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Results for “Traumatic brain injury”

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At least 19 recordsLinked to original sources

PubMed2004

A neuropsychological comparison of psychotic disorder following traumatic brain injury, traumatic brain injury without psychotic disorder, and schizophrenia.

Neuropsychological functioning in individuals with psychotic disorder following traumatic brain injury (PDFTBI), traumatic brain injury without psychosis (TBIWP), and schizophrenia were compared against each other and to the means of normal subjects. It was predicted that the PDFTBI group would be similar to the schizophrenic group in patterns of deficits, but milder in severity. Compared to scores from a normal sample, the PDFTBI group scored significantly lower in intelligence, vocabulary, verbal memory, and executive functioning, while the schizophrenic group scored significantly lower in intelligence, working memory, verbal memory, visual spatial abilities, and executive functioning. No differences were found between normal subjects and the TBIWP group. Implications of our findings for the conceptualization of psychotic disorders are discussed.

Adult↗

PubMed2006

[Anti-inflammatory modulators in traumatic brain injury].

Traumatic brain injury leads to primary and secondary brain injuries. Primary brain injury results from mechanical forces applied to the head at the time of impact. Secondary brain injury occurs at some time after the primary impact. Numerous pathophysiological mechanisms have been postulated to explain the progressive tissue damage produced by secondary injuries. The endogenous neuroinflammatory response after traumatic brain injury contributes to the development of blood-brain barrier breakdown, cerebral oedema and neuronal cell death and this has led to various pharmacological therapies to try to limit this type of damage. Studies employing glutamate receptor antagonist for cerebral protection have yielded promising results in laboratory animals but failed to produce clinically significant improvements. The present review will summarize the mechanisms of post traumatic cerebral inflammation with a special focus on the anti-inflammatory drug targets.

Adrenal Cortex Hormones↗

PubMed2004

Cerebral vascular and metabolic response to sustained systemic inflammation in ovine traumatic brain injury.

Traumatic brain injury (TBI) is frequently accompanied by a systemic inflammatory response secondary to multiple trauma, shock, or infections. This study investigated the impact of sustained systemic inflammation on cerebral hemodynamics and metabolism in ovine traumatic brain injury. Fifteen sheep were investigated for 14 hours. Head injury was induced with a nonpenetrating stunner in anesthetized, ventilated animals. One group (TBI/Endo, n = 6) subsequently received a continuous endotoxin infusion for 12 hours, whereas a second group (TBI, n = 6) received the carrier. Three instrumented animals served as sham controls. Head impact significantly increased intracranial pressure from 9 +/- 4 mm Hg to 21 +/- 15 mm Hg (TBI/Endo) and from 10 +/- 3 mm Hg to 24 +/- 19 mm Hg (TBI) (means +/- SD). Internal carotid blood flow increased and cerebral vascular resistance decreased (P < 0.05) during the hyperdynamic inflammatory response between 10 and 14 hours in the TBI/Endo group, whereas these parameters were at baseline level in the TBI group. Intracranial pressure remained unchanged during this period, but increased during hypercapnia. The CMRO2, PaCO2, and arterial hematocrit values were identical among the groups between 10 and 14 hours. It is concluded that chronic endotoxemia in ovine traumatic brain injury was associated with cerebral vasodilation uncoupled from global brain metabolism. Different mechanisms appear to induce cerebral vasodilation in response to inflammation and hypercapnia.

Animals↗

PubMed2005

Apoptosis and traumatic brain injury.

Traumatic brain injury is a cause of high mortality and morbidity and is an area of intense research. Apoptosis plays a crucial role in the pathogenesis of head injury, and the inhibition of apoptosis can potentially reverse the deleterious effects and lead to better functional outcome. Elucidation of the apoptotic pathway and its role in traumatic brain injury will provide potential targets for therapeutic intervention. This article aims to review the current wealth of literature on apoptosis and traumatic head injury and explores the current status of therapeutic strategies available.

