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 505 records · Page 28Linked to original sources
PubMed1995

Role of excitatory amino acid-mediated ionic fluxes in traumatic brain injury.

One major event taking place at the moment of traumatic brain injury in neuronal cells is the occurrence of massive ionic fluxes across the plasma membrane, which can be referred to as traumatic depolarization (TD). Unlike spreading depression, TD can occur over wide brain areas simultaneously. Furthermore, recovery from TD often takes far longer than recovery from ionic perturbation elicited by the passage of a single wave of spreading depression. Neuronal cell damage caused by ischemic brain injury is also initiated by massive ionic fluxes, termed anoxic depolarization. The occurrence of similar ionic events in these two forms of brain injury may account for the genesis of diffuse ischemia-like damage without actual episodes of hypoxia or ischemia in traumatic brain injury. We review the data indicating that excitatory amino acids (EAA) may play a vital role in producing TD, and that such EAA-mediated ionic perturbation is responsible for a number of posttraumatic events including subcellular metabolic dysfunction and cellular responses such as microglial activation and astrocytic transformation. TD may represent one of the most important mechanisms of diffuse neuronal cell dysfunction and damage associated with traumatic brain injury.

Animals↗
PubMed2006

Alteration of postural responses to visual field motion in mild traumatic brain injury.

OBJECTIVE: Balance deficits in individuals experiencing mild traumatic brain injury have been documented in numerous recent studies. However, long-lasting balance deficits and specific mechanisms causing these deficits have not been systematically examined. This article aimed to present empirical evidence showing destabilizing effects of visual field motion in concussed individuals up to 30 days postinjury. METHODS: Sixty student athletes participated in the pilot (n = 12) and major experiments (n = 48) before injury. Eight of these 48 subjects who experienced mild traumatic brain injury in athletic events were tested again on Days 3, 10, and 30 after the incident. Postural responses to visual field motion were recorded using a virtual reality environment in conjunction with balance (AMTI force plate) and motion tracking (Flock of Birds) technologies. RESULTS: The area of the center of pressure during upright stance did not change from Day 3 to 30 postinjury with respect to pre-injury status (P > .05). However, balance deficits induced by visual field motion were present up to 30 days postinjury. Destabilizing effect of visual field motion was observed via significant increase of the center of pressure data (P < .05) and reduced coherence value. CONCLUSION: Our data suggest the presence of residual sensory integration dysfunction in concussed individuals at least 30 days postinjury and may indicate a lower threshold for brain reinjury.

Adult↗
PubMed2005

Peculiarities of physical therapy for patients after traumatic brain injury.

Literature review data about methods and means of physical therapy for patients after traumatic brain injury is presented in this article. Traumatic brain injury is an urgent medical and social problem all over the world. It is the most common cause of disability in Lithuania. Patient rehabilitation after traumatic brain injury is divided into two periods: acute and subacute. In the beginning of rehabilitation physical therapist evaluates patient's functional status, later he uses methods and means of treatment, and evaluates effectiveness of rehabilitation. Early verticalisation is very important for patients with coma. Physical therapy consists of prevention of complications, improvement of muscle force, and range of motions, balance, movement coordination, endurance and cognitive functions. Early rehabilitation is necessary for traumatic brain injury patients and use of physical therapy methods can help to regain lost functions and to come back to the society.

Adolescent↗
PubMed2006

Compensation and malingering in traumatic brain injury: a dose-response relationship?

The purpose of this study was to determine if there is a dose-response relationship between potential monetary compensation and failure on psychological indicators of malingering in traumatic brain injury. 332 traumatic brain injury patients were divided into three groups based on incentive to perform poorly on neuropsychological testing: no incentive; limited incentive as provided by State law; high incentive as provided by Federal law. The rate of failure on five well-validated malingering indicators across these groups was examined. Cases handled under Federal workers compensation laws showed considerably higher rates of failure and diagnosable malingering than cases handled under State law. The findings indicate that monetary compensation associated with workers compensation claims is a major motive for exaggeration and malingering of problems attributed to work-related brain injuries. The clinician's index of suspicion regarding exaggeration and malingering of symptoms and deficits should be much higher in the context of Federal workers compensation claims, particularly in patients who have suffered only mild traumatic brain injury.

Adult↗
PubMedDate not supplied

Severity of injury and service utilization following traumatic brain injury: the first 3 months.

