Abstract
Hemianopia patients have lost vision from the contralateral hemifield, but make behavioural adjustments to compensate for this field loss. As a result, their visual performance and behaviour contrast with those of hemineglect patients who fail to attend to objects contralateral to their lesion. These conditions differ in their ocular fixations and perceptual judgments. During visual search, hemianopic patients make more fixations in contralesional space while hemineglect patients make fewer. During line bisection, hemianopic patients fixate the contralesional line segment more and make a small contralesional bisection error, while hemineglect patients make few contralesional fixations and a larger ipsilesional bisection error. Hence, there is an attentional failure for contralesional space in hemineglect but a compensatory adaptation to attend more to the blind side in hemianopia. A challenge for models of visual attentional processes is to show how compensation is achieved in hemianopia, and why such processes are hindered or inaccessible in hemineglect. We used a neurophysiology-derived computational model to examine possible cortical compensatory processes in simulated hemianopia from a V1 lesion and compared results with those obtained with the same processes under conditions of simulated hemineglect from a parietal lesion. A spatial compensatory bias to increase attention contralesionally replicated hemianopic scanning patterns during visual search but not during line bisection. To reproduce the latter required a second process, an extrastriate lateral connectivity facilitating form completion into the blind field: this allowed accurate placement of fixations on contralesional stimuli and reproduced fixation patterns and the contralesional bisection error of hemianopia. Neither of these two cortical compensatory processes was effective in ameliorating the ipsilesional bias in the hemineglect model. Our results replicate normal and pathological patterns of visual scanning, line bisection, and differences between hemianopia and hemineglect, and may explain why compensatory processes that counter the effects of hemianopia are ineffective in hemineglect.
Highlights
Patients with homonymous hemianopia have lost vision in the field contralateral to their lesion, most frequently from damage to the optic radiations or striate cortex (V1), less commonly from damage to the optic tract or lateral geniculate nucleus
When the model sustained a V1 lesion resulting in a left hemianopia with no compensatory processes in place, the scanpath was altered: it favoured the intact ipsilesional hemispace and omitted the blind side, similar to hemineglect scanpaths produced by the model with a parietal lesion
We found that the small contralesional bisection error seen in hemianopia was linked to the extrastriate form completion process, which influenced cortical perception of line length, and that the activity of V1 endstopping cells alone could not account for pathological traits in judging line length
Summary
Patients with homonymous hemianopia have lost vision in the field contralateral to their lesion, most frequently from damage to the optic radiations or striate cortex (V1), less commonly from damage to the optic tract or lateral geniculate nucleus. Hemineglect results typically from a lesion of the right posterior parietal cortex [1,2,3] but sometimes with frontal [4,5,6] or thalamic [7] lesions, and far less commonly from left-sided lesions. Despite their visual loss, hemianopic patients direct more eye movements towards their contralesional blind side during visual search [2,8]. The processes by which hemianopic patients are able to adapt and preferentially attend to the blind side are still unclear
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