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Impaired reading in patients with right hemianopia

Lookup NU author(s): Professor David Howard

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Abstract

A left occipital stroke may result in alexia for two reasons, which may coexist depending on the distribution of the lesion. A lesion of the left lateroventral prestriate cortex or its afferents impairs word recognition ('pure alexia). If the left primary visual cortex or its afferents are destroyed, resulting in a complete right homonymous hemianopia, rightward saccades during text reading are disrupted ('hemianopic' alexia). By using functional imaging, we showed two separate but interdependent systems involved in reading. The first, subserving word recognition, involved the representation of foveal vision in the left and right primary visual cortex and the ventral prestriate cortex. The second system, responsible for the planning and execution of reading saccades, consisted of the representation of right parafoveal vision in the left visual cortex, the bilateral posterior parietal cortex (left > right), and the frontal eye fields (right > left). Disruption of this distributed neural system was demonstrated in patients with severe right homonymous hemianopia, commensurate with their inability to perform normal reading eye movements. Text reading, before processes involved in comprehension, requires the integration of perceptual and motor processes. We have demonstrated these distributed neural systems in normal readers and have shown how a right homonymous hemianopia disrupts the motor preparation of reading saccades during text reading.

Publication metadata

Author(s): Leff AP, Scott SK, Crewes H, Hodgson TL, Cowey A, Howard D, Wise RJS

Publication type: Article

Publication status: Published

Journal: Annals of Neurology

Year: 2000

Volume: 47

Issue: 2

Pages: 171-178

ISSN (print): 0364-5134

ISSN (electronic): 1531-8249

Publisher: John Wiley & Sons, Inc.

URL: http://dx.doi.org/10.1002/1531-8249(200002)47:2<171::AID-ANA6>3.0.CO;2-P

DOI: 10.1002/1531-8249(200002)47:2<171::AID-ANA6>3.0.CO;2-P

PubMed id: 10665487

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