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Specific motor cortex hypoexcitability and hypoactivation in COPD patients with peripheral muscle weakness
Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations. Although peripheral alterations cannot totally explain peripheral muscle weakness in COPD, the existence of an activation deficit remains controversial. The heterogeneity of muscle weakness (between 32 and 57%...
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| Published in: | BMC pulmonary medicine 2020-01, Vol.20 (1), p.1-1, Article 1 |
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| creator | Alexandre, Francois Héraud, Nelly Tremey, Emilie Oliver, Nicolas Bourgouin, Dominique Varray, Alain |
| description | Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations. Although peripheral alterations cannot totally explain peripheral muscle weakness in COPD, the existence of an activation deficit remains controversial. The heterogeneity of muscle weakness (between 32 and 57% of COPD patients) is generally not controlled in studies and could explain this discrepancy. This study aimed to specifically compare voluntary and stimulated activation levels in COPD patients with and without muscle weakness.
Twenty-two patients with quadriceps weakness (COPD
), 18 patients with preserved quadriceps strength (COPD
) and 20 controls were recruited. Voluntary activation was measured through peripheral nerve (VA
) and transcranial magnetic (VA
) stimulation. Corticospinal and spinal excitability (MEP/Mmax and Hmax/Mmax) and corticospinal inhibition (silent period duration) were assessed during maximal voluntary quadriceps contractions.
COPD
exhibited lower VA
and lower MEP/Mmax compared with COPD
(p |
| doi_str_mv | 10.1186/s12890-019-1042-0 |
| format | article |
| fullrecord | <record><control><sourceid>gale_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_b5e8450871e740a5b5232142e527ac40</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A618765748</galeid><doaj_id>oai_doaj_org_article_b5e8450871e740a5b5232142e527ac40</doaj_id><sourcerecordid>A618765748</sourcerecordid><originalsourceid>FETCH-LOGICAL-c594t-99150efd030981da72c965ffa52a9c552e8ee747545563881f485b9b92517c6f3</originalsourceid><addsrcrecordid>eNptUstu1DAUjRCIPuAD2KBIbNpFit-xN0ij4dFKIxUJWFuOczPjIYmDnZl2_h6nU6qZCnlh3-tzzn3oZNk7jK4wluJjxEQqVCCsCowYKdCL7BSzEheECfHy4H2SncW4RgiXktPX2QnFKgVEnWbrHwNY1zibd370Ibc-jHCfr3aDh3vrRlO51o273PT1Q9LY0W3N6Hyfuz6f337_nA8phH6M-Z0bV_kAwQ0rCKbNu020LeR3YH73EOOb7FVj2ghvH-_z7NfXLz_n18Xi9tvNfLYoLFdsLJTCHEFTI4qUxLUpiVWCN43hxCjLOQEJULKSM84FlRI3TPJKVYpwXFrR0PPsZq9be7PWQ3CdCTvtjdMPCR-W2oTRpdZ0xUEyjmSJkyIyvOKEEswIcFIay1DS-rTXGjZVB7VNc6bJjkSPf3q30ku_1UIxQjFOApd7gdUz2vVsoaccopgqIcV2wl48Fgv-zwbiqDsXLbSt6cFvoiaUUoEEpzxBPzyDrv0m9GmtCcWwSKXFAWpp0rCub3zq0U6ieiawLAUvmUyoq_-g0qmhc9b30LiUPyLgPcEGH2OA5mkwjPRkTL03pk7G1JMx9bTI94eLfGL8cyL9C5VU2-k</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2341631165</pqid></control><display><type>article</type><title>Specific motor cortex hypoexcitability and hypoactivation in COPD patients with peripheral muscle weakness</title><source>Publicly Available Content Database</source><source>PubMed Central</source><creator>Alexandre, Francois ; Héraud, Nelly ; Tremey, Emilie ; Oliver, Nicolas ; Bourgouin, Dominique ; Varray, Alain</creator><creatorcontrib>Alexandre, Francois ; Héraud, Nelly ; Tremey, Emilie ; Oliver, Nicolas ; Bourgouin, Dominique ; Varray, Alain</creatorcontrib><description>Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations. Although peripheral alterations cannot totally explain peripheral muscle weakness in COPD, the existence of an activation deficit remains controversial. The heterogeneity of muscle weakness (between 32 and 57% of COPD patients) is generally not controlled in studies and could explain this discrepancy. This study aimed to specifically compare voluntary and stimulated activation levels in COPD patients with and without muscle weakness.
Twenty-two patients with quadriceps weakness (COPD
), 18 patients with preserved quadriceps strength (COPD
) and 20 controls were recruited. Voluntary activation was measured through peripheral nerve (VA
) and transcranial magnetic (VA
) stimulation. Corticospinal and spinal excitability (MEP/Mmax and Hmax/Mmax) and corticospinal inhibition (silent period duration) were assessed during maximal voluntary quadriceps contractions.
