Experimental investigation of cerebral contusion: Histopathological and immunohistochemical evaluation of dynamic cortical deformation

We used a new approach, termed dynamic cortical deformation (DCD), to study the neuronal, vascular, and glial responses that occur in focal cerebral c ontusions. DCD produces experimental contusion by rapidly deforming the cer ebral cortex with a transient, nonablative vacuum pulse of short duration ( 25 milliseconds) to mimic the circumstances of traumatic injury. A neuropat hological evaluation was performed on brain tissue from adult rats sacrific ed 3 days following induction of either moderate (4 psi, n = 6) or high (8 psi, n = 6) severity DCD. In all animals, DCD produced focal hemorrhagic le sions at the vacuum site without overt damage to other regions. Examination of histological sections showed localized gross tissue and neuronal loss i n the cortex at the injury site, with the volume of cell loss dependent upo n the mechanical loading (p < 0.001). Axonal pathology shown with neurofila ment immunostaining (SMI-31 and SMI-32) was observed in the subcortical whi te matter inferior to the injury site and in the ipsilateral internal capsu le. No axonal injury was observed in the contralateral hemisphere or in any remote regions. Glial fibrillary acidic protein (GFAP) immunostaining reve aled widespread reactive astrocytosis surrounding the necrotic region in th e ipsilateral cortex. This analysis confirms that rapid mechanical deformat ion of the cortex induces focal contusions in the absence of primary damage to remote areas 3 days following injury. Although it is suggested that mas sive release of neurotoxic substances from a contusion may cause damage thr oughout the brain, these data emphasize the importance of combined injury m echanisms, e.g. mechanical distortion and excitatory amino acid mediated da mage, that underlie the complex pathology patterns observed in traumatic br ain injury.