Articles: traumatic-brain-injuries.
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Arch Phys Med Rehabil · Oct 2013
Functional outcomes in traumatic disorders of consciousness: 5-year outcomes from the National Institute on Disability and Rehabilitation Research Traumatic Brain Injury Model Systems.
To characterize the 5-year outcomes of patients with traumatic brain injury (TBI) not following commands when admitted to acute inpatient rehabilitation. ⋯ Substantial proportions of patients admitted to acute inpatient rehabilitation before following commands recover independent functioning over as long as 5 years, particularly if they begin to follow commands before hospital discharge.
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J Emerg Trauma Shock · Oct 2013
Risk factors for cervical spine injury among patients with traumatic brain injury.
Diagnosis of cervical spine injury (CSI) is difficult in patients with an altered level of consciousness as a result of a traumatic brain injury (TBI). Patients with TBI and older adults are at increased risk for CSI. This study examined the various risk factors for CSI among trauma patients with TBI and whether adults who were older (≥55 years) were at higher risk for CSI when they sustained a fall-related TBI. ⋯ The identification of associated injuries and factors may assist physicians in evaluating CSI in patients with TBI.
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Traumatic brain injury (TBI) initiates a neuroinflammatory response that increases the risk of TBI-related mortality. Acute alcohol intoxication at the time of TBI is associated with improved survival. Ethanol is recognized as a systemic immunomodulator that may also impart neuroprotection. The effects of alcohol on TBI-induced neuroinflammation, however, are unknown. We hypothesized that ethanol treatment prior to TBI may provide neuroprotection by diminishing the neuroinflammatory response to injury. ⋯ Alcohol treatment prior to TBI reduces the local neuroinflammatory response to injury. The decreased neurologic and inflammatory impact of TBI in acutely intoxicated patients may be responsible for improved clinical outcomes.
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The mechanisms underlying the protective effects of hyperbaric oxygen (HBO) therapy on traumatic brain injury (TBI) are unclear. TBI initiates a neuroinflammatory cascade characterized by activation of microglia and increased production of proinflammatory cytokines. In this study, we attempted to ascertain whether the occurrence of neuroinflammation exhibited during TBI can be reduced by HBO. ⋯ Our results demonstrate that treatment of TBI during the acute phase of injury can attenuate microgliosis and proinflammatory cytokine TNF-α expression resulting in a neuroprotective effect. Even treating TBI with HBO after 8 h had a therapeutic effect.
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Neuroscience letters · Sep 2013
Distinct patterns of expression of traumatic brain injury biomarkers after blast exposure: role of compromised cell membrane integrity.
Glial fibrillary acidic protein (GFAP), a protein enriched in astrocytes, and Tau, a protein abundant in neuronal microtubules, are being widely studied as biomarkers of brain injury, and persistent severity-dependent increases in brain and blood have been reported. Studies on the acute changes of these proteins after blast exposure are limited. Using a mouse model of closely-coupled repeated blast exposures, we have evaluated acute changes in the levels of GFAP and total Tau by Western blotting. ⋯ Liver and spleen tissue showed significant increases in the levels of GFAP and Tau protein at 6 and 24 h post-blast exposures whereas semi-quantitative RT-PCR analysis of liver showed no significant changes in the levels of GFAP or Tau mRNAs. These results suggest that blast exposure causes transient changes in cell membrane integrity in multiple organs leading to abnormal migration of proteins from the tissues to the plasma and vice versa. This transient changes in cell membrane permeability and subsequent bidirectional movement of molecules may contribute to the pathophysiology of TBI and polytrauma after blast exposure.