Apoptosis↗

PubMedDate not supplied

Therapeutic hypothermia in traumatic brain injury.

Traumatic brain injury is a leading cause of death by trauma in adults in the United States and a major contributor to permanent physical, emotional, and psychological disabilities. Therapeutic hypothermia, defined as cooling of the body to less than 36 degrees C, has been shown to decrease mortality and morbidity and improve long-term outcomes by protecting the brain from secondary brain injury. The most commonly seen benefits of hypothermic temperatures of 32 degrees C to 33 degrees C are a significant reduction in intracranial hypertension and improved cerebral perfusion and oxygenation. Although evidence to date is insufficient to recommend the routine use of therapeutic hypothermia outside of the research setting, therapeutic hypothermia is used in multiple healthcare facilities in the world. The following article will define hypothermia and provide critical information necessary to provide care for the critically ill patient under therapeutic hypothermia. It will define the processes of brain injury and how hypothermia is thought to counteract those to protect the brain. Also included is a review of 2 major randomized, controlled trials of hypothermia for traumatic brain injury that have been instrumental in establishing guidelines and directing further research.

Adult↗

PubMed1998

Blood-free magnesium concentration declines following graded experimental traumatic brain injury.

Traumatic brain injury has been shown to result in a decrease in brain-free magnesium concentration that is associated with the development of neurologic motor deficits. Although these changes have been well characterized in the brain, changes in free magnesium homeostasis have not been characterized in other fluid compartments. The current experiments use ion selective electrodes to measure alterations in blood-free magnesium concentration following graded experimental brain injury in rats and to compare these changes with subsequent neurologic outcome. After severe impact-acceleration-induced injury, blood-free magnesium levels significantly declined (p < 0.05) by 25% and remained depressed for at least 4 days after injury. After moderate injury, the decline in blood-free magnesium was less than that observed in the severe injury group with respect to both degree of decline and duration of decline. The post-traumatic blood-free magnesium concentration correlated to observed motor deficits as assessed by rotarod evaluation (p < 0.001). We conclude that blood-free magnesium levels may be a prognostic indicator of outcome following severe traumatic brain injury.

Animals↗

PubMed2006

Epidemiology and outcomes of pediatric traumatic brain injury.

Traumatic brain injury is a leading cause of death and disability in the pediatric age group. Causes of injury vary with child developmental age, with more inflicted injuries in infants, fall-related injuries among toddlers, sports-related injuries among middle-school-aged children and motor vehicle crashes in older children. Prevention strategies exist for some pediatric traumatic brain injury; however, all suffer from lack of compliance and enforcement. Neuropsychological and behavioral outcomes for injured children vary with the severity of injury, child age at injury, premorbid child characteristics, family factors and the families' socioeconomic status. Each of these factors needs to be taken into account when designing rehabilitation strategies and assessing factors related to outcome.

Accidental Falls↗

PubMed1999

Traumatic brain injury.

Traumatic brain injury, caused by motor vehicle accidents, falls, assaults, or sports injuries affects approximately 7 million people each year. Early and rapid management of the initial brain injury and reduction in secondary insults can lead to improved outcomes. Nursing has an integral role in the care of the patient with traumatic brain injury and can have a positive impact on the outcome for the patient and the family. Types of injuries, treatment modalities, interdisciplinary management, and expected outcomes are discussed.

Algorithms↗

PubMed1997

The use of hyperventilation and its impact on cerebral ischemia in the treatment of traumatic brain injury.

Traumatic brain injury is a common occurrence in the United States, leading to approximately 190,000 deaths or long-term disabilities. Following the primary insult, secondary disturbances in cerebral blood flow (CBF) and metabolism may have deleterious effects on potentially viable neurons. Recent studies evaluating CBF immediately following head injury have revealed flows low enough to produce cerebral ischemia. Hyperventilation is used routinely to lower suspected increased intracranial pressure (ICP). Aggressive hyperventilation produces a marked reduction in CBF, which may give rise to or exacerbate cerebral ischemia, thus enhancing rather than reducing secondary injury. This article reviews the role of hyperventilation in the treatment of increased ICP and its impact on cerebral ischemia following traumatic brain injury.

