An anatomically detailed rhesus monkey brain FE model was developed to simulate in vivo responses of the brain of sub-human primates subjected to rotational accelerations resulting in diffuse axonal injury (DAI). The material properties used in the monkey model are those in the GHBMC 50th percentile male head model (Global Human Body Model Consortium). The angular loading simulations consisted of coronal, oblique and sagittal plane rotations with the center of rotation in neck to duplicate experimental conditions. Maximum principal strain (MPS) and Cumulative strain damage measure (CSDM) were analyzed for various white matter structures such as the cerebrum subcortical white matter, corpus callosum and brainstem. The MPS in coronal rotation were 45% to 54% higher in the brainstem, 8% to 48% higher in the corpus callosum, 13% to 22% higher in the white matter when compared to those in oblique and sagittal rotations, suggesting that more severe DAI was expected from coronal and oblique rotations as compared to that from sagittal rotation. The level 1+ DAI was associated with 1.3 to 1.42 MPS and 50% CSDM (0.5) responses in the brainstem, corpus callosum and cerebral white matter.
The mass scaling method, sometimes referred to as Holbourn's inverse 2/3 power law, used for development of human brain injury criterion was evaluated to understand the effect of geometrical and anatomical differences between human and animal head. Based on simulations conducted with the animal and human models in three different planes - sagittal, coronal and horizontal - the scaling from animal to human models are not supported due to lack of geometrical similitude between the animal and human brains. Thus, the scaling method used in the development of brain injury criterion for rotational acceleration/velocity is unreliable.