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Results for “Brain Injuries, Traumatic”

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PubMed2003

Heme oxygenase-2 protects against lipid peroxidation-mediated cell loss and impaired motor recovery after traumatic brain injury.

After traumatic brain injury (TBI), substantial extracellular heme is released from hemoproteins during hemorrhage and cell injury. Heme oxygenase (HO) isozymes are thought to detoxify the pro-oxidant heme to the potent antioxidant, bilirubin. HO-1, the inducible isozyme, is expressed in glial populations after injury and may play a protective role. However, the role of HO-2, the predominant and constitutively expressed isozyme in the brain, remains unclear after TBI. We used a controlled cortical impact injury model to determine the extent and mechanism of damage between HO-2 knock-out (KO) (-/-) and wild-type (WT) (+/+) mice. The specific cellular and temporal expressions of HO-2 and HO-1 were characterized by immunocytochemistry and Western blots. HO-2 was immunolocalized in neurons both before and after TBI, whereas HO-1 was highly upregulated in glia only after TBI. HO activity determined by gas chromatography using brain sonicates from injured HO-2 KO mice was significantly less than that of HO-2 wild types, despite the induction of HO-1 expression after TBI. Cell loss was significantly greater in KO mice in areas including the cortex, the CA3 region of hippocampus, and the lateral dorsal thalamus. Furthermore, motor recovery after injury, as measured by the rotarod assay and an inclined beam-walking task, was compromised in the KO mice. Finally, brain tissue from injured HO-2 KO mice exhibited decreased ability to reduce oxidative stress, as measured with an Fe(2+)/ascorbic acid-mediated carbon monoxide generation assay for lipid peroxidation susceptibility. These findings demonstrate that HO-2 expression protects neurons against TBI by reducing lipid peroxidation via the catabolism of free heme.

Animals↗

PubMedDate not supplied

Human responses to traumatic brain injury.

A traumatic brain injury can have devastating effects on the patient and the family. The patient with TBI faces deficits that influence life after hospitalization. With the use of specific nursing therapies, human responses to TBI can be treated and a patient can return to a satisfactory lifestyle.

Adolescent↗

PubMed2006

Natural history of the long-term cognitive, affective, and physical sequelae of mild traumatic brain injury.

Mild traumatic brain injury (MTBI) is associated with cognitive,affective, and physical sequelae. When symptoms persist for more than 3 months, a diagnosis of Post-Concussion Syndrome (PCS) is often given. The current study tracked symptom development to explore the natural sequelae of MTBI. Twenty-six MTBI patients received a comprehensive neuropsychological assessment at three intervals: within 1 week, at 4 months and at 7 months post-concussion. Based on DSMIV criteria and clinical judgment, two external raters diagnosed five MTBI participants with PCS. Results suggested that aspects of cognitive functioning of the symptomatic MTBI (i.e., PCS) participants were different from matched normal control (NC) subjects, and from the 21 MTBI patients who were asymptomatic, at 4 months. Asymptomatic MTBI participants improved in overall level of functioning from 4 to 7 months, but remained significantly different from NC participants in their reduced verbal fluency and working memory functioning.

Affective Symptoms↗

PubMed2000

Influences of secondary injury following traumatic brain injury in developing versus adult rats.

