Altered functional connectivity in the motor network after traumatic brain injury
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Abstract
Background: A large proportion of survivors of traumatic brain injury (TBI) have persistent cognitive impairments, the profile of which does not always correspond to the size and location of injuries. One possible explanation could be that TBI-induced damage extends beyond obvious lesion sites to affect remote brain networks. We explored this hypothesis in the context of a simple and well-characterized network, the motor network. The aim of this cross-sectional study was to establish the residual integrity of the motor network as an important proof of principle of abnormal connectivity in TBI.
Methods: fMRI data were obtained from 12 right-handed patients and 9 healthy controls while they performed the finger-thumb opposition task with the right hand. We used both conventional and psychophysiologic interaction (PPI) analyses to examine the integrity of functional connections from brain regions we found to be activated in the paradigm we used.
Results: As expected, the analysis showed significant activations of the left primary motor cortex (M1), right cerebellum (Ce), and bilateral supplementary motor area (SMA) in controls. However, only the activation of M1 survived robust statistical thresholding in patients. In controls, the PPI analysis revealed that left M1, SMA, and right Ce positively interacted with the left frontal cortex and negatively interacted with the right supramarginal gyrus. In patients, we observed no negative interaction and reduced interhemispheric interactions from these seed regions.
Conclusions: These observations suggest that patients display compromised activation and connectivity patterns during the finger-thumb opposition task, which may imply functional reorganization of motor networks following TBI.
Footnotes
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Study funding: This study was undertaken at the Wolfson Brain Imaging Centre and Wellcome Trust Clinical Research Facility, Cambridge, and was supported by research funds from the Evelyn Trust, Medical Research Council (G9439390), and by funds given to the Neuroscience theme of the Cambridge Biomedical Research Centre by the National Institute for Health Research. M.K. is supported by the Addenbrooke's Charitable Trust and E.A.S. is supported by the Stephen Erskine Fellowship, Queens' College Cambridge.
Disclosure: Author disclosures are provided at the end of the article.
Received November 17, 2009. Accepted in final form March 10, 2010.
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