Sagittal plane rotational acceleration induced diffuse axonal injury threshold was investigated using an animal model in which the heads of the rats were exposed to selected rotation accelerations. Post-trauma survival times ranged from 3 to 120 h. Numerous S100 serum concentrations, brain tissue stained for β-Amyloid Precursor Protein (β-APP), and probes for Cyclooxygenase 2 (COX2) mRNA were used to detect affected nerve cells, decaying axons, and cytoskeletal changes, respectively. Scaling laws were applied to estimate injury thresholds for the human brain.

Confocal imaging revealed bands of β-APP-positive axons in the corpus callosum and its edges in animals exposed to rotational accelerations >1.1 Mrad/s2. Similarly, for COX2 presence and S100 concentrations at >0.9 Mrad/s2, the numbers of stained cells in the cortex and hippocampus and the concentrations increased. The data clearly indicate that the rat brain is injured at a specific rotational acceleration. Scaled to that of humans this would be 10 krad/s2 with a duration of 4 ms.