PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “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 199 records · Page 11Linked to original sources
PubMed2003

Changes of metabotropic glutamate receptor subtype 1a in diffuse brain injury with secondary brain insults and the effects of 2-methyl-4-carboxyphenylglycine.

OBJECTIVE: To observe the changes of metabotropic glutamate receptor 1a in rat brain in a rodent model of diffuse head injury with secondary insults and the effects of 2-methyl-4-carboxyphenylglycine (MCPG). METHODS: Based on Marmarous rodent model of diffuse brain injury (DBI), hypotension was made by blood withdrawal as secondary brain insults (SBI). 105 male SD rats were randomized into A and B groups. The changes of mGluR(1a) in cerebral cortex were studied by immunohistochemistry and the effect of MCPG by HE. Each group was divided into different subgroups at different time after injury. RESULTS: Compared with that of sham group, the number of mGluR(1a) positive neuron increased by 12.9+/-3.2 (P<0.05) 1 day after injury in the injured cerebral cortex in DBI group. However, in DBI and SBI group there was a more significant increase in the number of mGluR(1a) positive neuron at 4 hours after injury (15.6+/-3.0, P<0.05) and then the number of mGluR(1a) positive neuron gradually decreased. Administration of MCPG reduced total cortical necrotic neurons counts on the 7th day after injury (5.21+/-2.52, P<0.05). CONCLUSIONS: Brain injury can increase the gene expression of mGluR(1a) and the role of mGluR(1a) may be a key factor in the aggravation of head injury with SBI, and that MCPG may have therapeutic potential in head injury.

Analysis of Variance↗
PubMed1992

Traumatic brain injury crisis intervention and family therapy--management and outcome. Brain Injury Treatment and Research Group.

This article presents a model for crisis intervention and family therapy after traumatic brain injury. Our program, firmly rooted in object-relations theory and transactional analysis, included patients and family members (significant others) living within 100 miles from the University Hospital of Umeå. The effects of the interventions were gauged at one and two years after the trauma are presented in terms of agreement/disagreement between the patient and the significant other concerning inter- and intrapersonal relationships as well as through a short case presentation. As a conclusion of our study a point is made to expand the scope of intervention to include also other segments of the social network of the patient.

Adult↗
PubMed2005

Differential activation of ERK, p38, and JNK MAPK by nociceptin/orphanin FQ in the potentiation of prostaglandin cerebrovasoconstriction after brain injury.

Fluid percussion brain injury elevates the cerebrospinal fluid (CSF) concentration of the opioid nociceptin/orphanin FQ (N/OFQ), which potentiates vasoconstriction to the prostaglandins U 46619, a thromboxane A(2) mimic, and prostaglandin (PG)F(2a). This study investigated the role of the extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) isoforms of mitogen activated protein kinase (MAPK) in potentiated prostaglandin vasoconstriction after brain injury and the relationship of brain injury induced release of N/OFQ to MAPK. Pial artery diameter was measured with a video microscaler by observation through a glass coverslip cranial window placed in the parietal cortex of newborn pigs. Brain injury potentiated U 46619 induced pial artery vasoconstriction but U 0126 and SB 203580 (10(-6) and 10(-5) M, respectively) (ERK and p38 MAPK inhibitors) blocked the potentiation. In contrast, administration of SP 600125 (10(-6) and 10(-5) M) (JNK MAPK inhibitor) only attenuated brain injury induced U 46619 potentiation and such responses were significantly different than that in the presence of either U 0126 or SB 203580 after FPI. Co-administration of N/OFQ (10(-10) M), the CSF concentration observed after brain injury, with U 46619 or PGF(2a) under non brain injury conditions potentiated prostaglandin vasoconstriction but U 0126 and SB 203580 blocked such potentiation. Administration of SP 600125 modestly attenuated prostaglandin potentiation by N/OFQ. These data show that activation of ERK and p38 primarily contribute to potentiation of prostaglandin constriction after brain injury. These data suggest that N/OFQ differentially activates ERK, p38, and JNK MAPK to contribute to potentiated prostaglandin vasoconstriction after fluid percussion brain injury.