OBJECTIVE: To describe the medical and rehabilitation service use of model systems by brain injured participants 1 to 3 months postdischarge from inpatient rehabilitation. DESIGN: Prospective follow-up study. SETTING: Georgia Model Brain Injury System (GAMBIS). PARTICIPANTS: Seventy-three GAMBIS subjects consenting to participate in the utilization substudy. MAIN OUTCOME MEASURES: Receipt of services and intensity of service use. ANALYSIS: Chi-square analysis of receipt of services by severity of injury. RESULTS: The likelihood of service use did not vary with severity of injury. Data suggest that intensity of service use was a function of injury severity. CONCLUSIONS: Subjects with mild and moderate injuries were as likely to use a range of medical and rehabilitation services during the 3-month postdischarge period as those with severe injuries. Traditional rehabilitation services, such as physical therapy, were far more likely to be used, than nontraditional services, such as psychological counseling, in spite of the high level of cognitive and social disability associated with traumatic brain injury.

Adolescent↗
PubMed2001

Executive function in traumatic brain injury and obsessive-compulsive disorder: an overlap?

Thirteen individuals with traumatic brain injury, 13 individuals with obsessive-compulsive disorder (OCD) and 10 normal controls were compared on neuropsychological measures of executive function. Individuals with a traumatic brain injury performed significantly poorer than the other two groups on a test measuring visuo-spatial strategy. Although the traumatic brain injury group made more errors on a test of maze learning and the OCD group less than the control group, this did not reach statistical significance. No support for an overlap in executive dysfunction in traumatic brain injury and OCD was found. It may be that the 'error prevention system' in the brain was influenced in a contrasting way by executive dysfunction in these disorders. This difference may reveal itself clinically in impulsivity/perseveration and slowness, respectively. Further studies were needed to test this hypothesis.

Adolescent↗
PubMed2004

The pathobiology of moderate diffuse traumatic brain injury as identified using a new experimental model of injury in rats.

Experimental models of traumatic brain injury have been developed to replicate selected aspects of human head injury, such as contusion, concussion, and/or diffuse axonal injury. Although diffuse axonal injury is a major feature of clinical head injury, relatively few experimental models of diffuse traumatic brain injury (TBI) have been developed, particularly in smaller animals such as rodents. Here, we describe the pathophysiological consequences of moderate diffuse TBI in rats generated by a newly developed, highly controlled, and reproducible model. This model of TBI caused brain edema beginning 20 min after injury and peaking at 24 h post-trauma, as shown by wet weight/dry weight ratios and diffusion-weighted magnetic resonance imaging. Increased permeability of the blood-brain barrier was present up to 4 h post-injury as evaluated using Evans blue dye. Phosphorus magnetic resonance spectroscopy showed significant declines in brain-free magnesium concentration and reduced cytosolic phosphorylation potential at 4 h post-injury. Diffuse axonal damage was demonstrated using manganese-enhanced magnetic resonance imaging, and intracerebral injection of a fluorescent vital dye (Fluoro-Ruby) at 24-h and 7-day post-injury. Morphological evidence of apoptosis and caspase-3 activation were also found in the cerebral hemisphere and brainstem at 24 h after trauma. These results show that this model is capable of reproducing major biochemical and neurological changes of diffuse clinical TBI.

Animals↗
PubMed2000

Effect of neutropenia and granulocyte colony stimulating factor-induced neutrophilia on blood-brain barrier permeability and brain edema after traumatic brain injury in rats.

