Please use this identifier to cite or link to this item: https://repositorio.ufrn.br/jspui/handle/123456789/23127
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dc.contributor.authorSantos-Pontelli, Taiza Elaine Grespan-
dc.contributor.authorPontes-Neto, Octavio Marques-
dc.contributor.authorAraujo, Draulio Barros de-
dc.contributor.authorSantos, Antonio Carlos dos-
dc.contributor.authorLeite, João Pereira-
dc.date.accessioned2017-05-26T17:34:23Z-
dc.date.available2017-05-26T17:34:23Z-
dc.date.issued2011-
dc.identifier.issn1807-5932-
dc.identifier.urihttp://hdl.handle.net/123456789/23127-
dc.languageengpt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectPusher behaviorpt_BR
dc.subjectStrokept_BR
dc.titlePersistent pusher behavior after a strokept_BR
dc.typearticlept_BR
dc.description.resumoPusher behavior (PB) is a postural control disorder characterized by actively pushing away from the nonparetic side and resisting passive correction with a tendency to fall toward the paralyzed side.1 These patients have no awareness that their active pushing is counterproductive, which precludes the patients from standing without assistance. Several studies have already demonstrated that PB can occur in patients with lesions in both hemispheres, and PB is distinct from neglect and anosognosia.2-8 The high frequency of the association between PB and neurophysiological deficits might reflect an increased vulnerability of certain regions to stroke-induced injury rather than any direct involvement with the occurrence of PB.9,10 Traditionally, PB has only been reported in stroke patients; however, it has also been described under nonstroke conditions.8 Previous imaging studies have suggested the posterolateral thalamus as the brain structure that is typically damaged in pusher patients.4,11 Nevertheless, other cortical and subcortical areas, such as the insular cortex and post-central gyrus, have also been highlighted as structures that are potentially involved in the pathophysiology of PB.2,12-16pt_BR
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