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 379 records · Page 21Linked to original sources
PubMed1999

Does the face protect the brain? A case-control study of traumatic brain injury and facial fractures.

BACKGROUND: The relationship between facial fractures and traumatic brain injury is controversial. Some studies show an increased risk of brain injury with the presence of facial fractures while others claim that facial fractures protect against brain injury. OBJECTIVE: To examine the association between facial fractures and traumatic brain injuries. DESIGN: Case-control study. SETTING: Subjects were recruited from the emergency departments of 7 hospitals in the Seattle, Wash, area. PATIENTS: Three thousand eight hundred forty-nine injured bicyclists and 5 scene deaths were identified from March 1, 1992, to August 31, 1994, with complete data available on 3388 bicyclists. INTERVENTIONS: None. RESULTS: The study group was composed of 1602 cases with injuries to the head, face, or brain and 1540 control subjects. There were 203 bicyclists with traumatic brain injuries, of whom 62 had an identifiable intracranial injury and 141 suffered a concussion. A total of 81 patients sustained facial fractures. The odds ratio for the risk of intracranial injury associated with facial fractures after adjustment for significant confounders was 9.9 (95% confidence interval, 5.1-19.3). The effect was less strong but still present when all traumatic brain injuries including concussions were considered (odds ratio, 2; 95% confidence interval, 1.1-3.7). No association was found for concussion only. CONCLUSIONS: This study demonstrates no evidence that facial fractures help prevent traumatic brain injury. Data indicate that facial fractures are markers for increased risk of brain injury.

Adolescent↗
PubMed2001

Activation of cyclo-oxygenase-2 contributes to motor and cognitive dysfunction following diffuse traumatic brain injury in rats.

1. Post-traumatic inflammation may play a significant role in the development of delayed secondary brain damage following traumatic brain injury. 2. During post-traumatic inflammation, metabolic products of arachidonic acid, known as prostanoids (prostaglandins and thromboxanes) are released and aggravate the injury process. Prostanoid synthesis is regulated by the enzyme cyclo-oxygenase (COX), which is present in at least two isoforms, COX-1 (the constitutive form) and COX-2 (the inducible form). 3. In the present study, we examine the temporal and spatial profiles of COX-2 expression and the effects of the COX-2 inhibitor nimesulide on motor and cognitive outcome following diffuse traumatic brain injury in rats. 4. Adult male Sprague-Dawley rats were injured using the 2 m impact acceleration model of diffuse traumatic brain injury. At preselected time points after injury, animals were killed and the expression of COX-2 was measured in the cortex and hippocampus by western blotting techniques. 5. Increased expression of COX-2 was found in the cortex at 3 days and in the hippocampus as early as 3 h postinjury and this persisted for at least 12 days. 6. Administration of nimesulide (6 mg/kg, i.p.) at 30 min after injury and daily over a 10 day post-traumatic neurological assessment period resulted in a significant improvement compared with vehicle (2% dimethylsulphoxide diluted in isotonic saline)-treated controls in cognitive deficits, as assessed by the Barnes circular maze. There was also a significant improvement in motor dysfunction as assessed by the rotarod test on days 1 and 2 post-trauma compared with vehicle-treated controls. 7. These results implicate the involvement of COX-2 in cognitive and motor dysfunction following diffuse traumatic brain injury.

Animals↗
PubMed2006

Modified experimental mild traumatic brain injury model.

