Literature DB >> 17069479

Neural correlates of modality-specific spatial extinction.

Argye E Hillis1, Shannon Chang, Jennifer Heidler-Gary, Melissa Newhart, Jonathan T Kleinman, Cameron Davis, Peter B Barker, Eric Aldrich, Lynda Ken.   

Abstract

Sites of lesions responsible for visual, tactile, and/or motor extinction have not been clearly identified. We sought to determine the frequency of extinction in various modalities immediately after acute ischemic stroke, the rate of co-occurrence of extinction across modalities, and areas of infarct and/or hypoperfusion associated with each modality of extinction. A total of 148 patients with right supratentorial stroke were studied. In Study 1, 88 patients without hemiplegia, hemianesthesia, or visual field cuts were tested within 24 hours of onset for visual, tactile, and motor extinction, and underwent magnetic resonance diffusion and perfusion imaging. Associations between modality of extinction and areas of neural dysfunction (hypoperfusion/infarct) were identified. Of the 88 patients, 19 had only tactile extinction, 8 had only visual extinction, 12 had only motor extinction, 14 had extinction in two or more modalities, and 35 had no extinction. Tactile extinction was associated with neural dysfunction in the inferior parietal lobule; visual extinction was associated with dysfunction in the visual association cortex; and motor extinction was associated with neural dysfunction in the superior temporal gyrus. In Study 2, data from 60 patients who were excluded from Study 1 because of motor deficits were analyzed in the same way to determine whether frontal lesions contributed to visual or tactile extinction. Results again demonstrated that tactile extinction is associated with inferior parietal dysfunction, and visual extinction is associated with dysfunction of the visual association cortex. Potential accounts of the results, based on the "hemisphere rivalry" model of extinction and the limited attentional capacity model, are considered.

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Year:  2006        PMID: 17069479     DOI: 10.1162/jocn.2006.18.11.1889

Source DB:  PubMed          Journal:  J Cogn Neurosci        ISSN: 0898-929X            Impact factor:   3.225


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