Rl. Sutton et al., UNILATERAL CORTICAL CONTUSION INJURY IN THE RAT - VASCULAR DISRUPTIONAND TEMPORAL DEVELOPMENT OF CORTICAL NECROSIS, Journal of neurotrauma, 10(2), 1993, pp. 135-149
Cerebrovascular disruption and cortical pathology resulting from eithe
r moderate (M-TBI) or severe (S-TBI) traumatic brain injury produced b
y a pneumatically-driven cortical contusion device were assessed in ad
ult male rats sacrificed at 6 and 24 h or 8 and 30 days after injury t
o the right sensorimotor cortex. Epidural, subdural, subarachnoid, pet
echial (cortex and corpus callosum), and/or intraventricular hemorrhag
e was present in all animals, more extensively and severely following
S-TBI. At 6 or 24 h after TBI, acidophilic (acid fuchsin-positive) neu
rons were numerous and widespread (S-TBI > M-TBI) in the ipsilateral c
ontused cortex. By 8 days few acidophilic neurons were present in peri
-impact regions of the ipsilateral neocortex, and none were detected i
n cortex 30 days postinjury. Both M-TBI and S-TBI groups had enlarged
ipsilateral cortical volumes (edema) at 6 and 24 h postcontusion. Eigh
t and 30 days after injury the mean volume of cortical necrosis was si
gnificantly larger in S-TBI than in M-TBI rats, and cortical necrosis
in both TBI conditions increased between 8 to 30 days postinjury. Thes
e results indicate that this pneumatically-driven contusion device pro
duces reliable and consistent primary and secondary cortical histopath
ology, the extent of which is related to the severity of initial injur
y.