BACKGROUND: Experimental models of traumatic brain injury (TBI), using a variety of techniques and species, have been devised with the aim of producing repeatable lesions resembling those found in head injuries. There are various TBI models mentioned in the literature. In experimental head trauma models, emphasis has been placed on the severe head injuries. There are only a few models developed to study mild traumatic brain injury (MTBI). In fact, MTBI is as important a problem as severe head injuries for neurosurgeons. METHODS: Fifty-six male Sprague-Dawley rats were subjected to MTBI with a weight-drop device, which was described by Marmarou et al. The said model was used in its original form as well as in modified forms by employing different weights dropped from the same height. Animals were divided into four groups of 14 rats as follows: Group I (n=14), head injury was induced using 450 g-1 m weight-height impact; Group II (n=14), head injury was induced using 350 g-l m weight-height impact; Group III (n=14), head injury was induced using 300 g-1 m weight-height impact; Group IV (n=14), control group, no injury was applied. Animals were evaluated neurologically, physiologically, electrophysiologically, and histopathologically. RESULTS: Group I and II animals (450 and 350 g-1m weight-height impact, respectively) showed the symptoms of severe head injury, whereas Group III animals (300 g-l m) showed more MTBI symptoms. CONCLUSION: We recommend the application of the modified MTBI model used for group III (300 g-l m weight-height impact) as the most appropriate and the simplest model for future MTBI studies.

Animals↗
PubMed2004

Language and memory profiles of adolescents with traumatic brain injury.

The performance of adolescents who suffered a traumatic brain injury in childhood, on language comprehension tasks with varying working memory demands, was examined. It was hypothesized that adolescents with a traumatic brain injury would perform more poorly than their non-injured peers, particularly on those tasks with high working memory demands. A case study design allowed for both group and intra-participant comparisons. A battery of language comprehension and working memory tasks was administered to six adolescents aged 12-16 years. Their performance was compared with six individually age-matched peers with typical development and to the normative data of the standardized tests. Intra-participant performance was examined by comparing results across language tasks that varied in working memory demands. Analysis revealed that individuals with traumatic brain injury performed poorly compared with their age-matched peers. However, the pattern of listening comprehension impairment differed across individuals and marked variability within the comprehension profiles for some individuals with traumatic brain injury was evident. Language comprehension tasks with high working memory demands generally posed the most difficulty for individuals with traumatic brain injury.

Adolescent↗
PubMed2003

Alterations of intestinal mucosa structure and barrier function following traumatic brain injury in rats.

AIM: Gastrointestinal dysfunction is a common complication in patients with traumatic brain injury (TBI). However, the effect of traumatic brain injury on intestinal mucosa has not been studied previously. The aim of the current study was to explore the alterations of intestinal mucosa morphology and barrier function, and to determine how rapidly the impairment of gut barrier function occurs and how long it persists following traumatic brain injury. METHODS: Male Wistar rats were randomly divided into six groups (6 rats each group) including controls without brain injury and traumatic brain injury groups at hours 3, 12, 24, and 72, and on day 7. The intestinal mucosa structure was detected by histopathological examination and electron microscopy. Gut barrier dysfunction was evaluated by detecting serum endotoxin and intestinal permeability. The level of serum endotoxin and intestinal permeability was measured by using chromogenic limulus amebocyte lysate and lactulose/mannitol (L/M) ratio, respectively. RESULTS: After traumatic brain injury, the histopathological alterations of gut mucosa occurred rapidly as early as 3 hours and progressed to a serious state, including shedding of epithelial cells, fracture of villi, focal ulcer, fusion of adjacent villi, dilation of central chyle duct, mucosal atrophy, and vascular dilation, congestion and edema in the villous interstitium and lamina propria. Apoptosis of epithelial cells, fracture and sparseness of microvilli, loss of tight junction between enterocytes, damage of mitochondria and endoplasm, were found by electron microscopy. The villous height, crypt depth and surface area in jejunum decreased progressively with the time of brain injury. As compared with that of control group (183.7 +/- 41.8 EU/L), serum endotoxin level was significantly increased at 3, 12, and 24 hours following TBI (434.8 +/- 54.9 EU/L, 324.2 +/- 61.7 EU/L and 303.3 +/- 60.2 EU/L, respectively), and peaked at 72 hours (560.5 +/- 76.2 EU/L), then declined on day 7 (306.7 +/- 62.4 EU/L, P<0.01). Two peaks of serum endotoxin level were found at hours 3 and 72 following TBI. L/M ratio was also significantly higher in TBI groups than that in control group (control, 0.0172 +/- 0.0009; 12 h, 0.0303 +/- 0.0013; 24 h, 0.0354 +/- 0.0025; 72 h, 0.0736 +/- 0.0105; 7 d, 0.0588 +/- 0.0083; P<0.01). CONCLUSION: Traumatic brain injury can induce significant damages of gut structure and impairment of barrier function which occur rapidly as early as 3 hours following brain injury and lasts for more than 7 days with marked mucosal atrophy.

