Articles: brain-injuries.
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Journal of neurotrauma · Oct 1994
Neurofilament 68 and neurofilament 200 protein levels decrease after traumatic brain injury.
We have examined the effect of lateral cortical impact injury on the levels of axonal cytoskeletal proteins in adult rats. Traumatic brain injury (TBI) causes a significant decrease in the protein levels of two prominent neurofilament (NF) proteins, NF68 and NF200. We employed quantitative immunoreactivity measurements on Western blots to examine NF68 and NF200 levels in homogenates of hippocampal and cortical tissue taken at several intervals postinjury. ⋯ This NF68 antigenicity pattern suggests the production of NF68 breakdown products caused by the pathologic activation of neuronal proteases, such as calpain. Putative NF68 breakdown products increase significantly until 1 day postinjury, suggesting that NF degradation may be ongoing until that time and indicating that a potential therapeutic window may exist within the first 24 h postinjury. In summary, these data identify specific biochemical alterations of the neuronal cytoskeleton following TBI and lay a foundation for further investigation of postinjury cytoskeletal changes in neuronal processes.
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Neurosurg. Clin. N. Am. · Oct 1994
ReviewIntegrated multimodality monitoring in the neurosurgical intensive care unit.
The selection of variables for continuous monitoring in the neurosurgical intensive care unit is based upon the requirement for constant perfusion and oxygenation of the brain and knowledge of the frequency and prognostic significance of abnormal values. Both arterial and intracranial pressure must be considered in the form of cerebral perfusion pressure. Body temperature and arterial oxygen saturation are essential to monitoring. Measurement of jugular venous oxygen saturation and cerebral blood flow velocity provide information of value in determining the source of raised intracranial pressure, the most appropriate means of treating it, and the safety of therapy.
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The sources of fever and infection in neurosurgical patients in the intensive care unit are varied and complex. Benign postoperative fever due to atelectasis of the lungs or from central nervous system sources are difficult to define. Distinguishing between these "benign" sources and true nosocomial bacterial infections can be a difficult clinical process. Empiric antibiotic regimens are outlined, and some guidelines are proposed for the management of infected catheters.
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Journal of neurotrauma · Oct 1994
Lateral cortical impact injury in rats: pathologic effects of varying cortical compression and impact velocity.
Direct lateral cortical impact through the intact leptomeninges using a pneumatically driven piston produces increasingly severe pathophysiologic derangements with increasing cortical deformation. We studied the histopathologic correlates of cortical impact injury produced by 2 mm, 2.5 mm, and 3 mm deformation in the rat at 5 m/sec. Additionally, the effect of impact velocity at a 2.5 mm deformation was assessed at 1 m/sec, 3 m/sec, and 5 m/sec. ⋯ Impact velocities of 1, 3, and 5 m/sec produced neuronal loss of 18.25%, 33.75%, and 48.3%, respectively. Hippocampal CA1 neuronal loss was also seen and paralleled cortical deformation and impact velocity. Cortical deformation and impact velocity are critical parameters in producing cortical contusion and must be considered when comparing results using this model.