Introduction

Human head injury involves different forms of focal and diffuse injury to the brain, and the great majority of patients display more than one abnormality upon neuropathological investigation. Focal injury is characterized pathologically by the presence of contusions and lacerations, often accompanied by hematoma. In contrast, the term diffuse injury is most often used for the finding of diffuse axonal injury (DAI) observed in the direct vicinity and also remote from the injury site. Classification becomes even more complex because TBI is often classified according to different grades of injury severity, and the pathologic sequelae after TBI can be separated into primary and secondary (delayed) injury. The term primary injury encompasses the immediate damage to the central nervous system (CNS) that occurs at the moment of impact. This damage to the brain cells and tissues is nonreversible and, therefore, not curable. In contrast, secondary or delayed injury is initiated at the moment of the traumatic insult and progresses for days or months. This secondary injury to the CNS is a complex and poorly understood network of interacting cellular, structural, functional, and molecular changes, including breakdown of the blood-brain barrier, formation

Encyclopedia of the Human Brain Volume 3

Copyright 2002, Elsevier Science (USA).

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of edema, impairment of energy metabolism, changes in cerebral perfusion and intracranial pressure, ionic dyshomeostasis, activation and/or release of autodestructive neurochemicals and enzymes, inflammation, and pathologic-protective genomic changes. Alone or in combination these events may lead to delayed cell death, but because many are potentially reversible a chance exists for therapeutic intervention to attenuate cellular damage directed at improving functional recovery during rehabilitation and in the chronic phase of the injury.

Experimental models of TBI have been designed to mimic closely the clinical sequelae of human TBI and play a crucial role in the process of evaluating and understanding the physiological, behavioral, and his-topathologic changes associated with TBI. Because human TBI is very much a heterogeneous disease, no single animal model of TBI can mimic the whole spectrum of clinical TBI. Rather, the concurrent use of a number of distinct yet complementary models is necessary to reliably reproduce the whole range of injury severity and characteristic features observed upon clinical and post mortem examination of TBI patients. Experimental models have contributed to our insight into the posttraumatic sequelae and have prompted the development of several novel diagnostic and treatment strategies that are now either part of standard clinical practice or under intense preclinical and clinical investigation.

This article attempts to provide a broad overview of the most widely used and popular experimental models of mechanically induced TBI in whole animals. Because rodents are the species of choice in the vast majority of studies due to their obvious advantages (small size, modest cost, extensive normative data available), this article will mainly focus on results obtained in studies with rodents, except where such data are not available. Moreover, this description will not extensively review the existing literature concerning nonmechanical models to produce brain damage (thermal, chemical, or electrical), in vitro models, or inanimate finite element computational model characterizations.

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