Motor cortex excitability and BDNF levels in chronic musculoskeletal pain according to structural pathology
Autor(a) principal: | |
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Data de Publicação: | 2016 |
Outros Autores: | , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UFRGS |
Texto Completo: | http://hdl.handle.net/10183/187800 |
Resumo: | The central sensitization syndrome (CSS) encompasses disorders with overlapping symptoms in a structural pathology spectrum ranging from persistent nociception [e.g., osteoarthritis (OA)] to an absence of tissue injuries such as the one presented in fibromyalgia (FM) and myofascial pain syndrome (MPS). First, we hypothesized that these syndromes present differences in their cortical excitability parameters assessed by transcranial magnetic stimulation (TMS), namely motor evoked potential (MEP), cortical silent period (CSP), short intracortical inhibition (SICI) and short intracortical facilitation (SICF). Second, considering that the presence of tissue injury could be detected by serum neurotrophins, we hypothesized that the spectrum of structural pathology (i.e., from persistent nociception like in OA, to the absence of tissue injury like in FM and MPS), could be detected by differential efficiency of their descending pain inhibitory system, as assessed by the conditioned pain modulation (CPM) paradigm. Third, we explored whether brain-derived neurotrophic factor (BDNF) had an influence on the relationship between motor cortex excitability and structural pathology. This cross-sectional study pooled baseline data from three randomized clinical trials We included females (n = 114), aged 19–65 years old with disability by chronic pain syndromes (CPS): FM (n = 19), MPS (n = 54), OA (n = 27) and healthy subjects (n = 14). We assessed the serum BDNF, the motor cortex excitability by parameters the TMS measures and the change on numerical pain scale [NPS (0–10)] during CPM-task. The adjusted mean (SD) on the SICI observed in the absence of tissue injury was 56.36% lower than with persistent nociceptive input [0.31(0.18) vs. 0.55 (0.32)], respectively. The BDNF was inversely correlated with the SICI and with the change on NPS (0–10) during CPM-task. These findings suggest greater disinhibition in the motor cortex and the descending pain inhibitory system in FM and MPS than in OA and healthy subjects. Likewise, the inter-hemispheric disinhibition as well as the dysfunction in the descending pain modulatory system is higher in chronic pain without tissue injury compared to a structural lesion. In addition, they suggest that a greater level of serum BDNF may be involved in the processes that mediate the disinhibition of motor cortex excitability, as well as the function of descending inhibitory pain modulation system, independently of the physiopathology mechanism of musculoskeletal pain syndromes. |
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Caumo, WolneiDeitos, AlíciaCarvalho, SandraLeite, JorgeCarvalho, FabianaSarria, Jairo Alberto DussánTarragó, Maria da Graça LopesSouza, Andressa deTorres, Iraci Lucena da SilvaFregni, Felipe2019-01-16T04:09:25Z20161662-5161http://hdl.handle.net/10183/187800001003420The central sensitization syndrome (CSS) encompasses disorders with overlapping symptoms in a structural pathology spectrum ranging from persistent nociception [e.g., osteoarthritis (OA)] to an absence of tissue injuries such as the one presented in fibromyalgia (FM) and myofascial pain syndrome (MPS). First, we hypothesized that these syndromes present differences in their cortical excitability parameters assessed by transcranial magnetic stimulation (TMS), namely motor evoked potential (MEP), cortical silent period (CSP), short intracortical inhibition (SICI) and short intracortical facilitation (SICF). Second, considering that the presence of tissue injury could be detected by serum neurotrophins, we hypothesized that the spectrum of structural pathology (i.e., from persistent nociception like in OA, to the absence of tissue injury like in FM and MPS), could be detected by differential efficiency of their descending pain inhibitory system, as assessed by the conditioned pain modulation (CPM) paradigm. Third, we explored whether brain-derived neurotrophic