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Complete validation of any finite element (FE) model of the human brain is very difficult due to the lack of adequate experimental data. However, more animal brain injury data, especially rat data, obtained under well-defined mechanical loading conditions, are available to advance the understanding of the mechanisms of traumatic brain injury. Unfortunately, internal response of the brain in these experimental studies could not be measured. The aim of this study was to develop a detailed FE model of the rat brain for the prediction of intracranial responses due to different impact scenarios. Model results were used to elucidate possible brain injury mechanisms. An FE model, consisting of more than 250,000 hexahedral elements with a typical element size of 100 to 300 microns, was developed to represent the brain of a rat. The model was first validated locally against peak brain deformation data obtained from nine unique dynamic cortical deformation (vacuum) tests.

The pia-arachnoid complex (PAC) covering the brain plays an important role in the mechanical response of the brain due to impact or inertial loading. However, the mechanical properties of the pia-arachnoid complex and its influence on the overall response of the brain have not been well characterized. Consequently, finite element (FE) brain models have tended to oversimplify the response of the pia-arachnoid complex, possibly resulting in a loss of accuracy in the model predictions. The aim of this study was to determine, experimentally, the material properties of the pia-arachnoid complex under quasi-static and dynamic loading conditions. Specimens of the pia-arachnoid complex were obtained from the parietal and temporal regions of freshly slaughtered bovine subjects with the specimen orientation recorded. Single-stroke, uniaxial quasi-static and dynamic tensile experiments were performed at strain-rates of 0.05, 0.5, 5 and 100 s-1 (n = 10 for each strain rate group).

A modified Marmarou impact acceleration injury model was developed to study the kinematics of the rat head to quantify traumatic axonal injury (TAI) in the corpus callosum (CC) and brainstem pyramidal tract (Py), to determine injury predictors and to establish injury thresholds for severe TAI. Thirty-one anesthetized male Sprague-Dawley rats (392 ± 13 grams) were impacted using a modified impact acceleration injury device from 2.25 m and 1.25 m heights. Beta-amyloid precursor protein (β-APP) immunocytochemistry was used to assess and quantify axonal changes in CC and Py. Over 600 injury maps in CC and Py were constructed in the 31 impacted rats. TAI distribution along the rostro-caudal direction in CC and Py was determined. Linear and angular responses of the rat head were monitored and measured in vivo with an attached accelerometer and angular rate sensor, and were correlated to TAI data.