Measuring and inducing brain plasticity in chronic aphasia

Julius Fridriksson, Julius Fridriksson

Abstract

Brain plasticity associated with anomia recovery in aphasia is poorly understood. Here, I review four recent studies from my lab that focused on brain modulation associated with long-term anomia outcome, its behavioral treatment, and the use of transcranial brain stimulation to enhance anomia treatment success in individuals with chronic aphasia caused by left hemisphere stroke. In a study that included 15 participants with aphasia who were compared to a group of 10 normal control subjects, we found that improved naming ability was associated with increased left hemisphere activity. A separate study (N = 26) revealed similar results in that improved anomia treatment outcome was associated with increased left hemisphere recruitment. Taken together, these two studies suggest that improved naming in chronic aphasia relies on the damaged left hemisphere. Based on these findings, we conducted two studies to appreciate the effect of using low current transcranial electrical stimulation as an adjuvant to behavioral anomia treatment. Both studies yielded positive findings in that anomia treatment outcome was improved when it was coupled with real brain stimulation as compared with a placebo (sham) condition. Overall, these four studies support the notion that the intact cortex in the lesioned left hemisphere supports anomia recovery in aphasia.

Learning outcomes: Readers will (a) be able to appreciate the possible influence of animal research upon the understanding of brain plasticity induced by aphasia treatment, (b) understand where functional changes associated with anomia treatment occur in the brain, (c) understand the basic principles of transcranial direct current stimulation, and (d) understand how brain stimulation coupled with aphasia treatment may potentially improve treatment outcome.

Copyright © 2011 Elsevier Inc. All rights reserved.

Figures

Fig. 1
Fig. 1
A box-plot showing treatment related change in RT associated with A-tDCS (light gray) and S-tDCS (dark gray). The error bars show the data range, the median is shown as the dark line in the middle of each box, and the inter-quartile range is represented as the top to bottom of each box. Printed by permission from Stroke.
Fig. 2
Fig. 2
A 4 × 2 electrode array setup: (A) The electrode array shown on the scalp of the subject with four cathodal electrodes (cyan) around two anode electrodes (red). (B) The same electrode array shown in relation to the underlying cortex. Notice the cortical lesion lying anterior to the anode electrodes. (C) The FEM model showing the greatest AC concentration (in red) directly under the anode electrodes on the posterior peri-lesional cortex. (D) An enhanced view of the peri-lesional regions seen in panel C showing a more detailed representation of the current concentration in relation to the cortical lesion.

Source: PubMed

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