Animals↗
PubMed1999

Consensus conference. Rehabilitation of persons with traumatic brain injury. NIH Consensus Development Panel on Rehabilitation of Persons With Traumatic Brain Injury.

OBJECTIVE: To provide biomedical researchers and clinicians with information regarding and recommendations for effective rehabilitation measures for persons who have experienced a traumatic brain injury (TBI). PARTICIPANTS: A nonfederal, nonadvocate, 16-member panel representing the fields of neuropsychology, neurology, psychiatry, behavioral medicine, family medicine, pediatrics, physical medicine and rehabilitation, speech and hearing, occupational therapy, nursing, epidemiology, biostatistics, and the public. In addition, 31 experts from these same fields presented data to the panel and a conference audience of 883 members of the public. The conference consisted of (1) presentations by investigators working in areas relevant to the consensus questions during a 2-day public session; (2) questions and statements from conference attendees during open discussions that were part of the public session; and (3) closed deliberations by the panel during the remainder of the second day and part of the third. Primary sponsors of the conference were the National Institute of Child Health and Human Development and the National Institutes of Health Office of Medical Applications of Research. EVIDENCE: The literature was searched through MEDLINE for articles from January 1988 through August 1998 and an extensive bibliography of 2563 references was provided to the panel and the conference audience. Experts prepared abstracts for their conference presentations with relevant citations from the literature. The panel prepared a compendium of evidence, including a patient contribution and reports from federal agencies. Scientific evidence was given precedence over clinical anecdotal experience. CONSENSUS PROCESS: The panel, answering predefined questions, developed their conclusions based on the scientific evidence presented during the open forum (October 26-28, 1998) and in the scientific literature. The panel composed a draft statement that was read in its entirety and circulated to the experts and the audience for comment. Thereafter, the panel resolved conflicting recommendations and released a revised statement at the end of the conference. The panel finalized the revisions within a few weeks after the conference. The draft statement was made available on the Internet immediately following its release at the conference and was updated with the panel's final revisions. CONCLUSIONS: Traumatic brain injury results principally from vehicular incidents, falls, acts of violence, and sports injuries and is more than twice as likely to occur in men as in women. The estimated incidence rate is 100 per 100000 persons, with 52000 annual deaths. The highest incidence is among persons aged 15 to 24 years and 75 years or older, with a less striking peak in incidence in children aged 5 years or younger. Since TBI may result in lifelong impairment of physical, cognitive, and psychosocial functioning and prevalence is estimated at 2.5 million to 6.5 million individuals, TBI is a disorder of major public health significance. Mild TBI is significantly underdiagnosed and the likely societal burden is therefore even greater. Given the large toll of TBI and absence of a cure, prevention is of paramount importance. However, the focus of this conference was the evaluation of rehabilitative measures for the cognitive and behavioral consequences of TBI. Evidence supports the use of certain cognitive and behavioral rehabilitation strategies for individuals with TBI. This research needs to be replicated in larger, more definitive clinical trials and, thus, funding for research on TBI needs to be increased.

Adolescent↗
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↗
PubMed1987

Endogenous opioids may mediate secondary damage after experimental brain injury.

Although endogenous opioids have been implicated in the pathophysiology of spinal cord injury and brain ischemia, the role of specific opioid peptides and opiate receptors in the pathophysiology of traumatic brain injury remains unexplored. This study examined regional changes in brain opioid immunoreactivity and cerebral blood flow (CBF) after fluid-percussion brain injury in the cat and compared the effect of an opiate antagonist (Win 44,441-3 [Win-(-)]) with its dextroisomer Win 44,441-2 [Win-(+)] (which is inactive at opiate receptors) in the treatment of brain injury. Dynorphin A immunoreactivity (Dyn A-IR) but not leucine-enkephalin-like immunoreactivity accumulated in injury regions after traumatic injury; Dyn-IR increases also occurred predominantly in those areas showing significant decreases in regional CBF. Administration of Win-(-) but not Win-(+) or saline at 15 min after injury significantly improved mean arterial pressure, electroencephalographic amplitude, and regional CBF and reduced the severity and incidence of hemorrhage. Win-(-) also significantly improved survival after brain injury. Taken together, these findings suggest that dynorphin, through actions at opiate receptors, may contribute to the pathophysiology of secondary brain injury after head trauma and indicate that selective opiate-receptor antagonists may be useful in treatment of traumatic brain injury.

