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Results for “Traumatic Brain Injuries”

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PubMed1990

Impaired awareness of behavioral limitations after traumatic brain injury.

Sixty-four traumatically brain injured patients were divided into three groups. Patients in Group I overestimated their behavioral competencies. Patients in Group II showed behavioral ratings similar to relatives' reports concerning behavioral competencies. Patients in Group III underestimated their behavioral competencies. Group I patients had greater evidence of bilateral and multiple-site lesions than group II and III patients. Speed of left-hand finger tapping was also worse in Group I than groups II and III, but other standard neuropsychologic test findings failed to separate the groups. Specific brain lesion sites were not related to group membership. Impaired awareness of behavioral limitations after traumatic brain injury may be related to neuropsychologic changes not measured by standard tests. Bilateral impairment of heteromodal cortex may be important to this phenomenon when it exists several months or years postinjury.

Adult↗

PubMedDate not supplied

Proton MR spectroscopic findings correspond to neuropsychological function in traumatic brain injury.

BACKGROUND AND PURPOSE: Traumatic brain injury (TBI) causes substantial irreversible damage to neurons. Our aim was to investigate whether proton MR spectroscopic measures of diffuse cellular integrity were related to neuropsychological dysfunction after TBI. METHODS: Twelve patients with TBI (mean, 53 +/- 23 days postinjury) and 14 control subjects were included in the study using paired MR spectroscopy and neuropsychological assessment. N-acetylaspartate (NAA), creatine, and choline were measured in normal-appearing occipitoparietal white and occipital gray matter using short-echo quantitative spectroscopy. A composite measure of neuropsychological function was calculated from z-scored individual tests probing the major functional domains commonly impaired after head trauma. RESULTS: Patients with TBI displayed reduced NAA in white matter and elevated choline in gray matter, suggestive of neuronal injury and inflammation, respectively. NAA and creatine in white and gray matter were significantly associated with composite neuropsychological function and many individual neuropsychological tests. Gray matter choline, although abnormal, was not related to neuropsychological function. CONCLUSION: The concordance between neurometabolic levels and behavioral function supports the hypothesis that diffuse axonal injury is an important contributor to brain dysfunction after TBI.

Adolescent↗

PubMedDate not supplied

The child with traumatic brain injury returns to school.

Traumatic brain injury (TBI) continues to be the leading cause of acquired disability in childhood (Lazar & Menaldino, 1995). As children with TBI return to home and schools, primary care clinicians and educators who often lack information about their long term abilities to function are encountering them more frequently. This article describes the pathophysiology of pediatric TBI and difficulties that can be encountered when the child returns to school and offers suggestions for nurses who can assist the child in receiving appropriate educational services.

Brain Injuries↗

PubMed2006

Activation of Rho after traumatic brain injury and seizure in rats.

Traumatic brain injury (TBI) is characterized by a progressive cell loss and a lack of axonal regeneration. In the central nervous system (CNS), the Rho signaling pathway regulates the neuronal response to growth inhibitory proteins and regeneration of damaged axons, and Rho activation is also correlated with an increased susceptibility to apoptosis. To evaluate whether traumatic brain injury (TBI) results in changes in Rho activation in vulnerable regions of the brain, GTP-RhoA pull down assays were performed on rat cortical and hippocampal tissue homogenates obtained from 24 h to 3 days following lateral fluid percussion brain injury (FPI). Following FPI, a significantly increased RhoA activation was observed from 24 h to 3 days post-injury in the cortex and by 3 days in the hippocampus ipsilateral to the injury. We also detected activated RhoA in the cortex and hippocampus contralateral to the injury, without concomitant changes in total RhoA levels. To determine if immediate post-traumatic events such as seizures may activate Rho, we examined RhoA activation in the brains of rats with kainic acid-induced seizures. Severe seizures resulted in bilateral RhoA activation in the cortex and hippocampus. Together, these results indicate that RhoA is activated in vulnerable brain regions following traumatic and epileptic insults to the CNS.

Animals↗

PubMed2000

Age-dependent cerebral hemodynamic effects of traumatic brain injury in newborn and juvenile pigs.

