Journal of neurotrauma
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Journal of neurotrauma · Apr 2010
Hyperoxic reperfusion after global cerebral ischemia promotes inflammation and long-term hippocampal neuronal death.
In this study we tested the hypothesis that long-term neuropathological outcome is worsened by hyperoxic compared to normoxic reperfusion in a rat global cerebral ischemia model. Adult male rats were anesthetized and subjected to bilateral carotid arterial occlusion plus bleeding hypotension for 10 min. The rats were randomized to one of four protocols: ischemia/normoxia (21% oxygen for 1 h), ischemia/hyperoxia (100% oxygen for 1 h), sham/normoxia, and sham/hyperoxia. ⋯ Behavioral deficits were also observed following hyperoxic, but not normoxic, reperfusion. We conclude that early post-ischemic hyperoxic reperfusion is followed by greater hippocampal neuronal death and cellular inflammatory reactions compared to normoxic reperfusion. The results of these long-term outcome studies, taken together with previously published results from short-term experiments performed with large animals, support the hypothesis that neurological outcome can be improved by avoiding hyperoxic resuscitation after global cerebral ischemia such as that which accompanies cardiac arrest.
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Journal of neurotrauma · Apr 2010
A new rat model for diffuse axonal injury using a combination of linear acceleration and angular acceleration.
Diffuse axonal injury (DAI) is a frequent form of traumatic brain injury, and is usually associated with long-lasting neurological impairments. A new experimental model was developed in the present study to induce DAI in rats by combining low linear and angular accelerations. In most clinical scenarios, DAI is caused by these two forms of acceleration in combination. ⋯ Although macroscopic damage was observed in all brain-injured animals, axonal damage and hemorrhagic tissue tears were only noted in the animals sustaining the combined accelerations. All rats survived the purely linear or angular acceleration, whereas the mortality rate reached 21.7% following the combined accelerations. These results show that this model is capable of reproducing the major histological and neurological changes that are associated with DAI, and that the combination of low linear and angular accelerations can produce non-linear and synergistic effects to induce moderate/severe DAI.
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Journal of neurotrauma · Apr 2010
Outcome prediction in mild traumatic brain injury: age and clinical variables are stronger predictors than CT abnormalities.
Mild traumatic brain injury (mTBI) is a common heterogeneous neurological disorder with a wide range of possible clinical outcomes. Accurate prediction of outcome is desirable for optimal treatment. This study aimed both to identify the demographic, clinical, and computed tomographic (CT) characteristics associated with unfavorable outcome at 6 months after mTBI, and to design a prediction model for application in daily practice. ⋯ Furthermore, we showed that the predictive value of a scheme based on a modified Injury Severity Score (ISS), alcohol intoxication, and age equalled the value of one that also included CT characteristics. In fact, it exceeded one that was based on CT characteristics alone. We conclude that, although valuable for the identification of the individual mTBI patient at risk for deterioration and eventual neurosurgical intervention, CT characteristics are imperfect predictors of outcome after mTBI.
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Journal of neurotrauma · Apr 2010
Loss of GABAergic interneurons in laminae I-III of the spinal cord dorsal horn contributes to reduced GABAergic tone and neuropathic pain after spinal cord injury.
Abstract In this study we explore if loss of GABAergic inhibitory interneurons in the superficial dorsal horn of the spinal cord contributes to reduced GABAergic tone and neuropathic pain following spinal cord injury (SCI). A moderate contusion injury to T11 resulted in the development of mechanical hyperalgesia and thermal hyperalgesia below the level of the lesion in gad1:GFP mice that were alleviated by IP administration of the GABA transporter antagonist tiagabine. Six weeks following SCI a decreased number of GFP(+) neurons were observed in the dorsal horn of SCI animals relative to sham mice. ⋯ Reversal of post-SCI neuropathic pain by tiagabine suggests that reduced GABAergic tone may contribute to hyperalgesia symptoms. This is supported by the subsequent observation that SCI reduced the number of GFP(+) inhibitory neurons, and the finding that some GABAergic GFP(+) neurons undergo cell death at a time point consistent with the development of neuropathic pain following SCI. Concordantly, reductions in both GAD65 and GAD67 and GAT1 immunoreactivity also support the observation of a loss of GABAergic inhibition and the associated spinal interneurons.