Hypoxia and hypotension are both common findings following traumatic brain injury occurring with a frequency of up to 46% according to data of the Traumatic Coma Data Bank. In the present study the influence of secondary injury on intracranial pressure and the cardiovascular response is investigated in developing rats. Differences from adult rats are determined. Diffuse brain injury was produced in intubated and ventilated 17-20 days old Sprague-Dawley rats (N = 16) using a modification of the Marmarou-model. Hypoxia was induced by reducing O2-concentration to 8% lasting for 15/30 min. Mean arterial blood pressure recordings and intracranial pressure recordings were performed continuously. Animals were divided into two groups, sustaining hypoxia alone (N = 9) and trauma/hypoxia (N = 7). The results were compared to readings in adult animals subjected to hypoxia (N = 5) and trauma/hypoxia (N = 5) (450 gm/150 cm). Immediately following the onset of hypoxia in the developing rat, MABP decreased from 76.5 +/- 13 mm Hg to 35.8 +/- 7 mm Hg. In the adult rat the decrease was more marked (from 93.3 +/- 8 mm Hg to 33.5 +/- 5.7 mm Hg) (p < 0.05). Mortality rate in developing rats with trauma/hypoxia was 43% with no significant change of ICP (from 13 +/- 5.2 to 22.3 +/- 11). All adult animals recovered following trauma/hypoxia with no relevant ICP-increase within one hour post-trauma. Hypoxia induces hypotension in adult and developing rats. However, developing rats appear to be more vulnerable to hypoxia associated with trauma.

Age Factors↗

PubMed2002

Course of functional improvement after stroke, spinal cord injury, and traumatic brain injury.

OBJECTIVE: To examine functional improvement patterns of persons with stroke, traumatic brain injury (TBI), and spinal cord injury (SCI). DESIGN: Statistical analysis of data from a multisite study evaluating rehabilitation outcomes. SETTING: Eight inpatient rehabilitation facilities. PARTICIPANTS: A total of 314 consecutive admissions of persons with stroke, SCI, and TBI who received acute medical rehabilitation between 1994 and 1998. INTERVENTION: Calibration of motor and cognitive items from the FIM instrument, grouping of cases by number of weeks of rehabilitation (length of stay [LOS] groups), and plotting of weekly averages across time. MAIN OUTCOME MEASURES: Weekly motor and cognitive functional status. RESULTS: With the exception of cognitive functioning for persons with SCI, LOS was related to initial functional status, with patients with greater disability having longer LOS (eg, initial motor status for persons with stroke was 48.3 for those with a 2-week stay, 36.8 for a 6-week stay, with the averages between decreasing monotonically). With the exception of cognitive gains for person with TBIs, the amount of functional gain during rehabilitation was essentially the same for all LOS groups (eg, the overall average total motor gain for persons with SCI is 22.3, with no patterns of increase or decrease across LOS groups); however, the rate of improvement in motor (but not cognitive) functioning differed across LOS groups, with patients with shorter stays having the greater rates of improvement (eg, the overall average weekly motor gain for persons with SCI was 3.6, with the averages by LOS group monotonically decreasing from 6.4 for those with 4-week stays to 2.7 for those with 9-week stays). CONCLUSIONS: When examined separately for persons grouped by LOS, functional status improved linearly during the rehabilitation stay, with differences in rate of improvement depending on initial functional status.

Adult↗

PubMed1992

Driving evaluation after traumatic brain injury.

Traumatic closed head injury results in a variety of cognitive and behavioral deficits that may be difficult to assess fully. Adequately evaluating driving safety is a common and important problem for health care professionals. The purpose of this study was to examine the relationship between standardized measures of cognitive function and measures of driving performance in patients with closed head injuries and in their age-matched relative or friend cohorts. Thirteen patients were evaluated. They had each sustained a closed head injury (followed by more than 1 h of coma) 3 to 6 months before testing. Their scores were analyzed along with those of seven cohorts. Assessments of cognitive function and behind-the-wheel driving performance were conducted by examiners blinded to subjects' group membership and medical condition. There was a significant relationship (r = 0.44) between the sum of rated scores of the Tactual Performance Test and Trail Making Test and the global pass/fail ratings of the behind-the-wheel driving test, but it was not related to the driving performance score. The difference between the verbal and performance IQs, and the difference between the block design and other performance tests of the Wechsler Adult Intelligence Scale-Revised were also not significantly related to driving performance. These results suggest that tests of cognitive function alone are not adequate to predict driving performance, and should be used along with standardized driving performance evaluations before recommendations are made.

Adolescent↗

PubMed2005

Cognitive appraisal accuracy moderates the relationship between injury severity and psychosocial outcomes in traumatic brain injury.