COPD
exhibited lower VA
and lower MEP/Mmax compared with COPD
(p < 0.05). Hmax/Mmax was not significantly different between groups (p = 0.25). Silent period duration was longer in the two groups of COPD patients compared with controls (p < 0.01). Interestingly, there were no significant differences between all COPD patients taken together and controls regarding VA
and MEP/Mmax.
COPD patients with muscle weakness have reduced voluntary activation without altered spinal excitability. Corticospinal inhibition is higher in COPD regardless of muscle weakness. Therefore, reduced cortical excitability and a voluntary activation deficit from the motor cortex are the most likely cortical mechanisms implicated in COPD muscle weakness. The mechanisms responsible for cortical impairment and possible therapeutic interventions need to be addressed.</description><identifier>ISSN: 1471-2466</identifier><identifier>EISSN: 1471-2466</identifier><identifier>DOI: 10.1186/s12890-019-1042-0</identifier><identifier>PMID: 31900129</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Brain ; Chronic obstructive lung disease ; Chronic obstructive pulmonary disease ; Cognitive science ; Complications and side effects ; Consortia ; Cortex (motor) ; Corticospinal excitability ; Development and progression ; Diseases ; Excitability ; Health aspects ; Human health and pathology ; Hypotheses ; Life Sciences ; Lung diseases ; Motor cortex ; Motor evoked potentials ; Muscle weakness ; Neuroscience ; Peripheral muscle weakness ; Peripheral nerves ; Physiological aspects ; Pulmonology ; Pulmonology and respiratory tract ; Pyramidal tracts ; Quadriceps muscle ; Studies ; Therapeutic applications ; Tissues and Organs</subject><ispartof>BMC pulmonary medicine, 2020-01, Vol.20 (1), p.1-1, Article 1</ispartof><rights>COPYRIGHT 2020 BioMed Central Ltd.</rights><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Attribution</rights><rights>The Author(s). 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c594t-99150efd030981da72c965ffa52a9c552e8ee747545563881f485b9b92517c6f3</citedby><cites>FETCH-LOGICAL-c594t-99150efd030981da72c965ffa52a9c552e8ee747545563881f485b9b92517c6f3</cites><orcidid>0000-0003-4453-3004 ; 0000-0003-3876-1211</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6942311/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2341631165?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25752,27923,27924,37011,37012,44589,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31900129$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-03139686$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Alexandre, Francois</creatorcontrib><creatorcontrib>Héraud, Nelly</creatorcontrib><creatorcontrib>Tremey, Emilie</creatorcontrib><creatorcontrib>Oliver, Nicolas</creatorcontrib><creatorcontrib>Bourgouin, Dominique</creatorcontrib><creatorcontrib>Varray, Alain</creatorcontrib><title>Specific motor cortex hypoexcitability and hypoactivation in COPD patients with peripheral muscle weakness</title><title>BMC pulmonary medicine</title><addtitle>BMC Pulm Med</addtitle><description>Peripheral muscle weakness can be caused by both peripheral muscle and neural alterations. Although peripheral alterations cannot totally explain peripheral muscle weakness in COPD, the existence of an activation deficit remains controversial. The heterogeneity of muscle weakness (between 32 and 57% of COPD patients) is generally not controlled in studies and could explain this discrepancy. This study aimed to specifically compare voluntary and stimulated activation levels in COPD patients with and without muscle weakness.
Twenty-two patients with quadriceps weakness (COPD
), 18 patients with preserved quadriceps strength (COPD
) and 20 controls were recruited. Voluntary activation was measured through peripheral nerve (VA
) and transcranial magnetic (VA
) stimulation. Corticospinal and spinal excitability (MEP/Mmax and Hmax/Mmax) and corticospinal inhibition (silent period duration) were assessed during maximal voluntary quadriceps contractions.
COPD
exhibited lower VA
and lower MEP/Mmax compared with COPD
(p < 0.05). Hmax/Mmax was not significantly different between groups (p = 0.25). Silent period duration was longer in the two groups of COPD patients compared with controls (p < 0.01). Interestingly, there were no significant differences between all COPD patients taken together and controls regarding VA
and MEP/Mmax.
