Time course of cellular pathology after controlled cortical impact injury.
Several different models of brain trauma are currently used and each simulates different aspects of the clinical condition and to varying degrees of accuracy. While numerous studies have characterized the cellular pathology after weight-drop or fluid percussion injury, detailed information on the histopathology that evolves after the controlled cortical impact model is incomplete. We have determined the spatiotemporal pathologies of neuronal, axonal, vascular, and macro- and microglial elements at 1, 4, 7, and 28 days after moderate controlled cortical impact injury. Neuronal injury identified by pyknotic perikarya and disrupted neurofilament-stained axonal profiles were evident by 1 day in ipsilateral cortex and hippocampus and at later times in the thalamus. glial fibrillary acidic protein-reactive astrocytes were more widespread, reaching a maximum immunointensity at 4 days across the ipsilateral hemisphere but declining to control levels thereafter. Microglia/macrophage-OX42 staining was initially restricted to the contusion site and then later to the thalamus, consistent with the pattern of neuronal injury. Increases in nestin immunoreactivity-a postulated marker of neural progenitor cells, and in NG2 proteoglycan-a marker of oligodendrocyte precursor cells, were detected by 1 day, reaching maximal immunointensity at 4-7 days after injury. Mean density and diameter of cortical microvessels was significantly reduced and increased respectively but only at the initial time points, suggesting that some degree of vascular remodeling takes place after injury. We discuss these results in light of recent evidence that suggests there may be some degree of endogenous repair after central nervous system injury.
Chen
S
S
Academic Neurosurgery, Centre for Brain Repair, University of Cambridge, Cambridge, UK.
Pickard
J D
JD
Harris
N G
NG
D000818:Animals; D001369:Axons / Q000473:pathology; D015415:Biomarkers / Q000032:analysis; D001930:Brain Injuries / Q000473:pathology*; D002540:Cerebral Cortex / Q000098:blood supply / Q000293:injuries* / Q000473:pathology*; D002560:Cerebrovascular Circulation; D003337:Corpus Callosum / Q000473:pathology; D004195:Disease Models, Animal; D018450:Disease Progression; D006624:Hippocampus / Q000473:pathology; D008297:Male; D017628:Microglia / Q000473:pathology; D009457:Neuroglia / Q000473:pathology; D009474:Neurons / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013788:Thalamus / Q000473:pathology
D015415:Biomarkers