theor & Appl TIMC Lab, CNRS, UMR 5525 Univ Hosp Grenoble Grenoble France heor & Appl TIMC Lab, CNRS, UMR 5525 Univ Montreal, Hotel Dieu Montreal, Dept Resp Med, Montreal, PQ, Canada Univ Montreal Montreal PQ Canada al, Dept Resp Med, Montreal, PQ, Canada
Titolo Testata:
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
fascicolo: 1, volume: 159, anno: 1999,
pagine: 213 - 219
SICI:
1073-449X(199901)159:1<213:PNISA->2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIC CONDUCTION FAILURE; EXPERIMENTAL DIABETIC NEUROPATHY; HYPOXIC NEUROPATHY; ENERGY-METABOLISM; NERVE; RESISTANCE; INSULIN; DISEASE; EXCITOTOXICITY; HYPERTENSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Levy, P CHU09,enoble, Dept Pneumol, Unite Sommeil & Resp, BP 217, F-38043 Grenoble CHU Grenoble BP 217 Grenoble France 09 , BP 217, F-38043 Grenoble
Citazione:
P. Mayer et al., "Peripheral neuropathy in sleep apnea - A tissue marker of the severity of nocturnal desaturation", AM J R CRIT, 159(1), 1999, pp. 213-219

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 highersupramaximal 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 Sa(O2) and a higher body mass index (BMI) and duration of Sa(O2) < 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-NRpatients. 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.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 14:21:18