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Results for “Traumatic Brain Injuries”

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PubMed2006

[Incomplete protective effects of minocycline on traumatic brain injury in rats and mice].

OBJECTIVE: To evaluate protective effect of minocycline,a semisynthetic tetracycline derivative on different traumatic brain injuries in rats and mice. METHODS: The opened brain trauma was induced in rats and the closed head injury and cold brain injury were induced in mice. In 3 brain trauma models, minocycline (45 mg/kg, ip) was administered twice daily for 2 d before the operation, at 30 min before and 1 h after the operation, and once daily for 2 d following the operation (totally 8 doses in 5 d). After the operation, the behavioral alteration was observed daily, lesion area and survival neuron density were measured at the end of the experiments (14 d after the injuries). RESULT: For rat opened traumatic injury, minocycline promoted the recovery of hindlimb motor activity (inclined board angle), but did not alter other indexes. For mouse closed head traumatic injury, minocycline reduced the neuron loss, but did not improve behavioral dysfunction. For mouse cold injury-induced trauma, minocycline reduced death rate and lesion area, but did not remarkably improve behavior and neuron loss. CONCLUSION: Minocycline only has an incomplete neuroprotective effect on different brain traumatic injuries in rats and mice.

Animals↗

PubMed2006

Magnesium for acute traumatic brain injury.

BACKGROUND: Acute traumatic brain injury is a leading cause of death and disability in young adults. Magnesium had been considered as a potential therapeutic tool because of its activity on NMDA-receptors, calcium channels and neuron membranes. Animals studies have indicated a beneficial effect of magnesium on outcome after brain injury, but its efficacy in humans is unknown. OBJECTIVES: To quantify the effect of magnesium administration on mortality and morbidity in patients with acute traumatic brain injury. SEARCH STRATEGY: We searched the Cochrane Injuries Group's specialised register, Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, National Research Register, Current Controlled Trials, SIGLE, LILACS, Zetoc. The searches were conducted in July 2005. SELECTION CRITERIA: We included all randomized controlled trials comparing any magnesium salt with no magnesium or with placebo, in patients following acute traumatic brain injury. DATA COLLECTION AND ANALYSIS: Two authors independently screened search results and assessed the full texts of potentially relevant studies for inclusion. Data were extracted and methodological quality was examined. MAIN RESULTS: Three studies met the inclusion criteria, one of which is an ongoing study. Two studies were included in the analysis. No data on mortality were available. For Glasgow Outcome Score at six months the pooled WMD = 0.55 (95% CI -0.15 to 1.26), P = 0.12. AUTHORS' CONCLUSIONS: There is currently no evidence to support the use of magnesium salts in patients with acute traumatic brain injury.

Acute Disease↗

PubMed2003

Violent traumatic brain injury: occurrence, patient characteristics, and risk factors from the Traumatic Brain Injury Model Systems project.

OBJECTIVES: To examine the occurrence of and characteristics associated with violent traumatic brain injury (TBI) in the Traumatic Brain Injury Model Systems (TBIMS) project for 4 of the 5 original Model Systems centers and to determine the patient characteristics of this group, as well as the risk factors for sustaining such an injury. DESIGN: Prospective evaluation of individuals with violent TBI over a 10-year period. SETTING: Four TBIMS centers. PARTICIPANTS: A total of 1,229 individuals who received acute hospitalization and inpatient rehabilitation care for TBI. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURE: The occurrence of a violent TBI. RESULTS: Twenty-six percent of the participants in the TBIMS project sustained a violent TBI. This type of injury was more common in African-American men who were single and slightly older than the average TBI patient, were unemployed before injury, and had had a previous TBI. A higher injury rate was noted in the earlier part of the evaluation period. Those who sustained a violent TBI had higher levels of caregiver burden and disability, as well as decreased productivity and community reintegration at rehabilitation discharge and at 1 and 2 years postinjury. CONCLUSIONS: The occurrence of violent TBI in the TBIMS project is consistent with national trends of decreasing incidence of violent injuries in the 1990s. These results present a profile of those who have been injured through violence. The relative risks for sustaining such an injury appear to be well defined when considering demographic and temporal factors.

Adult↗

PubMed2004

Incidence, risk factors and prevention of mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury.

