ABSTRACT
A specific temporal order of events at the cellular and molecular level occurs in response to primary impact forces when applied to the neuraxis. TBI initiates secondary reactive biochemical, molecular and genetic responses that may be autodestructive or neuroprotective. Therefore neurotrauma has effects on cell membranes, ion channels of axons, neurons and astrocytes, and also on whole brain systems affecting substrate delivery, blood flow, brain metabolism and neurological function. Accumulating evidence over the last two decades from in vitro and in vivo models and from human studies has led to improved understanding of the pathophysiological processes that promote the secondary sequelae of TBI. In this chapter we review the mechanisms, and complex biochemical, molecular and genomic responses generated to primary impact acceleration forces when applied to the neuraxis.
