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PubMed2003

Real-time PCR quantitation of FE65 a beta-amyloid precursor protein-binding protein after traumatic brain injury in rats.

In cases of traumatic brain injury (TBI) in which the patient survived for only a short period of time and was without macroscopic changes at autopsy, it is difficult to diagnose TBI. To detect early diagnostic markers of diffuse axonal injury (DAI), real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) in an experimental head trauma model of rat was chosen. The beta-amyloid precursor protein (beta-APP) is a well-known diagnostic marker of DAI which can be detected by immunolabeling as early as 1.5 h after injury. beta-APP has a binding protein, FE65, which is expressed in the brain of Alzheimer's disease patients along with beta-APP, but no involvement with brain injury has been reported. Neuron-specific enolase (NSE) is also a useful marker of DAI. We found that FE65 expression increased dramatically as early as 30 min after injury and decreased after peaking 1 h post-injury, although NSE showed no significant changes. These results suggest that real-time PCR of FE65 mRNA is useful for the diagnosis of DAI in forensic cases.

Amyloid beta-Protein Precursor↗

PubMed2005

Hypopituitarism and growth hormone deficiency in adult subjects after traumatic brain injury: who and when to test.

Traumatic brain injury (TBI) was traditionally considered an infrequent cause of hypopituitarism. However recent reports strongly suggest that TBI-mediated pituitary hormones deficiency may well be more frequent than previously thought. As the prevalence of hypopituitarism is not dependent on the severity of the trauma and considering the high number of TBI events in all industrialized countries a screening procedure for detecting hormone deficiencies in all TBI patients is not possible. In the present work a suggestion for screening a subgroup of TBI patients is discussed in order to increase the effectiveness of the whole procedure.

Brain Injuries↗

PubMed1995

Sustained arousal and attention after traumatic brain injury.

Clinicians report that patients with traumatic brain injury (TBI) often have difficulty with tasks requiring sustained attention, and there are neuroanatomical and neurophysiological reasons to expect such deficits. Nevertheless, laboratory measures of sustained attention or vigilance in TBI have produced conflicting results. These inconsistencies may be due to patient heterogeneity as well as the fact that vigilance performance is dependent on highly specific features of the task design. We developed a visual vigilance task in which the influence of non-attentional factors was minimized and task difficulty for patients and controls made comparable. Performance was characterized with respect to vigilance level as well as vigilance decrement, using measures of perceptual discrimination, response bias, reaction time and reaction time variability. Twenty-six patients with recent TBI and 18 control subjects were tested on this task. A MANOVA of ranked scores revealed significantly different patient and control performance overall. Initial level of performance (vigilance level) was slower and more variable for patients than controls, and patients showed more conservative response biases. Deterioration over time (vigilance decrement) was steeper for patients than controls for reaction time, reaction time variability, and response bias. Deterioration in accuracy (D') did not differ significantly between patients and controls. Performance was not related to available measures of injury severity. Hypotheses relating arousal mechanisms to vigilance performance are discussed.

Adolescent↗

PubMed2007

Intensive care unit management of fever following traumatic brain injury.

Fever, in the presence of traumatic brain injury (TBI), is associated with worsened neurologic outcomes. Studies prior to the publication of management guidelines revealed an undertreatment of fever in patients with neurologic insults. Presently the adult TBI guidelines state that maintenance of normothermia should be a standard of care therefore improvement in management of fever in these patients would be expected. The specific aims of the study were to: (1) determine the incidence of fever (T>or=38.5 degrees C) in a population of critically ill patients with TBI; (2) describe what interventions were recorded by intensive care unit (ICU) nurses in managing fever; (3) ascertain the rate of adherence with published normothermia guidelines. Medical record review of available hospital records was conducted on patients admitted to a level I trauma center following severe TBI (N=108) from the parent study. Temperature data was abstracted and contemporaneous nursing documentation was examined for evidence of intervention for fever and adherence with published standards. Data analyses were performed that included descriptive statistics. Seventy-nine percent of TBI patients (85/108) had at least one recorded fever event while in the ICU. However in only 31% of events did the patient receive any documented intervention by nursing staff for the elevated temperature. The most frequently documented intervention was pharmacologic (358/1166 elevations). Other nursing actions (e.g. use of fan) accounted for a minority (<1%) of nursing interventions documented. Patients were more likely to have a high temperature that exceeded 40 degrees C (13%) than a temperature that was normothermic (5%). There continues to be an under treatment of fever in patients with TBI by critical care nurses despite our knowledge of its negative effects on outcomes. There remains a gap in translation between patient outcomes research and bedside practice that needs to be overcome, thus research efforts need to now focus on understanding nurses' decision-making processes and the best methods of fever reduction in patients with TBI.

