Journal of neurotrauma
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Journal of neurotrauma · Oct 1995
ReviewSystemic hypothermia in treatment of severe brain injury: a review and update.
Laboratory studies of moderate hypothermia (30-33 degrees C) after injury show diminished neuronal loss after ischemia, diminished excessive neurotransmitter release after ischemia, prevention of blood-brain barrier disruption after ischemia and brain injury, and behavioral improvement after brain injury. Clinical literature suggests that brief periods of moderate hypothermia (> or = 30 degrees C) in humans are not associated with cardiovascular, hematologic, metabolic, or neurological toxicity. Clinical studies were, therefore, organized to investigate the potential application of moderate systemic hypothermia in patients after severe brain injury. ⋯ A randomized study of moderate hypothermia in 46 patients with Glasgow Coma Score (GCS) 4-7 gave an indication of improved neurologic outcome in the hypothermia group. A multicenter, randomized protocol to test the effect of moderate systemic hypothermia in patients with severe brain injury is in progress. Funded by the National Institutes of Health, The National Acute Brain Injury Study: Hypothermia tests the hypothesis that systemic hypothermia to 32-33 degrees C if rendered within 6 h of injury improves Glasgow Outcome Scores (GOS) at 6 months after injury in patients with severe brain injury (GCS 3-8).
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Journal of neurotrauma · Aug 1995
ReviewA new application for near-infrared spectroscopy: detection of delayed intracranial hematomas after head injury.
Clinical studies have documented the importance of secondary brain insults in determining neurologic outcome after head injury. Delayed intracranial hematomas are one of the most easily remediable causes of secondary injury if identified early, but can cause significant disability or death if not promptly recognized and treated. Early identification and treatment of these lesions that appear or enlarge after the initial CT scan may improve neurological outcome. ⋯ The hematomas appeared between 2 and 72 h after admission. In 24 of the 27 patients, a significant increase (>0.3) in the deltaOD occurred prior to an increase in intracranial pressure or a change in the neurological examination, or a change on CT scan. Early diagnosis using MRS may allow early treatment and reduce secondary injury caused by delayed hematomas.
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Journal of neurotrauma · Aug 1995
ReviewNew magnetic resonance imaging techniques for the evaluation of traumatic brain injury.
Although current computerized tomography (CT) and magnetic resonance imaging (MRI) techniques have shown great utility in diagnosing various aspects traumatic brain injury, damage resulting from mild diffuse brain injury often goes undetected with these procedures. Newly developed MRI techniques, including magnetization transfer imaging (MTI) and diffusion-weighted imaging (DWI), have been proposed to have enhanced sensitivities for identifying damage induced by both diffuse and focal brain injury. Results from recent initial studies with experimental models of brain injury suggest that MTI may be useful for evaluating diffuse white matter damage, while DWI may demonstrate regions of focal contusion more acutely and with greater accuracy than conventional MRI procedures.
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Journal of neurotrauma · Aug 1995
ReviewThe pathobiology of traumatically induced axonal injury in animals and humans: a review of current thoughts.
This manuscript provides a review of those factors involved in the pathogenesis of traumatically induced axonal injury in both animals and man. The review comments on the issue of primary versus secondary, or delayed, axotomy, pointing to the fact that in cases of experimental traumatic brain injury, secondary, or delayed, axotomy predominates. This review links the process of secondary axotomy to an impairment of axoplasmic transport which is initiated, depending upon the severity of the injury, by either focal cytoskeletal. misalignment or axolemmal permeability change with concomitant cytoskeletal. collapse. ⋯ The implications of diffuse axonal injury and its attendant deafferentation are considered by noting that with mild injury such deafferentation may lead to an adaptive neuroplastic recovery, whereas in more severe injury a disordered and/or maladaptive neuroplastic re-organization occurs, consistent with the enduring morbidity associated with severe injury. In closing, the review focuses on the implications of the findings made in experimental animals for our understanding of those events ongoing in traumatically brain-injured humans. It is noted that the findings made in experimental animals have been confirmed, in large part, in humans, suggesting the relevance of animal models for continued study of human traumatically induced axonal injury.