Journal of neurotrauma
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Journal of neurotrauma · Jul 2011
Novel model to investigate blast injury in the central nervous system.
Blast-induced neurotrauma (BINT) is a common injury modality associated with the current war efforts and increasing levels of terrorist activity. Exposure to the primary blast wave generated by explosive devices causes significant neurological deficits and is responsible for many of the war-related pathologies. Despite research efforts, the mechanism of injury is still poorly understood. ⋯ Our findings demonstrate that direct exposure to the blast wave compressed nervous tissue at a rate of 60 m/sec and led to significant functional deficits. Damage to the isolated spinal cord was marked by increased axonal permeability, suggesting rapid compression from the shockwave-generated high strain rates that resulted in membrane disruption. The model provides new insight into the mechanism of BINT and permits direct observation that may contribute to the development of appropriate treatment regimens.
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Journal of neurotrauma · Jul 2011
Review Meta Analysis Comparative StudyIntensive insulin therapy in brain injury: a meta-analysis.
Many studies have addressed the question of whether intensive insulin therapy (IIT) provides better outcomes for brain-injured patients than does conventional insulin therapy (CIT), with conflicting results. We performed a systematic review and meta-analysis of the literature to estimate the effect of IIT on patients with brain injury. We searched MEDLINE, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), and citations of key articles and selected "all randomized controlled trials" (RCTs) comparing the effect of IIT to CIT among adult patients with acute brain injury (traumatic brain injury, stroke, subarachnoid hemorrhage, and encephalitis). ⋯ IIT increased the rate of hypoglycemic episodes (RR=1.72, 95% CI=1.20, 2.46) however there was intractable heterogeneity present (I(2)=89%), which did not resolve upon sensitivity analysis. We found no evidence of publication bias by Egger's test (p=0.50). To conclude, IIT has no mortality or LTNO benefit to patients with brain injury, but is beneficial at decreasing infection rates.
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Journal of neurotrauma · Jul 2011
Clinical TrialNormobaric hyperoxia in traumatic brain injury: does brain metabolic state influence the response to hyperoxic challenge?
This study sought to investigate whether normobaric hyperoxia (NH) improves brain oxygenation and brain metabolism in the early phase of severe and moderate traumatic brain injury (TBI) and whether this effect occurs uniformly in all TBI patients. Thirty patients (9 women and 21 men) with a median initial Glasgow Coma Score (GCS) of 6 (range, 3-12) were monitored using a brain microdialysis (MD) catheter with a brain tissue oxygen sensor (PtiO(2)) placed in the least-injured hemisphere. The inspired oxygen fraction was increased to 100% for 2 h. ⋯ In patients with normal baseline brain lactate levels, we did not find any significant changes in the metabolic variables after NH. This suggests that the baseline metabolic state should be taken into account when applying NH to patients with TBI. This maneuver may only be effective in a specific group of patients.
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Journal of neurotrauma · Jul 2011
Predictive and associated factors of psychiatric disorders after traumatic brain injury: a prospective study.
Psychiatric disorders are common and often debilitating following traumatic brain injury (TBI). However, there is little consensus within the literature regarding the risk factors for post-injury psychiatric disorders. A 1-year prospective study was conducted to examine which pre-injury, injury-related, and concurrent factors were associated with experiencing a psychiatric disorder, diagnosed using the Structured Clinical Interview for DSM-IV-TR Axis I Disorders, at 1 year post-injury. ⋯ Limb injury also emerged as a useful early indicator of later psychiatric disorder. Post-injury psychiatric disorders were associated with concurrent unemployment, pain, poor quality of life, and use of unproductive coping skills. The clinical implications of these findings are discussed.
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Journal of neurotrauma · Jul 2011
Traumatic axonal injury in the optic nerve: evidence for axonal swelling, disconnection, dieback, and reorganization.
Traumatic axonal injury (TAI) is a major feature of traumatic brain injury (TBI) and is associated with much of its morbidity. To date, significant insight has been gained into the initiating pathogenesis of TAI. However, the nature of TAI within the injured brain precludes the consistent evaluation of its specific anterograde and retrograde sequelae. ⋯ Concomitant with this evolving axonal pathology, focal YFP fluorescence quenching occurred and mapped precisely to immunoreactive loci positive for Texas-Red-conjugated-IgG, indicating that blood-brain barrier disruption and its attendant edema contributed to this phenomenon. This was confirmed through the use of antibodies targeting endogenous YFP, which demonstrated the retention of intact immunoreactive axons despite YFP fluorescence quenching. Collectively, the results of this study within the injured optic nerve provide unprecedented insight into the evolving pathobiology associated with TAI.