Journal of neurotrauma
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Journal of neurotrauma · Mar 2014
Injury pattern, hospital triage and mortality of 1,250 patients with severe traumatic brain injury caused by road traffic accidents.
This epidemiological study analyzed the incidence, risk factors, hospital triage, and outcome of patients with severe traumatic brain injuries (sTBIs) caused by road traffic accidents (RTAs) admitted to hospitals in the Trauma Center West-Netherlands (TCWN) region. Trauma registry data were used to identify TBI in all RTA victims admitted to hospitals in the mid-West region of the Netherlands from 2003 to 2011. Type of head injury and severity were classified using the Abbreviated Injury Scale (AIS). ⋯ Hemorrhage and contusion both occur in over 50% of patients with sTBI. Specific brain injury patterns can be distinguished for specific road user groups, and independent prognostic risk factors for sTBI were identified. This knowledge may be used to improve vigilance for particular injuries in specific patient groups and stimulate development of focused diagnostic strategies.
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Journal of neurotrauma · Mar 2014
Correlations between blood-brain barrier disruption and neuroinflammation in an experimental model of penetrating ballistic-like brain injury.
Abstract Blood-brain barrier (BBB) disruption is a pathological hallmark of severe traumatic brain injury (TBI) and is associated with neuroinflammatory events contributing to brain edema and cell death. The goal of this study was to elucidate the profile of BBB disruption after penetrating ballistic-like brain injury (PBBI) in conjunction with changes in neuroinflammatory markers. Brain uptake of biotin-dextran amine (BDA; 3 kDa) and horseradish peroxidase (HRP; 44 kDa) was evaluated in rats at 4 h, 24 h, 48 h, 72 h, and 7 days post-PBBI and compared with the histopathologic and molecular profiles for inflammatory markers. ⋯ This profile was most closely associated with markers for adhesion (mRNA for intercellular adhesion molecule-1) and infiltration of peripheral granulocytes (mRNA for matrix metalloproteinase-9 [MMP-9] and myeloperoxidase staining). Improvement of BBB dysfunction coincided with increased expression of markers implicated in tissue remodeling and repair. The results of this study reveal a uniphasic and gradient opening of the BBB after PBBI and suggest MMP-9 and resident inflammatory cell activation as candidates for future neurotherapeutic intervention after PBBI.
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Journal of neurotrauma · Mar 2014
Neuroimaging, Behavioral, and Psychological Sequelae of Repetitive Combined Blast/Impact Mild Traumatic Brain Injury in Iraq and Afghanistan War Veterans.
Abstract Whether persisting cognitive complaints and postconcussive symptoms (PCS) reported by Iraq and Afghanistan war veterans with blast- and/or combined blast/impact-related mild traumatic brain injuries (mTBIs) are associated with enduring structural and/or functional brain abnormalities versus comorbid depression or posttraumatic stress disorder (PTSD) remains unclear. We sought to characterize relationships among these variables in a convenience sample of Iraq and Afghanistan-deployed veterans with (n=34) and without (n=18) a history of one or more combined blast/impact-related mTBIs. Participants underwent magnetic resonance imaging of fractional anisotropy (FA) and macromolecular proton fraction (MPF) to assess brain white matter (WM) integrity; [(18)F]-fluorodeoxyglucose positron emission tomography imaging of cerebral glucose metabolism (CMRglu); structured clinical assessments of blast exposure, psychiatric diagnoses, and PTSD symptoms; neurologic evaluations; and self-report scales of PCS, combat exposure, depression, sleep quality, and alcohol use. ⋯ Neuroimaging metrics did not differ between participants with versus without PTSD. Iraq and Afghanistan veterans with one or more blast-related mTBIs exhibit abnormalities of brain WM structural integrity and macromolecular organization and CMRglu that are not related to comorbid PTSD. These findings are congruent with recent neuropathological evidence of chronic brain injury in this cohort of veterans.
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Journal of neurotrauma · Mar 2014
Reversal of established traumatic brain injury-induced anxiety-like behavior in rats following delayed, post-injury neuroimmune suppression.
Abstract Traumatic brain injury (TBI) increases the risk of neuropsychiatric disorders, particularly anxiety disorders. Yet, there are presently no therapeutic interventions to prevent the development of post-traumatic anxiety or effective treatments once it has developed. This is because, in large part, of a lack of understanding of the underlying pathophysiology. ⋯ We examined the efficacy of an anti-inflammatory treatment in decreasing anxiety-like behavior and reactive gliosis when introduced at 1 month after injury. Delayed treatment substantially reduced established LFPI-induced freezing behavior and reactive gliosis in brain regions associated with anxiety and continued neuroprotective effects were evidenced 6 months post-treatment. These results support the conclusion that neuroinflammation may be involved in the development and maintenance of anxiety-like behaviors after TBI.