Journal of neurotrauma
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Journal of neurotrauma · Jun 2016
The UCLA Study of Children with Moderate to Severe Traumatic Brain Injury: Event-Related Potential Measure of Interhemispheric Transfer Time.
Traumatic brain injury (TBI) frequently results in diffuse axonal injury and other white matter damage. The corpus callosum (CC) is particularly vulnerable to injury following TBI. Damage to this white matter tract has been associated with impaired neurocognitive functioning in children with TBI. ⋯ This subgroup of TBI children with slow IHTT also had significantly poorer neurocognitive functioning than healthy controls-even after correction for premorbid intellectual functioning. We discuss alternative models for the relationship between IHTT and neurocognitive functioning following TBI. Slow IHTT may be a biomarker that identifies children at risk for poor cognitive functioning following moderate/severe TBI.
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Journal of neurotrauma · Jun 2016
CONTRECOUP TRAUMATIC INTRACEREBRAL HEMORRHAGE: A GEOMETRIC STUDY OF THE IMPACT SITE AND ASSOCIATION WITH HEMORRHAGIC PROGRESSION.
Traumatic intracerebral hemorrhage (TICH) represents 13-48% of the lesions after a traumatic brain injury (TBI). The frequency of TICH-hemorrhagic progression (TICH-HP) is estimated to be approximately 38-63%. The relationship between the impact site and TICH location has been described in many autopsy-based series. ⋯ Factors independently associated with TICH-HP obtained through logistic regression included an initial volume of <1 cc, cisternal compression, falls, acute subdural hematoma, multiple TICHs, and contrecoup TICHs. We demonstrated a significant association between the TICH location and impact site. The contrecoup represents a risk factor independently associated with hemorrhagic progression.
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Journal of neurotrauma · Jun 2016
Neuropsychological, metabolic, and GABAA receptor studies in subjects with repetitive traumatic brain injury.
Repetitive traumatic brain injury (rTBI) occurs as a result of mild and accumulative brain damage. A prototype of rTBI is chronic traumatic encephalopathy (CTE), which is a degenerative disease that occurs in patients with histories of multiple concussions or head injuries. Boxers have been the most commonly studied patient group because they may experience thousands of subconcussive hits over the course of a career. ⋯ Glucose metabolism was impaired in frontal areas associated with cognitive dysfunction, similar to findings in Alzheimer's disease. Low binding potential (BP) of (18)F-flumazenil (FMZ) was found in the angular gyrus and temporal cortical regions, revealing neuronal deficits. These results suggested that cognitive impairment and motor dysfunction reflect chronic damage to neurons in professional boxers with rTBI.
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Journal of neurotrauma · Jun 2016
Neuroprotective effects of the glutamate transporter activator, MS-153, following traumatic brain injury in the adult rat.
Traumatic brain injury (TBI) in humans and in animals leads to an acute and sustained increase in tissue glutamate concentrations within the brain, triggering glutamate-mediated excitotoxicity. Excitatory amino acid transporters (EAATs) are responsible for maintaining extracellular central nervous system glutamate concentrations below neurotoxic levels. Our results demonstrate that as early as 5 min and up to 2 h following brain trauma in brain-injured rats, the activity (Vmax) of EAAT2 in the cortex and the hippocampus was significantly decreased, compared with sham-injured animals. ⋯ Administration of (R)-(-)-5-methyl-1-nicotinoyl-2-pyrazoline (MS-153), a GLT-1 activator, beginning immediately after injury and continuing for 24 h, significantly decreased neurodegeneration, loss of microtubule-associated protein 2 and NeuN (+) immunoreactivities, and attenuated calpain activation in both the cortex and the hippocampus at 24 h after the injury; the reduction in neurodegeneration remained evident up to 14 days post-injury. In synaptosomal uptake assays, MS-153 up-regulated GLT-1 activity in the naïve rat brain but did not reverse the reduced activity of GLT-1 in traumatically-injured brains. This study demonstrates that administration of MS-153 in the acute post-traumatic period provides acute and long-term neuroprotection for TBI and suggests that the neuroprotective effects of MS-153 are related to mechanisms other than GLT-1 activation, such as the inhibition of voltage-gated calcium channels.
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Journal of neurotrauma · Jun 2016
Environmental Enrichment Attenuates Traumatic Brain Injury-Induced Neuronal Hyperexcitability in Supragranular Layers of Sensory Cortex.
We have previously demonstrated that traumatic brain injury (TBI) induces significant long-term neuronal hyperexcitability in supragranular layers of sensory cortex, coupled with persistent sensory deficits. Hence, we aimed to investigate whether brain plasticity induced by environmental enrichment (EE) could attenuate abnormal neuronal and sensory function post-TBI. TBI (n = 22) and sham control (n = 21) animals were randomly assigned housing in either single or enriched conditions for 7-9 weeks. ⋯ However, single-cell responses demonstrated EE-induced hypoexcitation in L4 post-TBI. EE was also able to fully ameliorate sensory hypersensitivity post-TBI, although it was not found to improve motor function. Long-term enrichment post-TBI induces changes at both the population and single-cell level in the sensory cortex, where EE may act to restore the excitation/inhibition balance in supragranular cortical layers.