Animals↗
PubMed1999

Rate of psychiatric illness 1 year after traumatic brain injury.

OBJECTIVE: Neurobehavioral symptoms are not uncommon after a traumatic brain injury. However, psychiatric syndromes per se have rarely been studied in patients with such an injury. The purpose of this study was to evaluate the type and extent of psychiatric syndromes in patients with traumatic brain injury. METHOD: One hundred ninety-six hospitalized adults were studied 1 year after a traumatic brain injury with the use of a two-stage psychiatric diagnostic procedure. Psychiatric diagnoses were made according to ICD-10 criteria on the basis of data from the Schedules for Clinical Assessment in Neuropsychiatry interview. RESULTS: Of 164 patients interviewed, 30 (18.3%) had an ICD-10 diagnosis of a psychiatric illness. Among the 120 patients who were 18-64 years old, 21.7% had a psychiatric illness, compared with 16.4% in a study of the general population. A depressive illness was present in 13.9% of the traumatic brain injury patients, compared with 2.1% of the general population, and panic disorder was present in 9.0%, compared with 0.8% of the general population. CONCLUSIONS: In comparison with the general population, a higher proportion of adult patients had developed psychiatric illnesses 1 year after a traumatic brain injury; the rates of depressive episode and panic disorder were significantly higher in the study group. A history of psychiatric illness, an unfavorable global outcome according to the Glasgow Outcome Scale, a lower score on the Mini-Mental State examination, and fewer years of formal education seemed to be important risk factors in the development of a psychiatric illness. Compensation claims, however, were not associated with the rate of psychiatric illness.

Adolescent↗
PubMed2002

Working memory after traumatic brain injury in children.

To investigate the effects of traumatic brain injury on working memory in children, we administered semantic (letter identity) and phonological (letter rhyme) N-back tasks to children who were on average 5 years post-mild (n = 54) or -severe (n = 26) traumatic brain injury and 44 typically developing children who were comparable in age. The correct detection of targets and false alarms were measured for each task. Memory load (which varied from 0 to 3 letters back) and age significantly affected the detection of targets and false alarms in both tasks. The severity of traumatic brain injury affected the correct detection of letters on the identity task and false alarms on the rhyme task. Traumatic brain injury severity also interacted with memory load in its effect on false alarms on the rhyme task. Traumatic brain injury results in impaired working memory and diminished inhibition in children. The N-back working memory task is feasible for administration to brain-injured children and potentially could be useful for studying brain activation associated with working memory and effects of drug therapy in this group of patients.

Adolescent↗
PubMed2006

[The undetected brain lesion in sports. Minor traumatic brain injury and its sequelae].

The minor traumatic brain injury (mTBI) in sports is often looked at as a bagatelle. The treating physician underestimates the severity of the injury suspecting that a mTBI is a nonstructural lesion with an overall excellent prognosis in the majority of the cases. This paper shows that the minor traumatic brain injury may be a structural brain lesion with potentially life-threatening dangers. The therapy should follow exactly defined guidelines, e.g., stepwise protocol of the Concussion in Sports (CIS-) Group. Return to sports activities should happen only when all physical but also cognitive symptoms have subsided. All mTBIs that have been sustained prior to the actual injury have to be recorded properly because repeated mTBIs may cause chronic degenerative brain damage. Neuropsychological testing will aid in the correct diagnosis of a mTBI and is a useful parameter in the course of the injury. In the future biochemical markers may serve as indicators of the severity of the brain injury and may also aid in predicting the outcome after TBI. Today biochemical markers do not serve as a substitute for neuroimaging.

Adolescent↗
PubMed1999

Experimental animal models of traumatic brain injury: medical and biomechanical mechanism.

