Chronic Hypoxemia Triggers a Neuropathic Process in Chronic Obstructive Pulmonary Disease: Insight From In Vivo Neurophysiological Assessments

Background and Purpose Peripheral neuropathies (PNs) are a common but poorly un-derstood complication of chronic obstructive pulmonary disease (COPD). To clarify the ini-tial trigger of a PN in COPD, we investigated the excitability of peripheral nerves in patients with COPD.Methods The automated nerve excitability test (NET) using the threshold-tracking paradigm was applied to 20 COPD patients. The recording protocol calculated the strength-duration time constant, threshold electrotonus (TE), current-threshold relationship, and recovery cycle (RC). Each NET parameter was compared with two control groups: normal controls group (NC group) and smokers without COPD group (smoker group).Results In the motor NETs, the change in the threshold in the mid-depolarizing phase of TE (40-60 ms) was smaller in the COPD group (50.7%+/- 1.2%, mean +/- SEM; n=20) than in the NC group (54.5%+/- 0.7%, n=25; p<0.01), as was the prominence of superexcitability in the RC (-22.6%+/- 1.5% and-26.4%+/- 1.1%, respectively; p=0.04). There were no significant differences in the sensory NETs. Comparisons between the COPD and smoker groups (n=25) also showed no differences in either the motor or sensory NETs.Conclusions The pattern of excitability in COPD revealed a membrane depolarization attribut-able to Na+-K+-ATPase failure in the axolemma of distal motor nerves. This finding suggests that chronic hypoxemia and adaptative process can alter axonal excitability and trigger a resultant neu-ropathic process that is antecedent to PN in COPD.

Automated summary

This study aimed to investigate the initial trigger of peripheral neuropathies (PNs) in chronic obstructive pulmonary disease (COPD). The automated nerve excitability test (NET) was conducted on 20 COPD patients, and it was found that COPD patients exhibited abnormal nerve excitability, characterized by smaller threshold changes in the mid-depolarizing phase and a prominent superexcitability in the recovery cycle. There were no significant differences in sensory nerve excitability between COPD patients and control groups.