OBJECTIVE: Granulocyte colony stimulating factor (GCSF) has been used to increase systemic absolute neutrophil count (ANC) in patients with severe traumatic brain injury to reduce nosocomial infection risk. However, the effect of increasing systemic ANC on the pathogenesis of experimental traumatic brain injury has not been studied. Thus, we evaluated the effect of systemic ANC on blood-brain barrier (BBB) damage and brain edema after traumatic brain injury in rats. DESIGN: Experimental study. SETTING: Research laboratory at the University of Pittsburgh, PA. SUBJECTS: Forty-three adult male Sprague-Dawley rats. INTERVENTIONS: Protocol I: rats were randomized to receive either vinblastine sulfate to reduce ANC, GCSF to increase ANC, or saline before controlled cortical impact (CCI) of moderate overall severity. Evans blue was used to assess BBB damage at 4-24 hrs after CCI. Protocol II: rats received GCSF or saline before CCI. Brain edema was estimated at 24 hrs using wet - dry) / wet weight method. Protocol III: rats received GCSF or saline before CCI. Brain neutrophil accumulation was estimated at 24 hrs using a myeloperoxidase assay. MEASUREMENTS AND MAIN RESULTS: Physiologic variables were controlled before CCI was maintained at normal in all animals before traumatic brain injury. No rats were anemic, hypoglycemic, or hypotensive before CCI. Protocol I: compared with control, systemic ANC decreased in vinblastine-treated rats and increased in GCSF-treated rats. BBB damage correlated with systemic ANC. Protocol II: mean systemic ANC before traumatic brain injury increased 15-fold in rats given GCSF vs. control; however no difference in brain edema was observed at 24 hrs after injury between groups. Protocol III: median systemic ANC at the time of CCI was increased ten-fold in rats given GCSF vs. control. No difference in brain myeloperoxidase activity 24 hrs after CCI was observed in rats treated with GCSF vs. control. CONCLUSIONS: Systemic ANC influences BBB damage after traumatic brain injury produced by CCI. Because BBB damage and brain edema are discordant, mechanisms other than BBB damage likely predominate in the pathogenesis of brain edema after contusion. The implications of increased BBB permeability with the administration of GCSF in our model remains to be determined. Increasing systemic ANC before CCI with GCSF administration does not increase posttraumatic brain neutrophil accumulation or brain edema after CCI in rats. The finding that neutrophil infiltration is not enhanced by systemic neutrophilia suggests that the ability of GCSF-stimulated neutrophils to migrate into injured tissue may be impaired. Further studies are needed to evaluate the effects of GCSF administration on secondary injury and functional outcome in experimental models of traumatic brain injury.

Animals↗
PubMed2006

Delayed, post-injury treatment with aniracetam improves cognitive performance after traumatic brain injury in rats.

Chronic cognitive impairment is an enduring aspect of traumatic brain injury (TBI) in both humans and animals. Treating cognitive impairment in the post-traumatic stages of injury often involves the delivery of pharmacologic agents aimed at specific neurotransmitter systems. The current investigation examined the effects of the nootropoic drug aniracetam on cognitive recovery following TBI in rats. Three experiments were performed to determine (1) the optimal dose of aniracetam for treating cognitive impairment, (2) the effect of delaying drug treatment for a period of days following TBI, and (3) the effect of terminating drug treatment before cognitive assessment. In experiment 1, rats were administered moderate fluid percussion injury and treated with vehicle, 25, or 50 mg/kg aniracetam for 15 days. Both doses of aniracetam effectively reduced injury-induced deficits in the Morris water maze (MWM) as measured on postinjury days 11-15. In experiment 2, injured rats were treated with 50 mg/kg aniracetam or vehicle beginning on day 11 postinjury and continuing for 15 days. MWM performance, assessed on days 26-30, indicates that aniracetam-treated animals performed as well as sham-injured controls. In experiment 3, animals were injured and treated with aniracetam for 15 days. Drug treatment was terminated during MWM testing on postinjury days 16-20. In this experiment, aniracetam-treated rats did not perform better than vehicle-treated rats. The results of these experiments indicate that aniracetam is an effective treatment for cognitive impairment induced by TBI, even when treatment is delayed for a period of days following injury.

Animals↗
PubMed2005

Traumatic brain injury induced hypopituitarism: the need and hope of rehabilitation.

Traumatic brain injury is a leading cause of death and disability in developed countries. Damage caused by focal and diffuse lesions produces symptoms involving most major medical systems as well as symptoms of neurological and psychological origin. The severity of a traumatic brain injury is difficult to assess, and therefore, an initial accurate prognosis is difficult as well. Present treatments focus on relieving symptoms without adequately addressing the underlying cause of those symptoms. Recent studies have shown anterior pituitary deficiencies to be common amongst survivors of TBI. As many symptoms ascribed to a TBI are similar to the symptoms of hypopituitarism, it is possible that treatment of these deficiencies will improve functioning and the quality of life for survivors of traumatic brain injuries.

Brain Injuries↗
PubMed2026

Role of Polygenic Risk Scores in Predicting Cognitive Functioning after Mild Traumatic Brain Injury: A TRACK-TBI Study.

