Publicação
Measuring spinal presynaptic inhibition in human subjects
| dc.contributor.author | Swash, Michael | |
| dc.contributor.author | Carvalho, Mamede | |
| dc.date.accessioned | 2021-10-18T14:05:12Z | |
| dc.date.available | 2021-10-18T14:05:12Z | |
| dc.date.issued | 2020 | |
| dc.description | © 2020 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved | pt_PT |
| dc.description.abstract | In recent years an increased level of motor neuronal excitation has been proposed as important in the neuronal degeneration so characteristic of amyotrophic lateral sclerosis (ALS/MND) (Van Den Bosch et al., 2006). This notion derives from the finding that levels of glutamate, an excitatory neurotransmitter, are raised in the cerebrospinal fluid in about 20% of patients with ALS/MND (Plaitakis and Caroscio, 1987) and glutamate transport is abnormal in brain and spinal cord tissue at autopsy (Rothstein et al., 1992; Yamanaka and Komine, 2018). Further, measurements of short interval cortical inhibition (SICI) in ALS/MND, using a threshold tracking protocol involving paired pulse transcranial magnetic stimulation of motor cortex, have shown that increased cortical excitability, determined by reduced cortical inhibition, may precede the clinical onset of ALS, and that this becomes more marked as the disease progresses (Vucic et al., 2008; Shibuya et al., 2017). | pt_PT |
| dc.description.version | info:eu-repo/semantics/publishedVersion | pt_PT |
| dc.identifier.citation | Clin Neurophysiol. 2020 Aug;131(8):1966-1967 | pt_PT |
| dc.identifier.doi | 10.1016/j.clinph.2020.04.015 | pt_PT |
| dc.identifier.eissn | 1872-8952 | |
| dc.identifier.issn | 1388-2457 | |
| dc.identifier.uri | http://hdl.handle.net/10451/49935 | |
| dc.language.iso | eng | pt_PT |
| dc.peerreviewed | yes | pt_PT |
| dc.publisher | Elsevier | pt_PT |
| dc.relation.publisherversion | https://www.sciencedirect.com/journal/clinical-neurophysiology | pt_PT |
| dc.title | Measuring spinal presynaptic inhibition in human subjects | pt_PT |
| dc.type | journal article | |
| dspace.entity.type | Publication | |
| oaire.citation.endPage | 1967 | pt_PT |
| oaire.citation.issue | 8 | pt_PT |
| oaire.citation.startPage | 1966 | pt_PT |
| oaire.citation.title | Clinical Neurophysiology | pt_PT |
| oaire.citation.volume | 131 | pt_PT |
| person.familyName | Swash | |
| person.familyName | de Carvalho | |
| person.givenName | Michael | |
| person.givenName | Mamede | |
| person.identifier.orcid | 0000-0002-8717-8914 | |
| person.identifier.orcid | 0000-0001-7556-0158 | |
| person.identifier.scopus-author-id | 7101990692 | |
| person.identifier.scopus-author-id | 7101893769 | |
| rcaap.rights | restrictedAccess | pt_PT |
| rcaap.type | article | pt_PT |
| relation.isAuthorOfPublication | c6014014-de11-4f31-ac1a-096c54052517 | |
| relation.isAuthorOfPublication | dd7f55d4-c2b5-4fd2-9bd1-a9542a62f58f | |
| relation.isAuthorOfPublication.latestForDiscovery | dd7f55d4-c2b5-4fd2-9bd1-a9542a62f58f |
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