Adult↗

PubMed2006

Facilitation of glutamatergic synaptic transmission in hippocampal CA1 area of rats with traumatic brain injury.

We investigated the effects of traumatic brain injury (TBI) on the glutamatergic synaptic transmission in the hippocampal CA1 area. A moderate impact (3.8-4.8atm) was applied onto the left parietal cerebral cortex by a fluid percussion injury (FPI) device. Conventional intracellular recordings were made from hippocampal CA1 pyramidal neurons in vitro. Electrophysiological properties of these neurons were compared between three groups (control, FPI-ipsilateral, and FPI-contralateral). The excitability of postsynaptic membrane of CA1 pyramidal neurons was not altered by the moderate FPI; however, the evoked glutamatergic excitatory synaptic transmission in the pyramidal neurons of post-FPI-CA1 was enhanced. Paired-pulse facilitation (PPF) was significantly suppressed in both the FPI-ipsilateral and FPI-contralateral groups and the frequencies of mEPSPs in neurons from the bilateral FPI groups were greater than the frequency in the control group. These results suggest that the glutamatergic synaptic transmission in the hipppocampal CA1 area is facilitated through presynaptic mechanisms after TBI.

Action Potentials↗

PubMed2005

Neural correlates of self-evaluative accuracy after traumatic brain injury.

Individuals who have sustained a traumatic brain injury (TBI) often exhibit an array of cognitive deficits, yet perhaps most maladaptive of these sequelae is the frequent occurrence of reduced insight into one's own condition. In such cases, TBI individuals may overestimate their post-injury level of socio-cognitive functioning, leading to disparities between how they perceive themselves and what others observe. This functional MRI (fMRI) investigation examined the relationship between level of insight into one's post-injury condition (i.e. trait/ability status) and neural activation evoked during an fMRI task involving self-appraisal of one's traits and abilities. Twenty TBI patients (8-12 weeks post-injury, ER Glasgow Coma Scale Average = 10.9+/-2.8) were selected on the criterion that they overestimate their current trait/abilities (as detected on the patient competency rating scale, PCRS). fMRI activation on the self-appraisal task was compared between the TBI patients and 20 matched controls. For both groups, the fMRI task evoked activation at mid-line prefrontal and retrosplenial cortices. TBI patients exhibited greater signal change in the anterior cingulate, precuneus and right temporal pole. Subsequently, a linear regression analysis was conducted for the TBI group, with the PCRS and a measure of cognitive speed entered as predictor variables to determine the selective effect of insight on self-evaluative brain activation. A more accurate level of trait/ability-based insight was related to increased signal change in the right anterior dorsal prefrontal cortex (PFC). The results suggest that one's post-injury level of self-referential insight is related to a network inclusive of the medial and right dorsal PFC.

Adolescent↗

PubMed1993

Mild traumatic brain injury syndrome.

The mild post-traumatic brain injury syndrome has continued to pose clinical management problems for medical specialists from the emergency physician to the family practitioner. The contribution of preinjury medical and psychosocial factors, along with the concomitant risk of litigation, complicates the diagnostic task. This review examines selected aspects of this problem, including definition and classification, pathophysiology, symptom constellation, medicolegal pitfalls, diagnostic procedures, and treatment recommendations. Practitioners need to be particularly alert to the optimal strategies for emergency department management to prevent "mild" injuries from becoming major disabilities.

Brain Injuries↗

PubMed2002

Modeling both the mechanical and hypoxic features of traumatic brain injury in vitro in rats.

