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PubMed2004

Memory functioning in children with traumatic brain injuries: a TOMAL validity study.

Traumatic brain injury (TBI) leads the causes of death and disability among children and adolescents. Despite the prevalence of TBI among children, few studies have examined memory in children. The purpose of this study was to compare memory functioning, as measured by the Test of Memory and Learning (TOMAL), of children with and without TBI and with moderate and severe TBI to determine if differences existed. Of the 140 participants, 70 had sustained a head trauma and 70 served as controls. The results indicated that, when the TBI and control group were compared, significant differences were found on all of the TOMAL indexes. With the exception of the verbal delayed recall items, significant differences were demonstrated on all the TOMAL subtests. No differences were identified when moderate and severe groups were compared. These findings further the understanding of memory following pediatric TBI, as well as have implications for interventions with this population.

Adolescent↗
PubMed2004

Parametric manipulation of working memory load in traumatic brain injury: behavioral and neural correlates.

Traumatic brain injury (TBI) is often associated with enduring impairments in high-level cognitive functioning, including working memory (WM). We examined WM function in predominantly chronic patients with mild, moderate and severe TBI and healthy comparison subjects behaviorally and, in a small subset of moderate-to-severe TBI patients, with event-related functional magnetic resonance imaging (fMRI), using a visual n-back task that parametrically varied WM load. TBI patients showed severity-dependent and load-related WM deficits in performance accuracy, but not reaction time. Performance of mild TBI patients did not differ from controls; patients with moderate and severe TBI were impaired, relative to controls and mild TBI patients, but only at higher WM-load levels. fMRI results show that TBI patients exhibit altered patterns of activation in a number of WM-related brain regions, including the dorsolateral prefrontal cortex and Broca's area. Examination of the pattern of behavioral responding and the temporal course of activations suggests that WM deficits in moderate-to-severe TBI are due to associative or strategic aspects of WM, and not impairments in active maintenance of stimulus representations. Overall, results demonstrate that individuals with moderate-to-severe TBI exhibit WM deficits that are associated with dysfunction within a distributed network of brain regions that support verbally mediated WM.

Adult↗
PubMed2003

Epidemiological aspect of traumatic brain injury in Northeast Italy.

BACKGROUND: Traumatic brain injuries (TBIs) remain an important public health problem in developed countries. Hospital records were reviewed to ascertain the epidemiology of TBIs in Northeast Italy. METHODS: The annual rates of TBI-associated hospitalisation were estimated by analysing data collected from hospital records from 1996 to 2000. TBIs were identified according to the Centers for Disease Control and Prevention definition and the ICDMAP-90 was used to assess their severity. FINDINGS: 55,368 TBIs were collected between 1996 and 2000, with an overall 29.4% decline in the number of cases. As for severity, moderate TBIs dropped by 34.1%, whereas a less conspicuous decline was observed for mild injuries. Severe injuries remained stable between 1996 and 1999, but rose in 2000, when the unclassified injuries were better distributed. Concerning outcome, fatal TBIs dropped slightly, but only in 2000. Causes of TBI were recorded in 59.2% of cases: 48.5% were motor vehicle accidents, 8.8% occurred at work and 12.2% at home. There were more males than females in all age groups. The highest number of cases per 100,000 person of motor vehicle accidents was recorded among 16-25 year-old and 36.5% occurred at weekends. Domestic accidents showed two age peaks, in children and the elderly. Occupational accidents occurred at all working ages, tending to decline with older age. INTERPRETATION: Better health care and educational campaigns may have contributed to the declining rate of TBI-associated hospitalisation. Special efforts should be made to further reduce the motor vehicle accidents involving young people and welfare programs are needed to limit the risk of falls and contain functional impairment in the elderly.

Accidents↗
PubMed2000

Chronic traumatic brain injury associated with boxing.