Animals↗

PubMed1998

The role of the primary care physician in maximizing cognitive and behavioral recovery from moderate to severe pediatric traumatic brain injury.

Traumatic brain injury (TBI) is a major cause of death and the most common cause of acquired disability in children. Moderate to severe TBI typically results in cognitive deficits, and behavioral and psychosocial adjustment problems, sometimes compromising long term development. Although variable, considerable recovery can occur, especially over the first one to two years post-injury. Appropriate educational and psychological intervention is critical to positive outcome. The primary care physician (PCP) has a major role in monitoring progress and intervention, and therefore in maximizing outcome. The short term neurocognitive and neurobehavioral sequelae and recovery pattern for traumatic brain injury, and the role of the primary care physician in maximizing recovery based on risk factors are described. Some intervention resources are included.

Achievement↗

PubMed2000

Neuropsychiatric Aspects of Traumatic Brain Injury.

Traumatic brain injury (TBI) may produce a variety of neuropsychiatric problems, including impaired cognition, depression, mania, affective lability, irritability, anxiety, and psychosis. Despite the common occurrence of these symptoms following TBI, there are relatively few studies that provide clear guidance regarding management. Many symptoms (eg, irritability, affective lability, fatigue, sleep disturbance, and impaired cognition) are primarily consequences of brain injury rather than symptoms of a comorbid psychiatric disorder such as major depression. Although it is difficult to study the complicated treatments needed for such symptom complexes, we are able to recommend an approach to the evaluation and treatment of neuropsychiatric problems following traumatic brain injury. A thorough assessment of the patient is a prerequisite to the prescription of any treatment. This assessment should include a thorough developmental, psychiatric, and medication history; a detailed mental status examination; a complete neurologic examination; and quantification of neuropsychiatric symptoms using standardized and accepted inventories (eg, Neurobehavioral Rating Scale, Neuropsychiatric Inventory ). All symptoms must be evaluated in the context of the patient's premorbid history and current treatment because neuropsychiatric symptoms may be influenced by either factor or by both factors. Psychotherapy is an important component of the treatment of neuropsychiatric problems following TBI. Additionally, patients should be encouraged to become involved with local TBI support groups. When medications are prescribed, it is essential to use cautious dosing (low and slow) and empiric trials with continuous reassessment of symptoms using standardized scales and monitoring for drug-drug interactions. In general, medications with significant sedative, antidopaminergic, and anticholinergic properties should be avoided, and benzodiazepines should be used sparingly, if at all. Although patients with TBI may be particularly susceptible to adverse effects of psychopharmacologic medications, at times dosages similar to those used for the non-brain-injured psychiatric patient may be needed. When a single medication does not provide adequate relief of symptoms or cannot be tolerated at therapeutic doses, an alternative strategy is to augment the effect of one medication by using a second low-dose agent with a different mechanism of action.

Journal Article↗

PubMed2003

BAY 38-7271: a novel highly selective and highly potent cannabinoid receptor agonist for the treatment of traumatic brain injury.

Traumatic brain injury (TBI) is the most common cause of mortality and morbidity in adults under 40 years of age in industrialized countries. Worldwide the incidence is increasing, about 9.5 million people are hospitalized per year due to TBI, and the death rate is estimated to be more than one million people per year. Recently BAY 38-7271 has been characterized as a structurally novel, selective and highly potent cannabinoid CB1/CB2 receptor agonist in vitro and in vivo with pronounced neuroprotective efficacy in a rat traumatic brain injury model, showing a therapeutic window of at least 5 h. Furthermore, neuroprotective efficacy was also found in models of transient and permanent occlusion of the middle cerebral artery and brain edema models as well. In this article we review the in vitro and in vivo pharmacology of BAY 38-7271, the results from acute and subacute toxicity studies, pharmacokinetics and drug metabolism in animals and healthy male volunteers. In phase I studies BAY 38-7271 was safe and well tolerated when administered by i.v. infusion for either 1 or 24 h. As the doses of BAY 38-7271 in animals needed for maximal neuroprotective efficacy were significantly lower than those inducing typical cannabinoid-like side effects, it is to be expected that the compound will offer a novel therapeutic approach with a favorable therapeutic window for the treatment of TBI or cerebral ischemia.

