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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 understood complication of chronic obstructive pulmonary disease (COPD). To clarify the initial trigger of a PN in COPD, we investigated the excitability of peripheral nerves in patients with COPD. METHODS: The automated n...

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Autores principales: Yoon, Seon Min, Park, Young Bum, Ko, Yousang, Bae, Jong Seok
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Neurological Association 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9982175/
https://www.ncbi.nlm.nih.gov/pubmed/36854335
http://dx.doi.org/10.3988/jcn.2022.0249
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author Yoon, Seon Min
Park, Young Bum
Ko, Yousang
Bae, Jong Seok
author_facet Yoon, Seon Min
Park, Young Bum
Ko, Yousang
Bae, Jong Seok
author_sort Yoon, Seon Min
collection PubMed
description BACKGROUND AND PURPOSE: Peripheral neuropathies (PNs) are a common but poorly understood complication of chronic obstructive pulmonary disease (COPD). To clarify the initial 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 attributable 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 neuropathic process that is antecedent to PN in COPD.
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spelling pubmed-99821752023-03-04 Chronic Hypoxemia Triggers a Neuropathic Process in Chronic Obstructive Pulmonary Disease: Insight From In Vivo Neurophysiological Assessments Yoon, Seon Min Park, Young Bum Ko, Yousang Bae, Jong Seok J Clin Neurol Original Article BACKGROUND AND PURPOSE: Peripheral neuropathies (PNs) are a common but poorly understood complication of chronic obstructive pulmonary disease (COPD). To clarify the initial 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 attributable 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 neuropathic process that is antecedent to PN in COPD. Korean Neurological Association 2023-03 2023-02-13 /pmc/articles/PMC9982175/ /pubmed/36854335 http://dx.doi.org/10.3988/jcn.2022.0249 Text en Copyright © 2023 Korean Neurological Association https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0 (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Yoon, Seon Min
Park, Young Bum
Ko, Yousang
Bae, Jong Seok
Chronic Hypoxemia Triggers a Neuropathic Process in Chronic Obstructive Pulmonary Disease: Insight From In Vivo Neurophysiological Assessments
title Chronic Hypoxemia Triggers a Neuropathic Process in Chronic Obstructive Pulmonary Disease: Insight From In Vivo Neurophysiological Assessments
title_full Chronic Hypoxemia Triggers a Neuropathic Process in Chronic Obstructive Pulmonary Disease: Insight From In Vivo Neurophysiological Assessments
title_fullStr Chronic Hypoxemia Triggers a Neuropathic Process in Chronic Obstructive Pulmonary Disease: Insight From In Vivo Neurophysiological Assessments
title_full_unstemmed Chronic Hypoxemia Triggers a Neuropathic Process in Chronic Obstructive Pulmonary Disease: Insight From In Vivo Neurophysiological Assessments
title_short Chronic Hypoxemia Triggers a Neuropathic Process in Chronic Obstructive Pulmonary Disease: Insight From In Vivo Neurophysiological Assessments
title_sort chronic hypoxemia triggers a neuropathic process in chronic obstructive pulmonary disease: insight from in vivo neurophysiological assessments
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9982175/
https://www.ncbi.nlm.nih.gov/pubmed/36854335
http://dx.doi.org/10.3988/jcn.2022.0249
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