Journal of neurotrauma
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Journal of neurotrauma · May 2011
Early post-traumatic seizures in moderate to severe pediatric traumatic brain injury: rates, risk factors, and clinical features.
We performed a retrospective, observational study at a level I pediatric trauma center of children with moderate-to-severe traumatic brain injury (TBI) from January 2002 to September 2006 to identify clinical and radiographic risk factors for early post-traumatic seizures (EPTS). Two hundred and ninety-nine children ages 0-15 years were evaluated, with 24 excluded because they died before the initial head computed tomography (CT) was obtained (n=20), or because their medical records were missing (n=4). Records were reviewed for accident characteristics, pre-hospital hypoxia or hypotension, initial non-contrast head CT characteristics, seizure occurrence, antiepileptic drug (AED) administration, and outcome. ⋯ AED treatment was protective against EPTS (OR 0.2 [95% CI 0.07,0.5]). Twenty-three (68%) patients developed EPTS within the first 12 h post-injury. This early peak in EPTS activity and demonstrated protective effect of AED administration in this cohort suggests that to evaluate the maximal potential benefit among patients at increased risk for EPTS, future research should be randomized and prospective, and should intervene during pre-trauma center care with initiation of continuous EEG monitoring as soon as possible.
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Journal of neurotrauma · May 2011
High intracranial pressure effects on cerebral cortical microvascular flow in rats.
To manage patients with high intracranial pressure (ICP), clinicians need to know the critical cerebral perfusion pressure (CPP) required to maintain cerebral blood flow (CBF). Historically, the critical CPP obtained by decreasing mean arterial pressure (MAP) to lower CPP was 60 mm Hg, which fell to 30 mm Hg when CPP was reduced by increasing ICP. We examined whether this decrease in critical CPP was due to a pathological shift from capillary (CAP) to high-velocity microvessel flow or thoroughfare channel (TFC) shunt flow. ⋯ Decreasing CPP by MAP decreased TFC shunt flow with a smaller rise in NADH and no edema. Doppler flux decreased less with increasing ICP than decreasing MAP. The decrease seen in the critical CPP with increased ICP is likely due to a redistribution of microvascular flow from capillary to microvascular shunt flow or TFC shunt flow, resulting in a pathologically elevated CBF associated with tissue hypoxia and brain edema, characteristic of non-nutritive shunt flow.
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Journal of neurotrauma · May 2011
Rasch measurement analysis of the Mayo-Portland Adaptability Inventory (MPAI-4) in a community-based rehabilitation sample.
The precise measurement of patient outcomes depends upon clearly articulated constructs and refined clinical assessment instruments that work equally well for all subgroups within a population. This is a challenging task in those with acquired brain injury (ABI) because of the marked heterogeneity of the disorder and subsequent outcomes. Although essential, the iterative process of instrument refinement is often neglected. ⋯ Results indicated that the MPAI-4 is a valid, reliable measure of outcome following traumatic ABI, which measures a broad but unitary core construct of outcome after ABI. Further, the MPAI-4 is composed of items that are unbiased toward selected subgroups except where differences could be expected [e.g., more chronic traumatic brain injury (TBI) patients are better able to negotiate demands of transportation than more acute TBI patients]. We address the trade-offs between strict unidimensionality and clinical applicability in measuring outcome, and illustrate the advantages and disadvantages of applying single-parameter measurement models to broad constructs.
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Journal of neurotrauma · May 2011
Variants of the endothelial nitric oxide gene and cerebral blood flow after severe traumatic brain injury.
Experimental studies suggest that nitric oxide produced by endothelial nitric oxide synthase (NOS3) plays a role in maintaining cerebral blood flow (CBF) after traumatic brain injury (TBI). The purpose of this study was to determine if common variants of the NOS3 gene contribute to hypoperfusion after severe TBI. Fifty-one patients with severe TBI were studied. ⋯ The findings in this study support the importance of NO produced by NOS3 activity in maintaining CBF after TBI, since lower CBF values were found in patients having the -786C allele. The study suggests that a patient's individual genetic makeup may contribute to the brain's response to injury and determine the patient's chances of surviving the injury. The results here will need to be studied in a larger number of patients, but could explain some of the variability in outcome that occurs following severe TBI.
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Journal of neurotrauma · May 2011
Cyclosporin A preserves mitochondrial function after traumatic brain injury in the immature rat and piglet.
Cyclosporin A (CsA) has been shown to be neuroprotective in mature animal models of traumatic brain injury (TBI), but its effects on immature animal models of TBI are unknown. In mature animal models, CsA inhibits the opening of the mitochondrial permeability transition pore (MPTP), thereby maintaining mitochondrial homeostasis following injury by inhibiting calcium influx and preserving mitochondrial membrane potential. The aim of the present study was to evaluate CsA's ability to preserve mitochondrial bioenergetic function following TBI (as measured by mitochondrial respiration and cerebral microdialysis), in two immature models (focal and diffuse), and in two different species (rat and piglet). ⋯ In piglets, CsA also preserved lactate pyruvate ratios (LPR), as measured by cerebral microdialysis and CBF at sham levels 24 h after injury, in contrast to the significant alterations seen in injured piglets compared to shams (p<0.01). The administration of CsA to piglets following RNR promoted a 42% decrease in injured brain volume (p<0.01). We conclude that CsA exhibits significant neuroprotective activity in immature models of focal and diffuse TBI, and has exciting translational potential as a therapeutic agent for neuroprotection in children.