OBJECTIVE: We undertook a best-evidence synthesis on the incidence, risk factors and prevention of mild traumatic brain injury. METHODS: Medline, Cinahl, PsycINFO and Embase were searched for relevant articles. After screening 38,806 abstracts, we critically reviewed 169 studies on incidence, risk and prevention, and accepted 121 (72%). RESULTS: The accepted articles show that 70-90% of all treated brain injuries are mild, and the incidence of hospital-treated patients with mild traumatic brain injury is about 100-300/100,000 population. However, much mild traumatic brain injury is not treated at hospitals, and the true population-based rate is probably above 600/100,000. Mild traumatic brain injury is more common in males and in teenagers and young adults. Falls and motor-vehicle collisions are common causes. CONCLUSION: Strong evidence supports helmet use to prevent mild traumatic brain injury in motorcyclists and bicyclists. The mild traumatic brain injury literature is of varying quality, and the studies are very heterogeneous. Nevertheless, there is evidence that mild traumatic brain injury is an important public health problem, but we need more high-quality research into this area.

Adolescent↗

PubMed2004

Diagnostic procedures in mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury.

We examined diagnostic procedures in mild traumatic brain injury by a systematic literature search. After screening 38,806 abstracts, we critically reviewed 228 diagnostic studies and accepted 73 (32%). The estimated prevalence of intracranial CT scan abnormalities is 5% in patients presenting to hospital with a Glasgow Coma Scale score of 15 and 30% or higher in patients presenting with a score of 13. About 1% of all treated patients with mild traumatic brain injury require neurosurgical intervention. There is strong evidence that clinical factors can predict computerized tomography scan abnormalities and the need for intervention in adults, but no such evidence for mild traumatic brain injury in children. We found evidence that skull fracture is a risk factor for intracranial lesions, but the diagnostic accuracy of radiologically diagnosed skull fracture as an indication of intracranial lesions is poor. There is only a little evidence for the diagnostic validity of cognitive testing and other diagnostic tools for mild traumatic brain injury.

Adolescent↗

PubMed2005

Delayed inhibition of Nogo-A does not alter injury-induced axonal sprouting but enhances recovery of cognitive function following experimental traumatic brain injury in rats.

Traumatic brain injury causes long-term neurological motor and cognitive deficits, often with limited recovery. The inability of CNS axons to regenerate following traumatic brain injury may be due, in part, to inhibitory molecules associated with myelin. One of these myelin-associated proteins, Nogo-A, inhibits neurite outgrowth in vitro, and inhibition of Nogo-A in vivo enhances axonal outgrowth and sprouting and improves outcome following experimental CNS insults. However, the involvement of Nogo-A in the neurobehavioral deficits observed in experimental traumatic brain injury remains unknown and was evaluated in the present study using the 11C7 monoclonal antibody against Nogo-A. Anesthetized, male Sprague-Dawley rats were subjected to either lateral fluid percussion brain injury of moderate severity (2.5-2.6 atm) or sham injury. Beginning 24 h post-injury, monoclonal antibody 11C7 (n=17 injured, n=6 shams included) or control Ab (IgG) (n=16 injured, n=5 shams included) was infused at a rate of 5 microl/h over 14 days into the ipsilateral ventricle using osmotic minipumps connected to an implanted cannula. Rats were assessed up to 4 weeks post-injury using tests for neurological motor function (composite neuroscore, and sensorimotor test of adhesive paper removal) and, at 4 weeks, cognition was assessed using the Morris water maze. Hippocampal CA3 pyramidal neuron damage and corticospinal tract sprouting, using an anterograde tracer (biotinylated dextran amine), were also evaluated. Brain injury significantly increased sprouting from the uninjured corticospinal tract but treatment with monoclonal antibody 11C7 did not further increase the extent of sprouting nor did it alter the extent of CA3 cell damage. Animals treated with 11C7 showed no improvement in neurologic motor deficits but did show significantly improved cognitive function at 4 weeks post-injury when compared with brain-injured, IgG-treated animals. To our knowledge, the present findings are the first to suggest that (1) traumatic brain injury induces axonal sprouting in the corticospinal tract and this sprouting may be independent of myelin-associated inhibitory factors and (2) that post-traumatic inhibition of Nogo-A may promote cognitive recovery unrelated to sprouting in the corticospinal tract or neuroprotective effects on hippocampal cell loss following experimental traumatic brain injury.

