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Results for “Traumatic Brain Injuries”

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PubMed2002

Traumatic brain injury in older adults.

Traumatic brain injury (TBI) is a serious health risk for older adults, and the consequences of TBI range from full recovery to death. For many who survive, there is a legacy of cognitive, physical, and emotional disability. Falls are the major cause of head injury in older adults. There are many risk factors including pre-existing brain disease, other diseases, and, sometimes, iatrogenic factors. Efforts directed at prevention are of great importance. Outcome studies indicate that outcome is generally worse for older people than for younger people with similar injuries, but older individuals also deserve aggressive rehabilitation directed at the best possible recovery. This review will discuss the symptoms and syndromes that commonly result from TBI with comments about treatment.

Aged↗

PubMed1996

Cerebral uric acid increases following experimental traumatic brain injury in rat.

Following traumatic brain injury (TBI), cortical and thalamic areas were analyzed histologically and by high-performance liquid chromatography with electrochemical detection for uric acid at various survival times. Following TBI, cortical uric acid was elevated by ten-fold at 24 and 48 h, but not at 1 h post-TBI. Histological evidence of neurodegeneration was found not only in cortex but also in the anteroventral thalamus. These data suggest that as in stroke, uric acid measurements may be a convenient and sensitive method for measuring peroxidative status in TBI.

Animals↗

PubMed2005

Progesterone treatment inhibits the inflammatory agents that accompany traumatic brain injury.

Progesterone given after traumatic brain injury (TBI) has been shown to reduce the initial cytotoxic surge of inflammatory factors. We used Western blot techniques to analyze how progesterone might affect three inflammation-related factors common to TBI: complement factor C3 (C3), glial fibrillary acidic protein (GFAP), and nuclear factor kappa beta (NFkappaB). One hour after bilateral injury to the medial frontal cortex, adult male rats were given injections of progesterone (16 mg/kg) for 2 days. Brains were harvested 48 h post-TBI, proteins were extracted from samples, each of which contained tissue from both the contused and peri-contused areas, then measured by Western blot densitometry. Complete C3, GFAP, and NFkappaB p65 were increased in all injured animals. However, in animals given progesterone post-TBI, NFkappaB p65 and the inflammatory metabolites of C3 (9 kDa and 75 kDa) were decreased in comparison to vehicle-treated animals. Measures of NFkappaB p50 showed no change after injury or progesterone treatment, and progesterone did not alter the expression of GFAP. The therapeutic benefit of post-TBI progesterone administration may be due to its salutary effect on inflammatory proteins known to increase immune cell invasion and cerebral edema.

Analysis of Variance↗

PubMed2006

Molecular correlates of age-specific responses to traumatic brain injury in mice.

Aged traumatic brain injury (TBI) patients suffer higher rates of mortality and disability than younger patients. Cognitive problems common to TBI patients are associated with damage to the hippocampus, a central locus of learning and memory. To investigate the molecular mechanisms of age-related vulnerability to brain injury in a mouse model of TBI, we studied the effects of TBI on hippocampal gene expression in young and aged mice. Young and aged male C57Bl/6 mice were subjected to sham injury or TBI and sacrificed 24 h post-injury. We used laser capture microdissection to obtain pure populations of neurons from the CA1, CA3, and dentate gyrus subfields of the hippocampus. We compared injury-induced gene expression in hippocampal neurons of young and aged mice using quantitative ribonuclease protection assay analysis of linearly amplified mRNA from laser captured neurons. Both increased age and TBI were associated with increased expression of neuroprotective (brain-derived neurotrophic factor), pro-inflammatory (interleukin-1beta), and proapoptotic (caspase-3) genes in mouse hippocampal neurons. Our data support previous reports that suggested the CA3 subregion is highly susceptible to fluid percussion TBI and that age-related changes in gene expression are one potential mechanism of increased vulnerability of the aged brain to TBI.

Aging↗

PubMed2005

Comparison of subjective and objective measurements of balance disorders following traumatic brain injury.