Chronic traumatic brain injury (CTBI) associated with boxing occurs in approximately 20% of professional boxers. Risk factors associated with CTBI include increased exposure (i.e., duration of career, age of retirement, total number of bouts), poor performance, increased sparring, and apolipoprotein (APOE) genotype. Clinically, boxers exhibiting CTBI will present with varying degrees of motor, cognitive, and/or behavioral impairments. The severe form of CTBI is referred to as dementia pugilistica. The diagnosis of CTBI is dependent upon documenting a progressive neurological condition that is consistent with the clinical symptomatology of CTBI attributable to brain trauma and unexplainable by an alternative pathophysiological process. Pathologically, CTBI shares many characteristics with Alzheimer's disease (i.e., neurofibrillary triangles, diffuse amyloid plaques, acetylcholine deficiency, and/or tau immunoreactivity). The mainstay of treatment of CTBI is prevention, however medications used in the treatment of Alzheimer's disease and/or parkinsonism may be utilized.

Boxing↗
PubMed1996

Factors influencing failure to return to work due to traumatic brain injury.

About 63% of all traumatic brain injuries (TBI) occur in teenagers and adults aged 15-64 years, the primary working population. Since reports of failure to return to work (FTRTW) vary, understanding the factors that influence FTRTW is key to improving work outcomes for this primarily working-age population. Our study sample consists of 343 previously employed persons who were hospitalized following TBI and had either returned to work at 1 year or had failed to return to work because of their injury (injury-related FTRTW). Medical records were reviewed and participants were interviewed by telephone at 1 year post-discharge. Individuals with injury-related FTRTW were far more likely to report dependence or modified independence on the Functional Independence Measure (FIM) than those who were employed at 1 year. The joint distribution of motor and cognitive items suggests that, for a given level of cognitive function, the addition of a motor limitation will result in greater injury-related FTRTW. In addition as motor function declines, FTRTW is further increased. Injury-related FTRTW is also associated with being unmarried and not completing high school. While the importance of behavioural, economic, and psychosocial factors should not be minimized, services aimed at improving function can be expected to have an impact on RTW after TBI.

Absenteeism↗
PubMed1999

Moclobemide in the treatment of major depressive disorder (DSM-3) following traumatic brain injury.

Major depression (MDD) following traumatic brain injury (TBI) is a common phenomenon. There are no adequate studies in the literature defining optimum treatments for this condition following TBI. The opportunity arose to analyse a group of patients who were included in a larger study of an antidepressant (moclobemide). As the treatment, but not the delivery, was known, this has the status of an open study. Twenty-six patients with major depression of late onset (mean 4.67 years post-TBI) were identified (18 male, 8 female), with a mean age at injury 28.49 years. The group was moderately depressed with Hamilton Depression score (HAM-D) of 23.385 and moderately anxious with Hamilton Anxiety score (HAM-A) of 21.231. Mean HAM-D reduction was 81% and HAM-A reduction 81%. Of the 26 subjects 23 were defined as responders. Onset of action was rapid, with 17 responding by day 3. Irritability scores showed a mean reduction of 57% and pain scores a reduction of 39%. It is concluded that moclobemide may be an effective treatment for MDD following TBI, but properly controlled studies must be carried out to confirm this.

Adolescent↗
PubMed1997

Effects of nalmefene, CG3703, tirilazad, or dopamine on cerebral blood flow, oxygen delivery, and electroencephalographic activity after traumatic brain injury and hemorrhage.

