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Results for “Traumatic Brain Injuries”

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PubMed2005

Effect of traumatic subarachnoid haemorrhage on neuropsychological profiles and vocational outcome following moderate or severe traumatic brain injury.

OBJECTIVE: Traumatic subarachnoid haemorrhage (tSAH) frequently occurs in moderate or severe traumatic brain injury (TBI) and is related to worse outcome at time of discharge from the acute hospitalization. The current study compared neuropsychological impairment and vocational outcome at 1-year post-injury in patients with and without tSAH. DESIGN: Acute injury, neuroradiological, neuropsychological and vocational data were collected for 100 patients admitted for neurorehabilitation following TBI. RESULTS: Patients with tSAH had significantly worse vocational outcome than patients without tSAH. On neuropsychological measures, patients with tSAH generally performed worse than patients without tSAH across most neurocognitive domains. However, differences in neuropsychological test performance between patients with and without tSAH reached statistical significance on measures of visuospatial processing, verbal reasoning and mood only. CONCLUSION: The presence of tSAH appears to be associated with worse vocational outcome in survivors of moderate or severe TBI. As such, the presence of tSAH appears to have predictive value with respect to outcome following TBI.

Adult↗

PubMed1996

Swallowing problems in adults with traumatic brain injury.

In patients with traumatic brain injury, the anatomic and physiologic status of the swallowing mechanism may be impaired. Patients typically compensate for these impairments by learning and using compensatory strategies to ensure safe and efficient food intake. However, when cognitive-communicative and behavioral impairments are also present, the rehabilitation of dysphagia is more complex and challenging. To facilitate maximum recovery from dysphagia, an interdisciplinary team approach is essential. Teams may include several medical and allied healthcare professionals such as the physician, nurse, speech-language pathologist, clinical dietitian, and physical and occupational therapist. The psychologist may be consulted to provide expertise in behavioral management strategies. The patient and caregiver also are integral members of this treatment team. Each team member needs to be aware of the food consistencies that are appropriate and the specific feeding techniques that are required. It is critical that all team members be consistent in their approach to feeding for the patient to learn and generalize the use of compensatory strategies. This article has presented a review of the literature on swallowing problems in traumatic brain injury. It is apparent that there are relatively few data-based studies that describe the impairments and even fewer that discuss the efficacy of treatment for dysphagia in these patients. In view of the frequency of oral intake problems in individuals with traumatic brain injury, and the added challenge of the cognitive-communicative problems, further studies are needed to increase our understanding of swallowing problems, their treatment, and recovery in this patient population.

Brain Injuries↗

PubMed2006

Impact of additional extracranial injuries on outcome after mild traumatic brain injury.

Many patients with mild traumatic brain injury (MTBI) concurrently sustain extracranial injuries; however, little is known about the impact of these additional injuries on outcome. We assessed the impact of additional injuries on the severity of postconcussional symptoms (PCS) and functional outcome 6 months post-injury. A questionnaire (including the Rivermead Post-Concussion Questionnaire and SF-36) was sent to consecutive MTBI patients (hospital admission Glasgow Coma Score 13-15; age range 18-60 years) admitted to the emergency department of a level-I trauma center, and, to serve as a baseline for PCS, a control group of minor-injury patients (ankle or wrist distortion). Of the 299 MTBI respondents (response rate 52%), 89 had suffered additional injuries (mean Injury Severity Score [ISS] of 14.5 +/- 7.4). After 6 months, 44% of the patients with additional injuries were still in some form of treatment, compared to 14% of patients with isolated MTBI and 5% of the controls. Compared to patients with isolated injury, MTBI patients with additional injuries had resumed work less frequently and reported more limitations in physical functioning. Overall, they did not report higher levels of PCS, despite somewhat more severe head injury. Regardless of the presence of additional injuries, patients that were still in treatment reported significantly more severe PCS, with highest rates in patients with isolated MTBI. In conclusion, many patients with additional extracranial injuries are still in the process of recovery at 6 months after injury. However, despite more severe impact to the head and inferior functional outcomes, these patients do not report more severe PCS.