factor (BDNF) had an influence on the relationship between motor cortex excitability and structural pathology. This cross-sectional study pooled baseline data from three randomized clinical trials We included females (n = 114), aged 19–65 years old with disability by chronic pain syndromes (CPS): FM (n = 19), MPS (n = 54), OA (n = 27) and healthy subjects (n = 14). We assessed the serum BDNF, the motor cortex excitability by parameters the TMS measures and the change on numerical pain scale [NPS (0–10)] during CPM-task. The adjusted mean (SD) on the SICI observed in the absence of tissue injury was 56.36% lower than with persistent nociceptive input [0.31(0.18) vs. 0.55 (0.32)], respectively. The BDNF was inversely correlated with the SICI and with the change on NPS (0–10) during CPM-task. These findings suggest greater disinhibition in the motor cortex and the descending pain inhibitory system in FM and MPS than in OA and healthy subjects. Likewise, the inter-hemispheric disinhibition as well as the dysfunction in the descending pain modulatory system is higher in chronic pain without tissue injury compared to a structural lesion. In addition, they suggest that a greater level of serum BDNF may be involved in the processes that mediate the disinhibition of motor cortex excitability, as well as the function of descending inhibitory pain modulation system, independently of the physiopathology mechanism of musculoskeletal pain syndromes.application/pdfengFrontiers in human neuroscience. Lousanne. Vol. 10 (July 2016), article 357, 15 p.Dor musculoesqueléticaCórtex motorFator neurotrófico derivado do encéfaloShort intracortical inhibitionBrain-derived neurotrophic factorCentral sensitizationConditioned pain modulationOsteoarthritisFibromyalgiaMyofascial pain syndromeMotor cortex excitability and BDNF levels in chronic musculoskeletal pain according to structural pathologyEstrangeiroinfo:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFRGSinstname:Universidade Federal do Rio Grande do Sul (UFRGS)instacron:UFRGSTEXT001003420.pdf.txt001003420.pdf.txtExtracted Texttext/plain83231http://www.lume.ufrgs.br/bitstream/10183/187800/2/001003420.pdf.txtf0176fae90f4f51a45bf5c85f7563a30MD52ORIGINAL001003420.pdfTexto completo (inglês)application/pdf889094http://www.lume.ufrgs.br/bitstream/10183/187800/1/001003420.pdfc5fe5b7021b42545ba23bac108c824dcMD5110183/1878002019-01-17 04:22:50.457955oai:www.lume.ufrgs.br:10183/187800Repositório de PublicaçõesPUBhttps://lume.ufrgs.br/oai/requestopendoar:2019-01-17T06:22:50Repositório Institucional da UFRGS - Universidade Federal do Rio Grande do Sul (UFRGS)false |
dc.title.pt_BR.fl_str_mv |
Motor cortex excitability and BDNF levels in chronic musculoskeletal pain according to structural pathology |
title |
Motor cortex excitability and BDNF levels in chronic musculoskeletal pain according to structural pathology |
spellingShingle |
Motor cortex excitability and BDNF levels in chronic musculoskeletal pain according to structural pathology Caumo, Wolnei Dor musculoesquelética Córtex motor Fator neurotrófico derivado do encéfalo Short intracortical inhibition Brain-derived neurotrophic factor Central sensitization Conditioned pain modulation Osteoarthritis Fibromyalgia Myofascial pain syndrome |
title_short |
Motor cortex excitability and BDNF levels in chronic musculoskeletal pain according to structural pathology |
title_full |
Motor cortex excitability and BDNF levels in chronic musculoskeletal pain according to structural pathology |
title_fullStr |
Motor cortex excitability and BDNF levels in chronic musculoskeletal pain according to structural pathology |
title_full_unstemmed |
Motor cortex excitability and BDNF levels in chronic musculoskeletal pain according to structural pathology |
title_sort |
Motor cortex excitability and BDNF levels in chronic musculoskeletal pain according to structural pathology |
author |
Caumo, Wolnei |
author_facet |
Caumo, Wolnei Deitos, Alícia Carvalho, Sandra Leite, Jorge Carvalho, Fabiana Sarria, Jairo Alberto Dussán Tarragó, Maria da Graça Lopes Souza, Andressa de Torres, Iraci Lucena da Silva Fregni, Felipe |
author_role |
author |
author2 |
Deitos, Alícia Carvalho, Sandra Leite, Jorge Carvalho, Fabiana Sarria, Jairo Alberto Dussán Tarragó, Maria da Graça Lopes Souza, Andressa de Torres, Iraci Lucena da Silva Fregni, Felipe |
