Lateropulsion syndrome or Pusher syndrome?

Abstract

After a hemisphere stroke, Lateropulsion has been empirically described as part of the pusher syndrome (Davies, 1985), comprising a severe lateropulsion with active pushing to the contralesional side (pusher), resistance to passive corrections, and spatial neglect. Here we investigated whether the pushing behavior is the central sign of the pusher syndrome. Cohort study of consecutive patients admitted in a neurorehabilitation after a first hemispheric stroke. Retrospective analysis of data collected at M1 post-stroke. Lateropulsion was assessed with the SCP. We also assessed: spatial neglect, aphasia, apraxia, depression, visual field defect, motor weakness, spasticity, sensory loss. One hundred and seventy-eight persons met inclusion criteria: age 63.2 (12.2) years, 57 females, 150 with infarction, 71 with a right hemispheric stroke. Lateropulsion prevalence was 26%; 14% without and 12% with additional pushing. The multivariate analysis (ordinal logistic regression) retained only two variables significantly associated with Lateropulsion: overall spatial neglect then weakness. Severe and moderate spatial neglect increased the risk to show lateropulsion (with or without pushing): OR 5.7 ( P < 0.001) and 3 ( P = 0.004), respectively. Severe weakness increased the risk to show lateropulsion, with or without pushing, (OR 2.8; P = 0.001), but not moderate weakness (OR 0.8; P = 0.3). The association between spatial neglect and lateropulsion was confirmed by a frequency analysis ( F = 135.6, P < 0.001). None patient without neglect showed lateropulsion whereas 97% patients with severe neglect showed lateropulsion (with or without pushing). Conversely all patients showing lateropulsion had a spatial neglect (moderate or severe), and this was true both for lateropulsion without pushing and lateropulsion with pushing. Spatial neglect is strongly associated with lateropulsion, regardless the existence of an additional pushing behavior. Spatial neglect has nothing to do specifically with the pusher syndrome but more generally with lateropulsion. This strengthens the idea that additional pushing behavior is a dramatic form of lateropulsion, not an idiosyncratic disease.