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Neural Plasticity
Volume 2017, Article ID 2361691, 15 pages
Research Article

Intrahemispheric Perfusion in Chronic Stroke-Induced Aphasia

1Center for the Neurobiology of Language Recovery, Northwestern University, Evanston, IL, USA
2Department of Communication Sciences and Disorders, School of Communication, Northwestern University, Evanston, IL, USA
3Department of Neurology, Feinberg School of Medicine, Northwestern University, Evanston, IL, USA
4Department of Radiology, Feinberg School of Medicine, Northwestern University, Evanston, IL, USA
5Massachusetts General Hospital, Department of Neurology, Harvard Medical School, Boston, MA, USA
6Department of Speech, Language, and Hearing, College of Health & Rehabilitation, Boston University, Boston, MA, USA
7Department of Cognitive Science, Krieger School of Arts & Sciences, Johns Hopkins University, Baltimore, MD, USA
8Department of Psychology, Weinberg College of Arts and Sciences, Northwestern University, Evanston, IL, USA

Correspondence should be addressed to Cynthia K. Thompson; ude.nretsewhtron@mohtkc

Received 30 September 2016; Revised 17 January 2017; Accepted 26 January 2017; Published 5 March 2017

Academic Editor: Zygmunt Galdzicki

Copyright © 2017 Cynthia K. Thompson 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.


Stroke-induced alterations in cerebral blood flow (perfusion) may contribute to functional language impairments and recovery in chronic aphasia. Using MRI, we examined perfusion in the right and left hemispheres of 35 aphasic and 16 healthy control participants. Across 76 regions (38 per hemisphere), no significant between-subjects differences were found in the left, whereas blood flow in the right was increased in the aphasic compared to the control participants. Region-of-interest (ROI) analyses showed a varied pattern of hypo- and hyperperfused regions across hemispheres in the aphasic participants; however, there were no significant correlations between perfusion values and language abilities in these regions. These patterns may reflect autoregulatory changes in blood flow following stroke and/or increases in general cognitive effort, rather than maladaptive language processing. We also examined blood flow in perilesional tissue, finding the greatest hypoperfusion close to the lesion (within 0–6 mm), with greater hypoperfusion in this region compared to more distal regions. In addition, hypoperfusion in this region was significantly correlated with language impairment. These findings underscore the need to consider cerebral perfusion as a factor contributing to language deficits in chronic aphasia as well as recovery of language function.