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At least 289 records · Page 16Linked to original sources
PubMed2006

Interface parameters of impact-induced mild traumatic brain injury.

Commonly considered a continuum of injuries, diffuse brain injury (DBI) ranges from mild concussion to severe diffuse axonal injury. The lower end of the spectrum is generally referred to as mild traumatic brain injury (MTBI). More severe forms of DBI have garnered extensive experimentation while these milder cases are considerably less explored. Recently, a new device was designed to generate DBI in the rodent using impact-induced angular acceleration. This device is modifiable so the entire spectrum of DBI can be investigated. Severity of DBI is critically dependent on magnitude of angular acceleration. A small animal surrogate like a rodent has a relatively small brain mass. This constraint poses a unique problem because the angular acceleration necessary for DBI is inversely related to brain mass. Prior experimentation estimated an angular acceleration of approximately 350 krad/s2 is necessary for the induction of mild traumatic brain injury (MTBI) in the rodent. To induce these magnitudes of angular acceleration in a repeatable manner, the impacting interface must be critically analyzed. This investigation uses a mathematical model based on parameters of a previously developed experimental model to assess the impacting interface such that angular accelerations are sufficient to produce MTBI in the rodent.

Acceleration↗
PubMed1997

EBIC-guidelines for management of severe head injury in adults. European Brain Injury Consortium.

Guidelines for the management of severe head injury in adults as evolved by the European Brain Injury Consortium are presented and discussed. The importance of preventing and treating secondary insults is emphasized and the principles on which treatment is based are reviewed. Guidelines presented are of a pragmatic nature, based on consensus and expert opinion, covering the treatment from accident site to intensive care unit. Specific aspects pertaining to the conduct of clinical trials in head injury are highlighted. The adopted approach is further discussed in relation to other approaches to the development of guidelines, such as evidence based analysis.

Adult↗
PubMed2006

A clinical report of adverse health effects due to bed sharing in two children with spinal cord injury and traumatic brain injury.

This paper explores the possibility that bed sharing may carry particular risks for children with special healthcare needs (CSHCN). Two cases of CSHCN who may have sustained adverse health effects from bed sharing are described. These two case reports indicate that CSHCN may be particularly susceptible to risks associated with bed sharing. Healthcare providers for CSHCN may need to inquire about patients' sleeping arrangements and, when bed sharing is acknowledged, provide counseling regarding the potential risks and benefits. They may need to monitor more closely for adverse events when bed sharing is a factor and should consider reporting health problems that may have occurred in concurrence with bed sharing.

Beds↗
PubMed1990

[Clinical aspects of thoraco-abdominal injuries associated with brain injuries].

The results of treatment of 31 patients with thoraco-abdominal trauma in combination with the brain trauma were analysed. Detection of the leading injury which determined the severity of a state of the sufferers offered considerable difficulties. In choice of a method for treatment the preference was given to the least traumatic methods providing saving the life of a patient. Seven sufferers died.

Abdominal Injuries↗
PubMedDate not supplied

Awareness, emotional adjustment, and injury severity in postacute brain injury.

OBJECTIVE: Relationships among awareness of deficits, injury severity, and emotional adjustment in patients with traumatic brain injury were explored. PARTICIPANTS: One hundred sixty-six individuals were referred for postacute neurocognitive assessment. DESIGN: Retrospective file analysis identified injury severity, and data from the Patient Competency Rating Scale and Katz Adjustment Scale-Revised, utilizing self-ratings and significant others' ratings, were gathered. RESULTS: Significant others described emotional adjustment difficulties, regardless of the severity of injury. A positive association was noted between patients' acknowledgment of neurobehavioral problems and ratings of their emotional adjustment. CONCLUSIONS: Severity of TBI appeared less important than emotional adjustment in the awareness of deficit; mildly injured patients were more likely to report neurobehavioral deficits than were moderately and severely injured patients, relative to the reports of significant others.

Adaptation, Psychological↗
PubMed2004

Relationship between flow-metabolism uncoupling and evolving axonal injury after experimental traumatic brain injury.

Blood flow-metabolism uncoupling is a well-documented phenomenon after traumatic brain injury, but little is known about the direct consequences for white matter. The aim of this study was to quantitatively assess the topographic interrelationship between local cerebral blood flow (LCBF) and glucose metabolism (LCMRglc) after controlled cortical impact injury and to determine the degree of correspondence with the evolving axonal injury. LCMRglc and LCBF measurements were obtained at 3 hours in the same rat from 18F-fluorodeoxyglucose and 14C-iodoantipyrine coregistered autoradiographic images, and compared to the density of damaged axonal profiles in adjacent sections and in an additional group at 24 hours using beta-amyloid precursor protein (beta-APP) immunohistochemistry. LCBF was significantly reduced over the ipsilateral hemisphere by 48 +/- 15% compared with sham-controls, whereas LCMRglc was unaffected, apart from foci of elevated LCMRglc in the contusion margin. Flow-metabolism was uncoupled, indicated by a significant 2-fold elevation in the LCMRglc/LCBF ratio within most ipsilateral structures. There was a significant increase in beta-APP-stained axons from 3 to 24 hours, which was negatively correlated with LCBF and positively correlated with the LCMRglc/LCBF ratio at 3 hours in the cingulum and corpus callosum. Our study indicates a possible dependence of axonal outcome on flow-metabolism in the acute injury stage.

