Articles: traumatic-brain-injuries.
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Journal of neurotrauma · Aug 2015
Mortality following traumatic brain injury inpatient rehabilitation.
The aim of this study was to examine the rate and causes of mortality following mild to severe traumatic brain injury (TBI) rehabilitation and to develop a multivariate prognostic model of mortality. We conducted a cohort study of 3341 individuals with mild to severe TBI followed-up from a post-acute inpatient rehabilitation center. Rate of death and survival between one and 26 years following injury were examined using standardized mortality ratios (SMRs) and prognostic models developed using Cox regression. ⋯ Premorbid lifestyle factors exerted a greater influence on mortality following TBI, compared with injury-related factors. This risk was especially prominent for younger individuals, who died primarily due to external causes. These findings highlight the need for interventions that address premorbid issues, such as substance abuse and mental health issues.
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Journal of neurotrauma · Aug 2015
Neuronal DNA Methylation Profiling of Blast-related Traumatic Brain Injury (TBI).
Long-term molecular changes in the brain resulting from blast exposure may be mediated by epigenetic changes, such as deoxyribonucleic acid (DNA) methylation, that regulate gene expression. Aberrant regulation of gene expression is associated with behavioral abnormalities, where DNA methylation bridges environmental signals to sustained changes in gene expression. We assessed DNA methylation changes in the brains of rats exposed to three 74.5 kPa blast overpressure events, conditions that have been associated with long-term anxiogenic manifestations weeks or months following the initial exposures. ⋯ Functional validation via gene expression analysis of 30 differentially methylated neuronal and glial genes showed a 1.2 fold change in gene expression of the serotonin N-acetyltransferase gene (Aanat) in blast animals (p<0.05). These data provide the first genome-based evidence for changes in DNA methylation induced in response to multiple blast overpressure exposures. In particular, increased methylation and decreased gene expression were observed in the Aanat gene, which is involved in converting serotonin to the circadian hormone melatonin and is implicated in sleep disturbance and depression associated with traumatic brain injury.
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Journal of neurotrauma · Aug 2015
Comparative StudyPatterns of Depression Treatment in Medicare Beneficiaries with Depression Following Traumatic Brain Injury.
There are no clinical guidelines addressing the management of depression after traumatic brain injury (TBI). The objectives of this study were to (1) describe depression treatment patterns among Medicare beneficiaries with a diagnosis of depression post-TBI; (2) compare them with depression treatment patterns among beneficiaries with a diagnosis of depression pre-TBI; and (3) quantify the difference in prevalence of use. We conducted a retrospective analysis of Medicare beneficiaries hospitalized with TBI during 2006-2010. ⋯ There was no difference in receipt of psychotherapy between the two groups (OR 1.08; 95% CI 0.93, 1.26). Depression after TBI is undertreated among older adults. Knowledge about reasons for this disparity and its long-term effects on post-TBI outcomes is limited and should be examined in future work.
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Traumatic brain injury (TBI) is a major risk factor for dementia. Recently, TBI has also been suggested as a risk factor for frontotemporal dementia (FTD), and plasma immunoreactivity to the TAR-DNA binding protein 43 (TDP-43) has been observed in both patients with acute TBI and long-term survivors of this condition. We used a population-based study to estimate and compare the risk of FTD in individuals with and without TBI. ⋯ Further, the behavioral impairments were likely associated with TDP-43 short fragment mislocalization and accumulation. Our findings suggest that in humans, TBI is associated with a greater occurrence of FTD. Moreover, clinical FTD manifestations may be associated with TDP-43 proteolysis, since impaired behaviors in TBI rats were reminiscent of those in humans with FTD.
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Survivin, a unique member of the inhibitor of the apoptosis protein (IAP) family, has been suggested to play a crucial role in promoting the cell cycle and mediates mitosis during embryonic development. However, the role of survivin following traumatic brain injury (TBI) in adult neurogenesis and apoptosis in the mouse dentate gyrus (DG) remains only partially understood. We adopted adenovirus-mediated RNA interference (RNAi) as a means of suppressing the expression of survivin and observed its effects on adult regeneration and neurological function in mice after brain injury. ⋯ Furthermore, downregulation of survivin results in a significant increase in programmed cell death in the DG, as assessed using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and 4',6-diamidino-2-phenylindole (DAPI) double staining. The Morris water maze (MWM) test was adopted to evaluate neurological function, which confirmed that knockdown of survivin worsened the memory capacity that was already compromised following TBI. Survivin in adult mice brains after TBI can be successfully down-regulated by RNAi, which inhibited adult hippocampal neurogenesis, promoted apoptotic cell death, and resulted in a negative role in the recovery of dysfunction following injury.