[Biopathology of craniocerebral injuries: experimental models].
INTRODUCTION: In traumatic brain injury the secondary damage is responsible for the majority of the clinical and pathological sequels. This circumstance together with the difficulties of acquiring well preserved brain material for specialized neuropathological study impair the understanding of processes implied in their pathophysiology. DEVELOPMENT AND CONCLUSIONS: The development of experimental models has played an outstanding role for the better knowledge of these processes. For the development of standardized experimental models the biophysical and anatomical characteristics of brain and skull of the various utilized species have to be considered, but the physiological, neurochemical and molecular peculiarities must also be taken into account. Various in vivo models have been developed, inducing direct impact to the skull or to the brain, or mimicking lesions subsequent to craniocerebral trauma, such as subarachnoid hemorrhage, hematoma or necrosis. To analyze the molecular mechanisms of cellular response in vitro models have been developed. A great amount of cells in the contusional area die immediately following traumatic brain injury, but a still higher number of cells will undergo in the following hours. This second wave of neuronal death is induced by phenomena such as secondary axotomy and brain edema. In the pathogenesis of both the damage of cytoplasmic membrane is involved.