Literature DB >> 19580383

Elucidating the nature of deregulated semantic cognition in semantic aphasia: evidence for the roles of prefrontal and temporo-parietal cortices.

Krist A Noonan1, Elizabeth Jefferies, Faye Corbett, Matthew A Lambon Ralph.   

Abstract

Semantic cognition--semantically driven verbal and nonverbal behavior--is composed of at least two interactive principal components: conceptual representations and executive control processes that regulate and shape activation within the semantic system. Previous studies indicate that semantic dementia follows from a progressive yet specific degradation of conceptual knowledge. In contrast, multimodal semantic impairment in aphasic patients (semantic aphasia [SA]) reflects damage to the control component of semantic cognition [Jefferies, E., & Lambon Ralph, M. A. Semantic impairment in stroke aphasia versus semantic dementia: A case-series comparison. Brain, 129, 2132-2147, 2006]. The purpose of the present study was to examine the nature of the semantic control deficits in SA in detail for the first time. Seven patients with SA were tested on four comprehension and naming tasks that directly manipulated the requirement for executive control in different ways. In line with many theories of cognitive control, the SA patients demonstrated three core features of impaired control: (i) they exhibited poor on-line manipulation and exploration of semantic knowledge; (ii) they exhibited poor inhibition of strongly associated distractors; and (iii) they exhibited reduced ability to focus on or augment less dominant aspects of semantic information, although the knowledge itself remained and could be successfully cued by external constraints provided by the examiner. Our findings are consistent with the notion that the anterior temporal lobes are crucial for conceptual knowledge whereas the left prefrontal and temporo-parietal cortices, damaged in patients with SA, play a critical role in regulating semantic activation in a task-appropriate fashion.

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Year:  2010        PMID: 19580383     DOI: 10.1162/jocn.2009.21289

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


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