Journal of neurotrauma
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Journal of neurotrauma · Jan 2017
Multicenter StudyHypoaminoacidemia characterizes chronic traumatic brain injury.
Individuals with a history of traumatic brain injury (TBI) are at increased risk for a number of disorders, including Alzheimer's disease, Parkinson's disease, and chronic traumatic encephalopathy. However, mediators of the long-term morbidity are uncertain. We conducted a multi-site, prospective trial in chronic TBI patients (∼18 years post-TBI) living in long-term 24-h care environments and local controls without a history of head injury. ⋯ Many years after injury, TBI patients exhibit abnormal metabolic responses and altered relationships between circulating amino acids, cytokines, and hormones. This pattern is consistent with TBI, inducing a chronic disease state in patients. Understanding the mechanisms causing the chronic disease state could lead to new treatments for its prevention.
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Journal of neurotrauma · Jan 2017
Striatal Mitochondrial Disruption Following Severe Traumatic Brain Injury.
Traumatic brain injury (TBI) results in oxidative stress and calcium dysregulation in mitochondria. However, little work has examined perturbations of mitochondrial homeostasis in peri-injury tissue. We examined mitochondrial homeostasis after a unilateral controlled cortical impact over the sensorimotor cortex in adult male rats. ⋯ We detected an acute increase in superoxide dismutase 2 mRNA expression, as well as an induction of microRNA (miR)-21 and miR-155, which have been previously demonstrated to disrupt mitochondrial homeostasis. Behaviorally, rats with TBI exhibited marked error rates in contrainjury forelimb performance on the ladder test. These findings reveal that there may be differential susceptibilities of various peri-injury brain structures to mitochondrial dysfunction and associated behavioral deficits, and that molecular pathways demonstrated to interfere with mitochondrial homeostasis and function are activated subacutely post-TBI.
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Journal of neurotrauma · Jan 2017
The Effect of Underwater Blast on Aggregating Brain Cell Cultures.
Although the deleterious effects of primary blast on gas-filled organs are well accepted, the effect of blast-induced shock waves on the brain is less clear because of factors that complicate the interpretation of clinical and experimental data. Brain cell aggregate cultures are comprised of multiple differentiated brain cell types and were used to examine the effects of underwater blast. Suspensions of these cultures encased in dialysis tubing were exposed to explosive-generated underwater blasts of low (∼300 kPa), medium (∼2,700 kPa), or high (∼14,000 kPa) intensities and harvested at 1-28 days post-exposure. ⋯ The free-floating nature of the aggregates during blast wave exposure, coupled with their highly hydrolyzed dialysis tubing containment, results in minimized boundary effects, thus enabling accurate assessment of brain cell response to a simplified shock-induced stress wave. This work shows that, at its simplest, blast-induced shock waves produce subtle changes in brain tissue. This study has mechanistic implications for the study of primary blast-induced traumatic brain injury and supports the thesis that underwater blast may cause subtle changes in the brains of submerged individuals.
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Journal of neurotrauma · Jan 2017
Long-Term Neuropsychological Profiles and their Role as Mediators of Adaptive Functioning following Traumatic Brain Injury in Early Childhood.
The objectives of the study were to characterize long-term neuropsychological outcomes following traumatic brain injury (TBI) sustained during early childhood, and determine whether identified neuropsychological impairments mediated the effect of TBI on long-term adaptive functioning. Participants included 16 children with severe TBI, 42 children with moderate TBI, and 72 children with orthopedic injuries (OI) sustained between ages 3 and 7 years. Children completed neuropsychological tests and caregivers completed a structured interview of child adaptive functioning at 6.9 (±1.10) years post-injury. ⋯ No neuropsychological measure significantly mediated the effect of moderate TBI on adaptive functioning. Children sustaining early severe TBI demonstrate persisting neuropsychological impairments into adolescence and young adulthood. The impact of severe TBI on children's long-term adaptive functioning is mediated in part by its effects on fluid reasoning and processing speed.
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Journal of neurotrauma · Jan 2017
No effect of anodal tDCS on GABA levels in patients with recurrent mild traumatic brain injury.
In patients in the chronic phase after recurrent mild traumatic brain injury (mTBI), alterations in gamma-aminobutyric acid (GABA) concentration and receptor activity have been reported, possibly mediating subtle but persistent cognitive deficits and increased rate of dementia in older age. We evaluated whether anodal transcranial direct current stimulation (atDCS) over the primary motor cortex reduces GABA concentration and GABAB receptor activity in patients with recurrent mTBI. Seventeen patients (mean age 25, two women) in the chronic phase after recurrent mTBI and 22 healthy control subjects (mean age 26, two women) were included. ⋯ Moreover, no effects of atDCS on GABA concentration and receptor activity were seen in patients with mTBI or healthy control subjects. GABA concentration may increase with the number of mTBI, but atDCS did not modulate GABA concentration and receptor activity, as has been reported previously. Specifics of experimental design and analysis, but also characteristics of the respective samples, may account for these differential findings, and should be addressed in future larger studies.