Articles: brain-injuries.
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Journal of neurotrauma · Sep 1997
NMDA-receptor antagonist protects neurons from secondary degeneration after partial optic nerve crush.
Damage resulting from a partial acute lesion of white matter in the central nervous system (CNS) gradually spreads also to neurons that escaped the primary injury, resulting in their degeneration. Such spreading has been referred to as secondary degeneration. In order to demonstrate that this degeneration is indeed secondary to that caused by the acute insult, as well as to investigate the mechanism underlying the spread of damage and ways in which to protect neurons from such damage, we have proposed the use of partial lesion of the rodent optic nerve as a model. ⋯ A positive VEP response to light was obtained in 90% of the MK-801 treated animals and in only 50% of injured controls. The questions regarding whether the secondary degeneration of initially spared neurons starts in their cell bodies or in their axons, and consequently the identity of the primary site of their protection by MK-801, are discussed in relation to the absence of N-methyl-D-aspartate receptors on nerve fibers. The present findings may have implications for both acute and chronic injuries of the CNS.
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A total of 208 multiple trauma patients with head injury (HI) were investigated who had been treated in the period from 1990 to 1995. The average age was 35.2 +/- 17.7 years; the injury severity according to ISS was 30.2 +/- 8.6 points; 20.5% died as a result of the HI; the mortality of all patients was 26.5%. The Glasgow Coma Scale (GCS) was determined at an average of 22 min after trauma (8.0 +/- 4.3 points) at the scene of accident. ⋯ The analysis of correlation/regression and receiver operating characteristics was able to predict 79% of patients' outcome accurately using GCS (r 0.54; P < 0.0001) alone, using CCT (r 0.65; P < 0.0001) 87% were correctly predicted with significant variables Cal-Fx, EDB, SAB and BS. CCT with GCS (r 0.74; P < 0.0001) were able to predict 88% accurately with significant variables Cal-Fx, EDB, BS and GCS. The combination of CCT with GCS, age and ISS (r 0.78; P < 0.0001) was able to predict only 87% correctly, although the r value was the highest; significant variable were Kal-Fx, EDB, BS, VL, GCS, age and ISS.
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There is an established link between congenital heart disease and acquired brain injury, which relates to the dependence of the nervous system on a consistent and responsive supply of oxygen and glucose. The advances in the field of infant cardiac surgery have presented new and different challenges to the arena of child neurology. This review provides an overview of the mechanisms of neurologic injury and cerebral hemodynamics and metabolism during cardiac surgery. This review discusses current and future strategies for the management of children with congenital heart disease.
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Clinical Trial
Clinical trial of induced hypothermia in comatose survivors of out-of-hospital cardiac arrest.
To examine the effects of moderate hypothermia (33 degrees C), induced by surface cooling in the ED and maintained for 12 hours in the ICU, on patients with anoxic brain injury after out-of-hospital cardiac arrest. ⋯ Compared with historical normothermic controls, outcome was significantly improved and there was no increase in complications when moderate hypothermia was induced in comatose survivors of out-of-hospital cardiac arrest and maintained for 12 hours. Larger, prospective, randomized, controlled studies of induced moderate hypothermia in comatose survivors of out-of-hospital cardiac arrest are warranted.
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Journal of neurotrauma · Aug 1997
Cholinergic modulation of cerebral cortical blood flow changes induced by trauma.
These experiments tested the role of cholinergic mechanisms in the changes of cerebral cortical blood flow (CBF) induced by brain trauma. CBF was measured with Iodo-14C-antipyrine autoradiography, in 128 cerebral cortex regions of both hemispheres, distributed in eight coronal slices. The effects of a 6.3-mm diameter craniotomy over the left motor-sensory cortex with no weight drop, and of trauma (drop weight of 20 g from 30 cm height on left motor-sensory cortex through a 6.3 mm circular craniotomy) on CBF were studied at 2 and 24 h after the interventions. ⋯ The cerebral cortex contralateral to the trauma showed significantly higher CBF 24 h after trauma when compared to intact controls or craniotomy that peaked at the area symmetrical to the center of trauma. This phenomenon was also enhanced by physostigmine and completely blocked by scopolamine. These results suggest a prominent role of cholinergic mechanisms in the vascular adjustments that accompany cerebral trauma.