Diffuse axonal injury (DAI) is characterized by axonal damage in large regions of white matter. Such axonal damage is caused by strain fields developed within the brain due to rapid rotational acceleration of the head. DAI is manifested in varying degrees of severity as concussion, coma, and fatality. Reliable estimates of the acceleration tolerance of the human brain are particularly important in evaluating vehicle restraint systems and structural crashworthiness. Experimental data pertaining to head injury biomechanics is extremely scarce. A procedure is developed whereby an estimate of the human DAI acceleration tolerance is estimated from the only experimental data available in the literature on the DAI tolerance of primates. This procedure involves finite element modeling of primate brains as structural entities. These models are utilized to provide information on the strain response within the brain, caused by head accelerations experienced in typical vehicle crash environments. A constitutive model is developed to model the non-linear material property of brain tissue using experimental data available in the literature. A finite element baboon brain model is developed. This model is simulated using several angular acceleration profiles which correspond to different levels of DAI severity in the animal model. A characteristic strain measure which correlates with the severity level of DAI is identified in the simulation response of the model. The choice of this strain measure is based on the high susceptibility of primate brains to DAI under lateral angular acceleration of the head in the coronal plane. DAI thresholds are characterized in terms of the magnitude of the chosen strain measure. A finite element model of the human brain is developed. Based on the DAI thresholds obtained from the baboon model, the strain response of the human brain finite element model is utilized to estimate a corresponding human DAI threshold.