Figure 1.
A flowchart of the process for creating the finite element model and connectome from T1 and diffusion MRI.
(a) The T1 image is (b) segmented into different head materials. The segmented geometry is then used to create (c) a biofidelic three-dimensional finite element volume mesh. The mesh is required for (d) an explicit dynamic finite element simulation that captures the biomechanical response from frontal impact. (e) Diffusion tensor images are used to generate (f) axonal bundle fiber tractography which is used to inform finite element transversely isotropic constitutive descriptions of white matter tissue behavior (c). Tractography is also used to create (g) a network model of the brain that can be (h) degraded over time.
Figure 2.
Schematic showing how structural network edges are degraded over time.
Red voxels indicate that the chosen critical cellular death threshold, , is reached. For this study, DTI tracts that traverse a damaged voxel are removed, thus degrading the connection strength of the network edge.
Figure 3.
Orthographic view of the local three-dimensional response measured at various locations in the brain for (a–b) pressure, (c–d) axonal strain and (e–f) strain rate predicted using a finite element simulation for impact to the head.
Prediction of the intracranial pressure response is compared to cadaveric experiments [53] and is shown in (b).
Figure 4.
Evolution of damaged tracts and the corresponding structural networks.
Using empirically-based cellular death predictions obtained from in vitro models of neural tissues, local strain and strain rate values computed from finite element simulations are used to specify injury. A computed cellular death of 3% was used as a critical value for defining white matter disruption. Damage is shown in red and the node size represents the percent change of degree. The predicted evolution of damage is shown for the sagittal and corresponding transverse views for 24 (a and b), 48 (c and d), 72 (e and f), and 96 hours (g and h).
Table 1.
The percentage of fully degraded edges and percentage of voxels above the 3% threshold for 24, 48, 72, and 96 hrs post-injury.
Figure 5.
Distribution of (a) the number of voxels with predicted cellular death above 3% for each day as a function of angle between axonal fiber bundle direction and direction of impact to the head, and (b) the number of voxels with predicted cellular death above 3% for each day as a function of angle between axonal fiber bundle direction and direction of impact to the head normalized by the initial distribution of fiber angle with respect to the loading condition.
Figure 6.
Connection strength matrices showing degradation over time, .
Connection strengths were resampled to a Gaussian distribution with a mean of 0.5 and a standard deviation of 0.1. Because of the monotonic cellular death criterion, as long as regions have non-zero axonal strain and strain rate from the finite element simulation, edges in the network eventually become degraded. The connection strength matrices at is shown in (a). The evolution of connection strength matrices for 0 (a), 24 (b), 48 (c), 72 (d), and 96 hours (e) are shown, as well as (f) the connection strength matrix for the case when a
strain threshold is used.
Figure 7.
Global and local efficiency in terms of time from impact.
Table 2.
Structural measures of simulated lesions for the top ten regions ranked according to percent reduction in local efficiency.
Figure 8.
Changes in (a) total edge strength and (b) global efficiency with change in critical cell death threshold for 24, 48, 72, and 96 hours.