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Frontal and temporal lobe contusions that were caused by a single sagittal plane angular acceleration impulse were analyzed. At neuropathological exam the depth, extent, and location of contusions were mapped and described according to a classification previously developed for human use. Of 30 rhesus monkeys subjected to a single angular acceleration impulse, 13 had no frontal or temporal contusion (Group 1), 8 had only frontal contusion (Group 2) and 9 had temporal contusions (Group 3). Correlation with angular acceleration, tangential acceleration and tangential force showed that the three groups were statistically different. The mean peak positive tangential force for Groups 1-3 was 541, 659 and 766 newtons respectively (p<0.10). This suggested that as mechanical imput increased, frontal contusions occur before temporal contusions and that the threshold for frontal contusion is less than that for temporal contusion.

This report discusses the development of brain injury tolerance criteria based on the study of three model systems: the primate, inanimate physical surrogates, and isolated tissue elements. Although we are equally concerned with the neural and neurovascular tissue components of the brain, the report will focus on the former and, in particular, the axonal elements. Under conditions of distributed, impulsive, angularacceleration loading, the primate model exhibits a pathophysiological response ranging from mild cerebral concussion to massive, diffuse white matter damage with prolonged coma. When physical models are subjected to identical loading conditions it becomes possible to map the displacements and calculate the associated strains and stresses within the field simulating the brain. Correlating these experimental models leads to predictive levels of tissue element deformation that may be considered as a threshold for specific mechanisms of injury.