Experimental fluid percussion brain injury: vascular disruption and neuronal and glial alterations.
Because of the potential relationship between vascular disturbances and secondary tissue damage, we identified areas of brain which exhibited hemorrhage and leakage of protein during the acute stage after experimental brain injury and subsequently studied the development of pathologic changes, including cavity formation, neuronal necrosis, and gliosis within these regions. The development of pathologic changes was evaluated at 1, 6, and 24 h and 1, 2, and 4 weeks after lateral, fluid percussion (FP) brain injury of moderate severity in the rat. Vascular disruption in the acute stages, as evidenced by hemorrhage and leakage of Evans blue albumin, was most prominent 6 h postinjury and was maximal in the parieto-occipital cortex. From 1 to 24 h after injury, regions of the injured hemisphere, including the cortex and hippocampus, exhibited abnormal neurons which stained with acid fuchsin and Alizarin red, histochemical markers for injured neurons and calcium, respectively. These same regions suffered significant neuronal cell loss from 1 to 4 weeks after injury. The distribution of reactive astrocytes was also evaluated by immunocytochemical localization of glial fibrillary acidic protein (GFAP). By 2 weeks postinjury, a prominent cavity was present in the frontoparietal and occipital cortices. Although astrogliosis was most pronounced in the cortex surrounding the cavity, prominent reactive astrocytes were widely distributed throughout the injured hemisphere. This study characterized the pathological changes which occur after experimental traumatic brain injury. In particular, we propose that neuronal cell injury in the hippocampus serves as a useful 'window' to assess beneficial efficacy of pharmacological intervention in the treatment of brain injury.
Cortez
S C
SC
Department of Neurology, University of California, San Francisco.
McIntosh
T K
TK
Noble
L J
LJ
D000818:Animals; D001930:Brain Injuries / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D002543:Cerebral Hemorrhage / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D008297:Male; D009336:Necrosis; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology*; D009474:Neurons / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D005904:Glial Fibrillary Acidic Protein