Adult↗

PubMed2005

Proton MR spectroscopic imaging depicts diffuse axonal injury in children with traumatic brain injury.

BACKGROUND AND PURPOSE: Diffuse axonal injury (DAI) after traumatic brain injury (TBI) is important in patient assessment and prognosis, yet they are underestimated with conventional imaging techniques. We used MR spectroscopic imaging (MRSI) to detect DAI and determine whether metabolite ratios are accurate in predicting long-term outcomes and to examine regional differences in injury between children with TBI and control subjects. METHODS: Forty children with TBI underwent transverse proton MRSI through the level of the corpus callosum within 1-16 days after injury. T2-weighted, fluid-attenuated inversion recovery, and susceptibility-weighted MR imaging was used to identify voxels as normal-appearing or as nonhemorrhagic or hemorrhagic injury. Neurologic outcome was evaluated at 6-12 months after injury. Metabolite ratios for total (all voxels), normal-appearing, and hemorrhagic brain were compared and used in a logistic regression model to predict long-term outcome. Total and regional metabolite ratios were compared with control data. RESULTS: A significant decrease in N-acetylaspartate (NAA)/creatine (Cr) and increase in choline (Cho)/Cr (evidence of DAI) was observed in normal-appearing (P < .05) and visibly injured (hemorrhagic) brain (P < .001) compared with controls. In normal-appearing brain NAA/Cr decreased more in patients with poor outcomes (1.32 +/- 0.54) than in those with good outcomes (1.61 +/- 0.50, P = .01) or control subjects (1.86 +/- 0.1, P = .00). In visibly injured brains, ratios were similarly altered in all patients. In predicting outcomes, ratios from normal-appearing and visibly-injured brain were 85% and 67% accurate, respectively. CONCLUSION: MRSI can depict injury in brain that appears normal on imaging and is useful for predicting long-term outcomes.

Adolescent↗

PubMed2007

Magnesium sulfate for neuroprotection after traumatic brain injury: a randomised controlled trial.

BACKGROUND: Traumatic brain injuries represent an important and costly health problem. Supplemental magnesium positively affects many of the processes involved in secondary injury after traumatic brain injury and consistently improves outcome in animal models. We aimed to test whether treatment with magnesium favourably affects outcome in head-injured patients. METHODS: In a double-blind trial, 499 patients aged 14 years or older admitted to a level 1 regional trauma centre between August, 1998, and October, 2004, with moderate or severe traumatic brain injury were randomly assigned one of two doses of magnesium or placebo within 8 h of injury and continuing for 5 days. Magnesium doses were targeted to achieve serum magnesium ranges of 1.0-1.85 mmol/L or 1.25-2.5 mmol/L. The primary outcome was a composite of mortality, seizures, functional measures, and neuropsychological tests assessed up to 6 months after injury. Analyses were done according to the intention-to-treat principle. This trial is registered with , number . FINDINGS: Magnesium showed no significant positive effect on the composite primary outcome measure at the higher dose (mean=55 average percentile ranking on magnesium vs 52 on placebo, 95% CI for difference -7 to 14; p=0.70). Those randomly assigned magnesium at the lower dose did significantly worse than those assigned placebo (48 vs 54, 95% CI -10.5 to -2; p=0.007). Furthermore, there was higher mortality with the higher magnesium dose than with placebo. Other major medical complications were similar between groups, except for a slight excess of pulmonary oedema and respiratory failure in the lower magnesium target group. No subgroups were identified in which magnesium had a significantly positive effect. INTERPRETATION: Continuous infusions of magnesium for 5 days given to patients within 8 h of moderate or severe traumatic brain injury were not neuroprotective and might even have a negative effect in the treatment of significant head injury.

Adolescent↗

PubMedDate not supplied

Traumatic brain injuries in Alaska, 1996-1998.