In traumatic brain injury, the brain is subjected to mechanical shear and varying degrees of hypoxia/ischemia. To compare effects of stretch injury, hypoxia, and the combination of both insults on neurons, mixed neuronal and astrocytic cultures were established from day 17 fetal rat brains. On days 17-19 in vitro, cultures were subjected to stretch injury or hypoxia of varying degrees, alone and in combination. Cultures were assayed for lactate dehydrogenase release and Trypan Blue uptake. Hypoxia or Stretch injury alone induced a graded response (P<0.05) on both assays. Stretch+Hypoxia (4 or 6 h) resulted in significantly greater injury as compared with controls (P<0.05), and as compared with either isolated Stretch or Hypoxia (1, 2, 4 or 6 h) alone (P<0.05).

Animals↗

PubMed2004

Short- and long-term social outcomes following pediatric traumatic brain injury.

The social outcomes of pediatric traumatic brain injury (TBI) were examined in a prospective, longitudinal study that included 53 children with severe TBI, 56 with moderate TBI, and 80 with orthopedic injuries, recruited between 6 and 12 years of age. Child and family functioning were assessed at baseline, at 6- and 12-month follow-ups, and at an extended follow-up a mean of 4 years post injury. Growth curve analyses revealed that pediatric TBI yields negative social outcomes that are exacerbated by family environments characterized by lower socioeconomic status, fewer family resources, and poorer family functioning. After controlling for group membership, age, race, socioeconomic status, and IQ, path analyses indicated that long-term social outcomes were accounted for in part by specific neurocognitive skills, including executive functions and pragmatic language, and by social problem-solving. Deficits in these domains among children with TBI are likely to reflect damage to a network of brain regions that have been implicated in social cognition.

Adaptation, Psychological↗

PubMed1998

The effects of visual distraction following traumatic brain injury.

Clinical assessments of individuals with traumatic brain injury (TBI) typically report attentional difficulties, with distractibility prominent among these complaints. However, laboratory-based measures have often failed to find disproportionate distraction among patients with TBI, as compared to control participants. In this experiment, we tested 21 patients hospitalized for rehabilitation following recent TBI and 21 demographically comparable control subjects on a visual reaction time go-no-go task in which the target was preceded or followed by a brightly colored moving visual stimulus, appearing above the target location. Early distractors actually served as warning stimuli, improving accuracy and speed for both participant groups. Distractors occurring at or shortly after the time of target presentation had no significant impact on accuracy or response bias in either group, but did produce slowing of RT that was significantly greater for patients than for controls. The distractor that produced maximal slowing occurred 100 ms after the presentation of the target or foil. Repeated testing sessions led to reduction in the impact of the distractor and loss of the group difference in RT impact. The degree of RT slowing induced by distraction was modestly related to injury severity, as measured by the current score on the Disability Rating Scale, and the time until the patient first followed verbal commands. There was also a trend of greater RT slowing among individuals with focal orbitofrontal lesions, as assessed on neuroimaging studies. These results document a greater susceptibility to extraneous visual distraction among patients with TBI in comparison to controls. The fact that this difference appears only in the RT domain, and is greatest when the distractor follows the target, suggests that the primary impact of visual distractors is on response preparation and execution rather than target detection.

Adolescent↗

PubMed2004

Changes in working memory after traumatic brain injury in children.

The impact of traumatic brain injury (TBI) on working memory (WM) was studied in 144 children (79 with mild, 23 with moderate, and 42 with severe injuries) who underwent magnetic resonance imaging (MRI) at 3 months and were tested at baseline and at 3, 6, 12, and 24 months postinjury. An n-back WM task for letter identity was administered with memory load ranging from 1- to 3-back and a 0-back condition. A TBI Severity x Quadratic Tune interaction showed that net percentage correct (correct detections of targets minus false alarms) was significantly lower in severe than in mild TBI groups. The Left Frontal Lesions x Age interaction approached significance. Mechanisms mediating late decline in WM and the effects of left frontal lesions are discussed.

Adolescent↗

PubMed2006

Activation of calcium/calmodulin-dependent protein kinases after traumatic brain injury.