Patients with traumatic brain injury (TBI) and Glasgow Coma Scale scores of 13-15 (historically called mild TBI [mTBI]) commonly experience changes in cognitive functioning, including processing speed, memory, and executive functioning. In a prospective sample (N = 523) of individuals of European descent who had been treated in a U.S. level 1 trauma center for mTBI, we examined the prognostic value of four polygenic risk scores (PRS) for cognitive outcomes at 6-months postinjury. To estimate the impact of mTBI on cognition, primary cognitive outcomes were scaled as z-scores reflecting changes in performance relative to predicted preinjury performance. The PRS examined were previously developed and validated to predict cognition-related outcomes of educational attainment (Education-PRS), intelligence (Intelligence-PRS), and Alzheimer's disease (AD-mild traumatic brain injury (APOE)-PRS and AD + APOE-PRS). Both the Education-PRS and Intelligence-PRS displayed bivariate associations with all four cognitive outcomes (&#x3b2; = 0.19-0.32), whereas neither Alzheimer's disease PRS was significantly associated with any outcome. After controlling for other factors known to predict cognitive outcomes of TBI (e.g., sex, education, mTBI severity defined by a combination of Glasgow Coma Scale scores and the presence/absence of acute intracranial findings on clinical neuroimaging), the Education-PRS and Intelligence-PRS remained independently predictive of verbal episodic memory (&#x3b2; = 0.10-0.16), whereas their associations with processing speed and executive functioning were mostly nonsignificant and were mediated through educational attainment. Looking across primary z-score and secondary raw score outcomes, cognitive outcomes 6 months post-mTBI were good on average, and PRS made small independent contributions to outcome prediction. The mediation model findings may support theories of cognitive reserve, which propose that individuals with stronger preinjury cognitive processing abilities (often estimated by educational history) can better compensate for TBI. Moreover, findings indicate that PRS may contribute modestly to multivariable models predicting cognitive function after TBI.

Humans↗
PubMed2004

[The protective effect of p53 antisense oligonucleotide against neuron apoptosis secondary to traumatic brain injury].

OBJECTIVE: To observe the phenomenon of delayed neuron death secondary to traumatic brain injury, and the protective effect of p53 antisense oligonucleotide against neuron apoptosis secondary to traumatic brain injury. METHODS: This study was based on the rat diffuse brain trauma model established by a simple weight-drop device. The behavior scales of neural function of rats and TUNEL that examined the injury extent of DNA in the cortex were used as a general assessment of brain injury. Electron microscope was used to observe the histological and cellular morphology. mRNA and protein expression of p53 were detected by in situ hybridization and immunohistochemistry. In this model, the therapeutic effect of p53 antisense drug were observed. RESULTS: Following trauma, the behavior scores of rats decreased rapidly and remarkably. Apoptotic neurons appeared in the traumatized cortex as early as 2 hours after impact, and peaked at 24 hours. As early as 2 hours after impact, p53 mRNA and p53 protein in the cortex were expressed increasingly. CONCLUSION: Neural apoptosis plays an important role in delayed neuron death and is responsible for neural dysfunction following traumatic brain injury. So the inhibition of neural apoptisis would turn into a new therapic measure against delayed neuron death following traumatic brain injury.

Animals↗
PubMed2000

[An experimental study on traumatic brain injury for inducing neuronal apoptosis in rats].

This study was designed to explore the effect of traumatic brain injury and its mechanism for inducing neuronal apoptosis. The model of experimental traumatic brain injury was used. The rats were dispatched at different times(3 h, 12 h, 24 h, 48 h, 72 h) after traumatic brain injury, and the neuronal apoptosis was evaluated with microscope (HE staining), TUNEL method, flow cytometry, gel electrophoresis and immunohistochemistry assay. The results showed that the brain tissue neurons treated by traumatic brain injury underwent morphological changes of apoptosis, the DNA presented "ladder" break, the rate of neuronal apoptosis at different times ranged from 9.8% to 14.0%, but that of the control group was 1.7% and the expressions of related apoptosis genes(c-myc, fas and fasL) were increased. The findings of this study indicate that traumatic brain injury can induce neuronal apoptosis, and its molecular mechanism might be related to the expression of some apoptosis genes.

Animals↗
PubMed2004

Time interval of oral feeding recovery as a prognostic factor in severe traumatic brain injury.