Animals↗

PubMed2026

Development of a High-Sensitivity Glycoproteomics Approach for Fc-Specific Quantification of IgG Core Fucosylation in Traumatic Brain Injury.

Traumatic brain injury (TBI) triggers complex neuroinflammatory cascades that involve sustained immune activation and dysregulated antibody effector functions. Immunoglobulin G (IgG) Fc N-glycosylation, particularly core fucosylation, critically modulates immune signaling through altered Fcγ receptor (FcγR) interactions; however, its role in TBI remains unexplored. Here, we developed a high-sensitivity, mass spectrometry-based glycoproteomics method for the systematic analysis of IgG Fc core fucosylation dynamics following TBI. The approach integrates Fc-specific enzymatic truncation with GlycINATOR (EndoS2) and tryptic digestion, followed by high-resolution LC-MS/MS profiling, enabling confident identification of truncated Fc glycopeptides. Furthermore, a targeted parallel reaction monitoring (PRM) strategy allowed direct quantification of core fucosylated and afucosylated glycopeptides from 10 μg of crude serum protein, eliminating the need for IgG purification. Our results reveal time-dependent and subclass-specific remodeling of IgG Fc fucosylation postinjury, characterized by an overall reduction in fucosylated species and a relative increase in afucosylation. Collectively, this study establishes a scalable analytical platform for Fc-specific glycosylation profiling and identifies IgG core fucosylation as a candidate molecular indicator of immune dysregulation in TBI, providing new insights into post-traumatic immune regulation.

Brain Injuries, Traumatic↗

PubMed2026

Artificial Intelligence-Driven Multi-Omics Analysis Reveals Hydroxytyrosol Targeting of the TXNIP-NLRP3 Inflammasome Axis in Traumatic Brain Injury.

Traumatic brain injury (TBI) induces secondary neuroinflammation driven by oxidative stress, inflammasome activation, and immune remodeling, yet specific mechanism-guided pharmacological interventions remain limited. This study established an artificial intelligence (AI)-integrated network pharmacology and multi-omics framework to evaluate whether hydroxytyrosol (HT), an olive-derived natural polyphenol, may regulate TBI-related neuroinflammatory targets centered on the TXNIP/NLRP3 inflammasome axis. Starting from the SMILES structure of HT, potential targets were predicted using PharmMapper, SwissTargetPrediction, and the Similarity Ensemble Approach and were standardized to UniProt identifiers. TBI-associated genes were integrated from GeneCards, DisGeNET, OMIM, and the Therapeutic Target Database. The overlapping target set was analyzed using STRING-based protein-protein interaction (PPI) networks, MCODE, CytoHubba, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. Public GEO transcriptomic datasets (GSE123831 and GSE104687) were used for cross-platform expression validation, differential expression analysis, and exploratory CIBERSORT-based immune infiltration estimation. Random forest (RF), multilayer perceptron (MLP), graph convolutional network (GCN), graph attention network (GAT), SHAP/LIME explainability analysis, LASSO inflammatory-risk scoring, and two-sample Mendelian randomization (MR) were further applied for target prioritization, immune phenotype mapping, and genetic association analysis. Seventy-three overlapping HT-TBI targets were identified. PPI and topology analyses prioritized TXNIP, NLRP3, CASP1, MAPK1, and TP53 as key hubs enriched in inflammasome activation, oxidative stress, apoptosis, and NOD-like receptor signaling. TXNIP, NLRP3, and CASP1 were consistently upregulated in both TBI transcriptomic datasets. LM22-based immune deconvolution suggested increased pro-inflammatory immune signatures and a positive TXNIP-M1 macrophage association (r = 0.63, p < 0.001), which should be interpreted as a transcriptome-derived hypothesis rather than validated murine immune-cell proportions. AI-based models consistently ranked TXNIP/NLRP3 as high-contribution features under internal validation, and removal of these targets reduced model performance. A five-gene inflammatory score achieved an internally evaluated AUC of 0.87, while two-sample MR supported positive genetic associations involving TXNIP expression, TBI risk, NLRP3 and IL-1β expression. Collectively, these findings prioritize the TXNIP/NLRP3/CASP1 module as a computationally supported candidate mechanism through which HT may influence oxidative stress-inflammasome-immune coupling in TBI. This study provides an interpretable drug-target-pathway-phenotype framework and identifies TXNIP, NLRP3, and CASP1 as priority nodes for future experimental validation.

