Di. Shreiber et al., Experimental investigation of cerebral contusion: Histopathological and immunohistochemical evaluation of dynamic cortical deformation, J NE EXP NE, 58(2), 1999, pp. 153-164
Citations number
33
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
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.