Patients with mild traumatic brain injury (TBI) often complain of dizziness. However, these problems may be undetected by a clinical exam. Therefore, the purpose of this study was to evaluate the relationships between the subjective and objective measures of balance impairment. Ten patients with TBI (6 men and 4 women) and 10 matched controls participated in this study. Average duration since the TBI was 2.8 years (range 0.4-14.4). Six of the 10 subjects with TBI had abnormal imaging studies. All subjects and controls had a normal neuromuscular exam. Tinetti Balance Assessments were obtained and the TBI group was not significantly different from the control group. The Dizziness Handicap Inventory (DHI) score supported their complaints of "unsteadiness" and "imbalance" from the subjects with TBI. The DHI score was 32 +/- 23 (range 4-68) out of a maximum possible score of 100. Balance was tested using computerized dynamic posturography. The Sensory Organization Test score was significantly lower for subjects who had a TBI (70 +/- 12) compared to the control subjects (80 +/- 8), which indicated that the subjects with TBI had poorer balance than the control subjects. A 13-link biomechanical model of the human body was used to compute the kinematics of the whole body center of mass (COM) while walking on a level surface. The subjects with TBI had significantly less displacement in the anterior/posterior direction, walked significantly slower, had significantly greater medial/lateral sway and velocity than the normal controls, and had significantly greater medial/lateral imbalance. There was a significant relationship between the physical aspects of the DHI and posturography. There was also significant relationship between the physical, functional, and total DHI and the motion of the COM. Overall, the motion of the COM predicted between 42 and 69% of the DHI score. The present study has demonstrated that objective measurements can quantify the patient's functional deficits. Therefore, these objective measurement techniques should be used to assess the clinical complaints of imbalance from patients with TBI.

Adult↗

PubMed1997

Activating the posttraumatic cholinergic system for the treatment of cognitive impairment following traumatic brain injury.

Cognitive impairment after traumatic brain injury (TBI) is correlated with decreased cholinergic markers of neuronal viability. The purpose of this experiment was to test the hypothesis that pharmacological activation of the muscarinic cholinergic system during the recovery period after TBI will improve cognitive performance. LU 25-109-T is a partial muscarinic M1 agonist that also acts as an antagonist at presynaptic M2 autoreceptors (thus increasing ACh release). Injured rats were injected subcutaneously daily for 15 days with either 0.0, 3.6, or 15 mumol/kg of LU 25-109-T beginning 24 h after a receiving a moderate (2.1 +/- 0.1 atm) level of central fluid percussion brain injury. Cognitive performance was assessed on days 11-15 postinjury in a Morris water maze (MWM). Injured rats treated with 15 mumol/kg, but not those treated with 3.6 mumol/kg, showed a significant improvement (p < 0.01) in MWM performance as compared with injured vehicle-treated rats. This result supports the hypotheses that a decrease in posttraumatic cholinergic neurotransmission contributes to TBI-induced cognitive deficits and that increasing cholinergic tone during the recovery period following TBI will improve cognitive performance.

Animals↗

PubMed2002

Sequelae following traumatic brain injury. The cerebrovascular perspective.

Traumatic brain injury (TBI) initiates a huge repertoire of biochemical perturbations. On one hand, destructive events are set into motion while on the other hand, protective and recovery mechanisms are evoked, each with their own temporal and spatial characteristics. The brain exists as a finely tuned balance between vascular, neuronal and glial interactions and so a complex interplay between these factors will dictate the final evolution of pathogenesis. Although vascular damage is a key event, it remains a somewhat neglected component to the underlying degenerative processes that evolve following injury to the brain. The present review will act to integrate the current knowledge of the vascular events proceeding injury to the brain, with an emphasis on how this impacts the control of vascular function and thus cerebral blood flow.

Animals↗

PubMed2003

Cerebral blood flow in chronic symptomatic mild traumatic brain injury.

