Articles: brain-injuries.
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Isotonic fluids have been thoroughly studied and for the vast majority of neurosurgical patients are both safe and effective. Conversely, HS may have some transient beneficial effects on cerebral physiology in animal models of brain injury. ⋯ Until the risk-benefit ratio of HS is better defined in humans, physicians should exercise caution and adhere to the Hippocratic oath. However, if this risk-benefit ratio is defined, HS may hold promise for the clinical conditions cited herein as well as other novel uses (cardiopulmonary bypass, spinal trauma [55,56]).
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Persistent vegetative state (PVS, apallic syndrome) has become a significant medical and social problem. The outcome of young people with PVS is a matter of great interest. Therefore, we analysed the outcome of 127 children and adolescents who were in PVS for at least 30 days following traumatic (n = 82) or hypoxic (n = 45) brain injury. ⋯ Thirteen patients (16%) with TBI became independent in everyday life versus only two (4%) with HBI. These results underline the important contribution of hypoxia in severe and permanent brain impairment. They also may help to establish the prognosis of children in PVS.
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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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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.