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
Because chronic obstructive pulmonary disease (COPD) is well known to induc
e peripheral neuropathy and resistance to ischemic nerve conduction failure
(RICF), we performed a case-control study examining peripheral nerve funct
ion during ischemia in 17 patients with severe obstructive sleep apnea (OSA
) without daytime hypoxemia and 10 control subjects. Median nerve conductio
n was studied before, during, and after a 30-min period of ischemia. Preisc
hemic sensory and mixed nerve potential amplitudes and sensory conduction v
elocity were lower in OSA patients than in control subjects despite higher
supramaximal stimulation. During ischemia, seven OSA patients manifested RI
CF (OSA-RICF), whereas both the other 10 patients, who were nonresistant to
ischemic conduction failure (OSA-NR), and control subjects did not. OSA-RI
CF patients had the lowest initial nerve-potential amplitude, whereas OSA-N
R 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-N
R patients. Seven patients (four OSA-RICF and three OSA-NR) were reevaluate
d after at least 2 mo of treatment with nasal continuous positive airway pr
essure (nCPAP). RICF disappeared in all OSA-RICF patients, whereas preische
mic nerve conduction parameters were unchanged in both OSA-RICF and OSA-NR
patients. Thus OSA patients have peripheral nerve dysfunction whose severit
y is partly related to the level of nocturnal hypoxemia. Abnormal preischem
ic 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.