Animals↗
PubMed2005

A single dose, three-arm, placebo-controlled, phase I study of the bradykinin B2 receptor antagonist Anatibant (LF16-0687Ms) in patients with severe traumatic brain injury.

Traumatic brain injury (TBI) mortality and morbidity remains a public health challenge. Because experimental studies support an important role of bradykinin (BK) in the neurological deterioration that follows TBI, a double-blind, randomized, placebo-controlled study of Anatibant (LF16- 0687Ms), a selective and potent antagonist of the BK B(2) receptor, was conducted in severe (Glasgow Coma Scale [GCS] < 8) TBI patients (n = 25) at six sites in the United States. At 8-12 h after injury (9.9 +/- 2.8 h), patients received a single subcutaneous injection of Anatibant (3.75 mg or 22.5 mg, n = 10 each) or placebo (n = 5). The primary objective was to investigate the pharmacokinetics of Anatibant; general safety, local tolerability, levels of the bradykinin metabolite BK1-5 in plasma and cerebrospinal fluid (CSF), intracranial pressure (ICP), and cerebral perfusion pressure were also assessed. We observed a dose-proportionality of the pharmacokinetics, Cmax, and AUC of Anatibant. V(d)/F, Cl/F, and t(1/2) were independent on the dose and protein binding was >97.7%. Anatibant, administered as single subcutaneous injections of 3.75 g and 22.5 mg, was well tolerated in severe TBI patients with no unexpected clinical adverse events or biological abnormalities observed. Interestingly, plasma and CSF levels of BK1-5 were significantly and markedly increased after trauma (e.g., 34,700 +/- 35,300 fmol/mL in plasma vs. 34.9 +/- 5.6 fmol/mL previously reported for normal volunteers), supporting the use of Anatibant as a treatment of secondary brain damage. To address this issue, a dose-response trial that would investigate the effects of Anatibant on the incidence of raised ICP and on functional outcome in severe TBI patients is needed.

Adolescent↗
PubMed1999

Accumulation of amyloid beta and tau and the formation of neurofilament inclusions following diffuse brain injury in the pig.

Brain trauma in humans increases the risk for developing Alzheimer disease (AD) and may induce the acute formation of AD-like plaques containing amyloid beta (A beta). To further explore the potential link between brain trauma and neurodegeneration, we conducted neuropathological studies using a pig model of diffuse brain injury. Brain injury was induced in anesthetized animals via nonimpact head rotational acceleration of 110 degrees over 20 ms in the coronal plane (n = 15 injured, n = 3 noninjured). At 1, 3, 7, and 10 days post-trauma, control and injured animals were euthanized and immunohistochemical analysis was performed on brain sections using antibodies specific for A beta, beta-amyloid precursor protein (betaPP), tau, and neurofilament (NF) proteins. In addition to diffuse axonal pathology, we detected accumulation of A beta and tau that colocalized with immunoreactive betaPP and NF in damaged axons throughout the white matter in all injured animals at 3-10 days post-trauma. In a subset of brain injured animals, diffuse A beta-containing plaque-like profiles were found in both the gray and white matter, and accumulations of tau and NF rich inclusions were observed in neuronal perikarya. These results show that this pig model of diffuse brain injury is characterized by accumulations of proteins that also form pathological aggregates in AD and related neurodegenerative diseases.

Amyloid beta-Peptides↗
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 Fc&#x3b3; receptor (Fc&#x3b3;R) 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 &#x3bc;g 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↗
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↗
PubMed1999

Relations between traumatic brain injury and the environment: feedback reduces maladaptive behaviour exhibited by three persons with traumatic brain injury.

