Neuroimaging in stroke and non-stroke pusher patients

Arquivos de Neuro-Psiquiatria, Jan 2011

Pusher 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.

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Neuroimaging in stroke and non-stroke pusher patients

Article Arq Neuropsiquiatr 2011;69(6):914-919 Neuroimaging in stroke and non-stroke pusher patients Taiza Elaine Grespan Santos-Pontelli, Octavio Marques Pontes-Neto, Draulio Barros de Araujo, Antonio Carlos dos Santos, João Pereira Leite ABSTRACT Pusher 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. Análise de neuroimagens de pacientes com síndrome do empurrador decorrente de AVC e outras etiologias RESUMO A síndrome do empurrador (SE) é um distúrbio de controle postural que acomete indivíduos com lesões encefálicas. Os objetivos deste estudo foram identificar as estruturas encefálicas envolvidas na SE, analisar a influência dos desvios de linha média (DLM) e volume do hematoma (VH) na gravidade e duração da SE. Dentre os pacientes internados na enfermaria de neurologia, foram identificados 31 pacientes com SE, idade média 67,4±11,89, 61,3% homens. Foram realizados exames neurológico e funcional. As análises das neuroimagens incluíram medidas de VH em pacientes com doença cerebrovascular (DC) hemorrágica, DLM, análise do território vascular, etiologia e lado da lesão. Lesão nas regiões parietal (p=0,041) e talâmica (p=0,001) foram significativamente mais frequentes nos pacientes com SE. Não foi observada correlação dos DLM e volume do hematoma com a gravidade e duração da SE. Palavras-Chave: síndrome do empurrador, doenças cerebrovasculares, controle postural. Correspondence João P. Leite Department of Neuroscience and Behavior Campus Universitário Ribeirão Preto 14049-900 Ribeirão Preto SP - Brasil E mail: Received 1 December 2010 Received in final form 4 July 2011 Accepted 11 July 2011 914 The pusher behavior (PB) may be the most intriguing disorder that impairs postural balance after acute encephalic lesions. Patients with PB lean towards the paretic side actively pushing with the nonparetic arm and leg and resist to any attempt of passive correction of their tilted body while sitting or standing1. Traditionally, the occurrence of PB had been only reported in stroke patients, though this disorder has also been described in non-stroke conditions2. Previous imaging studies have suggested the posterolateral thalamus as the typically damaged brain structure in pusher patients3,4. Nevertheless, other cortical and subcortical areas such as insular cortex and post-central gyrus5,6 have also been pointed out. Therefore, encephalic structures essentially affected in PB patients are still poorly understood. The aims of this study were to iden- Department of Neuroscience and Behavior, University of São Paulo School of Medicine at Ribeirão Preto, Ribeirão Preto SP, Brazil. Arq Neuropsiquiatr 2011;69(6) tify brain substrates that are critical for the occurrence of PB, to analyze the influence of the midline shift and hemorrhagic stroke volume on the signs and duration of the PB over a 3.5-year period of prospective follow-up. METHOD This was a prospective descriptive observational study that was approved by the ethics committee of our institution. Informed consent was obtained from all subjects or their legal responsible party. Patients with PB were prospectively identified from inpatients of a neurological emergency unit at a tertiary hospital of the University of São Paulo School of Medicine at Ribeirão Preto. All inpatients were screened by a physical therapist for any abnormal postural behavior by awaking and placing them in a seated position, as soon as clinically possible. If any instability appeared, they were further assessed for PB. Control group was composed by acute stroke patients with encephalic lesions confirmed by neuroimaging study that did not present PB and were matched for age and neurologic deficits with the group of patients with PB. Control group presented more previous encephalic lesions than PB group (p=0.027). Nevertheless, 95.66% of the control patients did not present neurologic deficits and were completely independent on their activities of daily living (ADL) before the lesion onset analyzed in this study. Patients were investigated by a unique qualified examiner (Santos-Pontelli, TEG). PB was assessed using a previously standardized Scale for Contraversive Pushing (SCP)7,8. The duration of PB was defined as the interval between injury onset and the complete resolution of PB signs (SCP=0). Pusher patients were periodically reevaluated (minimum 5; maximum 20 days). The reevaluation intervals were conducted within more than 10 days only after the 90th day post ictus onset. Severity of neurologic involvement of the patients was assessed by standardized scales such as the National Institutes of Health Stroke Scale (NIHSS) 9, Glasgow Coma Scale and Revised Trauma Score. Sensory deficits, visual field defects and aphasia were assessed as part of the NIHSS. The degree of paresis of the upper and lower limbs was scored with the usual clinical ordinal scale, where ‘0’ stands for no trace of movement and ‘5’ for normal movement. Patients were classified as having spatial neglect when there was clear evidence of a typical clinical behavior such as ‘1’ a spontaneous deviation of the head and eyes toward the ipsilesional side, ‘2’ orienting toward the ipsilesional side when addressed from the front or the contralesional side, and ‘3’ ignoring of contralesional located people or objects10. If the patient fulfilled these 3 first criteria and was conscious, another Stroke, non-stroke pusher, behavior Santos-Pontelli et al. four tests were further assessed: “Coping task”; “Clock Drawing test”; “Cancellation test” and “Line bisection test”10,11. Neglect was considered to be present in disoriented patients if they fulfilled the three clinical behaviors and, in conscious and oriented patients, if they fulfilled the criterion for spatial neglect in at least two of the four clinical tests, besides the clinical behavior. Anosognosia was rated by questioning the patient about limb weakness and confirmed only when no acknowledgement of motor weakness was obtained even after confrontation12. ADL function was assessed by the Barthel Index (BI) which evaluates 10 different abilities and ranges a total score from 0 to 100 points9,13. Un (...truncated)


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Taiza Elaine Grespan Santos-Pontelli, Octavio Marques Pontes-Neto, Draulio Barros de Araujo, Antonio Carlos dos Santos, João Pereira Leite. Neuroimaging in stroke and non-stroke pusher patients, Arquivos de Neuro-Psiquiatria, 2011, pp. 914-919, Volume 69, Issue 6, DOI: 10.1590/S0004-282X2011000700013