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Neural Plasticity
Volume 2017 (2017), Article ID 8740353, 17 pages
Research Article

Right Hemisphere Remapping of Naming Functions Depends on Lesion Size and Location in Poststroke Aphasia

1Department of Neurology, Georgetown University Medical Center, Washington, DC, USA
2Research Division, MedStar National Rehabilitation Hospital, Washington, DC, USA
3Department of Neurology, First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China

Correspondence should be addressed to Peter E. Turkeltaub

Received 8 July 2016; Accepted 24 November 2016; Published 12 January 2017

Academic Editor: Cynthia K. Thompson

Copyright © 2017 Laura M. Skipper-Kallal et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The study of language network plasticity following left hemisphere stroke is foundational to the understanding of aphasia recovery and neural plasticity in general. Damage in different language nodes may influence whether local plasticity is possible and whether right hemisphere recruitment is beneficial. However, the relationships of both lesion size and location to patterns of remapping are poorly understood. In the context of a picture naming fMRI task, we tested whether lesion size and location relate to activity in surviving left hemisphere language nodes, as well as homotopic activity in the right hemisphere during covert name retrieval and overt name production. We found that lesion size was positively associated with greater right hemisphere activity during both phases of naming, a pattern that has frequently been suggested but has not previously been clearly demonstrated. During overt naming, lesions in the inferior frontal gyrus led to deactivation of contralateral frontal areas, while lesions in motor cortex led to increased right motor cortex activity. Furthermore, increased right motor activity related to better naming performance only when left motor cortex was lesioned, suggesting compensatory takeover of speech or language function by the homotopic node. These findings demonstrate that reorganization of language function, and the degree to which reorganization facilitates aphasia recovery, is dependent on the size and site of the lesion.