The Effect of Traumatic Brain Injury on Functional Homotopy and Resting State Functonal Connectivity
1Department of Diagnostic Imaging, Sheba Medical Center, Israel
2The Joseph Sagol Neuroscience Center, Sheba Medical Center, Israel
3Department of Psychology, Tel-Aviv University, Israel
4Department of Neurosurgery, Rabin Medical Center, Belinson, Israel
5Sackler Faculty of Medicine, Tel-Aviv University, Israel
PURPOSE: Traumatic brain injury (TBI) experience varying degrees of residual neurological or cognitive deficits, ranging from impairments in simple alertness and vigilance to deficits in advanced complex executive functions. One mechanism by which TBI is thought to affect cognition and behavior is through alteration of functional connectivity (FC) between brain regions. Brain homotopy describes a fundamental characteristic of the intrinsic functional architecture of the brain. By measuring bilateral regional resting state functional connectivity (RSFC) studies have shown changes in functional homotopy in certain brain regions associated with age and a variety of diseases. Thus, it is reasonable to expect that an important aspect of TBI may be impairment of interhemispheric functional interactions. The present study aimed to: 1) Examine whether TBI patients exhibit decreased interhemispheric FC across several brain systems by using voxel mirrored homotopic connectivity (VMHC). 2) Examine whether decrease homotopy is associated with decreased FC in other areas of the brain.
MATERIAL & METHODS: Fifteen TBI patients were recruited from the department of neurosurgery at Sheba Medical Center, Tel-Hashomer (GCS<15). Thirty-four healthy controls matched by age and gender were recruited from the general population. First, in order to assess differences in functional homotopy between TBI and healthy control subjects, resting-state functional connectivity data was obtained and interhemispheric coordination was examined using voxel-mirrored homotopic connectivity, by calculating the correlation between each voxel and its counterpart on the opposite hemisphere. Second, seed-based FC was completed by placing regions-of- interest (ROIs) in clusters that exhibited significant group differences in the VMHC. Correlation analyses were conducted between the seed ROI and the remaining voxels within the brain.
RESULTS: TBI patients exhibited decreased VMHC in the hippocampus compared to controls. No voxel exhibited significantly higher VMHC in the TBI patients compared to controls. Subsequent seed-based functional connectivity analysis revealed disrupted functional connectivity between the hippocampus and frontal regions, including: the left frontal pole, lef frontal orbital and left inferior frontal gyrus in TBI patient.
CONCLUSION: Our present finding of reduced VMHC in the hippocampus is consistent with studies showing hippocampal impairment in TBI patients. Our results revealed disrupted functional connectivity between the hippocampus and frontal regions, which may underlie cognitive deficts of TBI patients.