Traumatic brain injury is one of the major causes of morbidity, mortality, and pediatric intensive care unit admissions of children. Although the effects of traumatic brain injury have been well described for adult animal models, few have investigated these effects in the newborn or have characterized such effects as a function of age using a single model of injury. Using a piglet model of brain injury, recent studies have shown that the cerebral hemodynamic effects and the corresponding mechanisms for such effects of injury vary as a functional of age. This review discusses the types of traumatic brain injury, their models, and the role of species in such model choice. This review also describes the effects of brain injury on cerebral blood flow, metabolism, and cerebrovascular regulation as a function of age. Finally, this review presents evidence for potential mechanisms that may contribute to age-dependent impaired cerebral hemodynamics following brain injury.

Age Factors↗

PubMed1997

Temporal and regional profiles of cytoskeletal protein accumulation in the rat brain following traumatic brain injury.

To characterize the cytoskeletal aberration due to traumatic injury, temporal and regional profiles of changes in immunoreactivity of microtubule-associated protein 2 (MAP2), neurofilament heavy subunit protein (NFH) and heat shock protein 72 (HSP72) were investigated after different magnitudes of traumatic brain injury by fluid percussion. The experimental rat brain was perfusion-fixed at 1, 6 and 24 hours after traumatic brain injury. Conventional histological staining has demonstrated that the mildest traumatic brain injury (1.0 atm) induced no neuronal loss at the impact site and that neuron loss was apparent when traumatic brain injury was increased to 4.3 atm. The mildest traumatic brain injury, however, caused a significant increase in HSP72 immunoreactivity in the superficial cortical layers at the impact site as early as 1 hour after the injury. In the case of severe traumatic brain injury (4.3 atm), neuron loss was apparent in the area at the impact site, but the increase in HSP72 immunoreactivity was moderate, and it was observed only after 6 hours in the deep cortical layers under the necrotic area. The increased immunostaining of MAP2 was demonstrated in damaged axons and neuronal perikarya in the wider area surrounding the impact site at 6 and 24 hours after the injury. Six and 24 hours after the injury, perikaryal accumulation of neurofilament was observed, and the accumulated neurofilament was mostly phosphorylated. These results indicate that the severe traumatic brain injury of 4.3 atm triggers the abnormal accumulation of cytoskeletal proteins in neuronal perikarya, most probably due to an impairment of axonal transport. It is implied that the increased expression of HSP72 may be involved in the protective process of neurons after traumatic brain injury.

Animals↗

PubMed2006

The incidence and severity of injury in children hospitalised for traumatic brain injury in Kashmir.

A large number of people experience traumatic brain injury each year, often with severe consequences. This is a public health problem that requires ongoing surveillance to follow trends in the incidence, risk factors, causes, and outcomes of these injuries. In 2003, a prospective study of all children below 15 years admitted to hospitals with a diagnosis of head injury was conducted in the Accident & Emergency Department of Sher-e-Kashmir Institute of Medical Sciences, Srinagar (India) to determine the incidence and severity of accidental head injury among children and the circumstances of injury. The highest incidence of head injury was seen at ages 6-10 years. Head injury rates were higher in males than in females. The leading causes include falls and motor vehicle accidents. More than 50% falls occurred in the age group of 4-6 years. Ninety per cent patients, who recovered, were discharged within 16-24 h after admission. Lack of supervision, non-implementation of safety measures and poor implementation of traffic rules leads to many injuries. The ability of the health care system to deal with increasing trauma in Jammu & Kashmir is limited. Nevertheless, prevention can be low cost strategy to overcome this problem. The results of epidemiological studies are affected by factors like demography, geographic region and socioeconomic status. This study emphasizes the need for intensified effort for prevention, minimising risk factors, strict legislative measures, observing traffic rules, implementation of safety measures, establishing appropriate trauma care at district level, adult supervision, and creating awareness.

Accidents↗

PubMed1998

Driving following traumatic brain injury: prevalence, exposure, advice and evaluations.