A prominent cognitive impairment after traumatic brain injury (TBI) is hippocampal-dependent memory loss. Although the histopathologic changes in the brain are well documented after TBI, the underlying biochemical mechanisms that contribute to memory loss have yet to be thoroughly delineated. Thus, we determined if calcium/calmodulin-dependent protein kinases (CaMKs), known to be necessary for the formation of hippocampal-dependent memories, are regulated after TBI. Sprague-Dawley rats underwent moderate parasagittal fluid-percussion brain injury on the right side of the parietal cortex. The ipsilateral hippocampus and parietal cortex were Western blotted for phosphorylated, activated alpha-calcium/calmodulin-dependent protein kinase II (alpha-CaMKII), CaMKIV, and CaMKI. alpha-Calcium/calmodulin-dependent protein kinase II was activated in membrane subcellular fractions from the hippocampus and parietal cortex 30 mins after TBI. CaMKI and CaMKIV were activated in a more delayed manner, increasing in phosphorylation 1 h after TBI. The increase in activated alpha-CaMKII in membrane fractions was accompanied by a decrease in cytosolic total alpha-CaMKII, suggesting redistribution to the membrane. Using confocal microscopy, we observed that alpha-CaMKII was activated within hippocampal neurons of the dentate gyrus, CA3, and CA1 regions. Two downstream substrates of alpha-CaMKII, the AMPA-type glutamate receptor GluR1, and cytoplasmic polyadenylation element-binding protein, concomitantly increased in phosphorylation in the hippocampus and cortex 1 h after TBI. These results demonstrate that several of the biochemical cascades that subserve memory formation are activated unselectively in neurons after TBI. As memory formation requires activation of CaMKII signaling pathways at specific neuronal synapses, unselective activation of CaMKII signaling in all synapses may disrupt the machinery for memory formation, resulting in memory loss after TBI.

Animals↗

PubMed2006

boc-Aspartyl(OMe)-fluoromethylketone attenuates mitochondrial release of cytochrome c and delays brain tissue loss after traumatic brain injury in rats.

The pathobiology of traumatic brain injury (TBI) includes activation of multiple caspases followed by cell death with a spectrum of apoptotic phenotypes. There are initiator (e.g. caspase-2, -8, and -9) and effector (e.g. caspase-3 and -7) caspases. Recently, caspase-2 and -8 have been shown to regulate cell death via provoking cytochrome c release from the mitochondria upstream of caspase-9. Here, we show that an intracerebral injection of the pan-caspase inhibitor boc-Aspartyl(OMe)-fluoromethylketone (BAF; 1 micromol) 1 min after TBI in rats reduces caspase-3-like activity, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and tissue damage, and cytochrome c release in ipsilateral cortex at 24 h versus vehicle. To investigate whether either caspase-2 and/or caspase-8 activation may contribute to cytochrome release, the effect of BAF treatment on caspase-2 and caspase-8 proteolysis was also examined. boc-aspartyl(OMe)-fluoromethylketone treatment inhibited proteolysis of caspase-2 but not caspase-8 24 h after TBI in rats versus vehicle. However, BAF with or without nerve growth factor (12.5 ng/h x 14 days intracerebrally via osmotic pump) did not result in differences in motor function, Morris water maze performance, hippocampal neuron survival, nor contusion volume at 14 days. These data suggest that BAF treatment reduces acute cell death after TBI by inhibiting mitochondrial release of cytochrome c, possibly via a mechanism involving initiator caspases; however, BAF appears to delay cell death, rather than result in permanent protection.

Amino Acid Chloromethyl Ketones↗

PubMed2000

Recovery of memory function following traumatic brain injury in pre-school 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. Ninety-six children with TBI were divided according to injury severity (mild, moderate, severe), and compared to age and SES matched healthy controls (n = 35). Children were evaluated acutely and at 6,12 and 18 months post-injury using intellectual and memory measures. Results showed a relationship between greater injury severity and poorer intellectual ability. This dose-response relationship was not clearly evident for memory function within the acute phase of recovery, but 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. Findings are discussed in the context of theories of plasticity and recovery of function.

Amnesia↗

PubMed2000

Behavioural differences between psychiatric patients with confirmed versus non-confirmed traumatic brain injuries.

The relationship between history of Traumatic Brain Injury (TBI) and BDI-2 depression scores at admission and discharge from the hospital was assessed in acutely hospitalized psychiatric patients. The participants were assigned to three groups: (1) no reported history of TBI (n = 18), (2) reported but not confirmed TBI history (n = 13), and (3) reported and confirmed TBI history (n = 15). It was found that confirmed history of TBI was associated with elevated BDI-2 depression scores. In contrast, the non-confirmed TBI group was characterized by over-reporting of psychological distress, as measured by MMPI-2 validity indices, 100% prevalence of alcohol use history, and depression scores that were intermediate between the control and confirmed TBI groups.