author2_role |
author author author author author author author author author |
dc.contributor.author.fl_str_mv |
Caumo, Wolnei Deitos, Alícia Carvalho, Sandra Leite, Jorge Carvalho, Fabiana Sarria, Jairo Alberto Dussán Tarragó, Maria da Graça Lopes Souza, Andressa de Torres, Iraci Lucena da Silva Fregni, Felipe |
dc.subject.por.fl_str_mv |
Dor musculoesquelética Córtex motor Fator neurotrófico derivado do encéfalo |
topic |
Dor musculoesquelética Córtex motor Fator neurotrófico derivado do encéfalo Short intracortical inhibition Brain-derived neurotrophic factor Central sensitization Conditioned pain modulation Osteoarthritis Fibromyalgia Myofascial pain syndrome |
dc.subject.eng.fl_str_mv |
Short intracortical inhibition Brain-derived neurotrophic factor Central sensitization Conditioned pain modulation Osteoarthritis Fibromyalgia Myofascial pain syndrome |
description |
The central sensitization syndrome (CSS) encompasses disorders with overlapping symptoms in a structural pathology spectrum ranging from persistent nociception [e.g., osteoarthritis (OA)] to an absence of tissue injuries such as the one presented in fibromyalgia (FM) and myofascial pain syndrome (MPS). First, we hypothesized that these syndromes present differences in their cortical excitability parameters assessed by transcranial magnetic stimulation (TMS), namely motor evoked potential (MEP), cortical silent period (CSP), short intracortical inhibition (SICI) and short intracortical facilitation (SICF). Second, considering that the presence of tissue injury could be detected by serum neurotrophins, we hypothesized that the spectrum of structural pathology (i.e., from persistent nociception like in OA, to the absence of tissue injury like in FM and MPS), could be detected by differential efficiency of their descending pain inhibitory system, as assessed by the conditioned pain modulation (CPM) paradigm. Third, we explored whether brain-derived neurotrophic factor (BDNF) had an influence on the relationship between motor cortex excitability and structural pathology. This cross-sectional study pooled baseline data from three randomized clinical trials We included females (n = 114), aged 19–65 years old with disability by chronic pain syndromes (CPS): FM (n = 19), MPS (n = 54), OA (n = 27) and healthy subjects (n = 14). We assessed the serum BDNF, the motor cortex excitability by parameters the TMS measures and the change on numerical pain scale [NPS (0–10)] during CPM-task. The adjusted mean (SD) on the SICI observed in the absence of tissue injury was 56.36% lower than with persistent nociceptive input [0.31(0.18) vs. 0.55 (0.32)], respectively. The BDNF was inversely correlated with the SICI and with the change on NPS (0–10) during CPM-task. These findings suggest greater disinhibition in the motor cortex and the descending pain inhibitory system in FM and MPS than in OA and healthy subjects. Likewise, the inter-hemispheric disinhibition as well as the dysfunction in the descending pain modulatory system is higher in chronic pain without tissue injury compared to a structural lesion. In addition, they suggest that a greater level of serum BDNF may be involved in the processes that mediate the disinhibition of motor cortex excitability, as well as the function of descending inhibitory pain modulation system, independently of the physiopathology mechanism of musculoskeletal pain syndromes. |
publishDate |
2016 |
dc.date.issued.fl_str_mv |
2016 |
dc.date.accessioned.fl_str_mv |
2019-01-16T04:09:25Z |
dc.type.driver.fl_str_mv |
Estrangeiro info:eu-repo/semantics/article |
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http://hdl.handle.net/10183/187800 |
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1662-5161 |
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001003420 |
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http://hdl.handle.net/10183/187800 |
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eng |
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dc.relation.ispartof.pt_BR.fl_str_mv |
Frontiers in human neuroscience. Lousanne. Vol. 10 (July 2016), article 357, 15 p. |
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