Survivors of traumatic brain injury often have long-term sensory, cognitive and motor deficits that may impair vehicle operation. However, relatively little is known about the driving status and driving characteristics of brain injury survivors. To better understand driving following traumatic brain injury, a survey of driving status, driving exposure, advice received about driving and evaluations of driving competency was administered to a convenience sample of traumatic brain injury survivors (n = 83). The majority of survey participants had experienced either moderate or severe traumatic brain injuries based on the Glasgow Coma Scale. A total of 60% of the survey participants reported that they were currently active drivers. Most individuals (> 60%) who had returned to driving reported driving every day and more than 50 miles per week. Traumatic brain injury survivors frequently received advice about driving from family members, physicians or non-physician health care professionals, but over half (63%) had not been professionally evaluated for driving competency. The presence of high driving exposure, coupled with a lack of widespread driving fitness testing, suggests that some traumatic brain injury survivors have characteristics that may evaluate their risk for vehicle crashes. However, subsequent prospective studies that directly assess driver safety will be needed to confirm this possibility.

Adult↗

PubMed2003

Noradrenergic agonists for acute traumatic brain injury.

BACKGROUND: Although there have been considerable gains in understanding the cascade of events that lead to secondary injury after traumatic brain injury (TBI), efforts to translate this understanding into new therapeutic, so-called neuroprotective, approaches have so far proven disappointing. Animal models suggest an alternative strategy: agents enhancing monoaminergic transmission, particularly amphetamines, have been shown to promote motor recovery from focal brain injury and it has been suggested that this might represent a complementary means of therapeutic intervention in the later post-injury phase. OBJECTIVES: To evaluate the evidence that amphetamines improve final outcome after traumatic brain injury. SEARCH STRATEGY: We searched MEDLINE, EMBASE, Science Citation Index, Cochrane Controlled Trials Register and the Cochrane Injuries Group's Specialised Register of Controlled Trials. Researchers and authors of published trials were also contacted. SELECTION CRITERIA: Randomised controlled trials comparing the use of a noradrenergic agonist (together with conventional non-pharmacological rehabilitative therapy) versus conventional non-pharmacological rehabilitative therapy alone. DATA COLLECTION AND ANALYSIS: Two reviewers independently screened records, extracted data and assessed trial quality. MAIN RESULTS: Although there is a limited clinical literature addressing this topic, none of the studies identified fully meets inclusion criteria for this review. REVIEWER'S CONCLUSIONS: At present there is insufficient evidence to support the routine use of methylphenidate or other amphetamines to promote recovery from TBI.

Adrenergic alpha-Agonists↗

PubMed2006

Pediatric minor traumatic brain injury.

The literature surrounding minor traumatic brain injury is complex, methodologically challenging, and controversial. Although we lack a consistent standardized definition, the annual rate is likely in excess of 200 per 100,000 children. The proportion of children with minor traumatic brain injury who will require neurosurgery is certainly <1%. Several studies are underway that have the potential to significantly advance our understanding of the specific risk factors for intracranial injury and more specifically neurosurgical injury. The mortality within children is very low, with estimates of 0% to 0.25%. Virtually all studies of the prognosis of minor brain injury in children have reported no long-term behavioral or cognitive sequelae as a specific result of the brain injury. Symptoms fall in 4 domains: somatic, cognitive, sleep/fatigue, and affective. Limited pediatric studies are available to assist clinicians in the prognosis or in optimizing recovery. Until further studies are available, a conservative approach is recommended. Children with suspected concussions should be removed from activity and observed. Children with symptomatic concussions must be limited to no physical activity. Adolescents and families need to self-monitor symptoms and limit environments or circumstances that exacerbate any symptoms. When symptoms resolve, a gradual progressive return to play is currently recommended. The recurrence risk for subsequent concussions is elevated, but there is limited documentation of the effectiveness of preventative efforts. Much remains to be learned.

Brain Injuries↗

PubMed1992

Personality disturbances associated with traumatic brain injury.

Personality disturbances associated with traumatic brain injury are reviewed. The varied structural pathology of the brain in this patient group makes it difficult to specify how different brain lesions may result in specific emotional and motivational disturbances. However, an attempt to clarify terms and review empirical findings is made. Longitudinal prospective studies that utilize appropriate control groups are needed. Future research may especially benefit by considering the long-term effects of early agitation following traumatic brain injury as well as the problem of aspontaneity and impairment of self-awareness.

Adult↗

PubMed2005

Misdiagnosis of post-traumatic stress disorder following severe traumatic brain injury.

