Conclusion

The number of experimental and clinical studies attempting to gain insight into the posttraumatic sequelae following TBI has expanded enormously over the past decade and has generated an abundant amount of preclinical and clinical data suggestive of a number of divergent cascades involved in the delayed damage after TBI. However, no single animal model is entirely successful in reproducing the complete spectrum of pathological changes observed after clinical TBI. Together with the existing in vivo models of experimental TBI, in vitro models and finite element characterizations have contributed to the current theories of posttraumatic sequelae. Further effort will be necessary to elucidate the acute and chronic changes occurring after TBI in a number of different preclinical models to gain greater insight into the cellular cascades. These studies must be directed at clarifying and validating the present concepts, establishing new therapeutic strategies, and extending the pharmacological armamentarium toward more effective treatment for head-injured patients. New technical breakthroughs, including new methodologies in radiological examination and the use of genomic chip arrays or transgenic animals, seem to be powerful tools in this effort. However, the living animal remains necessary to prove new concepts and make clinical trials successful and safe.

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