2017
DOI: 10.21767/2471-8505.100064
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Effect of Early Correction of Hyponatremia on Neurological Outcome in Traumatic Brain Injury Patients

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Cited by 4 publications
(2 citation statements)
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“…Limited functional recovery after TBI is attributed to progressive neuronal damage following secondary injury-related inflammation [151,152]. Based on their previous work, one group of researchers [153] coupled dexamethasone (DX) with hyaluronic acid to obtain HA-DXM, which reduced neuroinflammation when loaded with degradable hydrogel poly (ethylene glycol-bis-(acryl-oxy-acetate)) (PEG-bis-AA). Furthermore, it improved neuronal survival and function 7 days after injury in a rat model of mild TBI, and an extension of the study showed that the animals treated with PEGbis-AA/HA-DXM had significantly improved motor function and reduced inflammatory response and lesion volume, making this a promising intervention strategy for TBI therapy.…”
Section: Brain Diseasesmentioning
confidence: 99%
“…Limited functional recovery after TBI is attributed to progressive neuronal damage following secondary injury-related inflammation [151,152]. Based on their previous work, one group of researchers [153] coupled dexamethasone (DX) with hyaluronic acid to obtain HA-DXM, which reduced neuroinflammation when loaded with degradable hydrogel poly (ethylene glycol-bis-(acryl-oxy-acetate)) (PEG-bis-AA). Furthermore, it improved neuronal survival and function 7 days after injury in a rat model of mild TBI, and an extension of the study showed that the animals treated with PEGbis-AA/HA-DXM had significantly improved motor function and reduced inflammatory response and lesion volume, making this a promising intervention strategy for TBI therapy.…”
Section: Brain Diseasesmentioning
confidence: 99%
“…The initial trauma results in a primary injury that includes cerebral contusion, axonal shearing, and damage to vasculature [ 4 , 5 , 6 , 7 ]. This initial damage provokes the release of excitatory neurotransmitters, calcium influx into neurons, and the initiation of a secondary injury phase characterized by progressive neuroinflammatory responses that lead to delayed cell death and tissue damage [ 8 , 9 , 10 ]. The primary injury damage is rapid and is often considered as preventable but not treatable.…”
Section: Introductionmentioning
confidence: 99%