Traumatic brain injuries often lead to severe disability or death. These injuries most often affect younger, more active people and are likely to have enduring physical, emotional, and financial costs. In order to determine the incidence, etiology and severity of traumatic brain injuries in Alaska, the Alaska Department of Health and Social Services has conducted a three-year study of the demographic and epidemiologic characteristics of traumatic brain injuries in Alaska. From 1996 through 1998, 1,932 hospitalized cases or out-of-hospital deaths occurred in the state among Alaska residents, for an average incidence rate of 105.2 per 100,000 population. To analyze the incidence of these injuries, the Traumatic Brain Injury Surveillance Project analyzed the location, demographics, and etiology.

Accidents↗

PubMed2000

Biochemical, cellular, and molecular mechanisms in the evolution of secondary damage after severe traumatic brain injury in infants and children: Lessons learned from the bedside.

OBJECTIVE: To present a state-of-the-art review of mechanisms of secondary injury in the evolution of damage after severe traumatic brain injury in infants and children. DATA SOURCES: We reviewed 152 peer-reviewed publications, 15 abstracts and proceedings, and other material relevant to the study of biochemical, cellular, and molecular mechanisms of damage in traumatic brain injury. Clinical studies of severe traumatic brain injury in infants and children were the focus, but reports in experimental models in immature animals were also considered. Results from both clinical studies in adults and models of traumatic brain injury in adult animals were presented for comparison. DATA SYNTHESIS: Categories of mechanisms defined were those associated with ischemia, excitotoxicity, energy failure, and resultant cell death cascades; secondary cerebral swelling; axonal injury; and inflammation and regeneration. CONCLUSIONS: A constellation of mediators of secondary damage, endogenous neuroprotection, repair, and regeneration are set into motion in the brain after severe traumatic injury. The quantitative contribution of each mediator to outcome, the interplay between these mediators, and the integration of these mechanistic findings with novel imaging methods, bedside physiology, outcome assessment, and therapeutic intervention remain an important target for future research.

Journal Article↗

PubMed2002

Intermediate and long-term outcome in traumatic brain injury is not influenced by additional multiple organ injury.

BACKGROUND: This investigation aims at evaluating the influence of additional multiple organ injury in traumatic brain injury on the outcome in terms of the ability to perform the activities of daily life, of the need of care, and of job ability. METHODS: 62 victims (male to female ratio 4 : 1; age range 15-68 years) of traumatic brain injury were studied. Group 1 (n = 24) consisted of patients who suffered from traumatic brain injury with additional multiple organ injury, group 2 (n = 38) comprised patients with isolated brain injury. Outcome was assessed at 6 and 12 months after trauma by means of different rehabilitation scores. RESULTS: After 6 as well as after 12 months, the majority of both groups were independent in the activities of daily living. Furthermore, no differences were observed concerning the need of care. Job ability was almost equal for both groups. CONCLUSION: Additional multiple organ injury does not pertain to prognosis of traumatic brain injury.

Activities of Daily Living↗

PubMed2003

Respiratory care in spinal cord injury with associated traumatic brain injury: bridging the gap in critical care nursing interventions.

Spinal cord injury (SCI) is a devastating and challenging condition. The events that lead to SCI, such as road traffic accidents, falls, sports and violence [Top. Spinal Cord Inj. Rehabil. 5 (1999) 83], are also the common aetiologies of traumatic brain injury (TBI). It's not surprising then, that 20-50% of those with cervical SCI have TBI [J. Trauma 46 (1999) 450]. The literature pertaining to the management of either injury in isolation is vast, but lacking where the two conditions are experienced together and require distinct adaptations to interventions. Consequently, a gap in the literature exists. This paper focuses on those patients with SCI of the cervical spine with associated head injury, and pay particular attention to respiratory difficulties, and presents interventions required to minimise and treat the effects of such pulmonary compromise.

Brain Injuries↗

PubMed2001

Neuronal injury and loss after traumatic brain injury: time course and regional variability.

