Sagittal anterior-posterior rotational acceleration induced head injuries in the rat

A new test device to produce sagittal plane rearward rotational acceleration induced diffuse braininjury to the rat has been developed. During trauma, the heads, which were fixed to a rotating barby means of curved plates that were glued to the skull bones, were exposed to rotationalacceleration between 0.3 and 2 Mrad/s2. The animals were sacrificed 3, 24 and 72 hours aftertrauma. Blood samples were collected for serum analyses prior to sacrifice and subsequentdissection of the brains. Transverse cryostat brain tissue sections were cut at three locations inthe brains. The sections were stained with β-Amyliod Precursor Protein (β-APP) andNeurofilament (NF) antibodies and probes for Cyclooxygenase 2 (COX2) mRNA in-situhybridisation to detect decaying axons, cytoskeleton changes and affected nerve cells.Bands of β-APP positive axons, i.e. axons with reduced plasma flow and hence probably dyingaxons, were seen in the corpus callosum, thalamus and hippocampus and in the border of theseregions in most animals exposed to rotational trauma at 1.1 Mrad/s2 or higher. Similarly for theCOX2 marker; above 0.9 Mrad/s2 the numbers of stained cells were large for a number oflocations in the cortex and hippocampus region. Only negligible β-APP and COX2 mRNAupregulation were observed in the sham exposed controls and normal animals. NF changes werenot observed in controls or exposed animals euthanized prior to 3 hours after trauma, but visible24 hours after trauma. The S100 serum analyses indicate that blood vessel and glia cell injuriesoccur at rotational accelerations above 1.1 Mrad/s2.The data clearly indicate that the rat brain is injured at a rearward rotational acceleration of 1.0Mrad/s2 when the rotational acceleration pulse have a duration of 0.4 ms. The scaledrepresentative global head rotational acceleration and duration for humans is estimated to be 9krad/s2 and 4 ms, respectively. However, the study also highlight that these threshold values arehighly influenced by the choice of brain dimensions used in the scaling equations. In addition,differences such as position of the cerebellum, lack of gyruses in the rat brain, and location andshape of the ventricles, etc were not taken into account. In order to improve the understandingthe effect on scaling laws of these differences between the human and the rat, it is recommendedto carry out a parametric study on these issues using detailed FE-models of the rat and humans