Brain injury biomechanics in closed-head impact : Studies on injury epidemiology, tolerance criteria, biomechanics and traffic injury prevention

Permanent disability from traumatic brain injury is a devastating consequence of traffic crashes. Injury prevention is a fruitful approach to reduce the incidence and severity of disabling brain injury. However, the development of effective prevention techniques requires better knowledge on the mechanisms and biomechanics of brain injury in closed-head impact. The overall aim of this study is focused on brain injury mechanisms, biomechanics, and tolerances in closed-head impact. The research was multifaceted. It assessed the importance of traffic-related causes for disabling brain injury, determined brain injury biomechanics, criteria, and tolerances, analyzed a physical model of brain impact responses, developed a mathematical model of brain displacement and deformation during head impact, and linked brain motion and deformation to clinical patterns of traumatic brain injury. Karolinska hospital records were analyzed for traffic accident victims admitted to the Department of Neurosurgery. 32.5% of the patients experienced severe cognitive disability (GOS <4) at discharge. A Prevention Priority Index (PPI) was developed and combines injury incidence and disability outcome. PPI was 40.7% for car occupants (27.0% drivers and 13.7% passengers) and 44.7% for other road users (33.6% pedestrians, 10.2% bicyclists, and 0.9% mopedists). Anesthetized animal tests showed that brain injury is primarily caused by rate-dependent tissue deformation measured by the viscous response (VC). VC is the time-varying product of tissue deformation velocity (V) and compression (C). Compression is another mechanism. Locally, VC is the product of strain and strain-rate, e~de/dt, and C is strain, e. Statistical analysis gave proposed tolerance levels of VC = 0.7 m/s, e*de/dt = 45 s-1, C = 25%, and E = 0.25 for traumatic brain injury. Physical and mathematical models demonstrated that brain responses depend on the translational and rotational acceleration of the head. In severe head impacts, brain displacement < 25 mm at the vertex and compressive strain e < 0.30 at the base of the skull, brainstem, and occiput were observed during rotational head acceleration. Different response patterns were observed for translational head acceleration. The observed responses are consistent with published literature. Analysis showed that cortical contusion is primarily related to translational head acceleration that rapidly displaces the skull and deforms the brain along the axis of impact. Bridging vein rupture is related to both translational and rotational head acceleration that causes slip between the skull and brain, and stretches bridging veins in the cortical region. Diffuse axonal injury (DAI), coma, and concussion are related to high, strain-rate deformation of the brain. Analysis of impact biomechanics shows that the brain is naturally protected by a low-friction CSF layer, smooth intracranial surface at the vertex, and compliant bridging veins that allows non-injurious cortical motion of 10-15 mm. An important teleologic role for the lateral ventricles was identified since the fluid inclusions relieve strain in brain tissue during cortical motion. This allows the lower regions of the brain to remain fixed, while the cortex displaces without high internal strain that would otherwise occur if the brain were continuous. New information is provided on brain injury mechanisms, tolerance criteria, and impact biomechanics that is useful to the evaluation of occupant protection systems for brain injury prevention. The research improves the understanding of brain injury biomechanics in closed-head impact. Key Words: Closed-head impact, brain injury, biomechanics, injury mechanisms, tolerance criteria, epidemiology, and primary prevention. ISBN 91-628-2573-