Patients with mild traumatic brain injury (MTBI) challenge physicians' skills and test their patience. Their manifold symptomatology is often not supported by objective neurological findings. We sought to compare regional cerebral blood flow (rCBF) between symptomatic subjects with longstanding MTBI and healthy controls, and to examine the correspondence between neuropsychological deficit and rCBF compromise. Twenty-eight clinically symptomatic male subjects with MTBI and twenty matched controls underwent neuropsychological testing and Tc-99m-HMPAO brain SPECT imaging. Neuropsychological test data were used to categorize subjects into sub-groups according to the presumed location of lesions based on their neurobehavioral deficits. Image subtraction comparisons were made between controls, all MTBI subjects and sub-groups. MTBI patients demonstrated regions of hypoperfusion in frontal, pre-frontal and temporal cortices, and sub-cortical structures. Hypoperfusion in 'frontal', 'left posterior' and to a lesser extent 'sub-cortical' sub-groups was concordant with neuropsychological localization. This was not the case for the 'right posterior' group, where no concordance was found. The rCBF is reduced in symptomatic patients with longstanding MTBI and unremarkable structural brain imaging. Although group analysis is appropriate for the generation of statistically significant differences, the clinical application of brain SPECT imaging in MTBI calls for a capability to associate clinical examination, neuropsychological assessment and cerebral perfusion at the individual subject level. Such competence is still to be attained.

Adult↗

PubMed2006

Alterations in mammalian target of rapamycin signaling pathways after traumatic brain injury.

In response to traumatic brain injury (TBI), neurons initiate neuroplastic processes through the activation of intracellular signaling pathways. However, the molecular mechanisms underlying neuroplasticity after TBI are poorly understood. To study this, we utilized the fluid-percussion brain injury (FPI) model to investigate alterations in the mammalian target of rapamycin (mTOR) signaling pathways in response to TBI. Mammalian target of rapamycin stimulates mRNA translation through phosphorylation of eukaryotic initiation factor 4E binding protein-1 (4E-BP1), p70 ribosomal S6 kinase (p70S6K), and ribosomal protein S6 (rpS6). These pathways coordinate cell growth and neuroplasticity via dendritic protein synthesis. Rats received sham surgery or moderate parasagittal FPI on the right side of the parietal cortex, followed by 15 mins, 30 mins, 4 h, 24 h, or 72 h of recovery. Using Western blot analysis, we found that mTOR, p70S6K, rpS6, and 4E-BP1 phosphorylation levels were significantly increased in the ipsilateral parietal cortex and hippocampus from 30 mins to 24 h after TBI, whereas total protein levels were unchanged. Using confocal microscopy to localize these changes, we found that rpS6 phosphorylation was increased in the parietal cortex and all subregions of the hippocampus. In accordance with these results, eIF4E, a key, rate-limiting mRNA translation factor, was also phosphorylated by mitogen-activated protein kinase-interacting kinase 1 (Mnk1) 15 mins after TBI. Together, these results suggest that changes in mRNA translation may be one mechanism that neurons use to respond to trauma and may contribute to the neuroplastic changes observed after TBI.

Animals↗

PubMed2003

The epidemiology of traumatic brain injury: a review.

PURPOSE: Traumatic brain injury (TBI) not only has considerable morbidity and mortality, but it is a major cause of epilepsy. We wish to determine the frequency of TBI, special groups at risk for TBI, and mortality from TBI. METHODS: We reviewed studies of TBI that are either population based or derived from definable catchment areas that allow determination of incidence, identification of risk groups, and mortality. We review methodology used in epidemiologic studies of TBI and try to distinguish this data from that of head injury not necessarily affecting the brain. We report epidemiologic characteristics of TBI, including incidence, differences by age, gender, race and ethnic group, and geographic variation, and mortality. RESULTS: Population-based studies in the United States suggest that the incidence of TBI is between 180 and 250 per 100,000 population per year. Incidence may be higher in Europe and South Africa. There are groups at high risk for TBI. This includes males and individuals living in regions characterized by socioeconomic deprivation. There are selective age groups at risk for TBI. This includes the very young, adolescents and young adults, and the elderly. Mortality varies by severity but is high in those with severe injury and in the elderly. CONCLUSIONS: TBI is a major public health problem as well as a major cause of epilepsy. If primary prevention is to be undertaken, we must understand the epidemiology of the condition. The primary causes of TBI vary by age, socioeconomic factors, and geographic region, so any planned interventions must be tailored accordingly.

Age Distribution↗

PubMed2001

Delayed diagnosis of concomitant rotator cuff tear and brachial plexopathy in a patient with traumatic brain injury: a case report.

