Journal of neurotrauma
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Journal of neurotrauma · Jun 2011
Comparative StudyChanges in cerebral compartmental compliances during mild hypocapnia in patients with traumatic brain injury.
The benefit of induced hyperventilation for intracranial pressure (ICP) control after severe traumatic brain injury (TBI) is controversial. In this study, we investigated the impact of early and sustained hyperventilation on compliances of the cerebral arteries and of the cerebrospinal (CSF) compartment during mild hyperventilation in severe TBI patients. We included 27 severe TBI patients (mean 39.5 ± 3.4 years, 6 women) in whom an increase in ventilation (20% increase in respiratory minute volume) was performed during 50 min as part of a standard clinical CO(2) reactivity test. ⋯ During sustained hyperventilation, ICP increased (13.9 ± 6.2 vs. 15.3 ± 6.4 mmHg; p < 0.001), which correlated with a reduction in Ci (r(2) = 0.297; p = 0.003), but no significant changes in Ca were found during that period. The early reduction in Ca persisted irrespective of the duration of hyperventilation, which may contribute to the lack of clinical benefit of hyperventilation after TBI. Further studies are needed to determine whether monitoring of arterial and CSF compartment compliances may detect and prevent an adverse ischemic event during hyperventilation.
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Journal of neurotrauma · Jun 2011
Interaction between brain chemistry and physiology after traumatic brain injury: impact of autoregulation and microdialysis catheter location.
Bedside monitoring of cerebral metabolism in traumatic brain injury (TBI) with microdialysis is gaining wider clinical acceptance. The objective of this study was to examine the relationship between the fundamental physiological neuromonitoring modalities intracranial pressure (ICP), cerebral perfusion pressure (CPP), brain tissue oxygen (P(bt)O(2)), and cerebrovascular pressure reactivity index (PRx), and cerebral chemistry assessed with microdialysis, with particular focus on the lactate/pyruvate (LP) ratio as a marker of energy metabolism. Prospectively collected observational neuromonitoring data from 97 patients with TBI, requiring neurointensive care management and invasive cerebral monitoring, were analyzed. ⋯ These differences remained significant following adjustment for the influences of other important physiological parameters (ICP, CPP, P(bt)O(2), P(bt)CO(2), PRx, and brain temperature; mixed linear model), suggesting that they may reflect inherent tissue properties related to the initial injury. Despite inherent biochemical differences between less-injured brain and "perilesional" cerebral tissue, both tissue types exhibited relationships between established physiological variables and biochemistry. Decreases in perfusion and oxygenation were associated with deteriorating neurochemistry and these effects were more pronounced in perilesional tissue and when cerebrovascular reactivity was impaired.
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Journal of neurotrauma · Jun 2011
Reactive astrocytes inhibit the survival and differentiation of oligodendrocyte precursor cells by secreted TNF-α.
Axonal demyelination is a consistent pathological characteristic of spinal cord injury (SCI). Although an increased number of oligodendrocyte progenitor cells (OPCs) is observed in the injured spinal cord, they fail to convert into mature oligodendrocytes. However, little is known about the underlying mechanism. ⋯ When TNF-α or TNF-R1 was neutralized with antibody, the effect of reactive astrocyte-conditioned medium or recombinant TNF-α protein on OPC differentiation was markedly attenuated. In addition, reactive astrocyte-conditioned medium was also shown to induce OPC apoptosis. All these findings provide the first evidence that reactive astrocytes release TNF-α to inhibit OPC survival and prevent them from differentiating into mature oligodendrocytes, suggesting a mechanism for the failure of remyelination after SCI.
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Journal of neurotrauma · Jun 2011
Impact of cervical spine management brain injury on functional survival outcomes in comatose, blunt trauma patients with extremity movement and negative cervical spine CT: application of the Monte Carlo simulation.
Cervical spine (CS) magnetic resonance imaging (MRI) and collar use may prevent quadriplegia, yet create brain injury. We developed a computer model to assess the effect of CS management strategies on outcomes in comatose, blunt trauma patients with extremity movement and a negative CS CT scan. Strategies include early collar removal (ECR), ECR & MRI, late collar removal (LCR), and LCR & MRI. ⋯ Quality-Adjusted Life Months for Unstable, High-Risk, and Stable Patients are greater with ECR. LCR and MRI brain injury results in losses of functional survivorship that exceed those from quadriplegia. Model results suggest that early collar removal without cervical spine MRI is a reasonable, and likely the preferable, cervical spine management strategy for comatose, blunt trauma patients with extremity movement and a negative cervical spine CT scan.
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Journal of neurotrauma · Jun 2011
Acute serum hormone levels: characterization and prognosis after severe traumatic brain injury.
Experimental traumatic brain injury (TBI) studies report the neuroprotective effects of female sex steroids on multiple mechanisms of injury, with the clinical assumption that women have hormonally mediated neuroprotection because of the endogenous presence of these hormones. Other literature indicates that testosterone may exacerbate injury. Further, stress hormone abnormalities that accompany critical illness may both amplify or blunt sex steroid levels. ⋯ Changes in the post-TBI adrenal response and peripheral aromatization influenced hormone TRAJ profiles and contributed to the abnormalities, including increased estradiol in men and increased testosterone in women. In addition to older age and greater injury severity, increased estradiol and testosterone levels over time were associated with increased mortality and worse global outcome for both men and women. These findings represent a paradigm shift when thinking about the role of sex steroids in neuroprotection clinically after TBI.