We have examined regional neuronal injury after traumatic brain injury using Fluoro-Jade, an acidic dye that exhibits a marked affinity for both the degenerating neuronal cell body and its processes and have determined the extent to which early injury corresponds to regional patterns of neuronal loss. Rats (n=45) were subjected to lateral fluid percussion brain injury and euthanized at 3 h to 28 days post injury. Complementary Fluoro-Jade, silver impregnation methods and TUNEL were used to assess neuronal injury. Neuronal loss was evaluated in sections immunostained for NeuN, a neuronal specific nuclear protein. Overt neuronal cell loss was evident by 7 days post injury in the cortex, hippocampus and thalamus. Injured neurons were apparent in the ipsilateral cortex bordering the impact site, hippocampus (CA1 and dentate), thalamus, and vermis of the cerebellum as early as 3 h post injury. Degenerating neurons were maximal by 1 and 3 days in the cortex and hippocampus, by 3 and 7 days in the cerebellum, and by 7 days in the thalamus. The regional distribution of Fluoro-Jade-labeled neurons corresponded to a similar pattern of silver and TUNEL staining. Together, these findings demonstrate a regionally specific temporal pattern of neuronal injury that results in overt neuronal cell loss within both cortical and subcortical regions.

Animals↗

PubMed1999

Neuroprotective effect of hypothermia on neuronal injury in diffuse traumatic brain injury coupled with hypoxia and hypotension.

It is well established in mechanical head trauma that posttraumatic secondary insults, such as hypoxia and hypotension exacerbate neuronal injury and lead to worse outcome. In this study, the neuroprotective effect of hypothermia on the reduction of supraventricular subcortical neuronal damage was evaluated using an impact-acceleration model of diffuse traumatic brain injury coupled with both moderate and severe periods of hypoxia and hypotension. A total of 135 adult male Sprague-Dawley rats (340-375 g) were divided into three experimental studies: (I) physiological evaluation (n = 36); (II) quantitative analysis of the effect of trauma coupled with moderate and severe hypotension on neuronal damage assessed at 4 (n = 39) and 24 h (n = 24); and (III) the neuroprotective effect of hypothermia following moderate secondary insult (n = 36). Induction of hypothermia occurred at 15 min postinjury, to a level of 30 degrees C for 60 min. At the designated time points (4 and 24 h), the animals were sacrificed via standard transcardial perfusion techniques for histological processing. Quantitative assessment of neuronal damage using routine H&E staining at 4 hours showed neuronal damage which correlated with the severity of secondary insult. Animals exposed to trauma alone had a mean number of damaged neurons of 7.61 +/- 3.08/high powered field (hpf) compared with a mean of 1.21 +/- 0.30/hpf in the sham operated group (p = 0.015). Animals exposed to trauma with 10 min of hypoxia and hypotension (THH-10) showed a statistically significant number of damaged neurons compared to the sham-operated animals (7.50 +/- 2.15 damaged neurons/hpf, p = 0.013), whereas, neuronal damage in animals undergoing trauma with a 30-min secondary insult of hypoxia and hypotension (THH-30) was markedly increased (100 +/- 30.20/hpf, p = 0.002). Statistical analysis showed no significant difference in neuronal damage in animals subjected to secondary insult alone. At 24 h, the evolution of neuronal damage in the trauma alone group (5.08 +/- 1.63/hpf) was relatively static; however, there was a remarkable increase in the neuronal damage of the THH-10 group (29.88 50 +/- 8.20/hpf). However, hypothermia provided nearly complete protection against secondary insults, and neuronal damage was equal to that of the trauma alone group (p = 0.42). The results of this study confirm that hypothermia provides remarkable protection against the adverse effects of neuronal damage exacerbated by secondary injury. This study also presents a new model of secondary insult, which can be used experimentally to further define the mechanism of increased vulnerability of the injured brain.

Animals↗

PubMed1988

Treatment of the elderly brain-injured patient. Experience in a traumatic brain injury unit.

Recovery from traumatic brain injury in the elderly is a subject rarely discussed in the medical literature, and existing data is conflicting. The Traumatic Brain Injury Unit at Gaylord Hospital routinely admits patients over 50 years of age for rehabilitation after significant closed head injury. Of the 26 elderly head-injured patients reviewed over a four-year period for this study, 85% eventually returned to a home setting, with more than half independent in activities of daily living. Based on this encouraging data, it is suggested that the older head-injured patient can recover from severe closed head injury.

