Journal of neurotrauma
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Journal of neurotrauma · Mar 2017
Activation of KCNQ channels suppresses spontaneous activity in DRG neurons and reduces chronic pain after spinal cord injury.
A majority of people who have sustained spinal cord injury (SCI) experience chronic pain after injury, and this pain is highly resistant to available treatments. Contusive SCI in rats at T10 results in hyperexcitability of primary sensory neurons, which contributes to chronic pain. KCNQ channels are widely expressed in nociceptive dorsal root ganglion (DRG) neurons, are important for controlling their excitability, and their activation has proven effective in reducing pain in peripheral nerve injury and inflammation models. ⋯ These results encourage the further exploration of U. S. Food and Drug Administration-approved KCNQ activators for treating SCI pain, as well as efforts to develop a new generation of KCNQ activators that lack central side effects.
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Journal of neurotrauma · Mar 2017
Randomized Controlled Trial Multicenter StudyAssociation between blood glucose levels the next day following targeted temperature initiation and outcome in traumatic brain injury: a post-hoc analysis of the B-HYPO study.
We investigated associations between blood glucose levels and clinical outcomes in participants of the multi-center randomized controlled Brain-Hypothermia (B-HYPO) study. Patients with severe traumatic brain injury (TBI, Glasgow Coma Scale 4-8) were assigned to therapeutic hypothermia (TH, 32-34°C, n = 98) or fever control (35.5-37.0°C, n = 50) groups. TH patients were cooled as soon as possible for ≥72 h and rewarmed at a rate of <1°C/d. ⋯ In the TH group, the initial stress hyperglycemia was sustained the next day after TH induction. Day 1 BG predicted outcome in TBI patients with TH and fever control. Our findings indicate the significance of BG control particularly during TH treatment.
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Journal of neurotrauma · Mar 2017
ReviewCerebral perfusion pressure targets individualised to pressure-reactivity index in moderate to severe traumatic brain injury: A systematic review.
Traumatic brain injury (TBI) frequently triggers a disruption of cerebral autoregulation. The cerebral perfusion pressure (CPP) at which autoregulation is optimal ("CPPopt") varies between individuals, and can be calculated based on fluctuations between arterial blood pressure and intracranial pressure. This review assesses the effect of individualizing CPP targets to pressure reactivity index (a measure of autoregulation) in patients with TBI. ⋯ Although the data suggest an association between variation from CPPopt and poor clinical outcome at 6 months, the quality of evidence prevents firm conclusions, particularly regarding causality, from being drawn. Available data suggest that targeting CPPopt might represent a technique to improve outcomes following TBI, but currently there is insufficient high-quality data to support a recommendation for use in clinical practice. Further prospective, randomized controlled studies should be undertaken to clarify its role in the acute management of TBI.
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Journal of neurotrauma · Mar 2017
ReviewPumping the brakes: Neurotrophic factors for the prevention of dementia following traumatic brain injury.
Traumatic brain injury (TBI) is the leading cause of disability and death worldwide, affecting as many as 54,000,000-60,000,000 people annually. TBI is associated with significant impairments in brain function, impacting cognitive, emotional, behavioral, and physical functioning. Although much previous research has focused on the impairment immediately following injury, TBI may have much longer-lasting consequences, including neuropsychiatric disorders and cognitive impairment. ⋯ Unfortunately, however, no such treatment is currently available, making this a major area of unmet medical need. Increasing the level of neurotrophic factor expression in key brain areas may be one potential therapeutic strategy. Of the neurotrophic factors, granulocyte-colony stimulating factor (G-CSF) may be particularly effective for preventing the emergence of long-term complications of TBI, including dementia, because of its ability to reduce apoptosis, stimulate neurogenesis, and increase neuroplasticity.