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Changes in connectivity after visual cortical brain damage underlie altered visual function
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DOI：10.1093/brain/awn063.png)
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The full extent of the brain's ability to compensate for damage or changed experience is yet to be established. One question particularly important for evaluating and understanding rehabilitation following brain damage is whether recovery involves new and aberrant neural connections or whether any change in function is due to the functional recruitment of existing pathways, or both. Blindsight, a condition in which subjects with complete destruction of part of striate cortex (V1) retain extensive visual capacities within the clinically blind field, is an excellent example of altered visual function. Since the main pathway to the visual cortex is destroyed, the spared or recovered visual ability must arise from either an existing alternative pathway, or the formation of a new pathway. Using diffusion-weighted MRI, we show that both controls and blindsight subject GY, whose left V1 is destroyed, show an ipsilateral pathway between LGN (lateral geniculate nucleus) and human motion area MT+/V5 (bypassing V1). However, in addition, GY shows two major features absent in controls: (i) a contralateral pathway from right LGN to left MT+/V5, (ii) a substantial cortico-cortical connection between MT+/V5 bilaterally. Both observations are consistent with previous functional MRI data from GYshowing enhanced ipsilateral activation in MT+/V5. There is also evidence for a pathway in GY from left LGN to right MT+/V5, although the lesion makes its quantification difficult. This suggests that employing alternative brain regions for processing of information following cortical damage in childhood may strengthen or establish specific connections.
Keyword:
visual cortex
blindsight
diffusion tensor imaging
functional MRI
lateral geniculate nucleus
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