Analysis of Variance↗

PubMed2005

Restoration of cerebral vasoreactivity by an L-type calcium channel blocker following fluid percussion brain injury.

Traumatic brain injury (TBI) results in significant acute reductions in regional cerebral blood flow (rCBF). However, the mechanisms by which TBI impairs CBF and cerebral vascular reactivity have remained elusive. In the present study, the effect of verapamil, an L-type calcium (Ca(2+)) channel blocker, on post-traumatic vascular reactivity was evaluated following a lateral fluid percussion injury (FPI) in rats. rCBF was measured by [(14)C]-iodoantipyrine autoradiography 1 h after FPI. Following FPI, significant rCBF reductions were documented in all examined cortical areas. These reductions were the most prominent (72.0%) at the primary injury site. Intravenous infusion of verapamil (VE; 200 microg/kg/min), and norepinephrine (NE; 20 microg/mL/min) to maintain normal blood pressure, increased rCBF by 141.5% at the primary injury site when compared to untreated, FPinjured animals. Under stimulated conditions, both the ipsilateral and contralateral hemispheres failed to show any increases in rCBF at 1 h following FPI. In direct contrast, following VE+NE treatment all cortical areas measured showed near normal vascular reactivity to direct cortical stimulation (normal reactivity = 45% increase in rCBF vs. 47% increase in FPI+VE+NE cases). These findings suggest that the majority of post-traumatic hemodynamic depressions are closely related to mechanisms involving vasoconstriction. Furthermore, Ca(2+) may play a causative role in this vasoconstriction and the loss of vasoreactivity.

Animals↗

PubMed2003

Deleterious poly(ADP-ribose)polymerase-1 pathway activation in traumatic brain injury in rat.

Traumatic brain injury produces nitric oxide and reactive oxygen species. Peroxynitrite, resulting from the combination of nitric oxide and superoxide anions, triggers DNA strand breaks, leading to the activation of poly(ADP-ribose)polymerase-1. As excessive activation of this enzyme induces cell death, we examined the production of nitrosative stress, the activation of poly(ADP-ribose)polymerase-1, and the role of this enzyme in the outcomes of traumatic brain injury produced by fluid percussion in rats. Immunohistochemistry showed that 3-nitrotyrosine, an indicator of nitrosative stress, and poly(ADP-ribose), a marker of poly(ADP-ribose)polymerase-1 activation, were present as early as 30 min post-injury, and that persisted for 72 h. The poly(ADP-ribose)polymerase inhibitor, 3-aminobenzamide, at 10 and 30 mg/kg, significantly improved the neurological deficit, with a 60% reduction in the brain lesion volume and inhibition of poly(ADP-ribose)polymerase-1 activation. Thus, poly(ADP-ribose)polymerase-1 is involved in the neurological consequences of traumatic brain injury and may be a promising therapeutic target in clinical treatment of acute brain trauma.

Animals↗

PubMed2004

Prognosis for mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury.

We searched the literature on the epidemiology, diagnosis, prognosis, treatment and costs of mild traumatic brain injury. Of 428 studies related to prognosis after mild traumatic brain injury, 120 (28%) were accepted after critical review. These comprise our best-evidence synthesis on prognosis after mild traumatic brain injury. There was consistent and methodologically sound evidence that children's prognosis after mild traumatic brain injury is good, with quick resolution of symptoms and little evidence of residual cognitive, behavioural or academic deficits. For adults, cognitive deficits and symptoms are common in the acute stage, and the majority of studies report recovery for most within 3-12 months. Where symptoms persist, compensation/litigation is a factor, but there is little consistent evidence for other predictors. The literature on this area is of varying quality and causal inferences are often mistakenly drawn from cross-sectional studies.

Adult↗

PubMed2004

Alzheimer's pathology in human temporal cortex surgically excised after severe brain injury.