Traumatic brain injury (TBI) is often accompanied by additional trauma that can be obscured by cognitive dysfunction or multiple injuries in the same region of the body. This report describes the case of an unhelmeted motorcycle rider who collided with a telephone pole. He sustained a diffuse subarachnoid hemorrhage, bilateral subdural hematomas (right frontal and left temporal), diffuse axonal injury in the subcortical and periventricular white matter, and a left tibial fracture. After medical and surgical stabilization, he was transferred to a subacute rehabilitation facility and then to a rehabilitation center. He was evaluated for pain and limited range of motion in his right shoulder, where both a rotator cuff tear and a brachial plexopathy were diagnosed. This report discusses concomitant injuries that occur with TBI, and the management of rotator cuff tears and brachial plexopathy.

Brachial Plexus Neuropathies↗

PubMed2002

Attention impairment following traumatic brain injury.

The incidence of traumatic brain injury (TBI) is approximately 2,000,000 cases annually, and approximately 5.3 million Americans are currently living with some degree of cognitive-linguistic impairment secondary to TBI. One frequent aspect of that impairment is disordered attention. Attention is a complex system comprised of several component skills, each of which may be compromised by TBI and thus must be carefully assessed to design appropriate treatment protocols. Attention treatments for patients with TBI frequently involve implementing environmental controls and designing individualized therapy tasks that vary in terms of information processing demands. This article provides a summary of those attention impairments frequently associated with TBI and outlines assessment and treatment guidelines for clinicians serving TBI patients with attention problems.

Aphasia↗

PubMed2003

Non-pharmacological management of psychiatric disturbances after traumatic brain injury.

Persons who suffer traumatic brain injury (TBI) often demonstrate a variety of psychiatric and neuropsychiatric disturbances. Some of those disturbances may be managed by non-pharmacological methods. The methods draw heavily on established principles of psychotherapy and behavioral modification. However, the unique problems imposed by neurocognitive deficits must be factored into any form of non-pharmacological intervention with this patient group. A simple model consolidates information about the important ingredients in the non-pharmacological management of psychiatric disturbances in TBI patients.

Adult↗

PubMed2006

Development and evaluation of a pictorial-based analogical problem-solving programme for people with traumatic brain injury.

BACKGROUND: People with traumatic brain injury (TBI) must often deal with cognitive problems, including social problem-solving. The study reported herein evaluated the effectiveness of a newly developed pictorial-based analogical problem-solving skills training programme. It is hypothesized that the programme can help people with TBI to learn better problem-solving skills through systematic, theoretically driven learning strategies. METHOD: Based on the instrumental enrichment model and the hierarchy of daily problem-solving as suggested by Holloran and Bressler, analogical problem-solving training software was developed. Thirty subjects with TBI then attended a 20-session interactive analogical problem-solving skills training programme. Another 20 subjects with TBI and of similar demographics formed the control group. The outcome measures included session-based quizzes on analogical problem-solving, the Category Test of the Halstead Reitan Test Battery (HRTB) and the Lawton IADL Scale. FINDINGS: The analogical problem-solving training strategies were found to be effective in improving problem-solving skills. The subjects generally demonstrated a selective improvement in their functional and overall problem-solving skills, but not in their basic problem-solving skills. The subjects in the control group showed stable problem-solving skills over a 4-week interval (no statistically significant changes). The findings indicated the therapeutic significance of the training programme. CONCLUSIONS: The results of the study suggested that innovative cognitive rehabilitation programmes can be customized to match the needs of clients with TBI. The applicability and implications of the interactive pictorial-based analogical problem-solving skill-training programme that was used in the study and possibilities for future study in this research area are also discussed.

Adolescent↗

PubMedDate not supplied

Functional memory skills following traumatic brain injury in young children.

Traumatic brain injury (TBI) may have a profound impact on a child's ongoing development. Various risk factors have been found to predict outcome, but considerable variability remains unexplained. This study used a prospective, longitudinal design to examine recovery of memory function following TBI within the pre-school period. Forty-four children with TBI were divided according to injury severity (mild, moderate, severe), and compared to age and SES matched healthy controls (n = 26). Children were evaluated acutely and at 12 months post-injury using the Rivermead Behavioural Memory Test for Children. Results failed to show a clear dose-response relationship between injury severity and memory function during the acute phase of recovery. However, this relationship developed over time, with greater memory impairments evident for children with more severe TBI by 12 months post-injury. Children with mild TBI exhibited few memory problems.