Feedback is a commonly used technique in neurorehabilitation. It functions to strengthen or weaken select relations between individuals' behaviour and their environment. The study of behaviour-environment relations is a focus of operant psychology, commonly referred to as behaviour analysis. Central to behaviour analysis is the analysis of interrelations among stimuli, behaviour, and consequences. The focus on behaviour-environment relations may have considerable benefits for designing clinical treatments and accounting for successful and unsuccessful treatments, especially psychological interventions for maladaptive behaviour. In the present investigation, three persons with traumatic brain injuries, diagnosed with depression and presenting mild cognitive impairments, received feedback about their maladaptive behaviour. Weekly feedback resulted in general reductions in the variability and frequency of maladaptive behaviour. The results support the utility of giving equal consideration to relations between persons with traumatic brain injury and their environment, despite existing psychological or cognitive impairments. Future research on variables that influence the development and maintenance of behaviour-environment relations, and more generally operant behaviour, may provide a unique perspective on the effects of traumatic brain injury.

Adaptation, Psychological↗
PubMed2000

Glucocorticoids modulate BDNF mRNA expression in the rat hippocampus after traumatic brain injury.

Brain-derived neurotrophic factor (BDNF) expression in rat hippocampus is increased after experimental traumatic brain injury (TBI) and may be neuroprotective. Glucocorticoids are important regulators of brain neurotrophin levels and are often prescribed following TBI. The effect of adrenalectomy (ADX) on the expression of BDNF mRNA in the hippocampus after TBI has not been investigated to date. We used fluid percussion injury (FPI) and in situ hybridization to evaluate the expression of BDNF mRNA in the hippocampus 4 h after TBI in adrenal-intact or adrenalectomized rats (with or without corticosterone replacement). FPI and ADX independently increased expression of BDNF mRNA. In animals undergoing FPI, prior ADX caused further elevation of BDNF mRNA and this upregulation was prevented by corticosterone replacement in ADX rats. These findings suggest that glucocorticoids are involved in the modulation of the BDNF mRNA response to TBI.

Adrenalectomy↗
PubMed2004

Traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarism: screening study at 3 months after the brain injury.

OBJECTIVE: Acquired hypopituitarism in adults is obviously suspected in patients with primary hypothalamic-pituitary diseases, particularly after neurosurgery and/or radiotherapy. That brain injuries (BI) can cause hypopituitarism is commonly stated and has been recently emphasized but the management of BI patients does not routinely include neuroendocrine evaluations. AIM: To clarify the occurrence of hypopituitarism in patients after traumatic brain injury (TBI) or subarachnoid haemorrhage (SAH) 3 months after the BI. SUBJECTS AND METHODS: The occurrence of hypopituitarism in conscious patients after traumatic brain injury [TBI, n = 100, 31 women, 69 men; age 37.1 +/- 1.8 years; body mass index (BMI) 23.7 +/- 0.4 kg/m(2); Glasgow Coma Scale (GCS) 3-15] or subarachnoid haemorrhage [SAH, n = 40, 14 men, 26 wpmen, 51.0 +/- 2.0 years; 25.0 +/- 0.6 kg/m(2); Fisher's scale 1-4] was studied in a multicentre study 3 months after the BI. All patients underwent wide basal hormonal evaluation; the GH/IGF-I axis was evaluated by GHRH + arginine test and IGF-I measurement. RESULTS: In TBI patients, some degree of hypopituitarism was shown in 35%. Total, multiple and isolated deficits were present in 4, 6 and 25%, respectively. Diabetes insipidus was present in 4%. Secondary adrenal, thyroid and gonadal deficit was present in 8, 5 and 17%, respectively. Severe GH deficiency (GHD) was the most frequent pituitary defect (25%). In SAH patients, some degree of hypopituitarism was shown in 37.5%. Despite no total hypopituitarism, multiple and isolated deficits were present in 10 and 27.5%, respectively. Diabetes insipidus was present in 7.5%. Secondary adrenal, thyroid and gonadal deficit was present in 2.5, 7.5 and 12.5%, respectively. Severe GHD was the most frequent defect (25%). CONCLUSIONS: TBI and SAH are conditions associated with high risk of acquired hypopituitarism. The pituitary defect is often multiple and severe GHD is the most frequent defect. Thus neuroendocrine evaluations are always mandatory in patients after brain injuries.