The numerous traumatic brain injury models were designed to study the nature of the human brain injury. The properties of six experimental injury models were reviewed in this article. Weight-drop models with or without skull protection were compared in terms of experimental setup, possible error source, and biomechanical prospect. The modified percussion models with or without rigid cortical impact were contrasted with regard to reliability, histopathological production, and deformation. The focal contusion model by mechanical suction force represented isolated cortical injury without compression brain injury. As a class of traumatic brain injury, brain retraction damage was reviewed in this article.

Journal Article↗
PubMed2001

Management of mild traumatic brain injury: lack of consensus in Europe.

Mild traumatic brain injury (MTBI) accounts for most traumatic brain injuries and is an important cause of morbidity. Recent studies in various European countries have shown that no consensus exists about management of patients with MTBI. This study describes the management of MTBI patients in various European hospitals. A short questionnaire covering the areas of interest was sent to several EFNS members in European countries. The results of the inquiry show that there is, at present, no consensus about criteria for, or management of MTBI in European hospitals.

Brain Injuries↗
PubMed2025

Exploring potential targets and molecular mechanisms of traumatic brain injury exacerbated by Benzo(a)pyrene via network toxicology and&#xa0;molecular&#xa0;dynamics simulation.

Benzo(a)pyrene (BaP) is a common environmental pollutant from combustion sources that promotes oxidative stress, neuroinflammation and disruption of blood-brain barrier (BBB). However, its contribution to worsening traumatic brain injury (TBI) remains unclear. In this study, we aimed to assess the contribution of BaP to secondary injury in TBI. By integrating data from e.g., the Comparative Toxicogenomics Database, GeneCards, and Online Mendelian Inheritance in Man, 121 overlapping core targets were identified between BaP and TBI. Enrichment analyses via Gene Ontology and Kyoto Encyclopedia of Genes and Genomes, combined with protein-protein interaction networks and topological algorithms (degree, closeness centrality, betweenness centrality, average shortest path length, topological coefficient and partner of multi-edged node pairs), highlighted five hub genes (TP53, EGFR, AKT1, ACTB, and TNF) implicated in mitogen-activated protein kinase signaling, oxidative stress, and neuroinflammation. Molecular docking showed strong binding affinities of BaP to these hub proteins, with energies from -9.3 to -12.1&#xa0;kcal/mol, tighter than co-crystal ligands and existing protein-binding drugs. Molecular dynamics simulations confirmed interaction stability through low root-mean-square deviation (<&#x2009;0.5&#xa0;nm), fluctuation, and radius of gyration values. Calculation of binding free energies using MM-PBSA validated the strong binding affinity between BaP and binding pockets of each hub genes. Toxicity prediction analysis revealed an oral LD50 of 316&#xa0;mg/kg for BaP, with high probabilities for neurotoxicity, BBB permeability, carcinogenicity, and mutagenicity, associated with aryl hydrocarbon receptor activation. These findings reveal a "neurovascular homeostasis disruption" network underlying BaP-exacerbated TBI pathology and highlight potential targets to reduce pollution-related risks in TBI management.

Benzo(a)pyrene↗
PubMed1995

Effects of ethanol on respiratory function in traumatic brain injury.