Analysis of Variance↗

PubMed1996

Voltage-dependent Na+/K+ ion channel blockade fails to ameliorate behavioral deficits after traumatic brain injury in the rat.

Traumatic brain injury (TBI) induces massive, transient ion flux, after impact. This may be via agonist gated channels, such as the muscarinic, cholinergic or NMDA receptor, or via voltage-dependent channels. Pharmacological blockade of the former, is neuroprotective in most TBI models, but the role of voltage-dependent Na+/K+ channels has not been tested. We have therefore tested the hypothesis that intraventricular tetrodotoxin (TTX) (20 microliters, 5 mM) induced blockade of post-TBI ion flux will prevent cytotoxic cell swelling, Na+ and K+ flux, and behavioral deficit. Microdialysis demonstrated blockade of [K+]d flux in the TTX group compared to controls. Behavioral evaluation of motor (days 1-5) and memory function (days 11-15) after TBI revealed no beneficial effect in the TTX group compared to controls. Thus, although evidence of reduced ionic flux was demonstrated in the TTX group, memory and behavior were unaffected, suggesting that agonist-operated channel-mediated ion flux is more important after TBI.

Animals↗

PubMed1999

Effects of L-NAME and 7-NI on NOS catalytic activity and behavioral outcome after traumatic brain injury in the rat.

Traumatic brain injury (TBI) produces transient increases in constitutive nitric oxide synthase (cNOS) activity and prolonged behavioral abnormalities. This study investigated the effects of nitro-L-arginine-methyl ester (L-NAME) and 3-bromo-7-nitroindazole (7-NI) treatment on cNOS catalytic activity and sensorimotor behavioral outcome after TBI. Rats underwent moderate (1.8-2.2 atm) parasagittal fluid percussion brain injury (FPI). At 5 min after FPI, cNOS activity was significantly increased within the damaged cerebral cortex of vehicle-treated rats compared to the noninjured contralateral cortex (206.7 +/- 150.5 % of contralateral, p < 0.01). Pretreatment with L-NAME and 7-NI significantly reduced injury-induced cNOS activation (47.7 +/- 42.6 %, p < 0.05, and 96.16 +/- 12.76, p < 0.05, respectively). Pretreatment with L-NAME and 7-NI also inhibited cNOS activity within the contralateral noninjured cerebral cortex compared to vehicle-treated rats (L-NAME 43.7 +/- 12.47%, p < 0.05; 7-NI 36.8 +/- 7.47%, p < 0.05). Furthermore, pretreatment with 7-NI, but not L-NAME, significantly reduced forelimb placing sensorimotor deficits (3.14 +/- 1.07, p < 0.05) at 1 day after TBI compared to vehicle-treated rats (5.38 +/- 0.42). These data indicate that inhibition of injury-induced elevations in neuronal NOS activity has a beneficial effect on neurological outcome after parasagittal FPI brain injury.

Animals↗

PubMed1999

Cyclosporin A significantly ameliorates cortical damage following experimental traumatic brain injury in rodents.

Experimental traumatic brain injury (TBI) results in a rapid and significant necrosis of cortical tissue at the site of injury. In the ensuing hours and days, secondary injury exacerbates the original damage, resulting in significant neurological dysfunction. Young adult animals were treated either 5 min before or immediately after a cortical injury with the immunosuppressant cyclosporin A (CsA). All animals treated with CsA demonstrated a significant reduction in the amount of cortical damage 7 days following TBI. The effect was observed in adult rats and in two different strains of adult mice following systemic administration of the drug. Cyclosporin A has known effects on mitochondria by inhibiting the opening of the permeability transition pore and maintaining calcium homeostasis. These results with a clinically approved drug demonstrate an almost 50% reduction in lesion volume and suggest that the mechanisms responsible for tissue necrosis following TBI are amenable to manipulation. Since CsA also has known interactions with calcineurin and may be providing neuroprotection through that mechanism, additional animals were treated with the immunosuppressant FK 506. FK 506 failed to protect against the cortical damage. Amelioration of cortical damage with CsA indicates that pharmacological therapies can be devised that will significantly alter neurological outcome after injury.

Animals↗