PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Traumatic Brain Injuries”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources
PubMed2001

Caspase-3 activity is present in cerebrospinal fluid from patients with traumatic brain injury.

Loss of neurons after traumatic brain injury (TBI) might involve dysregulated apoptosis. Activation of caspase-3 is one hallmark of apoptosis. Therefore, caspase-3 activity (cleavage of DEVD-afc) was measured in cerebrospinal fluid (CSF) samples (n=113) from 27 patients with TBI at day 1 to 14 after trauma. Caspase-3 activity was detected in 31 (27.4%) CSF samples with highest values (> 5.5 microM/min) seen at day 2-5 after trauma. No caspase-3 activity was found in serum from patients or CSF from controls. The presence of activated caspase-3 in CSF suggests ongoing apoptotic processes during traumatic brain injury.

Adult↗
PubMed2005

Functional neuroimaging and cognitive rehabilitation for people with traumatic brain injury.

Cognitive deficits are a common consequence of traumatic brain injury. Although such deficits are amenable to rehabilitation, methods for individualizing cognitive interventions are still unrefined. Functional neuroimaging methods such as positron emission tomography and functional magnetic resonance imaging are emerging as possible technologies for measuring and monitoring the cerebral consequences of plasticity associated with brain injury and for evaluating the effectiveness of rehabilitation interventions. Functional neuroimaging may even enable more customized and efficient selection, design, or adaptation of individual cognitive rehabilitation programs. We review the current literature on functional neuroimaging after traumatic brain injury, relating these findings to cognitive rehabilitation. Overall, functional neuroimaging after traumatic brain injury has shown reliable differences in brain activity within several regions of frontal cortex, partly but not uniformly consistent with neuropsychological and structural findings in traumatic brain injury. We also outline a number of promising research opportunities for applying functional neuroimaging in traumatic brain injury settings, along with associated challenges.

Brain Injuries↗
PubMed2001

Primary brain tumors following traumatic brain injury--a population-based cohort study in Sweden.

OBJECTIVES: The aim of this study was to explore the association between traumatic brain injury and brain tumor development. METHODS: A cohort of patients hospitalized for traumatic brain injury during 1965-1994 was compiled using the Swedish Inpatient Register. Complete follow-up through 1995 was attained through record linkage with the Swedish Cancer Register, the Cause of Death Register, and the Emigration Register. Standardized incidence ratios (SIRs), defined as the ratios of the observed to the expected numbers of brain tumors, were used as the measure of relative risk. The expected number of brain tumors was calculated by multiplying the observed person-time by age-, gender- and calendar year-specific incidence-rates derived from the general Swedish population. RESULTS: The cohort included 311,006 patients contributing 3,225,317 person-years. A total of 281 cases of brain tumors were diagnosed during follow-up. No associations were found between traumatic brain injury and the risk of primary brain tumors, neither overall (SIR: 1.0; 95% confidence interval (CI): 0.9-1.2), nor in analyses broken down by main groups of brain tumors. Stratified analyses according to age at entry into the cohort, year of follow-up, and severity of the brain injury all showed essentially the same null results. CONCLUSION: No association between traumatic head injury and primary brain tumors has been found.

Adolescent↗
PubMed2004

Mitochondrial dysfunction contributes to cell death following traumatic brain injury in adult and immature animals.

Secondary injury following traumatic brain injury (TBI) is characterized by a variety of pathophysiologic cascades. Many of these cascades can have significant detrimental effects on cerebral mitochondria. These include exposure of neurons to excitotoxic levels of excitatory neurotransmitters with intracellular calcium influx, generation of reactive oxygen species, and production of peptides that participate in apoptotic cell death. Both experimental and clinical TBI studies have documented mitochondrial dysfunction, and animal studies suggest this dysfunction begins early and may persist for days following injury. Furthermore, interventions targeting mitochondrial mechanisms have shown neuroprotection after TBI. Continued evaluation and understanding of mitochondrial mechanisms contributing to neuronal cell death and survival after TBI is indicated. In addition, important underlying factors, such as brain maturation, that influence mitochondrial function should be studied. The ability to identify, target, and manipulate mitochondrial dysfunction may lead to the development of novel therapies for the treatment of adult and pediatric TBI.

Aging↗
PubMed2006

Neuroprotection by resveratrol against traumatic brain injury in rats.