Traumatic brain injury (TBI) is a risk factor for the development of Alzheimer's disease (AD). This immunohistochemical study determined the extent of AD-related changes in temporal cortex resected from individuals treated surgically for severe TBI. Antisera generated against Abeta species (total Abeta, Abeta(1-42), and Abeta(1-40)), the C-terminal of the Abeta precursor protein (APP), apolipoprotein E (apoE), and markers of neuron structure and degeneration (tau, ubiquitin, alpha-, beta-, and gamma-synuclein) were used to examine the extent of Abeta plaque deposition and neurodegenerative changes in 18 TBI subjects (ages 18-64 years). Diffuse cortical Abeta deposits were observed in one third of subjects (aged 35-62 years) as early as 2 h after injury, with only one (35-year old) individual exhibiting "mature", dense-cored plaques. Plaque-like deposits, neurons, glia, and axonal changes were also immunostained with APP and apoE antibodies. In plaque-positive cases, the only statistically significant change in cellular immunostaining was increased neuronal APP (P = 0.013). There was no significant correlation between the distribution of Abeta plaques and markers of neuronal degeneration. Diffuse tau immunostaining was localized to neuronal cell soma, axons or glial cells in a larger subset of individuals. Tau-positive, neurofibrillary tangle (NFT)-like changes were detected in only two subjects, both of more advanced age and who were without Abeta deposits. Other neurodegenerative changes, evidenced by ubiquitin- and synuclein-immunoreactive neurons, were abundant in the majority of cases. Our results demonstrate a differential distribution and course of intra- and extra-cellular AD-like changes during the acute phase following severe TBI in humans. Abeta plaques and early evidence of neuronal degenerative changes can develop rapidly after TBI, while fully developed NFTs most likely result from more chronic disease- or injury-related processes. These observations lend further support to the hypothesis that head trauma significantly increases the risk of developing pathological and clinical symptoms of AD, and provide insight into the molecular mechanisms that initiate these pathological cascades very early during severe brain injury.

Adolescent↗

PubMed2001

An endogenous cannabinoid (2-AG) is neuroprotective after brain injury.

Traumatic brain injury triggers the accumulation of harmful mediators that may lead to secondary damage. Protective mechanisms to attenuate damage are also set in motion. 2-Arachidonoyl glycerol (2-AG) is an endogenous cannabinoid, identified both in the periphery and in the brain, but its physiological roles have been only partially clarified. Here we show that, after injury to the mouse brain, 2-AG may have a neuroprotective role in which the cannabinoid system is involved. After closed head injury (CHI) in mice, the level of endogenous 2-AG was significantly elevated. We administered synthetic 2-AG to mice after CHI and found significant reduction of brain oedema, better clinical recovery, reduced infarct volume and reduced hippocampal cell death compared with controls. When 2-AG was administered together with additional inactive 2-acyl-glycerols that are normally present in the brain, functional recovery was significantly enhanced. The beneficial effect of 2-AG was dose-dependently attenuated by SR-141761A, an antagonist of the CB1 cannabinoid receptor.

Animals↗

PubMed2000

Lactate/glucose dynamics after rat fluid percussion brain injury.

Traumatic brain injury (TBI) places enormous early energy demand on brain tissue to reinstate normal ionic balance. Clinical studies have demonstrated a decline in extracellular fluid (ECF) glucose and an increase in lactate after TBI. In vitro studies suggest that this increase in lactate is mediated by increased glutamate and may provide a metabolic substrate for neurons, to aid in ionic restoration. This led us to hypothesize that high ECF lactate may be beneficial in recovery following TBI, where major ionic flux has been shown to occur. In this study, we measured cerebral dialysate lactate and glucose, and arterial lactate and glucose, before and after rat lateral fluid percussion brain injury (FPI; 2.06 +/- 0.13 atm) with and without IV lactate infusion (100 mM X 0.65 mL/h X 5 h) to test the hypothesis that arterial lactate can influence ECF lactate. Dialysate lactate increased within 10 min following FPI, with higher values in the lactate infusion group. Following FPI, the dialysate lactate increase was 238% with lactate infusion versus 171% increase with saline infusion. Dialysate glucose fell immediately following FPI, with a more severe decline in the saline group. The glucose decrease was 231% greater in the IV saline group. Furthermore, in the lactate infusion group, the dialysate glucose levels recovered to baseline levels by 4 h after injury, whereas they remained depressed through out the experiment, in the saline infusion group. We conclude that arterial lactate augmentation can increase brain dialysate lactate, and result in more rapid recovery of dialysate glucose after FPI. This may indicate a beneficial role for lactate, that may be potentially useful in the clinical situation, after TBI.

Animals↗

PubMedDate not supplied

Preventing secondary brain injuries.

Traumatic brain injury is a leading cause of death from injury in the United States. This article reviews nursing interventions to prevent and minimize secondary brain injuries and improve patient outcomes.