It has been observed that traumatic brain injury (TBI) increases the susceptibility of the brain to subsequent hypoxia, and prolonged apnea occurs in ethanol (EtOH)-treated animals following brain injury. This investigation tests the hypothesis that EtOH suppresses ventilation and hypercapnic respiratory drive following TBI. Immature pigs were anesthetized with halothane and received a 2 to 3 atm fluid-percussion brain injury. Respiratory parameters, including tidal volume, frequency, ventilation (VE), and arterial blood gases were measured on 100% O2 and on 5% to 6% inspired CO2 in O2 prior to and at 10, 60, 120, and 180 minutes after TBI. Hypercapnic response sensitivity (S) was measured as the change in VE per mm Hg increase in PaCO2. Intracranial pressure, mean arterial blood pressure, heart rate, brain temperature, glucose, and EtOH levels were also monitored. Three groups were studied: the first group of six received EtOH (3.5 gm/kg, intragastrically) without brain injury; the second group of six received TBI without EtOH; the third group of eight received EtOH and TBI. Ethanol levels were 121 +/- 13 (standard error of the mean) mg/dl in the EtOH/TBI group (136 +/- 25 in the EtOH group) at the time of injury, and 175 +/- 12 mg/dl in the EtOH/TBI group (200 +/- 20 mg/dl in the EtOH group) at 120 minutes after injury. The EtOH/TBI animals had significantly lower VE and S, and higher PaCO2 following brain injury (p < 0.05, repeated-measures analysis of variance). No significant differences were identified between groups for pH, PaCO2, intracranial pressure, heart rate, brain temperature, or glucose levels. Ethanol intoxication leads to significant impairment of respiratory control following traumatic brain injury and may contribute to brain injury in intoxicated trauma victims.

Alcoholic Intoxication↗
PubMed2004

Biochemical markers of brain injury: could they be used as diagnostic adjuncts in cases of inflicted traumatic brain injury?

Child abuse is the leading cause of serious traumatic brain injury (TBI) in infants and young children (Billmire & Myers, 1985; Bruce & Zimmerman, 1989). The incidence of serious or fatal inflicted traumatic brain injury (iTBI) in children < 1 year of age is approximately 1 in 3,300 ( Keenan et al., 2003); since many cases of iTBI are of mild or moderate severity, the incidence is probably significantly higher. Even at an incidence of 1 in 3,300, iTBI is as common as the incidence of cystic fibrosis (CF), the most common genetic recessive disease in the Caucasian population. Proper diagnosis of iTBI is difficult even for experienced and astute physicians because its presentation can be subtle and important historical data are often lacking. As a result, misdiagnosis is common and can have catastrophic medical consequences for patients and significant financial consequences for society ( Ewing-Cobbs et al., 1998; Jenny, Hymel, Pitzen, Reinert, & Hay, 1999). Unlike CF for which there are several well established screening tests, there are currently no diagnostic adjuncts to help physicians screen for possible iTBI.

Adolescent↗
PubMed2003

[Mild traumatic brain injury and its psychiatric assessment].

Mild traumatic brain injuries without circumscripted necrotic areas in brain tissue were called concussion in classic terminology. It was generally assumed, that such lesions were to heal without any residues. This notion can not be upheld completely any longer, since according to today's state of knowledge on the pathogenesis of brain trauma, chronic troubles and impairments may occur even after mild traumatic brain injuries. Besides, a number of psychosocial stress factors making it more difficult to cope with the posttraumatic disturbances and the new challenging life situation, play a marked role as to the outcome. In mild brain injuries, these environmental factors as well as a general lack of internal resources may be even more crucial than the trauma's severity by itself.

Adaptation, Psychological↗
PubMed2006

Increased oculomotor deficits during target blanking as an indicator of mild traumatic brain injury.

Given the susceptibility of cerebellar-cortical tracts to shearing injury from traumatic brain injury (TBI), we investigated impairment in the generation of predictive eye movements and its relationship to cognitive deficits in mild TBI patients using a smooth pursuit target-blanking paradigm. Compared to a target-tracking paradigm without blanking, this paradigm more greatly necessitates the generation of predictive eye movements, which are subserved by brain regions involved in cognitive processing. Mild TBI patients showed impaired prediction of target trajectories during target blanking, demonstrated by generation of saccades at earlier and more variable time points, as well as greater and more variable oculomotor error compared to controls. In addition, California Verbal Learning Test (CVLT-II) scores related to working memory, learning, and executive function were more highly correlated with oculomotor variability during target blanking than during target tracking. Our results suggest that a disruption of cerebellar-cortical connections in TBI may account for both oculomotor and cognitive impairment, and that measures of predictive eye movements during target blanking may be a sensitive metric of cognitive deficits after mild TBI.

Adolescent↗