Oxidative stress after traumatic brain injury may contribute to many of the pathophysiologic changes. Resveratrol, naturally present at high concentration in grape skin, seeds, and red wine, has significant antioxidant properties in a variety of in vitro and in vivo models. In this study, we investigate the effect of resveratrol on oxidative stress after traumatic brain injury in rat model.A total of 54 adult Wistar albino male rats weighing 250-300 g were used. The rats were allocated into three groups. The first group was control (sham-operated) group in which only a craniotomy was performed, the others were trauma and resveratrol groups. A 100 mg/kg single dose of resveratrol, freshly prepared by dissolving in 50% ethanol and diluted in physiological saline (2%), for resveratrol group, and 1 ml ethanol (2%) for trauma group, was administered intraperitoneally immediately after trauma. Weight-drop method was used for achieving head trauma. Then, all groups were separated into three subgroups for biochemical analysis, brain water content and histopathological assessment following trauma. Twenty-four hours after trauma brain water content and malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO), xanthine oxidase (XO) levels of traumatic hemisphere were evaluated. Quantitative histopathological analysis was performed on 14th day postinjury. Trauma caused a significant increase in MDA, XO, NO levels and decrease in GSH level as compared to control group. Resveratrol administration significantly reduced MDA, XO and NO levels, increased GSH level, and also attenuated tissue lesion area. Our results indicate that treatment with resveratrol immediately after traumatic brain injury reduce oxidative stress and lesion volume. Future studies involving different doses and the dose-response relationship could promise better results.

Animals↗
PubMed1991

Effect of associated injuries and blood volume replacement on death, rehabilitation needs, and disability in blunt traumatic brain injury.

OBJECTIVE: To examine the effects of associated injuries on death, disability, rehabilitation needs, and cost in patients with blunt traumatic brain injury. DESIGN: A retrospective case series analysis of 1,709 patients with blunt traumatic brain injury, or 37.2% of 4,590 consecutive blunt trauma patients, was combined with a prospective study of a subset of 202 of the 1,709 brain-injured patients obtained during the same time period with regard to need for rehabilitation services, residual disability, and costs at 1 yr after discharge from the acute trauma center. SETTING: A level I regional trauma center that is also the statewide neurotrauma and multiple trauma unit serving a population of more than 3 million persons. RESULTS: Contingency table analysis showed the Glasgow Coma Scale to be highly predictive (p less than .0001) of likelihood of mortality, need for postacute inpatient rehabilitation, or discharge home. Of the blunt traumatic brain injury patients, 40.4% (691) had an isolated brain injury and 59.6% (1,018) had brain plus at least one other systemic injury. The mortality rate of the isolated brain injury group was 11.1% compared with 21.8% in all brain plus systemic injury groups (p less than .0001). Spine, lung, visceral, pelvis, or extremity injuries in blunt traumatic brain injury all increased mortality rate to greater than 25% (all simultaneously significant, p less than .0001). Analysis of the interaction of brain injury (quantified by Glasgow Coma Scale) with blood replacement in the initial 24 hrs showed that at any Glasgow Coma Scale range, percent mortality increased as the volume of blood increased. Hypovolemic shock increased the mortality rate from 12.8% to 62.1% (p less than .0001). The need for postacute inpatient rehabilitation in survivors also increased as blood replacement increased, and shock increased the percent of patients requiring post-acute inpatient rehabilitation from 39.7% to 60.3%. In 202 consecutive surviving brain trauma patients followed for 1 yr, isolated brain-injured patients with moderate brain injuries had a 4% need for posttrauma, postacute inpatient rehabilitation with a total cost per case of $12,489 compared with the brain plus extremity injury group, who had a 23% postacute inpatient rehabilitation rate and a total cost per case of $36,177 at 1 yr. With severe brain injury, isolated brain injury increased postacute inpatient rehabilitation to 29% and 1-yr cost to $59,274, but with the brain plus extremity injury group, postacute inpatient rehabilitation increased to 49% and cost to $84,950. CONCLUSIONS: In blunt traumatic brain injury, the addition of major visceral or extremity injuries, with need for blood replacement or shock, increases the risk of death, the need for rehabilitation, and the costs of disability.

Baltimore↗
PubMed1997

Cognitive effects of antipsychotic agents in persons with traumatic brain injury.