Artificial Intelligence↗

PubMed1996

Traumatic brain injury.

Traumatic brain injury (TBI) contributes significantly to the mortality and morbidity rates of traumatized patients. This article presents current concepts in the pathophysiology of TBI, including mechanisms of injury, biomolecular mediators of injury, and the occurrence of secondary injury. Emergency management, monitoring, and imaging of TBI also are reviewed.

Algorithms↗

PubMed2003

Psychotic disorder and traumatic brain injury.

Traumatic brain injury (TBI) can result in serious and disabling neuropsychiatric disorders, such as cognitive deficits and personality change, as well as severe and chronic psychosis. This review focuses on the relationship between TBI and schizophrenia-like psychosis (SLP) including its epidemiology, diagnostic criteria, clinical presentation, psychopathology, risk factors, and pathophysiology. The relationships between post-traumatic epilepsy and SLP, and brain trauma and schizophrenia, are also discussed. The risk of SLP does increase after TBI. The clinical presentation has considerable overlap with primary schizophrenic disorder, with a prominence of persecutory and other delusions and auditory hallucinations, as well as a lack of negative symptoms. The onset is often gradual, with a subacute or chronic course. More severe and diffuse brain injury, especially of the temporal and frontal lobes, is the most prominent risk factor. Genetic load may also play a role, but presence of epilepsy could be a protective factor. Further large and systematic longitudinal studies are needed.

Brain Injuries↗

PubMed1993

Motor performance in children after traumatic brain injury.

Traumatic brain injury can result in persistent impairments of motor performance that interfere with functional activities. This study compared the gross and fine motor performance of 14 traumatically brain-injured children (five to 15 years old, with loss of consciousness for at least 24 hours) to 14 normal children group matched for age and sex. All subjects had normal intelligence and no prior history of cognitive or motor delays. Subjects were assessed with the Bruininks-Oseretsky Test of Motor Proficiency at least 16 months after injury. Results were compared using the Wilcoxon rank sum test. Highly significant differences were found between groups on the Gross Motor Composite. Although no significant differences were found on the Fine Motor Composite, a highly significant difference also was found on one of the fine motor sub-tests, Upper-Limb Speed and Dexterity. Subtest analysis revealed that when speed was a component of either fine or gross motor tasks, a pattern of significant differences was found. This is consistent with previous research in neuropsychology, which has demonstrated problems in speeded motor performance of children with brain injuries. These findings provide direction for further research, clinical assessment, and treatment of this at-risk population.

Adolescent↗

PubMed2003

Neurologic aspects of traumatic brain injury.

Traumatic brain injury is a common neurologic condition that can have a significant emotional and financial burden. Neurologic injury is classified on the basis of initial clinical status by the Glasgow Coma Scale, and also by the type and location of head injury. Complications in the management of these patients are reviewed, ranging from intracranial pressure management and stroke to post-traumatic epilepsy. In addition, predictive prognostic variables that can be used to predict outcome based on a patient's presentation at the time of a head trauma are discussed. Finally, interventions such as induced hypothermia that can be undertaken to try to optimize outcome, are discussed along with current data in support of or against such techniques.

Brain Injuries↗