Articles: brain-injuries.
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J. Neurol. Neurosurg. Psychiatr. · Feb 2001
Preliminary experience of the estimation of cerebral perfusion pressure using transcranial Doppler ultrasonography.
The direct calculation of cerebral perfusion pressure (CPP) as the difference between mean arterial pressure and intracranial pressure (ICP) produces a number which does not always adequately describe conditions for brain perfusion. A non-invasive method of CPP measurement has previously been reported based on waveform analysis of blood flow velocity measured in the middle cerebral artery (MCA) by transcranial Doppler. This study describes the results of clinical tests of the prototype bilateral transcranial Doppler based apparatus for non-invasive CPP measurement (nCPP). ⋯ The device is of potential benefit for intermittent or continuous monitoring of brain perfusion pressure in situations where the direct measurement is not available or its reliability is in question.
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Chin. J. Traumatol. · Feb 2001
Randomized Controlled Trial Clinical TrialChanges of evoked potentials and evaluation of mild hypothermia for treatment of severe brain injury.
To observe the changes of evoked potentials after severe brain injury and the effect of mild hypothermia on acute severe brain injury. ⋯ These results demonstrate that mild hypothermia treatment (32-34 degrees C) in the Group B has a significant neuroelectrophysiological effect on severe brain injury. Nevertheless, the effect of mild hypothermia in the Group A is not apparent and needs further studying.
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Randomized Controlled Trial Clinical Trial
A randomized trial of very early decompressive craniectomy in children with traumatic brain injury and sustained intracranial hypertension.
The object of our study was to determine, in children with traumatic brain injury and sustained intracranial hypertension, whether very early decompressive craniectomy improves control of intracranial hypertension and longterm function and quality of life. ⋯ All children were managed from admission onward according to a standardized protocol for head injury management. Children with raised intracranial pressure (ICP) were randomized to standardized management alone or standardized management plus cerebral decompression. A decompressive bitemporal craniectomy was performed at a median of 19.2 h (range 7.3-29.3 h) from the time of injury. ICP was recorded hourly via an intraventricular catheter. Compared with the ICP before randomization, the mean ICP was 3.69 mmHg lower in the 48 h after randomization in the control group, and 8.98 mmHg lower in the 48 hours after craniectomy in the decompression group (P=0.057). Outcome was assessed 6 months after injury using a modification of the Glasgow Outcome Score (GOS) and the Health State Utility Index (Mark 1). Two (14%) of the 14 children in the control group were normal or had a mild disability after 6 months, compared with 7 (54%) of the 13 children in the decompression group. Our conclusion was that when children with traumatic brain injury and sustained intracranial hypertension are treated with a combination of very early decompressive craniectomy and conventional medical management, it is more likely that ICP will be reduced, fewer episodes of intracranial hypertension will occur, and functional outcome and quality of life may be better than in children treated with medical management alone (P=0.046; owing to multiple significance testing P <0.0221 is required for statistical significance). This pilot study suggests that very early decompressive craniectomy may be indicated in the treatment of traumatic brain injury.
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Journal of neurotrauma · Feb 2001
Injury severity and sensitivity to treatment after controlled cortical impact in rats.
We sought to determine sensitivity of the cortical impact injury model of traumatic brain injury (TBI) to severity of injury and to treatment. We examined the pattern of motor and cognitive deficits and recovery following TBI over a range of injury severities, and examined the efficacy of surface-induced moderate hypothermia at three disparate injury levels. In experiment I, Sprague-Dawley rats were injured at one of eight injury severity levels from 0 mm (sham) to 2.5 mm depth of penetration. ⋯ The 1.0-mm group exhibited small deficits that recovered completely by day 3; the 1.6-mm group recovered to the level of shams by day 5, and the 2.5-mm group did not show significant recovery during the testing period. Hypothermia effectively attenuated behavioral deficits for the 1.6-mm group, but had no effect on the other two groups. These three observations--that increasing injury severity is associated with increasing motor and cognitive deficits, that injury severity is related to recovery time, and that hypothermia treatment is selectively effective--have each been reported in the human TBI population; thus, moderate cortical impact injury in rats may be a model with clinical predictability for evaluating neuroprotective therapies.
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Experimental neurology · Feb 2001
Selective blockade of the mGluR1 receptor reduces traumatic neuronal injury in vitro and improvesoOutcome after brain trauma.
The effects of selective blockade of group I metabotropic glutamate receptor subtype 1 (mGluR1) on neuronal cell survival and post-traumatic recovery was examined using rat in vitro and in vivo trauma models. The selective mGluR1 antagonists (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester (CPCCOEt), and (S)-(+)-alpha-amino-4-carboxy-2-methylbezeneacetic acid (LY367385) provided significant neuroprotection in rat cortical neuronal cultures subjected to mechanical injury, in both pretreatment or posttreatment paradigms. Administration of the antagonists also attenuated glutamate-induced neuronal cell death in the cultures. ⋯ It appears that these compounds mediate their neuroprotective effect through an mGluR1 antagonist action, as demonstrated by inhibition of agonist induced phosphoinositide hydrolysis in our in vitro system. Moreover, AIDA, CPCCOEt, and LY367385, at concentrations shown to be neuroprotective, had no significant effects on the steady state NMDA evoked whole cell current. Taken together, these data suggest that modulation of mGluR1 activity may have substantial therapeutic potential in brain injury.