In order to apply what has already been learned to prevent or minimize injuries and to continue to attain a deeper understanding of the injury mechanisms involved in blunt impact to the head, the following specific aims are proposed: 1) To map brain motion during head impact for a variety of angular velocities and for different directions of impact to determine brain kinematics in terms of relative motion with respect to the skull. 2) To map brain motion during head impact while the head is protected by helmets, for a deeper understanding of the relative effects of linear and angular acceleration on the brain. 3) To compare the strain and strain rates from helmeted and non-helmeted impacts to determine the role played by these parameters in head injury. For the first specific aim, it is our hypothesis that because of the incompressibility of the brain and cerebral spinal fluid (CSF) and because of the relatively stiff skull, brain motion is limited to +/-5 mm relative to the skull, regardless of the severity of impact (level of angular acceleration) and direction of impact. However, the range of angular velocities used was limited to approximately 25 rad/s. Cadaveric testing is required to test this hypothesis over a range of angular velocities because previous suggestions for tolerance to angular acceleration included a maximum value for both angular acceleration and velocity (Lowenhielm, 1975). If the relative motion of the brain remains at +/-5 mm for a range of angular velocities, then, we can safely conclude that angular motion has a limited effect on brain injury and that other factors need to be considered to explain the whole picture of diffuse brain injury. As for the second specific aim, recent data from our cadaveric experiments have not shown a strong relationship between relative brain motion and angular acceleration of the head. One cadaveric head was subjected to angular accelerations, in excess of 10,000 rad/s, but the amount of relative brain motion with respect to the skull was limited to +/-5 mm, additionally, almost no brain motion was found in linear acceleration impacts. This raises the question of how the brain is protected by a helmet, since wearing a helmet would effect only small reductions in angular acceleration, which would not reduce relative brain motion inside the skull significantly. Therefore, it is hypothesized that one of the causes of brain injury is the rate at which the brain is being strained.
Specific Aim #2 will map brain motion during helmeted and non-helmeted impacts to establish the difference in response and to measure the strain and strain rate for a variety of input conditions.
Specific Aim #3 is based on the same strain rate hypothesis. It tests the hypothesis by comparing the strain, strain rate and the product of strain and strain rate to determine which of these parameters show a significant drop when a helmet is used. These results will limit the number of future animal experiments required to test this hypothesis further on living systems.
| Mao, Haojie; Jin, Xin; Zhang, Liying et al. (2010) Finite element analysis of controlled cortical impact-induced cell loss. J Neurotrauma 27:877-88 |
| Jin, Xin; Ma, Chunsheng; Zhang, Liying et al. (2007) Biomechanical response of the bovine pia-arachnoid complex to normal traction loading at varying strain rates. Stapp Car Crash J 51:115-26 |
| Hardy, Warren N; Mason, Matthew J; Foster, Craig D et al. (2007) A study of the response of the human cadaver head to impact. Stapp Car Crash J 51:17-80 |
| Jin, Xin; Lee, Jong B; Leung, Lai Yee et al. (2006) Biomechanical response of the bovine pia-arachnoid complex to tensile loading at varying strain-rates. Stapp Car Crash J 50:637-49 |
