Introduction

Yearly, about 2 million patients will suffer traumatic brain injury (TBI). Much research has been conducted in the field of TBI over the past decades, yet no specific therapy is available. Different experimental models of TBI have been devised over the past years. Since TBI is a heterogeneous condition no single model can depict the actual pathophysiological changes associated with its entire spectrum. Therefore, each model can be seen as representing a subset of injury. Thus, some models are more akin to represent diffuse axonal injury whereas others are more representative of closed head injury with contusions and still others involve traumatic skull fractures with secondary brain impact. Of note, although some in vitro models for TBI exist (for review see reference 8) this chapter will limit itself to discussion of in vivo models. Using each of these models the interested reader may evaluate the physiological, neurochemical, behavioral–cognitive, histological, and pathological sequelae of TBI. Using these methods one can also assess new diagnostic tools and new therapeutic options for neurotrauma. Furthermore, new diagnostic tools such as magnetic resonance imaging (MRI) or MR spectroscopy can be used to further outline TBI pathophysiology.

Closed head injury

TBI is induced in this model by dropping a weight on top of the exposed skull leading to closed head injury (CHI) Adjusting the height and weight of the free-falling weight can modify the severity of the injury.