Articles: brain-injuries.
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In traumatic axonal injury, Ca2+ influx across a focally damaged axolemma precipitates local mitochondrial failure, degradation of the subaxolemmal spectrin network and compaction of neurofilaments, which collectively contribute to axonal failure. In previous studies, cyclosporin A pretreatment preserved mitochondrial integrity and attenuated axonal failure following trauma. ⋯ CsA pretreatment dramatically reduced Ca2+-induced cytoskeletal damage following injury; CsA-treated rats, compared with vehicle-treated rats, displayed a 70% decrease in immunoreactive/damaged profiles. We suggest that CsA-mediated preservation of mitochondrial integrity enables the restoration of ionic and metabolic homeostasis thereby short-circuiting Ca2+-induced proteolysis in injured axons.
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Revista médica de Chile · Feb 1999
Review[Ventilatory support in patients with acute disease of the central nervous system].
Patients with severe head injury are prone to pulmonary complications that result in hypoxemia or hypercarbia, which could worsen their neurological condition. A rational ventilatory approach requires a good knowledge of respiratory and neurological pathophysiology. ⋯ The use of low or moderate positive and expiratory pressure levels apparently improves oxygenation without worsening intracranial pressure. Ventilatory management should be closely monitored and adjusted to hemodynamic, respiratory and neurological status to achieve a good outcome.
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Journal of neurotrauma · Feb 1999
One-year study of spatial memory performance, brain morphology, and cholinergic markers after moderate controlled cortical impact in rats.
Persistent cognitive deficits are one of the most important sequelae of head injury in humans. In an effort to model some of the structural and neuropharmacological changes that occur in chronic postinjury brains, we examined the longitudinal effects of moderate vertical controlled cortical impact (CCI) on place learning and memory using the Morris water maze (MWM) test, morphology, and vesicular acetylcholine (ACh) transporter (VAChT) and muscarinic receptor subtype 2 (M2) immunohistochemistry. Vertical CCI (left parietal cortex, 4 m/sec, 2.5 mm; n = 10) or craniotomy (sham) was produced in male Sprague-Dawley rats (n = 10). ⋯ This suggests a compensatory response of cholinergic neurons to increase the efficiency of ACh neurotransmission. Moderate CCI in rats produces subtle MWM performance deficits accompanied by persistent alteration in M2 and VAChT immunohistochemistry and progressive tissue atrophy. The inability of injured rats to benefit from repeated exposures to the MWM may represent a deficit in procedural memory that is independent of changes in hippocampal cholinergic systems.
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AACN clinical issues · Feb 1999
Review Case ReportsResuscitation of the multitrauma patient with head injury.
Head injury remains the leading cause of death from trauma. The definitive method for eliminating preventable death from traumatic brain injury remains elusive. New research underscores the danger of inadequate or inappropriate support of oxygenation, ventilation, and perfusion to cerebral tissues. ⋯ A search for optimal treatments based on prospective randomized trials will continue. Development of neuroprotective drugs and use of hypertonic saline may be on the horizon. In an effort to ensure optimal outcome, contemporary trauma nursing must embrace new concepts, shed outmoded therapy, and ensure compliance with the basic tenets of critical care for the multitrauma patient with head injury.
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To determine the incidence of clinically significant intracranial injury in the anticoagulated patient suffering minor head trauma without loss of consciousness (LOC) or acute neurologic abnormality. ⋯ The incidence of clinically significant intracranial injury is extremely low in the anticoagulated patient suffering minor blunt head trauma without LOC or acute neurologic abnormality. CT scanning may not be necessary in these patients. Larger prospective studies are needed to confirm these findings.