OBJECTIVE: Traumatic brain injury (TBI) frequently results in significant changes in physical, cognitive and emotional status. Outcomes after TBI may be related to accurate appraisal of these changes. This study examined the relationship between cognitive appraisal accuracy and psychosocial outcomes in TBI survivors. METHODS: Participants were male and female TBI survivors (n=103) who were at least 6 months post-injury and a family member of each survivor. Appraisal accuracy was assessed using self- and observer-report measures of perceived cognitive difficulties. Family members also completed a measure of psychosocial function. Hierarchical regression techniques were used to determine whether cognitive appraisal accuracy accounted for a significant proportion of variance in psychosocial outcomes. RESULTS: Study findings indicated cognitive appraisal accuracy moderated the relationship between injury severity and aspects of psychosocial function. CONCLUSIONS: The results suggest that brain injury outcomes may be improved when an individual is able to accurately assess limitations.

Adult↗

PubMed2001

Current concepts: diffuse axonal injury-associated traumatic brain injury.

OBJECTIVES: To review the probable physical, physiologic mechanisms that result in the medical and neuropsychologic complications of diffuse axonal injury (DAI)-associated traumatic brain injury (TBI). DATA SOURCES: Various materials were accessed: MEDLINE, textbooks, scientific presentations, and current ongoing research that has been recently reported. STUDY SELECTION: Included were scientific studies involving TBI, particularly direct injury to the axons and glia of the central nervous system (CNS) in both in vitro and in vivo models. These studies include pathologic findings in humans as well as the medical complications and behavioral outcomes of DAI. Studies that addressed animal models of DAI as well as cellular and/or tissue models of neuronal injury were emphasized. The review also covered work on the physical properties of materials involved in the transmission of energy associated with prolonged acceleration-deceleration injuries. DATA EXTRACTION: Studies were selected with regard to those that addressed the mechanism of TBI associated with DAI and direct injury to the axon within the CNS. The material was generally the emphasis of the article and was extracted by multiple observers. Studies that correlate the above findings with the clinical picture of DAI were included. DATA SYNTHESIS: Concepts were developed by the authors based on the current scientific findings and theories of DAI. The synthesis of these concepts involves expertise in physical science, basic science concepts of cellular injury to the CNS, acute medical indicators of DAI, neuropsychologic indicators of DAI, and rehabilitation outcomes from TBI. CONCLUSIONS: The term DAI is a misnomer. It is not a diffuse injury to the whole brain, rather it is predominant in discrete regions of the brain following high-speed, long-duration deceleration injuries. DAI is a consistent feature of TBI from transportation-related injuries as well as some sports injuries. The pathology of DAI in humans is characterized histologically by widespread damage to the axons of the brainstem, parasagittal white matter of the cerebral cortex, corpus callosum, and the gray-white matter junctions of the cerebral cortex. Computed tomography and magnetic resonance imaging scans taken initially after injury are often normal. The deformation of the brain due to plastic flow of the neural structures associated with DAI explains the micropathologic findings, radiologic findings, and medical and neuropsychologic complications from this type of injury mechanism. There is evidence that the types of cellular injury in TBI (DAI, anoxic, contusion, hemorrhagic, perfusion-reperfusion) should be differentiated, as all may involve different receptors and biochemical pathways that impact recovery. These differing mechanisms of cellular injury involving specific biochemical pathways and locations of injury may, in part, explain the lack of success in drug trials to ameliorate TBI.

Animals↗

PubMed2006

The use of state workers' compensation administrative data to identify injury scenarios and quantify costs of work-related traumatic brain injuries.

