Articles: traumatic-brain-injuries.
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NeuroImage. Clinical · Jan 2017
Activation of dominant hemisphere association cortex during naming as a function of cognitive performance in mild traumatic brain injury: Insights into mechanisms of lexical access.
Patients with a history of mild traumatic brain injury (mTBI) and objective cognitive deficits frequently experience word finding difficulties in normal conversation. We sought to improve our understanding of this phenomenon by determining if the scores on standardized cognitive testing are correlated with measures of brain activity evoked in a word retrieval task (confrontational picture naming). The study participants (n = 57) were military service members with a history of mTBI. ⋯ These findings may indicate weak afferent inputs to and within an extended cortical network including association cortex of the dominant hemisphere in patients with low cognitive performance. The association between word finding difficulties and low cognitive performance may therefore be the result of a diffuse pathophysiological process affecting distributed neuronal networks serving a wide range of cognitive processes. These findings also provide support for a parallel processing model of lexical access.
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Neurobiol Sleep Circadian Rhythms · Jan 2017
Circadian variability of the initial Glasgow Coma Scale score in traumatic brain injury patients.
The Glasgow Coma Scale (GCS) score is the primary method of assessing consciousness after traumatic brain injury (TBI), and the clinical standard for classifying TBI severity. There is scant literature discerning the influence of circadian rhythms or emergency department (ED) arrival hour on this important clinical tool. ⋯ Nighttime TBI patients present with decreased GCS scores and are admitted to ICU at higher rates, yet have fewer prior comorbidities and similar systemic injuries. The interaction between nighttime hours and decreased GCS score on ICU admissions has important implications for clinical assessment/triage.
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This study compared the ability of five injury severity measures, namely the Abbreviated Injury Scale to the Head (AIS-H), Glasgow Coma Scale (GCS), Glasgow Outcome Scale (GOS), Extended Glasgow Outcome Scale (GOSE), and Injury Severity Score (ISS), to predict return-to-work after a traumatic brain injury (TBI). Furthermore, factors potentially associated with return-to-work were investigated. In total, 207 individuals aged ≤65 years newly diagnosed with a TBI and employed at the time of injury were recruited and followed-up for 1year by telephone every 3 months. ⋯ A multivariable analysis revealed that individuals with higher injury severity as measured by the ISS (hazard ratio [HR], 0.94; 95% confidence interval [CI], 0.92-0.97), a lack of autonomy in transportation (HR, 2.55; 95% CI, 1.23-5.32), cognitive impairment (HR, 0.47; 95% CI, 0.28-0.79), and depression (HR, 0.97; 95% CI, 0.95-0.99) were significantly less likely to be employed after a TBI. In conclusion, of the five injury severity measures, the ISS may be the most capable measure of predicting return-to-work after a TBI. In addition to injury severity, autonomy in transportation, cognitive function, and the depressive status may also influence the employment status during the first year after a TBI.
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Chronic pain after traumatic brain injury (TBI) is very common, but the mechanisms linking TBI to pain and the pain-related interactions of TBI with peripheral injuries are poorly understood. Chemokine receptors play an important role in both pain and brain injury. In the current work, we pursued the hypothesis that the epigenetically regulated CXC chemokine receptor 2 (CXCR2) is a crucial modulator of nociceptive sensitization induced by TBI. ⋯ Chromatin immunoprecipitation experiments demonstrated TBI-enhanced association of the CXCR2 promoter with acetylated-H3K9 histone protein that was also reversible using anacardic acid. Taken together, our findings suggested that TBI causes the upregulation of spinal CXCR2 through an epigenetic mechanism ultimately supporting nociceptive sensitization. The use of CXCR2 antagonists may, therefore, be useful in pain resulting from TBI.
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Restor. Neurol. Neurosci. · Jan 2017
Diffuse traumatic brain injury in the mouse induces a transient proliferation of oligodendrocyte progenitor cells in injured white matter tracts.
Injury to the white matter may lead to impaired neuronal signaling and is commonly observed following traumatic brain injury (TBI). Although endogenous repair of TBI-induced white matter pathology is limited, oligodendrocyte progenitor cells (OPCs) may be stimulated to proliferate and regenerate functionally myelinating oligodendrocytes. Even though OPCs are present throughout the adult brain, little is known about their proliferative activity following axonal injury caused by TBI. ⋯ These results suggest that traumatic axonal injury in the mouse induces a transient proliferative response of residing OPCs. These proliferating OPCs may replace dead oligodendrocytes and contribute to remyelination, which needs evaluation in future studies.