Network analysis of human fMRI data suggests modular restructuring after simulated acquired brain injury
The pathophysiology underlying neurocognitive dysfunction following mild traumatic brain injury (TBI), or concussion, is poorly understood. In order to shed light on the effects of TBI at the functional network or modular level, our research groups are engaged in the acquisition and analysis of func...
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Published in | Medical & biological engineering & computing Vol. 54; no. 1; pp. 235 - 248 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
2016
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | The pathophysiology underlying neurocognitive dysfunction following mild traumatic brain injury (TBI), or concussion, is poorly understood. In order to shed light on the effects of TBI at the functional network or modular level, our research groups are engaged in the acquisition and analysis of functional magnetic resonance imaging data from subjects post-TBI. Complementary to this effort, in this paper we use mathematical and computational techniques to determine how modular structure changes in response to specific mechanisms of injury. In particular, we examine in detail the potential effects of focal contusions, diffuse axonal degeneration and diffuse microlesions, illustrating the extent to which functional modules are preserved or degenerated by each type of injury. One striking prediction of our study is that the left and right hemispheres show a tendency to become functionally separated post-injury, but only in response to diffuse microlesions. We highlight other key differences among the effects of the three modelled injuries and discuss their clinical implications. These results may help delineate the functional mechanisms underlying several of the cognitive sequelae associated with TBI. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0140-0118 1741-0444 |
DOI: | 10.1007/s11517-015-1396-2 |