Hemorrhage after traumatic brain injury (TBI) in cats produces significant decreases in cerebral oxygen delivery (DcereO2) and electroencephalographic (EEG) activity. To determine whether effective treatments for the separate insults of TBI and hemorrhagic shock would also prove effective after the clinically relevant combination of the two, we measured the effects of a kappa-opiate antagonist (nalmefene), an inhibitor of lipid peroxidation (tirilazad), a thyrotropin-releasing hormone analog (CG3703), a clinically useful pressor agent (dopamine) or a saline placebo on cerebral blood flow (CBF), and EEG activity after TBI and mild hemorrhagic hypotension. Cats (n = 40, 8 per group) were anesthetized with 1.6% isoflurane in N2O:O2 (70:30) and prepared for fluid-percussion TBI and microsphere measurements of CBF. Cats were randomized to receive nalmefene (1 mg/kg), tirilazad (5 mg/kg), CG3703 (2 mg/kg), dopamine (20 microg x kg(-1) x min[-1]) or a saline placebo (2 ml, 0.9% NaCl). Animals were injured (2.2 atm), hemorrhaged to 70% of preinjury blood volume, treated as just described and resuscitated with a volume of 10% hydroxyethyl starch equal to shed blood. CBF was determined and EEG activity recorded before injury, after hemorrhage, and 0, 60, and 120 min after resuscitation (R0, R60, and R120). CBF increased significantly after resuscitation (R0) in the nalmefene- and CG3703-treated groups. CBF did not differ significantly from baseline in any group at R60 or R120. DcereO2 was significantly less than baseline in the saline-, dopamine-, and tirilazad-treated groups at R60 and in the dopamine-, tirilazad-, and CG3703-treated groups at R120. EEG activity remained unchanged in the nalmefene-treated group but deteriorated significantly at R60 or R120 compared to baseline in the other groups. Nalmefene and CG3703 preserved the hyperemic response to hemodilution (otherwise antagonized by TBI), and nalmefene prevented the deterioration in DcereO2 and EEG activity that occurs after TBI and hemorrhage.

Animals↗
PubMed1998

Fentanyl infusion preserves cerebral blood flow during decreased arterial blood pressure after traumatic brain injury in cats.

Hypotension after traumatic brain injury (TBI) has been associated with significant reductions in cerebral blood flow (CBF) in experimental animals. In humans, posttraumatic hypotension is associated with significantly worsened outcome, possibly because of cerebral hypoperfusion. The existence of opioid receptor-mediated cerebrovascular dilatory effects in humans has been theorized. We studied the systemic and cerebral vascular effects of fentanyl after fluid-percussion injury (FPI) TBI in isoflurane-anesthetized cats. In an approved protocol, 17 fasted cats were anesthetized, mechanically ventilated with 1-1.5% isoflurane in 70% N2O/30% O2, and prepared for FPI. Electroencephalogram (EEG) and intracranial pressure (ICP) were monitored. Cerebral blood flow and cardiac output were measured with radiolabelled microspheres. Animals received moderate FPI (2.2 atm) followed by 15 min of stabilization. Cats were then randomized to control (isoflurane anesthesia plus saline placebo) or fentanyl (isoflurane anesthesia plus fentanyl 50 microg x kg(-1) h(-1)) groups. CBF, EEG, and ICP were recorded at baseline (Baseline), 15 min post-FPI (post-FPI), and at 15, 75, and 135 min after beginning fentanyl or saline placebo infusions (INF 15, INF 75, INF 135). EEG, ICP, PaCO2, PaO2, pH, and temperature were similar between groups. Mean arterial pressure was significantly lower than in the control group after fentanyl administration, while total CBF was not significantly different from control values. In a previous study, decreasing MAP to 80 mm Hg after TBI in isoflurane-anesthetized cats resulted in a 30% decrease in CBF. In this study, fentanyl after TBI significantly decreased MAP but not CBF. Fentanyl administration was associated with preservation of CBF despite hypotension. Further research is necessary to evaluate the effects of fentanyl on cerebral autoregulation after TBI.

Animals↗
PubMedDate not supplied

Risk of posthospitalization mortality among persons with traumatic brain injury, South Carolina 1999-2001.

