Literature DB >> 16313931

Visuospatial deficits in patients with early left-hemispheric lesions and functional reorganization of language: consequence of lesion or reorganization?

Karen Lidzba1, Martin Staudt, Marko Wilke, Ingeborg Krägeloh-Mann.   

Abstract

INTRODUCTION: Patients with early left-hemispheric lesions have repeatedly been reported to show spared language functions (which are then mediated by the right hemisphere), but exhibit deficits in visuospatial functions. The "crowding hypothesis" explains these deficits by a neuronal scarcity in the right hemisphere for the original right hemispheric functions. An alternative hypothesis suggests direct lesion effects as the sole reason for the visuospatial impairments. The scope of this study was to examine the relations between visuospatial skills and hemispheric preference for language, and between visuospatial skills and cerebral lesion size.
METHODS: In a sample of young adults with pre- or perinatally acquired focal lesions of the left hemisphere and unilateral spastic cerebral palsy on the right side, we assessed intelligence and neuropsychological functions in the verbal and visuospatial domains. The behavioural data was correlated with structural MRI information and language preference as assessed using fMRI.
RESULTS: Patients with right hemispheric language production were impaired in visuospatial functions, compared not only to normal controls, but also to patients without right hemispheric language preference. Additionally, the degree of right hemispheric language correlated negatively with performance in visuospatial tasks. Lesion size correlated negatively only with performance IQ, which again correlated negatively with motor impairment of the patients and thus does not seem to reflect true cognitive deficits.
CONCLUSION: Visuospatial deficits in patients with early left-hemispheric lesions are a consequence of lesion-induced right hemispheric language organization, thus lending further support to the "crowding hypothesis".

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Year:  2005        PMID: 16313931     DOI: 10.1016/j.neuropsychologia.2005.10.022

Source DB:  PubMed          Journal:  Neuropsychologia        ISSN: 0028-3932            Impact factor:   3.139


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