Acute Disease↗

PubMed1998

Effects of mild traumatic brain injury on narrative discourse production.

Mild traumatic brain injury (MTBI) and postconcussive syndrome can result in difficult to document complaints regarding subtle language use. Narrative discourse production has been shown to be a sensitive index of linguistic and cognitive deficits in the more severe TBI population. The narrative discourse production of MTBI subjects was investigated to determine whether cognitive changes were reflected in linguistic production. Eight MTBI, five moderate TBI, and five neurologically normal subjects were matched for age, education, and gender. The TBI subjects were matched on a number of neuropsychological measures. The subjects produced narratives about their correct picture sequences on five items from the Wechsler Adult Intelligence Scale-Revised picture arrangement subtest. The narratives were scored for correct arrangement, content essential information, correct story, and implied meaning. Significant differences were found between the normal control group and both the TBI groups on accuracy of narrative description of the correct picture sequences. Although differences in generation of implied meaning failed to reach significance, a trend was noted for both the TBI groups to produce fewer implied meanings than the control group. The results suggest that cognitive disruptions associated with MTBI may affect the quality of narrative discourse.

Adult↗

PubMed1994

Endogenous phosphorylation of a 61,000 dalton hippocampal protein increases following traumatic brain injury.

Acute biochemical consequences of moderate traumatic brain injury (TBI) include activation of kinases, including protein kinase C (PKC). To determine the possible consequences of PKC activation at the substrate level, we have examined protein phosphorylation patterns 1 h following injury. Although the phosphorylation of most proteins remained unchanged following injury, we observed a significant increase in the phosphorylation of a 61,000 dalton protein (TBI61) in injured rat hippocampus (121% higher than sham control) in vitro. TBI61 phosphorylation could be enhanced by phosphatidyl serine and diacylglycerol or by addition of exogenous PKC. In addition, TBI61 phosphorylation was inhibited by the PKC inhibitor, staurosporine, suggesting further that this protein may be a PKC substrate. These data suggest that TBI increases the phosphorylation of a 61 kD hippocampal protein in vitro. Increases in the protein level and activity of PKC could contribute to this increased phosphorylation.

Alkaloids↗

PubMed2006

Reduced collagen degradation in polytraumas with traumatic brain injury causes enhanced osteogenesis.

Patients with traumatic brain injury (TBI) and skeletal injuries have increased rates of excessive bone healing (EH = hypertrophic callus formation and/or heterotopic ossification). Polytrauma patients are often attributed higher rates of delayed fracture union. This study compares 182 total fractures in 29 isolated polytrauma patients (POLY) and 48 patients after TBI and polytrauma (TBI+POLY), examining the clinical parameters of EH versus delay. A subset of 28 patients (13 TBI+POLY, 15 POLY) underwent serological testing for the following bone turnover parameters: carboxy-terminal extension peptide of type 1 procollagen (P1CP), pyridinolene cross-linked carboxy-terminal telopeptide (1CTP), insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), and basic fibroblast growth factor (bFGF). There were higher rates of delayed union in the POLY patients (45% vs. 23%) and EH in the TBI+POLY patients (33% vs. 17%) (not significant = NS). More delayed unions were observed in diaphyseal fractures suffered by POLY (28%) than in TBI+POLY (15%) patients (NS). EH after pelvic fracture was apparent in 52% TBI+POLY and in 21% POLY fractures (NS). P1CP levels did not differ between the groups, but the collagen breakdown parameter 1CTP was significantly higher in the POLY group (p = 0.01-0.04). IGF-1 levels were below normal in both groups, and did not differ. IGFBP-3, an IGF-1-inhibiting and collagenase-3-activating protein, was significantly higher in POLY patients (p = 0.017-0.037). bFGF levels did not vary between groups. Increased serum levels of 1CTP and IGFBP-3 in POLY patients suggest that EH in TBI patients is secondary to decreased collagen breakdown rather than increased synthesis.

Adolescent↗