Adult↗
PubMed2026

Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.

Traumatic brain injury (TBI) initiates a complex secondary injury cascade that significantly contributes to long-term neurological deficits, with post-translational modifications (PTMs) emerging as pivotal molecular regulators of this process. Unlike primary mechanical damage, secondary injury evolves over hours to years and involves intricate proteomic alterations that changes in gene expression alone cannot fully explain. PTMs-including phosphorylation, ubiquitination, acetylation, SUMOylation, glycosylation, and emerging modifications such as succinylation, lactylation, and nitrosylation-serve as dynamic molecular switches that fine-tune protein function, stability, localization, and interactions in response to TBI-induced stressors. These modifications play dual roles: they can either promote neuroprotection and recovery or drive pathological processes such as neuronal cell death (via apoptosis, necroptosis, and ferroptosis), neuroinflammation through glial activation and inflammasome signaling, blood-brain barrier disruption, mitochondrial dysfunction, and impaired synaptic plasticity. Critically, extensive crosstalk exists among different PTM pathways-such as the interplay between phosphorylation and ubiquitination in protein degradation or the competitive balance between acetylation and SUMOylation-that collectively shape cellular fate after injury. This nuanced regulatory network presents both challenges and opportunities for therapeutic intervention. Targeting PTM-related enzymes, including kinases, phosphatases, E3 ligases, and histone deacetylases, has shown promise in preclinical models, while novel strategies like Proteolysis-Targeting Chimeras (PROTACs) and repurposed drugs (e.g., metformin, resveratrol) offer innovative avenues for modulating the PTM landscape. Advances in high-throughput proteomics and mass spectrometry are enabling the mapping of TBI-specific PTM signatures across spatiotemporal phases, facilitating the identification of pro-survival versus pro-death modification thresholds. Despite hurdles in clinical translation-such as blood-brain barrier penetration and off-target effects-the growing understanding of PTM dynamics underscores their potential as both biomarkers and therapeutic targets. Future TBI management may thus rely on precision medicine approaches that integrate multi-PTM profiling to guide combination therapies aimed at tipping the balance toward neural repair and functional recovery.

Brain Injuries, Traumatic↗
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↗
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↗
PubMed2005

Extracellular signal-regulated kinase-mediated IL-1-induced cortical neuron damage during traumatic brain injury.

Traumatic brain injury (TBI) is one of the most prevalent causes of morbidity and mortality in youth. Interleukin-1 (IL-1) has many roles in the brain in addition to mediating glial inflammatory response; it has also been implicated in neurodegenerative diseases. We demonstrated the signal transduction pathway of IL-1 overproduction-induced cortical neuron loss during TBI. A calibrated weight-drop device (450 g weight and 2m height) was used to induce TBI in adult male Sprague-Dawley rats under general anesthesia (sodium pentobarbital: 40 mg/kg, i.p.). Expression of interleukin-1alpha (IL-1alpha), interleukin-1beta (IL-1beta), extracellular signal-regulated kinase (ERK), Jun, and p-38 were determined by Western blotting and RT-PCR. Neuronal damage was evaluated by microscopic examination. We found both mRNA and proteins of cortical IL-1alpha and IL-1beta increased three hours after TBI. Phosphorylation of ERK significantly increased but there were no significant effects on cortical expression of ERK, Jun and p-38. Administration of ERK inhibitor, PD98059, IL-1alpha antibody and IL-1beta antibody protected animals from TBI-induced neuronal damage. Our results suggest that TBI-induced cortical neuron death was mediated by the IL-1 receptor through ERK phosphorylation.

Animals↗