Traumatic brain injury (TBI) negatively impacts long-term survival. However, little is known about the likelihood of death within the first year following hospital discharge. This study examined mortality among a representative sample of 3679 persons within 1 year of being discharged from any of 62 acute care hospitals in South Carolina following TBI and identified the factors associated with early death using a multivariable Cox proportional hazards model. The mortality experience of the cohort was also compared with that of the general population by using standardized mortality ratios for selected causes of death by age, adjusted for race and sex.

Adolescent↗
PubMedDate not supplied

The use of serum biomarkers to predict outcome after traumatic brain injury in adults and children.

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality in adults and children. Predicting outcome after TBI is difficult, but it is important for acute management, counseling of family members, and provision of rehabilitation services. Serum biomarkers may be useful alone or in combination with clinical variables to predict outcome after TBI. This article reviews the potential uses of serum biomarkers for the clinician, current literature related to the use of serum biomarkers for outcome prediction after adult and pediatric TBI, limitations of the literature, and future direction for this field.

Biomarkers↗
PubMed2006

Cerebral response to norepinephrine compared with fluid resuscitation in ovine traumatic brain injury and systemic inflammation.

OBJECTIVE: Traumatic brain injury is frequently accompanied by a systemic inflammatory response. Systemic inflammation was associated with cerebral hyperperfusion uncoupled to global oxygen metabolism in ovine head trauma. The present study investigated the cerebral effects of cerebral perfusion pressure (CPP) management performed by either fluid resuscitation or vasopressor treatment of low CPP induced by systemic inflammation. DESIGN: Nonrandomized experimental study. SETTING: University hospital laboratory. SUBJECTS: A total of 12 adult sheep. INTERVENTIONS, MEASUREMENTS, AND MAIN RESULTS: Sheep were anesthetized and ventilated throughout the experimental period (13 hrs). After baseline measurements (hour 0), blunt head trauma was induced by a nonpenetrating stunner. After postinjury measurements (hour 2), all animals received continuous endotoxin infusion. At hour 10, one group (n = 6) was infused with hydroxyethyl starch until CPP reached 60-70 mm Hg. A second group (n = 6) received norepinephrine for CPP elevation. In the norepinephrine group, blood was isovolemically exchanged by hydroxyethyl starch to achieve comparable hematocrit levels. Head trauma increased intracranial pressure and decreased brain tissue oxygen tension. Endotoxemia induced a hyperdynamic cardiovascular response with increased internal carotid blood flow in the presence of systemic hypotension and decreased CPP. Hydroxyethyl starch infusion further increased internal carotid blood flow from (mean +/- sd) 247 +/- 26 (hour 10) to 342 +/- 42 mL/min (hour 13) and intracranial pressure from 20 +/- 4 (hour 10) to a maximum of 25 +/- 3 mm Hg (hour 12) but did not significantly affect brain tissue oxygen tension, sinus venous oxygen saturation and oxygen extraction fraction. Norepinephrine increased internal carotid blood flow from 268 +/- 19 to 342 +/- 58 mL/min and intracranial pressure from 22 +/- 11 to 24 +/- 11 mm Hg (hour 10 vs. hour 13) but significantly increased sinus venous oxygen saturation from 49 +/- 4 (hour 10) to a maximum of 59 +/- 6 mm Hg (hour 12) and decreased oxygen extraction fraction. The increase in brain tissue oxygen tension during norepinephrine treatment was not significant. CONCLUSION: We conclude that despite identical carotid blood flows, only CPP management with norepinephrine reduced the cerebral oxygen deficit in this model.

Animals↗
PubMed2000

Positioning of patients with severe traumatic brain injury: research-based practice.

Traumatic brain injuries (TBIs) are the most common disabling injuries in the United States, accounting for 44% of all deaths due to trauma. Once inflicted, primary cerebral injury is immutable and irreversible. Consequently, initial critical care of TBI patients focuses on prevention of secondary cerebral injury through the treatment of intracranial hypertension, systemic resuscitation, and multisystem stabilization. Relationships exist between therapeutic positioning, multisystemic stability, and prevention of secondary cerebral injury in severe TBI. A critical review and synthesis of current research literature on multisystem responses to positioning led to development of clinical recommendations based on currently available evidence and generated best practices for positioning patients with severe TBI.

