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Stephen G. Lomber, Bertram R. Payne, Amee J. Hall, Shveta Malhotra, Jeffrey G. Mellott; Adaptive cortical plasticity underlying recovery from cerebral damage induced visual neglect. Journal of Vision 2006;6(6):516. doi: 10.1167/6.6.516.
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In humans, damage to cortex at the temporo-parieto-occipital junction in the right hemisphere often results in profound neglect of contralateral visual space. In cats, similar deficits are identified following reversible deactivation of cortex forming the banks of the posterior middle suprasylvian (pMS) sulcus. Cooling deactivation of none of the flanking cortices results in contralateral neglect. Neglect is also caused by permanent lesions of pMS sulcal cortex. However, these deficits are only profound for the first few days following the lesion and the deficits quickly attenuate to normal levels over the first two weeks post-lesion. In this study we tested the hypothesis that flanking cortex would assume the attentional functions normally mediated by pMS sulcal cortex. Cats were trained to perform a visual localization task, pMS sulcal cortex in the right hemisphere was ablated using ibotenic acid, and cooling loops were placed over four flanking cortices: anterior middle suprasylvian (aMS) sulcus, middle suprasylvian (MS) gyrus, the middle ectosylvian (ME) gyrus, and the dorsal posterior suprasylvian (dPS) gyrus. Neglect was profound for three days post-op. The deficit then attenuated and was absent by the end of the 2nd week. One month post-surgery, we found that cooling deactivation of aMS sulcal cortex, but not aMS sulcal cortex nor the MS or dPS gyri, resulted in a profound contralateral visual neglect. Therefore, we conclude that functions of visual attention normally mediated by pMS sulcal cortex relocate to aMS sulcal cortex following permanent damage to pMS sulcal cortex.
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