Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/74292
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dc.contributor.authorde Antonio-Palomero, A.en_US
dc.contributor.authorVictoria-Díaz, J.en_US
dc.date.accessioned2020-09-08T09:11:41Z-
dc.date.available2020-09-08T09:11:41Z-
dc.date.issued2001en_US
dc.identifier.issn0210-0010en_US
dc.identifier.otherWoS-
dc.identifier.urihttp://hdl.handle.net/10553/74292-
dc.description.abstractIntroduction. The long-term potentiation (LTP) of synaptic transmission constitutes a remarkable example of synaptic plasticity, and represents a learning model. The LTP has been described by several authors in the hippocampus through high frequency stimulation. Objectives, patients and methods. In the present paper we have used conventional EMG-biofeedback techniques which aims at investigating the rehabilitation of myopathies and the electrophysiological mechanism of neuromuscular learning at marrow level. Three experimental patients of progressive muscular dystrophy, aged between I I and 15, were systematically treated with EMG-biofeedback in several muscular groups. Special attention is given to the records corresponding to rest post-maximum effort (RPME). Results. For the principal muscular groups rehabilitated it has been verified that the motor unit potentials corresponding to RPME show intense activity, with average amplitudes of 600-700 muV and duration close to 15 ms, against a practically nonexistent activity before rehabilitation. The descent of the alkaline phosphatase (from 200 U/l to 50 U/l) and the lactic-deshydrogenase Conclusions. The EMG-biofeedback techniques allow its to (from 320 U/l to 210 U/l) are specially significant physical efficiency inpatients of progressive muscular dystrophy. The analysis of post-biofeedback motor unit potentials, and the strong descent of the enzymes in the last phase of treatment, allows us to deduce the establishment of LTP between the alpha-motoneurons and the axonic terminals of the microneurons of Renshaw. The mechanism of the LTP at marrow level is interpreted through two physiological hypotheses concerning the circuit of Renshaw.en_US
dc.languageengen_US
dc.relation.ispartofRevista de Neurologiaen_US
dc.sourceRevista de Neurologia [ISSN 0210-0010], v. 33 (12), p. 1125-1128, (Diciembre 2001)en_US
dc.subject320507 Neurologíaen_US
dc.subject.otherCircuit Of Renshawen_US
dc.subject.otherElectromyographic Biofeedbacken_US
dc.subject.otherMotor Unit Potentialsen_US
dc.subject.otherProgressive Muscular Dystrophyen_US
dc.subject.otherNervios periféricosen_US
dc.subject.otherUnión neuromuscular y músculoen_US
dc.titleLong-term potentiation at marrow level induced through EMG-biofeedbacken_US
dc.title.alternativeIncremento en la eficacia de las alfamotoneuronas inducido mediante biofeedback-EMGen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.33588/rn.3312.2001002en_US
dc.identifier.isi000173163700006-
dc.description.lastpage1128en_US
dc.identifier.issue12-
dc.description.firstpage1125en_US
dc.relation.volume33en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.contributor.daisngid34014253-
dc.contributor.daisngid16567711-
dc.description.numberofpages4en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:de Antonio-Palomero, A-
dc.contributor.wosstandardWOS:Victoria-Diaz, J-
dc.date.coverdateDiciembre 2001en_US
dc.identifier.ulpgces
dc.description.jcr0,26
dc.description.jcrqQ4
dc.description.scieSCIE
item.fulltextSin texto completo-
item.grantfulltextnone-
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