Activities of Daily Living↗

PubMed2002

Vision Disturbances Following Traumatic Brain Injury.

Vision disturbances following traumatic brain injury (TBI) include anomalies of accommodation, version, vergence (nonstrabismic, as well as strabismic), photosensitivity, visual field integrity, and ocular health. Traumatic brain injury patients with complex diplopia patterns, noncomitant strabismic anomalies, and advanced ocular health anomalies are either monitored by or referred to neuro-ophthalmologists and ophthalmologists for evaluation and possible surgical or medical intervention, as needed. Anomalies of accommodation, vergence, version, photosensitivity, and field of vision are amenable to noninvasive, rehabilitative interventions, such as vision therapy, which is rendered by optometrists and is described in this article. Further, vision therapy may be performed in isolation or in conjunction with the application of the following: Fusional prism spectacles (for diplopia) Tinted spectacles (for photosensitivity) Yoked prism spectacles (for visual-spatial hemispheric inattention, with or without a manifest visual field defect), as appropriate Dependent on the severity of vision impairment post-TBI, other types of rehabilitation, such as vestibular, physical, cognitive, and occupational rehabilitation, are deferred pending the stabilization of vision function to an appropriate level. Rehabilitative optometric intervention is appropriate and beneficial for many TBI patients. Therefore, it should be offered as a possible evaluation and treatment option to investigate the patient's symptoms and determine the prognosis for treatment, as would be done with any other therapeutic modality.

Journal Article↗

PubMed2006

Changes in white matter late after severe traumatic brain injury in childhood.

Severe traumatic brain injury in childhood, particularly that complicated by raised intracranial pressure, has significant long-term effects on the brain. Since magnetic resonance imaging provides a means of visualizing neuroanatomic structure in exquisite detail, the scope of this review is to revisit the pathology of traumatic brain injury described in recent clinical imaging studies. Acute imaging provides insight into the acute mechanism of focal and diffuse injury. There is some reduction in threshold for white matter pathology in the hemisphere ipsilateral to injury. After injury, there may be long-term effects on white matter architecture and the potential for brain growth. In this context, the pattern of hippocampal rather than parahippocampal gyrus tissue loss provides insight into the likely cause of white matter injury being cerebral hypoperfusion.

Atrophy↗

PubMed1995

Comparison of three measures of injury severity in children with traumatic brain injury.

Eighty-six traumatically brain-injured children aged 6 to 15 years who were consecutively admitted to a pediatric Level I trauma center were recruited for participation in the study. A comprehensive battery of behavioral, cognitive, communicative, social, motoric, and neurological tests was administered to the children from 12 to 36 months postinjury. The performance of three severity indices, the Glasgow Coma Scale (GCS), the ASCOT probability of survival, and the head injury component of the Anatomic Profile, was compared with respect to their association with long-term outcomes in five neurological domains, as assessed by linear regression models. The ASCOT probability of survival was correlated to test scores in all five domains. The GCS and the head injury component of the Anatomic Profile were each correlated to outcome in only one domain. The ASCOT probability of survival, which includes coded variables for the GCS, systolic blood pressure, and respiratory rates on admission, as well as a measure of multisystem anatomic injury, was the most sensitive indicator of head injury severity and was associated with outcomes beyond survival and death in this population. Probability of survival is a promising brain injury severity index that may be useful in efforts to assess new medical and rehabilitative therapies for children with traumatic brain injury.

Adolescent↗

PubMed1998

Reduction of tyrosine nitration after N(omega)-nitro-L-arginine-methylester treatment of mice with traumatic brain injury.

Oxygen free radicals and nitric oxide (NO) have been proposed to be involved in the cascade of injury elicited by traumatic brain injury. However, the mechanism(s) of injury remain to be explored. Since superoxide generation is triggered by traumatic brain injury, the cytotoxic peroxynitrite could be formed, but it is not known if this actually occurs. Dot blot and immunohistochemistry studies were performed to quantify tyrosine nitration and identify cell types in which such reactions occur in the brain of mice submitted to traumatic brain injury. Nitrotyrosine formation increased from 4 to 24 h after traumatic brain injury and was primarily observed in degenerating neurons, in areas corresponding to the sites of direct impact (frontal cortex) and diffuse impact (frontoparietal cortex and ventromedial hypothalamic nucleus). Furthermore, N omega-nitro-L-arginine-methylester (L-NAME), a NO-synthase inhibitor which has previously been shown to promote neurological recovery in traumatic brain injury, reduced nitrotyrosine formation and the number of nitrotyrosine-positive neurons. These results indicate that traumatic brain injury induces peroxynitrite formation which may contribute to cell damage.