BACKGROUND: The incidence of post-traumatic stress disorder (PTSD) after traumatic brain injury is unclear. One issue involves the validity of diagnosis using self-report questionnaires. AIMS: To compare PTSD'caseness' arising from questionnaire self-report and structured interview. METHOD: Participants (n=34) with traumatic brain injury were recruited. Screening measures and self-report questionnaires were administered, followed by the structured interview. RESULTS: Using questionnaires, 59% fulfilled criteria for PTSD on the Post-traumatic Diagnostic Scale and 44% on the Impact of Events Scale, whereas using structured interview (Clinician-Administered PTSD Scale) only 3% were 'cases'. This discrepancy may arise from confusions between effects of PTSD and traumatic brain injury. CONCLUSIONS: After traumatic brain injury, PTSD self-report measures might be used for screening but not diagnosis.

Adult↗

PubMed1993

Pediatric traumatic brain injury: acute and rehabilitation costs.

Pediatric traumatic brain injury constitutes an enormous public health problem, but little is known about the economic costs of such injury. Using charges as a proxy for cost, we prospectively collected data on initial hospital charges and professional fees for emergency department services, acute inpatient care, and acute inpatient rehabilitation for 96 patients with mild, moderate, and severe traumatic brain injuries. We also examined the relationship between these costs and injury severity and etiology. Acute care and rehabilitation median costs were $5,233 per child, $11,478 for hospitalized children, and $230 for those only seen in the emergency department. Median costs for injuries due to motor vehicles, bicycles, and falls were $15,213, $6,311, and $792, respectively. Using Glasgow Coma Scale criteria, median cost of mild, moderate, and severe traumatic brain injuries were $598, $12,022, and $53,332, respectively. Injury etiology added modestly but significantly to the prediction of cost over and above that predicted by injury severity alone. Rehabilitation costs accounted for 37% of the total for all children, but 45% of those with the most severe injuries.

Adolescent↗

PubMed1996

Reduced evoked release of acetylcholine in the rodent hippocampus following traumatic brain injury.

The chronic effects of traumatic brain injury on acetylcholine release were evaluated by using in vivo microdialysis. Acetylcholine release was measured in the hippocampus of anesthetized rats 2 weeks after lateral controlled cortical impact (n = 10) or sham surgery (n = 10). Prior to microdialysis, behavioral assessments of motor and spatial memory were performed. Cortical impact (6 meter/s, 2 mm deformation) produced beam balance deficits that persisted for 1 day and beam walking deficits that persisted for 3 days after injury. In addition, spatial memory, as measured by swim latencies in a Morris water maze, was compromised between 10-14 days after injury. Immediately following behavioral testing, the animals were anesthetized with halothane, and a microdialysis probe was placed into the dorsal hippocampus. After a 160 min equilibration period, extracellular levels of acetylcholine were measured prior to and after an intraperitoneal administration of scopolamine (1 mg/kg), which evokes acetylcholine release by blocking autoreceptors. Prior to scopolamine administration, there were no differences in extracellular levels of acetylcholine between injured and sham animals. However, there was a significant reduction of hippocampal acetylcholine release evoked by scopolamine in injured animals as compared to sham controls. In separate control groups, saline administration alone did not change hippocampal acetylcholine release in injured (n = 5) or sham (n = 5) animals. This study represents the first application of in vivo microdialysis to evaluate chronic neurotransmission deficits following TBI. The present study demonstrates that a magnitude of traumatic brain injury (TBI) sufficient to produce spatial memory deficits can result in a reduction in scopolamine-evoked release of acetylcholine within the hippocampus. The data further suggest that presynaptic mechanisms mediating release of acetylcholine could play a significant role in cholinergic neurotransmission deficits following TBI.

Acetylcholine↗

PubMed2006

Direct transport within an organized state trauma system reduces mortality in patients with severe traumatic brain injury.