Bed Rest↗
PubMed2006

Pediatric traumatic brain injury: past, present and future.

Traumatic brain injury (TBI) is the leading cause of death and disability in children. Evidence-based guidelines for the management of this population are available; however, the data highlight significant deficiencies with few treatment standards or guidelines. Considering the limited availability of resources, it is necessary to define realistic goals. Attention should be given to injury prevention, developing standardized pediatric admission and outcome evaluations, increasing the utility and spectrum of physiological and biochemical testing, and defining the evolving role of imaging in TBI.

Brain Injuries↗
PubMed2006

Mitochondrial heat shock protein 60 is increased in cerebrospinal fluid following pediatric traumatic brain injury.

Mitochondrial dysfunction occurs after traumatic brain injury (TBI) and contributes significantly to subsequent cell death. Heat shock protein 60 (hsp60) is a predominantly mitochondrial protein with important homeostatic functions. Induction of hsp60 has been demonstrated in cerebral ischemia models, possibly reflecting mitochondrial stress. We measured hsp60 concentration in the cerebrospinal fluid (CSF) of 34 infants and children after severe TBI and of 7 control patients by ELISA. Peak CSF hsp60 concentration was increased in TBI patients versus controls (0.84 ng/ml, range 0-44.59, vs. 0.0 ng/ml, range 0-0.48; p<0.05). Induction of hsp60 occurred early after the injury. Peak hsp60 concentration was independently associated with the severity of injury, defined as the admission Glasgow Coma Scale score. These data suggest that increased hsp60 in CSF might reflect the severity of early mitochondrial stress or damage after TBI.

Biomarkers↗
PubMed2006

Traumatic brain injury in the pediatric population.

Traumatic brain injury (TBI) is a common injury among children. Most TBIs are mild and do not require hospitalization. However, whether or not the patients require acute hospitalization, TBIs may have long-lasting consequences. There is little research on the nutrient needs of these patients, and recommendations are frequently based on data from adults with TBI. It is clear that calorie and protein needs are elevated with acute TBI. However, calorie needs are also decreased by therapies such as sedation, chemical paralysis, and barbiturate coma. Long-term calorie needs may be lower for "comatose" patients. Enteral feeding is preferred and possible for patients with TBI, though gastric feeding may be problematic in some patients. In the acute phase, patients with TBI can also have dysregulation of fluid and electrolyte balance, which may require alterations in nutrition care. Dysphagia is common after moderately severe TBI and requires a multidisciplinary approach for treatment. Future opportunities for research on pediatric TBI are numerous and may include ongoing clarification of macronutrient needs, as well as investigation into the roles of specific nutrients such as zinc, antioxidants, and anti-inflammatory compounds.

Adolescent↗
PubMed2002

Traumatic brain injury: assessment and management.

Suspected traumatic brain injury is a common presenting problem for emergency department staff. Sorting out who needs to have a computed tomography scan, who should be admitted and who should be followed up can be difficult. A framework for making these decisions is provided in this article.

Alcohol Drinking↗
PubMed2003

The current status and problems of rehabilitation for TBI (traumatic brain injury) patients in Japan.

Recently, traumatic brain injury (TBI) is one of the major topics of rehabilitation medicine. In the USA, a nationwide research project has already been underway since 1987. However, interest in the rehabilitation of TBI patients became a matter of concern in Japan from the 1990s. TBI patients do not only have physical impairments, but also impairments of higher cortical functions such as cognitive impairment and abnormal behavior, so both physical and cognitive rehabilitation are very important for TBI patients. The purpose of this paper is to report on the current status of and problems with TBI rehabilitation in Japan, and also to introduce a new TBI evaluation system that we originally developed in Japan.

Brain Injuries↗