Amyloid beta-Protein Precursor↗
PubMed1994

Brain injury.

Explore the source record for details and available documents.

Brain Injuries↗
PubMed1998

The relationship of soluble adhesion molecule concentrations in systemic and jugular venous serum to injury severity and outcome after traumatic brain injury.

UNLABELLED: Adhesion molecules control the migration of leukocytes into tissue after injury. This may result in further cellular damage. We hypothesized that altered serum concentrations of soluble intercellular adhesion molecule (sICAM)-1 and soluble L-selectin (sL-selectin) after traumatic brain injury would correlate with injury severity and neurological outcome. We investigated serum concentrations of sICAM-1 and sL-selectin in 22 patients with traumatic brain injury admitted to the intensive care unit. The Glasgow Coma Scale (GCS) score and Injury Severity Score were recorded. Paired arterial and jugular venous blood samples were taken on admission and 24, 48, and 96 h after injury. Mean systemic and jugular venous concentrations of sICAM-1 were normal on admission but became significantly increased by 96 h (P = 0.018). sL-selectin concentrations of injured patients were markedly below those of controls at all time points (P < 0.001). There were no significant differences between jugular venous and arterial concentrations of either sICAM-1 or sL-selectin. Serum sICAM-1 was significantly related to neurological outcome (P < 0.001) and to the GCS score (P < 0.001). These changes in adhesion molecule expression after acute brain injury may be important in the pathophysiology of secondary injury. The highly significant relationship between serum sICAM-1 and neurological outcome suggests that the inflammatory response to injury may be detrimental. Drugs that antagonize the actions of the adhesion molecules may have a role in therapy after traumatic brain injury. IMPLICATIONS: This observational study shows that there is a strong association between soluble intercellular adhesion molecule-1 in serum and poor neurological outcome after traumatic brain injury. This suggests that inflammation after brain injury may worsen the prognosis and that therapies directed against this inflammation may prove useful.

Adolescent↗
PubMed2005

Diffuse axonal injury in mild traumatic brain injury: a diffusion tensor imaging study.

OBJECT: Diffuse axonal injury (DAI) is a major complication of traumatic brain injury (TBI) that leads to functional and psychological deficits. Although DAI is frequently underdiagnosed by conventional imaging modalities, it can be demonstrated using diffusion tensor imaging. The aim of this study was to assess the presence and extent of DAI in patients with mild TBI. METHODS: Forty-six patients with mild TBI and 29 healthy volunteers underwent a magnetic resonance (MR) imaging protocol including: dual-spin echo, fluid-attenuated inversion recovery, T2-weighted gradient echo, and diffusion tensor imaging sequences. In 20 of the patients, MR imaging was performed at a mean of 4.05 days after injury. In the remaining 26, MR imaging was performed at a mean of 5.7 years after injury. In each case, mean diffusivity and fractional anisotropy were measured using both whole-brain histograms and regions of interest analysis. No differences in any of the histogram-derived measures were found between patients and control volunteers. Compared with controls, a significant reduction of fractional anisotropy was observed in patients' corpus callosum, internal capsule, and centrum semiovale, and there were significant increases of mean diffusivity in the corpus callosum and internal capsule. Neither histogram-derived nor regional diffusion tensor imaging metrics differed between the two groups. CONCLUSIONS: Although mean diffusivity and fractional anisotropy abnormalities in these patients with TBI were too subtle to be detected with the whole-brain histogram analysis, they are present in brain areas that are frequent sites of DAI. Because diffusion tensor imaging changes are present at both early and late time points following injury, they may represent an early indicator and a prognostic measure of subsequent brain damage.

Adolescent↗
PubMed1999

Effects of the bradykinin antagonist Bradycor (deltibant, CP-1027) in severe traumatic brain injury: results of a multi-center, randomized, placebo-controlled trial. American Brain Injury Consortium Study Group.