Over 1 million survivors of traumatic brain injury receive maintenance pharmacotherapy, of which a substantial number receive antipsychotic agents for the treatment of psychoses, agitation and aggression, and other maladaptive behaviours. In spite of the common clinical uses of antipsychotics, the cognitive risks versus benefits are unclear. The purpose of this study was to assess differences in cognitive functioning before, during, and after discontinuation of antipsychotic agents in inpatients undergoing rehabilitation for traumatic brain injury. Neuropsychiatric tests (Reys Auditory-Verbal Learning, Trail Making A&B, Digit Span Forwards and Backward) evaluating cognitive skills of verbal ability, visuomotor speed, memory, learning, attention, and spatial ability were administered to each subject at baseline (immediately prior to tapering or discontinuing antipsychotic), when taper reached 50% of baseline dose, 1 week after antipsychotic discontinuation, and 3 weeks after discontinuation. These data suggest that select areas of cognition improve after antipsychotic discontinuation in subjects with traumatic brain injury. The magnitude of improvement appeared to be greater after discontinuation with thioridazine, a low-potency agent, compared to haloperidol, a high-potency agent. Results, although very preliminary, support the hypothesis of cholinergic involvement in regulating cognitive processes, and this underscores the need for more systematic research in this area.

Adult↗
PubMedDate not supplied

Orally delivered baclofen to control spastic hypertonia in acquired brain injury.

To determine if oral/systemic delivery of baclofen can effectively decrease spastic hypertonia due to acquired brain injury (traumatic brain injury, stroke, anoxia, or encephalopathy). Tertiary care outpatient rehabilitation center directly attached to a university hospital. Patients were a convenience sample recruited consecutively who had been referred for treatment of their spastic hypertonia to our spasticity clinic over a 5-year period. The spastic hypertonia was due to an acquired brain injury by either traumatic brain injury (TBI), stroke, or anoxic brain injury. All patients were more than 6 months postinjury or illness. Retrospective review of patients before and after initiation of treatment with oral baclofen, per standardized clinical data sheets. Thirty-five patients (22 TBI patients) were started on oral baclofen and were reevaluated between 1 to 3 months after initiation of treatment. Data for motor tone (Ashworth scores), spasm scores (Penn spasm frequency score), and deep tendon reflex scores were collected on the affected upper extremity (UE) and lower extremity (LE) side(s). Normal extremities were not assessed. Differences over time were assessed via descriptive statistics and Wilcoxon signed-rank. After 1 to 3 months of treatment when subjects had reached their maximal tolerated dosage, the average LE Ashworth score in the affected lower extremities (LEs) decreased from 3.5 to 3.2 (P =.0003), the reflex score decreased from 2.5 to 2.2 (P =.0274), and there was no statistical difference in the spasm score (P >.05). When the 22 TBI patients are analyzed separately, the average LE Ashworth score decreased from 3.5 to 3.2 (P =.0044) and the reflex score decreased from 2.7 to 2.0 (P =.0003). There was no statistically significant change in UE tone, spasm frequency, or reflexes after 1 to 3 months of treatment (P >.05). The average dosage at follow-up was 57 mg/day of baclofen (range 15-120 mg/day). There was a 17% incidence of somnolence that limited the maximum daily dosage of the medication. The oral delivery of baclofen is capable of reducing LE spastic hypertonia resulting from acquired brain injury. The lack of effect upon the upper extremities may be due to receptor specificity issues. GABA-B receptors may be less involved in the modulation of UE spastic hypertonia.

Administration, Oral↗
PubMed2000

Evidence for cellular damage in normal-appearing white matter correlates with injury severity in patients following traumatic brain injury: A magnetic resonance spectroscopy study.

Neuropsychological studies in patients who have suffered traumatic brain injury show that the eventual clinical outcome is frequently worse than might be predicted from using conventional (CT or T(1)/T(2)-weighted MRI) imaging. Furthermore, patients who have sustained an initial mild or moderate injury may show long-term disability. This implies that there may be abnormalities in areas of the brain that actually appear normal on conventional imaging. Proton magnetic resonance spectroscopy studies have shown that N-acetylaspartate and choline-containing compounds can provide measures of cellular injury. We report MRI and proton magnetic resonance spectroscopy studies of 19 head-injured patients performed once the patients were clinically stable (mean 11 days after injury, range 3-38 days). Proton magnetic resonance spectra were acquired from frontal white matter that on conventional MRI appeared normal. The brain N-acetylaspartate/creatine ratio was reduced [patients (mean +/- standard deviation), 1.28 +/- 0.25; controls, 1.47 +/- 0. 24; P = 0.04] and the choline/creatine ratio was increased (patients, 0.85 +/- 0.18; controls, 0.63 +/- 0.10; P < 0.001) compared with controls. When the severity of the injury was assessed using either the Glasgow coma scale or the length of post-traumatic amnesia, the increase in the choline/creatine ratio was significant even in the mildly injured group (P = 0.008 and P = 0.04, respectively). Furthermore, there was a significant correlation (P = 0.008) between the severity of head injury and the N-acetylaspartate/choline ratio. We conclude that there is an early reduction in N-acetylaspartate and an increase in choline compounds in normal-appearing white matter which correlate with head injury severity, and that this may provide a pathological basis for the long-term neurological disability that is seen in these patients.

