Articles: traumatic-brain-injuries.
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Neurorehabil Neural Repair · Mar 2017
Proactive Response Inhibition and Subcortical Gray Matter Integrity in Traumatic Brain Injury.
Traumatic brain injury (TBI) has been associated with impairments in inhibiting prepotent motor responses triggered by infrequent external signals (ie, reactive inhibition). It is unclear whether proactive preparation to inhibit upcoming responses is also affected (ie, proactive inhibition). Successful inhibition relies on frontosubcortical interactions; therefore, impairments might be linked with gray matter atrophy in subcortical structures. ⋯ Our results reveal that proactive inhibition seems unaffected in TBI and that volume of subregions of subcortical nuclei is predictive for response inhibition proficiency and of clinical relevance in TBI.
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Observational Study
Longitudinal changes in anthropometrics and impact on self-reported physical function after traumatic brain injury.
Patients admitted to the ICU with a traumatic brain injury (TBI) are at risk of muscle wasting but this has not been quantified. Our aims were to describe longitudinal changes in anthropometrical data, compare the accuracy of non-invasive methodologies to the validated dual-energy x-ray absorptiometry (DXA), and assess the relationships between anthropometrical data and self-reported physical function. ⋯ Patients with a TBI lose muscle thickness while in the ICU but the trajectory of loss stabilises after ICU discharge. Ultrasound-derived QMLT is related to total lean mass and physical function after discharge. Further studies are needed to confirm that ultrasound measurement of QMLT is a useful surrogate measure of muscle mass and functional outcomes after trauma and critical illness.
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Moderate-to-severe traumatic brain injury is one of the strongest environmental risk factors for the development of neurodegenerative diseases such as late-onset Alzheimer's disease, although it is unclear whether mild traumatic brain injury, or concussion, also confers risk. This study examined mild traumatic brain injury and genetic risk as predictors of reduced cortical thickness in brain regions previously associated with early Alzheimer's disease, and their relationship with episodic memory. Participants were 160 Iraq and Afghanistan War veterans between the ages of 19 and 58, many of whom carried mild traumatic brain injury and post-traumatic stress disorder diagnoses. ⋯ Finally, analyses that examined the apolipoprotein E4 allele, post-traumatic stress disorder, and genetic risk for schizophrenia and depression confirmed the specificity of the Alzheimer's disease polygenic risk finding. These results provide evidence that mild traumatic brain injury is associated with greater neurodegeneration and reduced memory performance in individuals at genetic risk for Alzheimer's disease, with the caveat that the order of causal effects cannot be inferred from cross-sectional studies. These results underscore the importance of documenting head injuries even within the mild range as they may interact with genetic risk to produce negative long-term health consequences such as neurodegenerative disease.
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Randomized Controlled Trial
Intensive insulin therapy for preventing postoperative infection in patients with traumatic brain injury: A randomized controlled trial.
To assess the effect of intensive insulin therapy (IIT) for preventing postoperative infection in patients with traumatic brain injury (TBI). ⋯ IIT leads to a reduced infection rate, shorter stays in ICU, and improved neurological outcome.
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Journal of neurochemistry · Mar 2017
Transient receptor potential vanilloid type 4 channels mediate Na-K-Cl-co-transporter-induced brain edema after traumatic brain injury.
Na+ -K+ -2Cl- co-transporter (NKCC1) plays an important role in traumatic brain injury (TBI)-induced brain edema via the MAPK cascade. The transient receptor potential vanilloid type 4 (TRPV4) channel participates in neurogenic inflammation, pain transmission, and edema. In this study, we investigated the relationship between NKCC1 and TRPV4 and the related signaling pathways in TBI-induced brain edema and neuronal damage. ⋯ Administration of either the TRPV4 antagonist, RN1734, or NKCC1 antagonist, bumetanide, significantly attenuated TBI-induced brain edema through decreasing the phosphorylation of MEK, ERK, and Akt proteins. Bumetanide injection inhibited TRPV4 expression, which suggests NKCC1 activation is critical to TRPV4 activation. Our results showed that hippocampal NKCC1 activation increased TRPV4 expression after TBI and then induced severe brain edema and neuronal damage through activation of the MAPK cascade and Akt-related signaling pathway.