Traumatic brain injuries (TBI) account for over 50,000 deaths per year. Annually 70,000-90,000 TBI survivors sustain significant neurological deficits in the United States. Traumatic axonal injury (TAI) is a consequence of TBI. Most of these injuries occur due to motor vehicle accidents. There is a need to understand the underlying mechanisms of this type of injury. Injury of axons has been explained by two mechanisms, namely primary axotomy (immediate tearing of the axons) and secondary axotomy (delayed injury). Due to the inability to directly measure strain or displacement rate in brain, axonal injury tolerance due to trauma has still not been directly quantified at high displacement rates. There is a need to develop a better understanding of axonal injury tolerance in TBI so that finite element models can more accurately be used to design countermeasures that reduce the consequences of both linear and rotational brain motion during impact.

In this study an in-vivo TAI model was developed using spinal nerve roots of rats. In the first part of this study, the relationship between strain, displacement rate and morphological injury to spinal nerve roots were identified using histological techniques. The extent of injury was assessed based on damage to blood vessels and axons. It was found that as the displacement rate increased (from 20mm/sec to 200mm/sec) the extent of injury increased.

In the second part of the study, relationships between strain, displacement rate and functional injury to spinal nerve roots were determined using neurophysiological techniques. Decreases in area under the evoked compound action potential (AUC), in conduction velocity (CV) and in peak amplitude of compound action potential were observed after stretch, with variations in extent of recovery over the next 6 hours.