Articles: brain-injuries.
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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.
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Poor outcomes following transcranial gunshot wounds (TC-GSW) and the perception of significant financial loss have led some institutions to adopt a fatalistic attitude towards these patients. This study was undertaken to define those factors predictive of mortality following TC-GSW as well as to determine the costs and benefits associated with providing care to these individuals. We reviewed the medical records of 57 TC-GSW patients seen at our Level I Trauma Center between January 1990 and December 1992. ⋯ Nonsurvivors who became organ donors were clinically and demographically indistinguishable from those in whom organs/tissues could not be retrieved. Despite the poor outcome following TC-GSW, vigorous resuscitation and stabilization is justified in all patients, in that nearly one half of nonsurvivors will become organ and/or tissue donors. Concerns regarding excessive monetary looses by treating facilities are unfounded.
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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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The management of brain swelling that frequently occurs following severe traumatic brain injury (TBI) presents a difficult challenge for physicians treating these patients. A traditional cornerstone for the treatment of post-traumatic brain swelling has been prophylactic hyperventilation to reach PaCO2 levels of 25 to 28 torr. While there are anecdotal reports of improvement in intracranial pressure (ICP) and neurologic functioning following institution of this therapy, the only prospective, randomized trial of its use has found worse outcomes in those treated with prophylactic hyperventilation therapy for 5 days. ⋯ In some cases, TBI also causes an increase in cerebral vascular responsivity to hypocapnia, increasing the drop in regional CBF that occurs with hyperventilation. Thus, there is a well defined physiologic basis for expecting hyperventilation to cause worsened clinical outcomes following TBI. While this therapy clearly is indicated for the management of acute neurologic deterioration or intracranial hypertension refractory to all other forms of medical therapy, hyperventilation is no longer recommended as a first-line therapy for intracranial hypertension or as prophylactic therapy following severe TBI.
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Movement of water between the brain and the intravascular space is dependent on osmotic gradients, which may be established by the acute administration of either hyper- or hypo-osmolar solutions. Mannitol, a hypertonic crystalloid solution, is commonly used to decrease brain water content and reduce intracranial pressure (ICP). Hypertonic saline solutions also decrease brain water and ICP while temporarily increasing systolic blood pressure and cardiac output. ⋯ Colloid solutions exert little influence on either variable. Fluid restriction minimally affects cerebral edema and, if pursued to excess, may result in episodes of hypotension, which may increase ICP and are associated with worse neurologic outcome. Although there is no single best fluid for patients with traumatic brain injury, isotonic crystalloids are widely used and can be justified on a scientific basis.