PROBLEM: Traumatic brain injury (TBI) is a public health problem but little is known about the nature of that problem in the working population. METHOD: The author used a national definition to identify cases in Washington State from workers' compensation (WC) hospital billing data, quantified the cost of WC insurance benefits using actuarial cost estimates, and identified high risk industries using ANSI Z16.2 typology. RESULTS: There were 928 cases of TBI with a lifetime claim cost of $159 million from the Washington State Fund (1994-2001). Sixty percent of injuries resulted in death or disability. The highest risks of TBI are concentrated in 16 industrial insurance risk classes and the highest costs in 19 North American Industry Classification codes. Injury scenarios were identified for nine industrial insurance risk classes. CONCLUSIONS: TBI is a disabling and costly workplace injury in the state of Washington, affecting even teenagers and seniors who are not generally considered to be part of the workforce. Injury typology codes provide useful information for improving workplace safety. IMPACT ON INDUSTRY: This research provides industry with quantitative information regarding the cost of work-related traumatic brain injury and the usefulness of using workers' compensation claims data to reduce the burden of workplace injury.

Adult↗

PubMed2003

Incidence, risk factors, and outcomes of fecal incontinence after acute brain injury: findings from the Traumatic Brain Injury Model Systems national database.

OBJECTIVE: To investigate the incidence, risk factors, and outcome in patients with fecal incontinence after acute brain injury. DESIGN: A retrospective study of the incidence of and risk factors contributing to fecal incontinence, and outcomes at admission to and discharge from inpatient rehabilitation and at 1-year follow-up. SETTING: Medical centers in the federally sponsored Traumatic Brain Injury Model Systems (TBIMS). PARTICIPANTS: A total of 1,013 consecutively enrolled rehabilitation inpatients from 17 TBIMS centers who were admitted to acute care within 24 hours of traumatic brain injury and seen at 1-year postinjury between 1990 and 2000. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Incidence of fecal incontinence, length of coma, length of posttraumatic amnesia (PTA), admission Glasgow Coma Scale (GCS) score, length of stay (LOS), FIM instrument scores, disposition at discharge and follow-up, and incidences of pelvic fracture, frontal contusion, and urinary tract infection (UTI). RESULTS: The incidence of fecal incontinence was 68% at admission to inpatient rehabilitation, 12.4% at rehabilitation discharge, and 5.2% at 1-year follow-up. Analysis of variance and chi-square analyses revealed statistically significant associations between the incidence of fecal incontinence at rehabilitation admission and admission GCS score, length of coma and PTA, LOS, and incidence of UTI and frontal contusion. Fecal incontinence at rehabilitation discharge was significantly associated with several variables, including age, discharge disposition, admission GCS score, length of coma, PTA, LOS, FIM scores, and incidence of pelvic fracture and frontal contusion. Significant associations were also found between fecal incontinence at 1-year follow-up and age, discharge and current 1-year disposition, admission GCS score, length of coma, LOS, FIM scores, and incidence of UTI (P<.05). Although logistic regression analyses were significant (P<.001), and predicted continence with 100% accuracy, demographics, injury characteristics, medical complications, and functional outcomes did not predict incontinence at discharge and at 1-year follow-up. CONCLUSIONS: Fecal incontinence is a significant problem after brain injury. Certain factors may increase its likelihood. Further studies evaluating mechanisms of fecal incontinence and treatment or control interventions would be useful.

Amnesia↗

PubMedDate not supplied

A population-based outcomes study of persons hospitalized with traumatic brain injury: operations of the South Carolina Traumatic Brain Injury Follow-up Registry.

OBJECTIVE: To describe the design and operations of the South Carolina Traumatic Brain Injury (TBI) Follow-up Registry. DESIGN: Statewide prospective cohort study. SETTING: State of South Carolina. PARTICIPANTS: 2118 persons discharged from acute care hospitals after experiencing TBI. INTERVENTION: Telephone interviews. MAIN OUTCOME MEASURES: Service needs, alcohol and drug use, psychosocial health, health-related quality of life, functional status, symptoms of TBI, employment, global life satisfaction, and death. RESULTS: Selected initial and 1-year follow-up findings concerning demographic, insurance status, income, and employment factors. CONCLUSIONS: Population-based outcome studies that describe longer term problems associated with TBI, the need for services, and estimated disability could be useful to inform public policy.

Activities of Daily Living↗

PubMed2000

Evidence that synaptically-released zinc contributes to neuronal injury after traumatic brain injury.

