http://brain.oxfordjournals.org/content/early/2015/02/14/brain.awv022.abstract
DOI: http://dx.doi.org/10.1093/brain/awv022
First published online: 16 February 2015
Summary
Both
hemispheres are engaged in recovery from word production deficits in
aphasia. Lexical therapy has been shown to induce brain reorganization
even in patients with chronic aphasia. However, the interplay of factors
influencing reorganization patterns still remains unresolved. We were
especially interested in the relation between lesion site,
therapy-induced recovery, and beneficial reorganization patterns. Thus,
we applied intensive lexical therapy, which was evaluated with
functional magnetic resonance imaging, to 14 chronic patients with
aphasic word retrieval deficits. In a group study, we aimed to
illuminate brain reorganization of the naming network in comparison with
healthy controls. Moreover, we intended to analyse the data with joint
independent component analysis to relate lesion sites to therapy-induced
brain reorganization, and to correlate resulting components with
therapy gain. As a result, we found peri-lesional and contralateral
activations basically overlapping with premorbid naming networks
observed in healthy subjects. Reduced activation patterns for patients
compared to controls before training comprised damaged left hemisphere
language areas, right precentral and superior temporal gyrus, as well as
left caudate and anterior cingulate cortex. There were decreasing
activations of bilateral visuo-cognitive, articulatory, attention, and
language areas due to therapy, with stronger decreases for patients in
right middle temporal gyrus/superior temporal sulcus, bilateral
precuneus as well as left anterior cingulate cortex and caudate. The
joint independent component analysis revealed three components indexing
lesion subtypes that were associated with patient-specific recovery
patterns. Activation decreases (i) of an extended frontal lesion
disconnecting language pathways occurred in left inferior frontal gyrus;
(ii) of a small frontal lesion were found in bilateral inferior frontal
gyrus; and (iii) of a large temporo-parietal lesion occurred in
bilateral inferior frontal gyrus and contralateral superior temporal
gyrus. All components revealed increases in prefrontal areas. One
component was negatively correlated with therapy gain. Therapy was
associated exclusively with activation decreases, which could mainly be
attributed to higher processing efficiency within the naming network. In
our joint independent component analysis, all three lesion patterns
disclosed involved deactivation of left inferior frontal gyrus.
Moreover, we found evidence for increased demands on control processes.
As expected, we saw partly differential reorganization profiles
depending on lesion patterns. There was no compensatory deactivation for
the large left inferior frontal lesion, with its less advantageous
outcome probably being related to its disconnection from crucial
language processing pathways.
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