Effect of age on amount and distribution of diffuse axonal injury after rotational trauma
Poster (konferens), 2014
Traumatic brain injuries (TBI) are a major public health problem in term of suffering and cost for society. About 40% of the TBI patients admitted to hospitals are non-focal injuries, usually referred to as distributed brain injuries (DBI). Studies have hypothesized that the resulting strains in the brain tissue are the primary cause of neurological deficiencies following DBI. These strains commonly appear when the skull is accelerated and the brain mass, due to its inertia, lags behind or continues its motion relative the skull. It has been suggested that the severity of the injury correlates with the amplitude of the angular acceleration, or with the resulting angular velocity. Among DBI, diffuse axonal injury (DAI) is common and regularly results in unconsciousness or death. Past studies have suggested DAI injury criteria and thresholds that can be used with crash test dummies and mathematical models of the human. However, these past studies have been performed with rather young animals. In addition, some studies have shown that brain properties change as we grow older; it is likely that this have an effect on the risk of DAI following a rotational head injury. Therefore, the aim of this study is to investigate the distribution of axonal injuries in the brain following sagittal plane rotation trauma and to determine if the injury threshold changes when the subjects grow older. In this study rats were exposed to sagittal plane rotational acceleration head trauma and the outcome studied using Amyloid Precursor Protein to detect axonal injuries. For relatively young animals, DAI were found in and along the border of the corpus callosum and in the brainstem when rotational acceleration exceeded 1.1 Mrad/s2. Slightly older animals required higher accelerations to exhibit similar injury levels and the injury patterns were different. We hypothesise that the lower injury scores for the older subjects could be due to differences in tolerance to tissue strains or, as indicated in the literature, that the differences were due to changes in the constitutive properties of the brain tissue. The latter suggests, in combination with the observed differences between older and younger individuals, that additional studies on brain tissue properties, and studies on rotational acceleration induced DAI, should be carried out using even younger and older animals than used in this study. In conclusion, a previous study showed that the onset of diffuse axonal injuries started to appear at 10 krad/s2 with a duration of 4 ms, when data were scaled for humans, whereas new data indicate that this onset is slightly higher for occupants that are approximately 15 years older.
TRAUMATIC BRAIN INJURY
AMYLOID PRECURSOR PROTEIN