A phase II prospective, randomized, double blind clinical trial of Bradycor, a bradykinin antagonist, was conducted at 31 centers within North America in severely brain injured patients. Patients of Glasgow Coma Score (GCS) 3-8 (n = 139) with at least one reactive pupil were randomized to receive either Bradycor, 3 microg/kg/min or placebo as a continuous intravenous infusion for 5 days, with the infusion beginning within 12 h of the injury. The primary objective was to assess the efficacy of a continuous infusion of Bradycor (3.0 mc/kg/min) in preventing elevation of intracranial pressure (ICP). Other efficacy measures included the effect of Bradycor on the Therapy Intensity Level (TIL), mortality, and functional outcome. A secondary objective was to evaluate the safety of Bradycor in patients with severe brain injury. Randomization was carried out according to a computer generated randomization list. Patients were followed for the first 14 days of hospitalization with long-term outcome assessed at 3 and 6 months after injury. During the infusion and while the ICP monitor was in place, ICP measurements were recorded hourly along with blood pressure and heart rate. A modified version of the TIL was used to record therapeutic interventions hourly, while the ICP was being monitored. Outcome was assessed at 3 and 6 months after injury using the Glasgow Outcome Score (GOS). Bradycor was well tolerated in this patient population, and no adverse events were attributable to the compound. Although positive trends were seen for both ICP and TIL in the Bradycor group, these differences analyzed on a daily basis were not significant. However, a mixed model of variance which included treatment, day, treatment by day interaction, age and GCS revealed that the percentage time ICP of >15 mm Hg on days 4 and 5 was significantly lower in the Bradycor group compared to placebo (p = 0.035). There were fewer deaths in the Bradycor group, which had a 28-day all cause mortality of 20% versus 27% on placebo. Patients treated with Bradycor showed a 10.3% improvement in favorable outcome at 3 months and a 12% improvement in dichotomized GOS at 6 months (p = 0.26). The consistent positive trends seen in ICP, TIL, neuropsychological tests, and, most importantly, 3- and 6-month GOS provide supportive evidence that a bradykinin antagonist may play a neuroprotective role in severe brain injury.

Adolescent↗
PubMedDate not supplied

Diffuse axonal injury associated with chronic traumatic brain injury: evidence from T2*-weighted gradient-echo imaging at 3 T.

BACKGROUND AND PURPOSE: Diffuse axonal injury is frequently accompanied by tissue tear hemorrhages. We examined whether high field strength T2*-weighted gradient-echo imaging performed during the chronic stage of traumatic brain injury may have advantages in the evaluation of diffuse axonal injury as compared with T1- and T2-weighted MR imaging. METHODS: Prospective MR imaging of 66 patients (age range, 17-57 years) was performed using a 3-T system 3 to 292 months (median, 23.5 months) after traumatic brain injury. T1-, T2-, T2*-hypointense and T2-hyperintense foci of 1- to 15-mm diameter were registered in 10 brain regions by two readers separately. Foci that appeared hypointense both on the T1- and T2- and/or on the T2*-weighted images were defined as traumatic microbleeds. RESULTS: For 46 (69.7%) of the patients, T2*-weighted gradient-echo imaging revealed traumatic microbleeds. Hyperintense foci were observed on the T2-weighted images of only 15 (22.7%) patients. T2*-weighted imaging showed significantly more traumatic microbleeds (P =.000) than did T1- and T2-weighted imaging. Interobserver agreement was strong (kappa = 0.79, tau = 0.749, P =.000). For 14 (21.2%) of the patients, T2*-weighted gradient-echo imaging revealed traumatic microbleeds in the corpus callosum, whereas for only two (3%), hyperintense callosal lesions were seen on the T2-weighted images. Although a significant correlation existed between the total amount and callosal appearance of traumatic microbleeds and Glasgow Coma Scale scores (P =.000), no correlation existed with extended Glasgow Outcome Scale scores. CONCLUSION: T2*-weighted gradient-echo imaging at high field strength is a useful tool for the evaluation of diffuse axonal injury during the chronic stage of traumatic brain injury. Diffuse axonal injury-related brain lesions are mainly hemorrhagic. The relevance of diffuse axonal injury for long-term clinical outcome is uncertain.

Adolescent↗
PubMed2005

Brain death after severe traumatic brain injury: the role of systemic secondary brain insults.

Secondary brain insults predominantly due to hypotension are frequent among patients with fatal traumatic brain injury. We assessed the correlation between different systemic secondary brain insults and brain death in 404 patients admitted to our intensive care unit (ICU) after severe traumatic brain injury. We collated data on hypoxemia and hypotension prior to as well as the occurrence of hypoxemia, hypotension, shock, anemia, hyperglycemia, and hyperthermia within the first 24 hours after ICU admission. We also considered both the presence of extracranial injuries and the category of traumatic brain injury using computerized tomography. The 59 patients (14.6%) who developed brain death, were significantly older than patients without a fatal neurological outcome (46.1 +/- 22 vs 29.5 +/- 14.9 years; P < .0001). Intracranial mass lesions, whether surgically evacuated were more frequent among brain-dead patients. The systemic secondary brain insults significantly associated with brain death were hypoxemia, hypotension, shock, anemia, and hyperglycemia within the first 24 hours after ICU admission. After multivariate analysis, the factors that independently predicted brain death were the occurrence of shock (odds ratio [OR], 6.74; 95% confidence interval [CI], 2.85-15.84; P = .001) and older age (OR, 1.05; 95% CI, 1.03-1.07; P = .003). In conclusion, early shock seems to be the major systemic secondary brain insult associated with brain death in patients with severe traumatic brain injury. Prevention of or correction of shock might help to either decrease the occurrence of a fatal neurological outcome or in brain-dead patients to preserve organs in better condition for procurement.

Adult↗