Adolescent↗
PubMed2000

Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations.

Traumatic brain injury (TBI) is a public health problem of great concern, because it affects more than 2 million individuals each year. TBI occurs as a result of motor vehicle crashes, falls, and sports-related events. Biomechanical mechanisms occurring at the time of the injury initiate primary and secondary injuries that evolve over several days. In this article the relationship between an blunt injury event and the subsequent damage produced is addressed. Mechanisms of brain injury from biomechanics to cellular pathobiology are presented. Primary and secondary injuries are differentiated, and specific focal and diffuse clinical syndromes are described. Cellular mechanisms responsible for injury are also addressed, because they provide the unifying concepts across the many clinical syndromes so often discussed separately in reviews of traumatic brain injury.

Biomechanical Phenomena↗
PubMed2001

Long-term neuropsychological outcome after traumatic brain injury.

OBJECTIVE: To describe neuropsychological outcome 5 years after injury in persons with traumatic brain injury (TBI) who received inpatient medical rehabilitation. To determine the magnitude and pattern neuropsychological recovery from 1 year to 5 years after injury. DESIGN: Longitudinal cohort study with inclusion based on the availability of neuropsychological data at 1 year and 5 years after injury. SETTING: National Institute on Disability and Rehabilitation Research Traumatic Brain Injury Model Systems of Care. PARTICIPANTS: One hundred eighty-two persons with complicated mild to severe traumatic brain injury. PRIMARY OUTCOME MEASURES: Digits Forward and Backward, Logical Memory I and II, Token Test, Controlled Oral Word Association Test, Symbol Digit Modalities Test, Trail Making Test, Rey Auditory Verbal Learning Test, Visual Form Discrimination, Block Design, Wisconsin Card Sorting Test, and Grooved Pegboard. RESULTS: Significant variability in outcome was found 5 years after TBI, ranging from no measurable impairment to severe impairment on neuropsychological tests. Improvement from 1 year after injury to 5 years was also variable. Using the Reliable Change Index, 22.2% improved, 15.2% declined, and 62.6% were unchanged on test measures. CONCLUSIONS: Neuropsychological recovery after TBI is not uniform across individuals and neuropsychological domains. For a subset of persons with moderate to severe TBI, neuropsychological recovery may continue several years after injury with substantial recovery. For other persons, measurable impairment remains 5 years after injury. Improvement was most apparent on measures of cognitive speed, visuoconstruction, and verbal memory.

Adult↗
PubMed2001

Magnetization transfer imaging and proton MR spectroscopy in the evaluation of axonal injury: correlation with clinical outcome after traumatic brain injury.

BACKGROUND AND PURPOSE: Current imaging does not permit quantification of neural injury after traumatic brain injury (TBI) and therefore limits both the development of new treatments and the appropriate counseling of patients concerning prognosis. We evaluated the utility of magnetization transfer ratio (MTR) and proton MR spectroscopy in identifying patients with neuronal injury after TBI. METHODS: Thirty patients with TBI (21-77 years old; mean age, 42 years; admission Glasgow Coma Scale (GOS) scores 3-15; mean score, 11) were studied on a 1.5-T system with magnetization transfer imaging and MR spectroscopy of the splenium. Magnetization transfer imaging was also performed in the brain stem in all patients, and other areas of the brain were sampled in one patient. The splenium of the corpus callosum and brain stem were studied because these are often affected by diffuse axonal injury. Scans were obtained 2 to 1129 days after injury (median, 41 days). MTR was considered abnormal if it was more than 2 SD below normal. Proton MR spectroscopy was used to calculate the N-acetylaspartate (NAA)/creatine (Cr) ratio. GOS was determined at least 3 months after injury. RESULTS: In 10 patients with a GOS of 1 to 4, the mean NAA/Cr was 1.24 +/- 0.28; two of these patients had abnormal MTR in normal-appearing white matter (NAWM). In 20 patients with a GOS of 5, the mean NAA/Cr was 1.53 +/- 0.37 (P < .05); four of these patients had abnormal MTR in NAWM. MTR abnormalities in NAWM were identified in six patients, but these changes did not correlate with GOS or MR spectroscopy changes. CONCLUSION: MTR and MR spectroscopy can quantify damage after TBI, and NAA levels may be a sensitive indicator of the neuronal damage that results in a worse clinical outcome.

Aspartic Acid↗