Articles: brain-injuries.
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Complement Ther Nurs Midwifery · May 2001
Comparative StudyBrain injury: the uncertainties of using complementary therapies.
The use of complementary therapies is fast growing in the UK, but their place within health care is still unclear. This study explored the views of families using a specific complementary therapy in the care of their brain-injured children, and of professionals involved in the care of the children. The findings revealed an interesting comparison of views about the use of complementary therapies and attitudes towards their use.
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Acta neuropathologica · May 2001
Immunomorphological sequelae of severe brain injury induced by fluid-percussion in juvenile pigs--effects of mild hypothermia.
Severe traumatic brain injury (TBI) often leads to a bad outcome with considerable neurological deficits. Secondary brain injuries due to a rise of intracranial pressure (ICP) and global hypoxia-ischemia are critical and may be reduced in extent by mild hypothermia. A porcine animal model was used to study the effect of severe TBI, induced by fluid percussion (FP; 3.5+/-0.3 atm) in combination with a secondary insult, i.e., temporary blood loss with hypovolemic hypotension. ⋯ Thus, severe TBI caused by FP, combined with temporary blood loss, consistently produced traumatic axonal injury and focal brain damage. Mild hypothermia was able to prevent a secondary increase in ICP and its sequelae of diffuse hypoxic-ischemic brain injury. However, hypothermia did not afford protection from traumatic axonal injury.
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The role of metabotropic glutamate receptor activation after traumatic brain injury (TBI) is not well understood. In vitro studies suggest that activation of Groups II and III metabotropic glutamate receptors may provide some degree of neuroprotection and may be potential targets for the development of therapeutic strategies. Thus, we examined the effects of Group II and Group III selective agonists on neuronal degeneration after in vivo TBI. ⋯ Administration of selective Group II metabotropic glutamate receptor agonists protects neurons against in vivo TBI. These receptors may thus be a promising target for future neuroprotective drugs.
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Journal of neurotrauma · May 2001
Neuron-specific enolase serum levels after controlled cortical impact injury in the rat.
The aim of this study was to investigate the time course and the correlation of neuron-specific enolase (NSE) serum levels to the severity of traumatic brain injury in rats. Sixty-five male Wistar rats were subjected to severe cortical impact injury (100 PSI, 2 mm deformation). Blood samples were drawn directly after trauma and after 1, 6, 12, 24, and 48 h in the trauma group. ⋯ The highest NSE serum values were detected 6 h after trauma (31.5 microg/L mean, n = 10). In addition, we found a close relationship between NSE serum levels and the severity of traumatic brain injury in the cortical impact model. NSE serum levels reflect in a time-dependent manner the severity of brain trauma induced by cortical impact model in rat.
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Journal of neurosurgery · May 2001
Effects of tacrolimus on hemispheric water content and cerebrospinal fluid levels of glutamate, hypoxanthine, interleukin-6, and tumor necrosis factor-alpha following controlled cortical impact injury in rats.
Disturbance of calcium homeostasis contributes to evolving tissue damage and energetic impairment following traumatic brain injury (TBI). Calcium-mediated activation of calcineurin results in production of tissue-damaging nitric oxide and free oxygen radicals. Inhibition of calcineurin induced by the immunosuppressant tacrolimus (FK506) has been shown to reduce structural and functional damage after ischemia. The aims of the present study were to investigate time- and dose-dependent short-term antiedematous effects of tacrolimus following TBI. ⋯ Under the present study design, the potency of tacrolimus in reducing edema formation following CCII seems limited. However, its immunosuppressive effects could be of value in influencing the posttraumatic inflammatory response known to aggravate tissue damage.