Prior evidence indicates that synaptically-released zinc enters postsynaptic neurons in toxic excess during ischemia and seizures. In addition, prevention of this zinc translocation has been shown to be neuroprotective in both ischemia and seizures. Here we show evidence that the same translocation of zinc from presynaptic boutons into postsynaptic neurons occurs after mechanical injury to the brain. Specifically, using a rat model of traumatic brain injury, we show that trauma is associated with (i) loss of zinc from presynaptic boutons (ii) appearance of zinc in injured neurons, and (iii) neuroprotection by intraventricular administration of a zinc chelator just prior to brain impact. The possible use of zinc chelators for neuroprotection after head trauma is considered.

Aminoquinolines↗

PubMed2002

Secondary injury in traumatic brain injury patients--a prospective study.

OBJECTIVE: Secondary insults of hypotension and hypoxia significantly impact on outcome in patients with traumatic brain injury (TBI). More than 4 hours' delay in evacuation of intracranial haematomas has been demonstrated to have an additional impact on outcome. The objective of this study was to document the incidence of these preventable secondary insults in patients admitted with moderate or severe brain injury. METHODOLOGY: All moderate and severe head injury patients admitted to Groote Schuur Hospital over a 3-month period were studied prospectively. Data were obtained from ambulance dockets, referral letters, patient charts and attending medical staff. Preventable secondary insults (hypotension, hypoxia) and time delay to assessment and surgery were documented. Outcome was assessed using the Glasgow outcome scale (GOS) at discharge or outpatient follow-up. RESULTS: Ninety-six patients were studied. Forty-nine patients experienced at least one recorded preventable event of hypoxia or hypotension. Seventeen had an intracranial haematoma requiring evacuation. The mean time interval between injury and surgery was 455 minutes. No haematoma was evacuated within 4 hours of injury. Patients referred via a primary or secondary care facility experienced a mean additional delay of 70 minutes. These results demonstrated a significant incidence of secondary injury and delay to assessment and surgery. We believe that education and a raised awareness of the impact of secondary insults may have a positive impact on TBI outcome in our referral area.

Adolescent↗

PubMed2004

Functional outcomes following anoxic brain injury: a comparison with traumatic brain injury.

PRIMARY OBJECTIVE: To compare the functional outcomes of patients with anoxic brain injury (ABI) and patients with traumatic brain injury (TBI) following inpatient rehabilitation. RESEARCH DESIGN: Retrospective chart review. METHODS AND PROCEDURES: Data on 68 patients with brain injury (34 with ABI and 34 with TBI) were collected. MAIN OUTCOMES AND RESULTS: The ABI and TBI groups were demographically similar, except that patients with ABI were more likely to be married. Both groups significantly improved their function and were similar upon discharge. For the ABI group, there were trends toward a shorter length of stay, increased total FIM efficiency and decreased cost of stay when compared with the TBI group. The patients with ABI tended to be discharged to a sub-acute rehabilitation facility more than those in the TBI group. CONCLUSIONS: This study is important because it shows that patients with ABI benefit from inpatient rehabilitation and made significant functional gains comparable to the gains of patients with TBI.

Activities of Daily Living↗

PubMed2004

Methodological issues and research recommendations for mild traumatic brain injury: the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury.

The WHO Collaborating Centre for Neurotrauma Task Force on Mild Traumatic Brain Injury performed a comprehensive search and critical review of the literature published between 1980 and 2002 to assemble the best evidence on the epidemiology, diagnosis, prognosis and treatment of mild traumatic brain injury. Of 743 relevant studies, 313 were accepted on scientific merit and comprise our best-evidence synthesis. The current literature on mild traumatic brain injury is of variable quality and we report the most common methodological flaws. We make recommendations for avoiding the shortcomings evident in much of the current literature and identify topic areas in urgent need of further research. This includes the need for large, well-designed studies to support evidence-based guidelines for emergency room triage of children with mild traumatic brain injury and to explore more fully the issue of prognosis after mild traumatic brain injury in the elderly population. We also advocate use of standard criteria for defining mild traumatic brain injury and propose a definition.