Animals↗

PubMed2001

The impact of hypercarbia on the evolution of brain injury in a porcine model of traumatic brain injury and systemic hemorrhage.

Carbon dioxide is perhaps the most potent available modulator of cerebrovascular tone and thus cerebral blood flow (CBF). These experiments evaluate the impact of induced hypercarbia on the matching of blood flow and metabolism in the injured brain. We explore the hypothesis that hypercarbia will restore the relationship of CBF to metabolic demand, resulting in improved outcome following traumatic brain injury (TBI) and hemorrhage. A behavioral outcome score, hemodynamic, metabolic, and pathologic parameters were assessed in anesthetized and ventilated juvenile pigs. Animals were assigned to either normocarbia or hypercarbia and subdivided into TBI (via fluid percussion) with or without hemorrhage. The experimental groups were TBI; TBI + 40% hemorrhage (40%H); TBI + hypercarbia (CO2); and TBI + 40%H + CO2. Hemorrhaged animals were resuscitated with blood and crystalloid. Hypercarbia was induced immediately following TBI using 10% FiCO2. The normocarbic group demonstrated disturbance of the matching of CBF to metabolism evidenced by statistically significant increases in cerebral oxygen and glucose extraction. Hypercarbic animals showed falls in the same parameters, demonstrating improvement in the matching of CBF to metabolic demand. Parenchymal injury was significantly decreased in hypercarbic animals: 3/10 hypercarbic versus 6/8 normocarbic animals showed cerebral contusions at the gray/white interface (p = 0.05). The hypercarbic group had significantly better behavioral outcome scores, 10.5, versus 7.3 for the normocarbic groups (p = 0.005). The decreased incidence of cerebral contusion and improved behavioral outcome scores in our experiments appear to be mediated by better matching of cerebral metabolism and blood flow, suggesting that manipulations modulating the balance of blood flow and metabolism in injured brain may improve outcomes from TBI.

Animals↗

PubMed2005

Early Glasgow Outcome Scale scores predict long-term functional outcome in patients with severe traumatic brain injury.

Patients sustaining severe traumatic brain injury (TBI) have variable long-term outcomes. We examined the association between Glasgow Outcome Scale (GOS) assessed at 3 months and long-term outcomes at 12 months after TBI. We studied 159 patients with severe, closed traumatic brain injuries (Glasgow Coma Scale [GCS] <or= 8) who were treated at an academic medical center and survived for a minimum of 3 months after TBI. Demographics and admission clinical data and GOS at 3 and 12 months were analyzed. Multivariate logistic regression was used to asses the relationship between 3-month GOS, demographics, and clinical data and a poor outcome, defined as GOS 1-3 assessed at 12 months after injury. The patient population was predominantly male (77%), with a median age of 30 years and a median admission GCS of 6. The logistic regression model showed that the GOS at 3 months was the best predictor of 12-month outcomes (odds ratio = 15.22, p < 0.001). The presence of prolonged hypotension, diffuse axonal injury (DAI), and fixed and dilated pupils on admission were also significant independent predictors of poor 12-month outcome (for all, p <or= 0.047). The adjusted logistic model showed a steep gradient of long-term recovery potential depending upon GOS at 3 months, ranging from an 89.4% chance of poor outcome for patients with a GOS of 2, to a 0.11% chance of poor outcome for those with a GOS of 5. The 3-month GOS is a powerful independent predictor of long-term outcome for patients with severe TBI. Prolonged hypotension, DAI, and the presence of fixed and dilated pupils were also independent predictors of poor outcome.

Adolescent↗