Articles: brain-injuries.
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Journal of neurotrauma · Mar 1996
Diminished microtubule-associated protein 2 (MAP2) immunoreactivity following cortical impact brain injury.
This study employed Western blotting and qualitative immunohistochemistry to analyze the effects of cortical impact traumatic brain injury (TBI) on acute changes in MAP2 immunoreactivity in the rat cortex. We employed a lateral cortical impact injury device to induce severe TBI, which is associated with focal cortical contusion and neuronal death at the impact site. Three hours following TBI, Western blotting detected substantial MAP2 loss only in the cortex ipsilateral to the site of injury. ⋯ Alterations in MAP2 immunofluorescence were found both within and beyond areas of focal contusion and necrosis in the ipsilateral cortex. Thus, traumatic brain injury in rats can produce rapid and significant dendritic pathology within sites of contusion. However, immunohistochemical changes in MAP2 labeling outside of contused regions suggests that TBI-induced dendritic damage may not be exclusively associated with acute cell death.
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Journal of neurotrauma · Mar 1996
Laser-Doppler flowmetry measurements of subcortical blood flow changes after fluid percussion brain injury in rats.
Laser-Doppler flowmetry (LDF) was used to record subcortical cerebral blood flow in hippocampus and striatum immediately following parasaggital fluid percussion brain injuries of mild to moderate severity (2.58 +/- 0.09 atm, 10-11 msec duration) in spontaneously breathing anesthetized rats. At 5 min postinjury, mean blood flow decreased bilaterally by 20-30% in both brain structures, and remained significantly reduced during the remainder of the 60 min postinjury recording interval. Blood flow did not change in the sham-injured rats. ⋯ The microsphere measurements revealed that the preinjury baseline and postinjury right hippocampal blood flow changes were not significantly altered by the intrahippocampal presence of an LDF probe, verifying that the LDF probe was not by itself an unacceptably disruptive influence on local cerebrovascular reactivity. Moreover, when right hippocampal blood flow was simultaneously evaluated in injured rats by both techniques, the relative blood flow changes were significantly correlated. These results indicate that laser-Doppler flowmetry provides a potentially useful means to appreciate acute regional cerebrovascular changes relative to other measures of outcome after brain trauma.
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A case is described of a young male who suffered head injuries in a motor accident and subsequently displayed a severe anterograde amnesia in the presence of a relatively intact retrograde memory. He also demonstrated marked impairment of general intellectual ability, naming, perceptual skills and executive functioning. ⋯ It is further argued that while frontal impairment occurred in this case it lacks any of the hallmarks of frontal amnesia. The case is further evidence for the fractionation of amnesic syndromes.
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J. Cereb. Blood Flow Metab. · Mar 1996
Mild posttraumatic hypothermia reduces mortality after severe controlled cortical impact in rats.
The effect of posttraumatic hypothermia (brain temperature controlled at 32 degrees C for 4 h) on mortality after severe controlled cortical impact (CCI) was studied in rats. Four posttraumatic brain temperatures were compared: 37 degrees C (n = 10), 36 degrees C (n = 4), 32 degrees C (n = 10), and uncontrolled (UC; n = 6). Rats were anesthetized and subjected to severe CCI (4.0-m/s velocity, 3.0-mm depth) to the exposed left parietal cortex. ⋯ Posttraumatic hypothermia suppressed EEG during treatment and reduced mortality after severe CCI. The threshold for this protective effect appears to be a brain temperature < 36 degrees C. Thus, even mild hypothermia may be beneficial after severe brain trauma.
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Severe traumatic brain injuries are extremely heterogeneous. At least seven of the secondary derangements in the brain that have been identified as occurring after most traumatic brain injuries also occur after cardiac arrest. These secondary derangements include posttraumatic brain ischemia. ⋯ Stepwise measures to prevent lethal brain swelling after traumatic brain injury need experimental exploration, based on the multifactorial mechanisms of brain swelling. Novel treatments have so far influenced primarily healthy tissue; future explorations should benefit damaged tissue in the penumbra zones and in remote brain regions. The prehospital arena is unexplored territory for traumatic brain injury research.