PRIMARY OBJECTIVES: To assess the outcome of severe traumatic brain injury at least 1 year after trauma, in relation to some early clinical prognostic factors occurring during coma recovery. RESEARCH DESIGN: Retrospective study conducted at the post-coma unit of a rehabilitation hospital. METHODS AND PROCEDURES: A total of 43 patients were included. All of the patients sustained severe traumatic brain injury and prolonged coma, i.e. coma lasting at least 15 days. Outcome was assessed by means of Glasgow Coma Scale, Barthel Index and Mini Mental State 1 year after trauma, in relation to some early clinical prognostic factors occurring during coma recovery. MAIN OUTCOMES AND RESULTS: At the 1 year follow-up, a statistically significant correlation was found with both the Glasgow Outcome Scale and the Barthel Index for the time interval from brain injury to recovery of the following clinical variables: optical fixation, ability to obey commands, spontaneous motor activity and first safe oral feeding. Psychomotor agitation and bulimia were also favourable prognostic factors for the final outcome. CONCLUSIONS: In the present study, first safe oral feeding during coma recovery represents the clinical feature that better predicts the final outcome of patients with severe traumatic brain injury and prolonged coma.

Adolescent↗
PubMed1998

Executive functioning as outcome in patients after traumatic brain injury.

The present study was designed to determine how traumatic brain injury affect executive functioning, to know whether different treatments in the acute phase improve this functioning, and to check whether the severity of the neurocognitive impairment is detected by the Glasgow Outcome Scale (GOS). Ability for problem solving and executive functioning within 2 years after Traumatic Brain Injury (TBI) was examined in 35 conscious survivors. Two groups were formed. One group consisted of 13 patients who needed neurosurgery. The other group was made up of 22 patients without neurosurgical treatment. All were treated in the Neurosurgical Intensive Care Unit and in the Rehabilitation Service. The following variables were registered: Secondary Lesions, Glasgow Coma Scale (GCS), CT, subacute CT, and Glasgow Outcome Scale. Neuropsychological tests administered were Wisconsin Card Sorting Test (WCST) and the Tower of Hanoi/Sevilla. Comparing both groups' test performance (man Whitney U) we found that a severe traumatic brain injury, whatever the treatment applied in the acute phase, impairs the executive functioning of the patients; this impairment is related to acute pathophysiological events. The neurosurgical intervention does not improve the executive functioning. The Glasgow Outcome Scale does not detect more than 25% of the patients with severe impairment. It is suggested that the Tower of Hanoi/Sevilla could be a good tool to evaluate the executive functioning routinely in TBI patients as outcome. It also suggested that mild TBI patients must be referred for a complete neuropsychological examination.

Adult↗
PubMed2004

Effects of diffuse axonal injury on speed of information processing following severe traumatic brain injury.

To test the hypothesis that slowed information processing in traumatic brain injury is related to diffuse axonal injury (DAI), the authors compared 10 patients with predominant DAI (diffuse group) and minimal DAI (mixed injury group) on the Symbol Digit Modalities Test, simple and choice reaction time, Trail Making Tests A and B, and the Stroop Neuropsychological Screening Test. The diffuse group was slower than the mixed injury and control groups on basic speed of processing tasks. This difference was not apparent on complex speeded tasks once basic speed of processing was controlled for. The diffuse group's slower speed of processing was not accounted for by differences in injury severity, age, or time postinjury. The diffuse group showed greater recovery over time.

Adolescent↗
PubMed2004

Mild traumatic brain injuries presenting to Swedish hospitals in 1987-2000.

OBJECTIVE: To evaluate the incidence and causes of mild traumatic brain injury in Sweden. DESIGN: Retrospective, population-based incidence cohort study. SUBJECTS: All persons presenting to hospitals in Sweden between 1987 and 2000 with a discharge diagnosis of ICD-9 code 850 and ICD-10 code S0.60. METHODS: Data source was the Hospital Discharge Register at the National Board of Health and Welfare (Sweden). Incidence rates are stratified by age, gender, mechanism of injury and length of hospital stay. RESULTS: Men had a mean of 209 mild traumatic brain injuries per 100,000 inhabitants and women averaged 148 per 100,000. Men had more mild traumatic brain injury than women at all ages. There were 2 incidence peaks, in the age strata 16-20 years and those over 65 years. Falls were the most common cause of mild traumatic brain injury overall and occurred commonly under the age of 10 years and over the age of 65 years. Motor vehicle and bicycle injuries were the second and third most common causes of mild traumatic brain injury, and had their peak incidence in those aged 16-35 years. CONCLUSION: Preventative strategies for mild traumatic brain injury should be age and gender specific.

Adolescent↗