Navegando por Autor "Pontes-Neto, Octavio Marques"
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Artigo ArticleNeuroimaging in stroke and non-stroke pusher patients(2011-07-11) Santos-Pontelli, Taiza Elaine Grespan; Pontes-Neto, Octavio Marques; Araújo, Dráulio Barros de; Santos, Antonio Carlos dos; Leite, João PereiraPusher behavior (PB) is a disorder of postural control affecting patients with encephalic lesions. This study has aimed to identify the brain substrates that are critical for the occurrence of PB, to analyze the influence of the midline shift (MS) and hemorrhagic stroke volume (HSV) on the severity and prognosis of the PB. We identified 31 pusher patients of a neurological unit, mean age 67.4±11.89, 61.3% male. Additional neurological and functional examinations were assessed. Neuroimaging workup included measurement of the MS, the HSV in patients with hemorrhagic stroke, the analysis of the vascular territory, etiology and side of the lesion. Lesions in the parietal region (p=0.041) and thalamus (p=0.001) were significantly more frequent in PB patients. Neither the MS nor the HSV were correlated with the PB severity or recovery time. Key words: pusher behavior, stroke, postural control.Artigo Persistent pusher behavior after a stroke(2011) Santos-Pontelli, Taiza Elaine Grespan; Pontes-Neto, Octavio Marques; Araújo, Dráulio Barros de; Santos, Antonio Carlos dos; Leite, João PereiraPusher 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.2,12-16