Articles: brain-injuries.
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Ann Fr Anesth Reanim · Apr 2000
Review[Role of the regulation in the management of patients with severe head injuries].
The regulator of the emergency medical ambulance service is involved in the various steps of the initial management of severe head trauma patients: handling calls, basic life support, prehospital advance life support, transport and hospital admission. The management is rapid (helicopter transports) coherent and adapted (adherence to the guidelines for severe head injury), and considers of local difficulties (geographical, possibility of admission to trauma centres), with the aim of improving the outcome of severely head-injured patients.
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Traumatic brain injury (TBI) constitutes a major health and economic problem for developed countries, being one of the main causes of mortality and morbidity in children and young adults. Because of the immense importance and future consequences of TBI, the physician who sees a patient soon after brain injury must have a complete understanding of the pathophysiology and develop a practical knowledge of initial management of such patients. TBI may have intracranial and systemic effects that combine to give overall cerebral ischaemia. ⋯ The concept of 'cerebral protection' has been extended to encompass pretreatment of secondary injury. Preventing and treating cerebral ischaemia is the main goal of initial management of head-injured patients. Initial care focuses on achieving oxygenation, airway control and treatment of arterial hypotension.
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Ann Fr Anesth Reanim · Apr 2000
Review[Management of severely head-injured patients during the first 24 hours. Which specific therapeutics?].
Intracranial and systemic mechanisms of the secondary brain lesion are the targets of specific therapy for the head-injured patient. Recommendations for good clinical practice have recently defined the role of the main therapeutic measures. There is no indication for corticosteroids in head injury. ⋯ The place of hypothermia remains to be defined. Although controversial, optimized hyperventilation, induced systemic hypertension and vasoconstrictive therapy are optimally used under multimodal monitoring. New therapeutic perspectives, aimed at controlling biochemical disorders at a cellular level, are under investigation, but are still inconclusive at the present time.
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Ann. N. Y. Acad. Sci. · Apr 2000
Traumatic brain injury elevates the Alzheimer's amyloid peptide A beta 42 in human CSF. A possible role for nerve cell injury.
The increased risk for Alzheimer's Disease (AD) associated with traumatic brain injury (TBI) suggests that environmental insults may influence the development of this age-related dementia. Recently, we have shown that the levels of the beta-amyloid peptide (A beta 1-42) increase in the cerebrospinal fluid (CSF) of patients after severe brain injury and remain elevated for some time after the initial event. The relationships of elevated A beta with markers of blood-brain barrier (BBB) disruption, inflammation, and nerve cell or axonal injury were evaluated in CSF samples taken daily from TBI patients. ⋯ Similar or better correlations were observed between A beta 1-40 and the three aforementioned markers. These results imply that the degree of brain injury may play a decisive role in determining the levels of A beta 1-42 and A beta 1-40 in the CSF of TBI patients. Inflammation and alterations in BBB may play lesser, but nonetheless significant, roles in determining the A beta level in CSF after brain injury.
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J. Cereb. Blood Flow Metab. · Apr 2000
Expression of Fas and Fas ligand after experimental traumatic brain injury in the rat.
Apoptotic cell death plays an important role in the cascade of neuronal degeneration after traumatic brain injury (TBI), but the underlying mechanisms are not fully understood. However, increasing evidence suggests that expression of Fas and its ligand (FasL) could play a major role in mediating apoptotic cell death in acute and chronic neurologic disorders. To further investigate the temporal pattern of Fas and FasL expression after experimental TBI in the rat, male Sprague Dawley rats were subjected to unilateral cortical impact injury. ⋯ These results reveal induction of Fas and FasL expression in the cortex after TBI in the rat. Further, these data implicate an involvement of Fas and FasL in the pathophysiologic mechanism of apoptotic neurodegeneration after TBI. Last, these data suggest that strategies aimed to repress posttraumatic Fas- and FasL-induced apoptosis may open new perspectives for the treatment of TBI.