Articles: traumatic-brain-injuries.
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Population-based studies have supported the hypothesis that a positive history of traumatic brain injury (TBI) is associated with an increased incidence of neurological disease and psychiatric comorbidities, including chronic traumatic encephalopathy, Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. These epidemiologic studies, however, do not offer a clear definition of that risk, and leave unanswered the bounding criteria for greater lifetime risk of neurodegeneration. ⋯ Given this reality, multiple modalities and approaches must be combined to characterize who are at risk so that appropriate interventions to alter progression of neurodegeneration can be evaluated. This article presents data from a study that highlights uses of neuroimaging and areas of needed research in the link between TBI and neurodegenerative disease.
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Neurorehabil Neural Repair · Jun 2014
Rest-Activity Cycle Disturbances in the Acute Phase of Moderate to Severe Traumatic Brain Injury.
Sleep-wake disturbances are among the most persistent sequelae after traumatic brain injury (TBI) and probably arise during the hospital stay following TBI. These disturbances are characterized by difficulties sleeping at night and staying awake during the day. ⋯ Patients with acute moderate/severe TBI had an altered rest-activity cycle, probably reflecting severe fragmentation of sleep and wake episodes, which globally improved over time. A faster return to rest-activity cycle consolidation may predict enhanced brain recovery.
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Disturbed sleep pattern is a common symptom after head trauma and its prevalence in acute traumatic brain injury (TBI) is less discussed. Sleep has a profound impact on cognitive function recovery and the mediating effect of disturbed sleep on cognitive function recovery has not been examined after acute TBI. ⋯ Poor sleep efficiency, prolonged periods of daytime sleep, and a high prevalence of hypersomnia are common symptoms in acute TBI patients. The duration of daytime sleep mediates the relationship between the severity of brain injury and the recovery of cognition function.
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Arch Clin Neuropsychol · Jun 2014
Factors influencing postconcussion and posttraumatic stress symptom reporting following military-related concurrent polytrauma and traumatic brain injury.
The purpose of this study was to identify factors that are predictive of, or associated with, high endorsement of postconcussion and posttraumatic stress symptoms following military-related traumatic brain injury (TBI). Participants were 1,600 U. S. service members (age: M = 27.1, SD = 7.1; 95.4% male) who had sustained a mild-to-moderate TBI and who had been evaluated by the Defense and Veterans Brain Injury Center at one of six military medical centers. ⋯ Depression alone accounted for the vast majority of unique variance (60.0%) and was strongly associated with, and predictive of, clinically elevated posttraumatic stress symptoms (OR = 38.78; RR = 4.63). There was a very clear, strong, and clinically meaningful association between depression, posttraumatic stress, and postconcussion symptoms in this sample. Brain injury severity, however, was not associated with symptom reporting following TBI.
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Journal of neurochemistry · Jun 2014
2-Methoxyestradiol confers neuroprotection and inhibits a maladaptive HIF-1α response after traumatic brain injury in mice.
HIF-1α is pivotal for cellular homeostasis in response to cerebral ischemia. Pharmacological inhibition of HIF-1α may reduce secondary brain damage by targeting post-translational mechanisms associated with its proteasomal degradation and nuclear translocation. This study examined the neuroprotective effects of 2-methoxyestradiol (2ME2), the involved HIF-1α-dependent response, and alternative splicing in exon 14 of HIF-1α (HIF-1α∆Ex14) after traumatic brain injury (TBI) in mice. ⋯ Early 2ME2 administration reduced the secondary brain damage and neuronal HIF-1α probably involving ubiquitin proteasome system-mediated degradation. The up-regulation of neuropathological HIF-1α target genes and pro-apoptotic BNIP3 protein was attenuated. We propose that the inhibition of a maladaptive HIF-1α response may contribute to 2ME2-mediated neuroprotection.