Focal brain injury: histological evidence of delayed inflammatory response in a new rodent model of focal cortical injury.

Cortical contusions are one of the most common characteristics in head injury and are regarded by many as the hallmark of significant injury. No experimental study has clarified the roles of mechanical forces, haemorrhage and ischaemia in the process of progressive acute brain damage and later neurobehavioural dysfunction. We have devised a new, simple reproducible rodent model of focal cortical injury which employs a 'pure' mechanical/physical force applied through the intact dura. Using this model we have investigated the time course and pattern of changes in neurons, glia and microvasculature. With the exception of haemorrhage, this model closely reproduces the light- and electron microscopy features of human contusion. In the absence of perivascular haemorrhage we have demonstrated delayed perivascular protein leakage and polymorphonuclear-leukocyte infiltration of the damaged cortex. We postulate that a component of the delayed blood brain barrier breakdown demonstrated in human focal head injury (which may contribute to swelling and brain damage) is due to an acute inflammatory response, the magnitude of which is dependent on the amount of tissue injury.