COPD patients with muscle weakness have reduced voluntary activation without altered spinal excitability. Corticospinal inhibition is higher in COPD regardless of muscle weakness. Therefore, reduced cortical excitability and a voluntary activation deficit from the motor cortex are the most likely cortical mechanisms implicated in COPD muscle weakness. The mechanisms responsible for cortical impairment and possible therapeutic interventions need to be addressed.</description><subject>Brain</subject><subject>Chronic obstructive lung disease</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Cognitive science</subject><subject>Complications and side effects</subject><subject>Consortia</subject><subject>Cortex (motor)</subject><subject>Corticospinal excitability</subject><subject>Development and progression</subject><subject>Diseases</subject><subject>Excitability</subject><subject>Health aspects</subject><subject>Human health and pathology</subject><subject>Hypotheses</subject><subject>Life Sciences</subject><subject>Lung diseases</subject><subject>Motor cortex</subject><subject>Motor evoked potentials</subject><subject>Muscle weakness</subject><subject>Neuroscience</subject><subject>Peripheral muscle weakness</subject><subject>Peripheral nerves</subject><subject>Physiological aspects</subject><subject>Pulmonology</subject><subject>Pulmonology and respiratory tract</subject><subject>Pyramidal tracts</subject><subject>Quadriceps muscle</subject><subject>Studies</subject><subject>Therapeutic applications</subject><subject>Tissues and Organs</subject><issn>1471-2466</issn><issn>1471-2466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUstu1DAUjRCIPuAD2KBIbNpFit-xN0ij4dFKIxUJWFuOczPjIYmDnZl2_h6nU6qZCnlh3-tzzn3oZNk7jK4wluJjxEQqVCCsCowYKdCL7BSzEheECfHy4H2SncW4RgiXktPX2QnFKgVEnWbrHwNY1zibd370Ibc-jHCfr3aDh3vrRlO51o273PT1Q9LY0W3N6Hyfuz6f337_nA8phH6M-Z0bV_kAwQ0rCKbNu020LeR3YH73EOOb7FVj2ghvH-_z7NfXLz_n18Xi9tvNfLYoLFdsLJTCHEFTI4qUxLUpiVWCN43hxCjLOQEJULKSM84FlRI3TPJKVYpwXFrR0PPsZq9be7PWQ3CdCTvtjdMPCR-W2oTRpdZ0xUEyjmSJkyIyvOKEEswIcFIay1DS-rTXGjZVB7VNc6bJjkSPf3q30ku_1UIxQjFOApd7gdUz2vVsoaccopgqIcV2wl48Fgv-zwbiqDsXLbSt6cFvoiaUUoEEpzxBPzyDrv0m9GmtCcWwSKXFAWpp0rCub3zq0U6ieiawLAUvmUyoq_-g0qmhc9b30LiUPyLgPcEGH2OA5mkwjPRkTL03pk7G1JMx9bTI94eLfGL8cyL9C5VU2-k</recordid><startdate>20200103</startdate><enddate>20200103</enddate><creator>Alexandre, Francois</creator><creator>Héraud, Nelly</creator><creator>Tremey, Emilie</creator><creator>Oliver, Nicolas</creator><creator>Bourgouin, Dominique</creator><creator>Varray, Alain</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-4453-3004</orcidid><orcidid>https://orcid.org/0000-0003-3876-1211</orcidid></search><sort><creationdate>20200103</creationdate><title>Specific motor cortex hypoexcitability and hypoactivation in COPD patients with peripheral muscle weakness</title><author>Alexandre, Francois ; 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Although peripheral alterations cannot totally explain peripheral muscle weakness in COPD, the existence of an activation deficit remains controversial. The heterogeneity of muscle weakness (between 32 and 57% of COPD patients) is generally not controlled in studies and could explain this discrepancy. This study aimed to specifically compare voluntary and stimulated activation levels in COPD patients with and without muscle weakness.
Twenty-two patients with quadriceps weakness (COPD
), 18 patients with preserved quadriceps strength (COPD
) and 20 controls were recruited. Voluntary activation was measured through peripheral nerve (VA
) and transcranial magnetic (VA
) stimulation. Corticospinal and spinal excitability (MEP/Mmax and Hmax/Mmax) and corticospinal inhibition (silent period duration) were assessed during maximal voluntary quadriceps contractions.
COPD
exhibited lower VA
and lower MEP/Mmax compared with COPD
(p < 0.05). Hmax/Mmax was not significantly different between groups (p = 0.25). Silent period duration was longer in the two groups of COPD patients compared with controls (p < 0.01). Interestingly, there were no significant differences between all COPD patients taken together and controls regarding VA
and MEP/Mmax.
COPD patients with muscle weakness have reduced voluntary activation without altered spinal excitability. Corticospinal inhibition is higher in COPD regardless of muscle weakness. Therefore, reduced cortical excitability and a voluntary activation deficit from the motor cortex are the most likely cortical mechanisms implicated in COPD muscle weakness. The mechanisms responsible for cortical impairment and possible therapeutic interventions need to be addressed.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>31900129</pmid><doi>10.1186/s12890-019-1042-0</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-4453-3004</orcidid><orcidid>https://orcid.org/0000-0003-3876-1211</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Publicly Available Content Database; PubMed Central |
| subjects | Brain Chronic obstructive lung disease Chronic obstructive pulmonary disease Cognitive science Complications and side effects Consortia Cortex (motor) Corticospinal excitability Development and progression Diseases Excitability Health aspects Human health and pathology Hypotheses Life Sciences Lung diseases Motor cortex Motor evoked potentials Muscle weakness Neuroscience Peripheral muscle weakness Peripheral nerves Physiological aspects Pulmonology Pulmonology and respiratory tract Pyramidal tracts Quadriceps muscle Studies Therapeutic applications Tissues and Organs |
| title | Specific motor cortex hypoexcitability and hypoactivation in COPD patients with peripheral muscle weakness |
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