Adult↗

PubMed2005

Dose-dependent neuronal injury after traumatic brain injury.

The Fluoro-Jade (FJ) stain reliably identifies degenerating neurons after multiple mechanisms of brain injury. We modified the FJ staining protocol to quickly stain frozen hippocampal rat brain sections and to permit systematic counts of stained, injured neurons at 4 and 24 h after mild, moderate or severe fluid percussion traumatic brain injury (TBI). In adjacent sections, laser capture microdissection was used to collect uninjured (FJ negative) CA3 hippocampal neurons to assess the effect of injury severity on mRNA levels of selected genes. Rats were anesthetized, intubated, mechanically ventilated and randomized to sham, mild (1.2 atm), moderate (2.0 atm) or severe (2.3 atm) TBI. Four or 24 h post-TBI, ten frozen sections (10 microm thick, every 15th section) were collected from the hippocampus of each rat, stained with FJ and counterstained with cresyl violet. Fluoro-Jade-positive neurons were counted in hippocampal subfields CA1, CA3 and the dentate gyrus/dentate hilus. At both 4 and 24 h post-TBI, numbers of FJ-positive neurons in all hippocampal regions increased dose-dependently in mildly and moderately injured rats but were not significantly more numerous after severe injury. Although analysis of variance demonstrated no overall difference in expression of mRNA levels for heat shock protein 70, bcl-2, caspase 3, caspase 9 and interleukin-1beta in uninjured CA3 neurons at all injury levels, post hoc analysis suggested that TBI induces increases in neuroprotective gene expression that offset concomitant increases in deleterious gene expression.

Analysis of Variance↗

PubMed2001

Increased expression of neuronal glucose transporter 3 but not glial glucose transporter 1 following severe diffuse traumatic brain injury in rats.

Traumatic brain injury results in an increased brain energy demand that is associated with profound changes in brain glycolysis and energy metabolism. Increased glycolysis must be met by increasing glucose supply that, in brain, is primarily mediated by two members of the facilitative glucose transporter family, Glut1 and Glut3. Glut1 is expressed in endothelial cells of the blood-brain barrier (BBB) and also in glia, while Glut3 is the primary glucose transporter expressed in neurons. However, few studies have investigated the changes in glucose transporter expression following traumatic brain injury, and in particular, the neuronal and glial glucose transporter responses to injury. This study has therefore focussed on investigating the expression of the glial specific 45-kDa isoform of Glut1 and neuronal specific Glut3 following severe diffuse traumatic brain injury in rats. Following impact-acceleration injury, Glut3 expression was found to increase by at least 300% as early as 4 h after induction of injury and remained elevated for at least 48 h postinjury. The increase in Glut3 expression was clearly evident in both the cerebral cortex and cerebellum. In contrast, expression of the glial specific 45-kDa isoform of Glut1 did not significantly change in either the cerebral cortex or cerebellum following traumatic injury. We conclude that increased glucose uptake after traumatic brain injury is primarily accounted for by increased neuronal Glut 3 glucose transporter expression and that this increased expression after trauma is part of a neuronal stress response that may be involved in increasing neuronal glycolysis and associated energy metabolism to fuel repair processes.

Animals↗

PubMed1995

Enhanced vulnerability to secondary ischemic insults after experimental traumatic brain injury.

Both experimental traumatic brain injury and clinical traumatic brain injury appear to render the brain more vulnerable to a second ischemic insult. The mechanisms of enhanced vulnerability to subsequent ischemia appear to include a reduced ability to increase cerebral blood flow in response to hypotension, hypoxemia, or acute anemia and increased tissue sensitivity to ischemia. Although numerous mediators may be involved in increased tissue sensitivity, those that particularly merit investigation include oxygen free radicals, glutamate, arachidonate metabolites, calcium ions, and protein kinase C.

Animals↗