Journal of neurotrauma
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Journal of neurotrauma · Mar 2017
A Mouse Model of Bilateral Cervical Contusion-Compression Spinal Cord Injury.
Cervical spinal cord injury (cSCI) occurs in over half of all cases of traumatic spinal cord injury (SCI), yet we lack therapies that can generate significant functional recovery in these patients. The development of animal models of cSCI will aid in the pre-clinical assessment of therapies and in understanding basic pathophysiological mechanisms. Here, we describe a clinically relevant model of cervical contusion-compression injury in the mouse. ⋯ Volumetric analysis of protein kinase C gamma (PKCgamma)-stained axons revealed that this injury results in significant damage to the corticospinal tract caudal to the injury site. Finally, we used quantitative real-time polymerase chain reaction to show that genes associated with inflammation and glial scarring are upregulated as a result of injury. This study confirms that we can effectively model bilateral cervical injury in the mouse and provides a framework for future studies using this model to assess therapies.
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Journal of neurotrauma · Mar 2017
Primary blast injury depressed hippocampal long-term potentiation through disruption of synaptic proteins.
Blast-induced traumatic brain injury (bTBI) is a major threat to United States service members in military conflicts worldwide. The effects of primary blast, caused by the supersonic shockwave interacting with the skull and brain, remain unclear. Our group has previously reported that in vitro primary blast exposure can reduce long-term potentiation (LTP), the electrophysiological correlate of learning and memory, in rat organotypic hippocampal slice cultures (OHSCs) without significant changes to cell viability or basal, evoked neuronal function. ⋯ Blast also reduced the expression of postsynaptic density protein-95 (PSD-95) and phosphorylation of stargazin protein at the serine-239/240 site. Finally, we found that modulation of the cyclic adenosine monophosphate (cAMP) pathway ameliorated electrophysiological and protein-expression changes caused by blast. These findings could inform the development of novel therapies to treat blast-induced loss of neuronal function.
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Journal of neurotrauma · Mar 2017
Regional grey matter volume loss is associated with gait impairments in young brain-injured individuals.
Traumatic brain injury (TBI) often leads to impairments in gait performance. However, the underlying neurostructural pathology of these gait deficits is poorly understood. We aimed to investigate regional gray matter (GM) volume in young moderate-to-severe TBI participants (n = 19; age 13 years 11 months ±3 years 1 month), compared with typically developing (TD) participants (n = 30; 14 years 10 months ±2 years 2 months), and assess whether reduced volume was related to impaired gait performance in TBI participants. ⋯ Moreover, in the TBI group, volume losses in subcortical ROIs were highly inter-correlated, indicating that atrophy tends to occur in combined subcortical structures. Finally, it was demonstrated, for the first time, that gait abnormalities in TBI subjects were associated with reduced volume in specific GM structures, including the hippocampus, thalamus, and the cerebellar, superior frontal, paracentral, posterior cingulate, and superior parietal cortices. The present study is an important first step in the understanding of the neurostructural pathology underlying impaired gait in TBI patients.
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Journal of neurotrauma · Mar 2017
Controlled Clinical TrialCerebral Perfusion changes in Post-Concussion Syndrome: A prospective controlled cohort study.
The biology of post-concussive symptoms is unclear. Symptoms are often increased during activities, and have been linked to decreased cerebrovascular reactivity and perfusion. The aim of this study was to examine cerebral blood flow (CBF) in children with different clinical recovery patterns following mild traumatic brain injury (mTBI). ⋯ Symptomatic children have higher CBF. Children who "recovered" quickly, have decreased CBF suggesting that clinical recovery precedes the cerebral recovery. Further longitudinal studies are required to determine if these perfusion patterns continue to change over time.