ENDURING COGNITIVE, NEUROBEHAVIORAL AND HISTOPATHOLOGICAL CHANGES PERSIST FOR UP TO ONE-YEAR FOLLOWING SEVERE EXPERIMENTAL BRAIN INJURY IN RATS

Clinical studies have demonstrated that patients sustain prolonged beh avioral deficits following traumatic brain injury, in some cases culmi nating in the cognitive and histopathological hallmarks of Alzheimer's disease. However, few studies have examined the long-term consequence s of experimental traumatic brain injury. In the present study, anesth etized male Sprague-Dawley rats (,n=185) were subjected to severe late ral fluid-percussion brain injury (n=115) or sham injury (n=70) and ev aluated up to one year post-injury for cognitive and neurological defi cits and histopathological changes. Compared with sham-injured control s, brain-injured animals showed a spatial learning impairment that per sisted up to one year post-injury. In addition, deficits in specific n eurologic motor function tasks also persisted up to one year post-inju ry. Immunohistochemistry using multiple antibodies to the amyloid prec ursor protein and/or amyloid precursor protein-like proteins revealed novel axonal degeneration in the striatum, corpus callosum and injured cortex up to one year post-injury and in the thalamus up to six month s post-injury. Histologic evaluation of injured brains demonstrated a progressive expansion of the cortical cavity, enlargement of the later al ventricles, deformation of the hippocampus, and thalamic calcificat ions. Taken together, these findings indicate that experimental trauma tic brain injury can cause long-term cognitive and neurologic motor dy sfunction accompanied by continuing neurodegeneration. (C) 1998 IBRO. Published by Elsevier Science Ltd.