The perception–action model states that visual information is processed in different cortical areas depending on the purpose for which the information is acquired. Specifically, it was suggested that the ventral stream mediates visual perception, whereas the dorsal stream primarily processes visual information for the guidance of actions (Goodale & Milner, 1992). Evidence for the model comes from patient studies showing that patients with ventral stream damage (visualform agnosia) and patients with dorsal stream damage (optic ataxia) show divergent performance in action and perception tasks. Whereas DF, a patient suffering from visualform agnosia, was found to perform well in visuomotor tasks despite her inability to use vision for perceptual tasks, patients with optic ataxia show usually the opposite pattern, i.e. good perception but impairedvisuomotor control. The finding that both disorders seem to provoke a mirror-reversed pattern of spared and impairedvisual functions, led to the belief that optic ataxia and visualform agnosia can be considered as complementary disorders. However, the visuomotorperformance of patients with optic ataxia is typically only impaired when they are tested in visual periphery while being often preserved when tested in central vision. Here, we show that DF's visuomotorperformance is also only preserved when the target is presented centrally. Her reaching and grasping movements to targets in peripheralvision are abnormal. Our findings indicate that DF's visuomotorperformance is quite similar to the visuomotorperformance of patients with optic ataxia which undermines previous suggestions that the two disorders form a double-dissociation.
|Number of pages||8|
|Early online date||7 Nov 2011|
|Publication status||Published - Jan 2012|
- perception-action model
- visual form agnosia
- visual periphery
Hesse, C., Ball, K., & Schenk, T. (2012). Visuomotor performance based on peripheral vision is impaired in visual form agnosic patient DF. Neuropsychologia, 50(1), 90-97. https://doi.org/10.1016/j.neuropsychologia.2011.11.002