Brain Injuries↗

PubMed2004

Vitamin E reduces amyloidosis and improves cognitive function in Tg2576 mice following repetitive concussive brain injury.

Traumatic brain injury is a well-recognized environmental risk factor for developing Alzheimer's disease. Repetitive concussive brain injury (RCBI) exacerbates brain lipid peroxidation, accelerates amyloid (Abeta) formation and deposition, as well as cognitive impairments in Tg2576 mice. This study evaluated the effects of vitamin E on these four parameters in Tg2576 mice following RCBI. Eleven-month-old mice were randomized to receive either regular chow or chow-supplemented with vitamin E for 4 weeks, and subjected to RCBI (two injuries, 24 h apart) using a modified controlled cortical impact model of closed head injury. The same dietary regimens were maintained up to 8 weeks post-injury, when the animals were killed for biochemical and immunohistochemical analyses after behavioral evaluation. Vitamin E-treated animals showed a significant increase in brain vitamin E levels and a significant decrease in brain lipid peroxidation levels. After RBCI, compared with the group on regular chow, animals receiving vitamin E did not show the increase in Abeta peptides, and had a significant attenuation of learning deficits. This study suggests that the exacerbation of brain oxidative stress following RCBI plays a mechanistic role in accelerating Alphabeta accumulation and behavioral impairments in the Tg2576 mice.

Amyloid↗

PubMed1998

What happens after brain injury?

Traumatic brain injury is one of the leading causes of injury and death among the young in the United States. Severity can range from the brief confusion of a football player who has had his "bell rung" to the complete loss of voluntary behavior seen in the vegetative state. In this article, Dr Goldberg reviews the rehabilitation process used to restore the fullest function possible within the limits of the patient's injury, with emphasis on innovative assessment and treatment techniques. He also describes an approach to evaluation of minimally conscious patients that can be used to detect and confirm the presence of active cognition.

Brain Concussion↗

PubMed1992

Preventing secondary brain injury.

Traumatic brain injury affects approximately 500,000 persons each year. For those patients who survive until they reach the hospital, the major goal of the health care team is to prevent secondary injuries or insults that may follow the initial event and worsen the brain injury. Factors that can cause secondary insults to the brain include hypoxia, hypercapnia, hypotension, and intracranial hypertension. Prevention of these factors begins in the pre-hospital care phase and continues into the critical care unit. Early recognition of these factors and prompt intervention can improve the neurologic outcome of the patient with severe head injury. An understanding of the causes and effects of these secondary insults is critical to the appropriate medical and nursing management of these patients.

Brain Injuries↗

PubMed1995

Spatial memory deficits, increased phosphorylation of the transcription factor CREB, and induction of the AP-1 complex following experimental brain injury.

Traumatic brain injury causes both short- and long-term neurological impairments. A cascade of biochemical changes triggered by the injury may increase the expression of several genes, which has been hypothesized to contribute to the observed cognitive deficits. The mechanism(s) of induction for these genes is not yet known. We present evidence that lateral cortical impact injury in rats that produces spatial memory deficits also increases phosphorylation of the transcription factor CREB (cAMP response element binding). Subsequent to the phosphorylation of CREB, c-Fos expression and the AP-1 complex are enhanced. The temporal and spatial activation of c-Fos is consistent with it being induced by phosphorylated CREB proteins. Thus, CREB-mediated gene activation may contribute to the observed behavioral deficits. Further elucidation of the biochemical and pathophysiological changes will be of importance for clinical therapy.

Animals↗

PubMed1996

Verbal learning subtypes in traumatic brain injury: a replication.

Traumatic brain injury (TBI) has been associated with memory impairments, but the severity and qualitative aspects of such impairment do not appear homogeneous across patients. This study sought to replicate an earlier investigation that found distinct verbal learning subtypes in TBI using the California Verbal Learning Test (CVLT). CVLT data from 88 acute rehabilitation inpatients with mild, moderate, and severe traumatic brain injuries were analyzed with multiple cluster analytic techniques. Cluster analyses yielded five learning subtypes, three of which appeared similar to the subtypes previously identified as Active, Disorganized, and Passive subtypes, and two that appeared similar to the Deficient subgroup. Traumatic brain injury appears to be characterized by heterogeneous, but fairly reliable, verbal learning subtypes that can be detected early postinjury.

Adolescent↗