BACKGROUND: Prehospital management of traumatic brain injury (TBI) and trauma system development and organization are aspects of TBI care that have the potential to significantly impact patient outcome. This multi-center study was conducted to explore the effect of prehospital management decisions on early mortality after severe TBI. METHODS: This report is based on 1449 patients with severe TBI (GCS<9) treated at 22 trauma centers enrolled in a New York State quality improvement (QI) program between 2000 and 2004. The prehospital data collected on these patients include time of injury, time of arrival to the trauma center, mode of transport, type of EMS provider, direct or indirect transport, blood pressure and pulse oximetry values, GCS score, pupillary assessment, and airway management procedures. RESULTS: After exclusion criteria were applied, a total of 1,123 patients were eligible for analysis. The majority of patients were male (75%) with a mean age of 36 years. After controlling for arterial hypotension, age, pupillary status, and initial GCS score, direct transport was found to result in significantly lower mortality than indirect transport. Transport mode, time to admission, and prehospital intubation were not found to be related to 2-week mortality. CONCLUSIONS: The present study provides class II evidence that demonstrates a 50% increase in mortality associated with indirect transfer of TBI patients. Patients with severe TBI should be transported directly to a Level I or Level II trauma center with capabilities as delineated in the Guidelines for the Prehospital Management of Traumatic Brain Injury, even if this center may not be the closest hospital.

Adult↗

PubMed2001

Multicontextual occupational therapy intervention: A case study of traumatic brain injury.

Cognitive deficits after a traumatic brain injury can result in significant functional limitations in all areas of daily living. An individual's ability to generalize learning may be limited, thus making it harder to live independently in the community. Assessing a client's metacognitive skills and awareness level may help to establish a baseline understanding about the supervision required and the most suitable living arrangements. This study describes a multicontextual, community re-entry occupational therapy programme directed at awareness training and compensation for cognitive problems in a 34-year-old man with traumatic brain injury. Intervention consisted of metacognitive training, exploration and use of effective processing strategies, task gradations and practice of functional activities in multiple environmental contexts. Strategies such as self-prediction, self-monitoring, role reversal and the use of checklists were used. Results after six months of intervention show improvements in the client's awareness level, enhancement of his occupational function, increased satisfaction with performance and a decrease in the level of attendant care. Additional studies are recommended to validate the findings.

Journal Article↗

PubMed1997

Treatment of traumatic brain injury with moderate hypothermia.

BACKGROUND: Traumatic brain injury initiates several metabolic processes that can exacerbate the injury. There is evidence that hypothermia may limit some of these deleterious metabolic responses. METHODS: In a randomized, controlled trial, we compared the effects of moderate hypothermia and normothermia in 82 patients with severe closed head injuries (a score of 3 to 7 on the Glasgow Coma Scale). The patients assigned to hypothermia were cooled to 33 degrees C a mean of 10 hours after injury, kept at 32 degrees to 33 degrees C for 24 hours, and then rewarmed. A specialist in physical medicine and rehabilitation who was unaware of the treatment assignments evaluated the patients 3, 6, and 12 months later with the use of the Glasgow Outcome Scale. RESULTS: The demographic characteristics and causes and severity of injury were similar in the hypothermia and normothermia groups. At 12 months, 62 percent of the patients in the hypothermia group and 38 percent of those in the normothermia group had good outcomes (moderate, mild, or no disabilities). The adjusted risk ratio for a bad outcome in the hypothermia group was 0.5 (95 percent confidence interval, 0.2 to 1.2). Hypothermia did not improve the outcomes in the patients with coma scores of 3 or 4 on admission. Among the patients with scores of 5 to 7, hypothermia was associated with significantly improved outcomes at 3 and 6 months (adjusted risk ratio for a bad outcome, 0.2; 95 percent confidence interval, 0.1 to 0.9 at both intervals), although not at 12 months (risk ratio, 0.3; 95 percent confidence interval, 0.1 to 1.0). CONCLUSIONS: Treatment with moderate hypothermia for 24 hours in patients with severe traumatic brain injury and coma scores of 5 to 7 on admission hastened neurologic recovery and may have improved the outcome.

Adolescent↗

PubMed2001

Caspase-3 activity is present in cerebrospinal fluid from patients with traumatic brain injury.

Loss of neurons after traumatic brain injury (TBI) might involve dysregulated apoptosis. Activation of caspase-3 is one hallmark of apoptosis. Therefore, caspase-3 activity (cleavage of DEVD-afc) was measured in cerebrospinal fluid (CSF) samples (n=113) from 27 patients with TBI at day 1 to 14 after trauma. Caspase-3 activity was detected in 31 (27.4%) CSF samples with highest values (> 5.5 microM/min) seen at day 2-5 after trauma. No caspase-3 activity was found in serum from patients or CSF from controls. The presence of activated caspase-3 in CSF suggests ongoing apoptotic processes during traumatic brain injury.

Adult↗