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PubMed2006

Masculine role adherence and outcomes among men with traumatic brain injury.

PRIMARY OBJECTIVE: Traumatic brain injury (TBI) is a significant health problem disproportionately affecting men and is often associated with changes in masculine role functioning in life domains such as vocational functioning, sexual and inter-personal functioning and personal independence. These changes could have serious implications for men's adjustment following injury. The aim of this study was to examine the relations among traditional masculine role adherence, psychosocial adjustment and rehabilitation outcomes in men with TBI. RESEARCH DESIGN: A correlational design was chosen to examine the relations among variables. Spearman correlations and Wilcoxon Rank Sum tests were used to examine relationships between masculine role variables and outcome variables. METHODS AND PROCEDURES: The study included 33 men with TBI who had been discharged from inpatient rehabilitation within 5 years. Participants completed surveys on traditional masculine gender role adherence and gender role conflict and additional data, including measures of functional outcome, life satisfaction, psychosocial outcomes and earnings, were obtained through the TBI Model System longitudinal data collection system. MAIN OUTCOMES AND RESULTS: The results revealed significant associations between masculine role adherence and satisfaction with life, follow-up earnings and FIM change from admission to discharge. CONCLUSIONS: In the current study, particular masculine role variables corresponded to different functional and psychological outcomes. Understanding these differences provides new directions for treatment and offers important information about aspects of traditional masculine roles that may enhance or hinder adjustment to injury.

Adaptation, Psychological↗

PubMed1997

Visual electrodiagnostic findings in mild traumatic brain injury.

Patients with traumatic brain injury (TBI) frequently exhibit varied forms of visual system dysfunction including: binocular, oculomotor, accommodative, refractive error shift, visual field loss, and visual perceptual deficits. A 5-year collaborative study between optometry and ophthalmology was initiated to follow documented mild TBI patients utilizing diagnostic methods to assess the quantity and quality of visual system deficits and recovery. A group of patients with mild TBI receiving optometric rehabilitation were compared with a group of age-matched, gender-matched, and headsize-matched TBI patients not receiving such treatment. Eighteen patients diagnosed with mild TBI underwent a treatment regimen of optometric rehabilitation (group I); 32 patients diagnosed with mild TBI did not receive optometric rehabilitation (group II). Pattern visually evoked cortical potential (VECP) testing and electroretinography (ERG) evaluation were utilized initially, repeated 6-12 months later and then 12-18 months after baseline. All TBI patients' VECP and ERG results were compared to age-matched, headsize-matched controls. Once the ERG had been used to exclude retinal involvement, identification of visual pathway dysfunction was possible with the VECP. Full-field ERG results in all groups were not remarkable and not sensitive for patients with mild TBI. Initial testing results revealed that 72% of those TBI patients in group I demonstrated VECP waveform abnormalities and 81% of those patients in group II showed waveform dysfunction. In the testing performed 12-18 months later, 38% of group I TBI patients, after receiving a treatment regimen of optometric rehabilitation, showed VECP waveform abnormalities; 78% of group II TBI patients demonstrated waveform abnormalities. VECP evaluation in patients with mild TBI can provide a useful and reliable tool for objective assessment of visual system deficit and recovery. Significant differences in visual system recovery were shown when comparing group I and group II.

Adolescent↗

PubMed1998

Social and behavioural effects of traumatic brain injury in children.

Traumatic brain injury (TBI) is the leading cause of death and permanent disability in children and adolescents. Although cognitive and behavioural effects have now been reported for all degrees of TBI severity in children, other aspects of functioning which might be related (such as psychosocial adjustment), have been neglected. In the present study the social and behavioural effects of TBI were assessed by comparing 27 TBI children with 27 controls. TBI children demonstrated significantly lower levels of self-esteem and adaptive behaviour, and higher levels of loneliness, maladaptive behaviour and aggressive/antisocial behaviour. These findings confirm the previously demonstrated detrimental effects of TBI on children's behavioural functioning and offer new evidence for the detrimental effects of TBI on children's social functioning.

Adaptation, Psychological↗

PubMed2003

Developing experimental models to address traumatic brain injury in children.

Traumatic brain injury (TBI) is the leading cause of injury-related death and disability among children under the age of 15 years in the United States. Epidemiological studies have revealed that even within the pediatric population there are differences in incidence, gender differences, causes, types of injuries sustained, and mortality within age subdivisions. This heterogeneity must be taken into account when developing appropriate models to address TBI in children. This review explores the current developmental TBI models, including fluid percussion, weight drop, and controlled cortical impact. It also addresses unique considerations to modeling pediatric brain injury that require special attention when modeling and designing studies: age appropriateness, injury severity, evaluation of recovery, plasticity, and anesthesia.

Animals↗

PubMed2000

Enoxaparin reduces brain edema, cerebral lesions, and improves motor and cognitive impairments induced by a traumatic brain injury in rats.

Traumatic brain injury (TBI) is often accompanied by secondary ischemia due, in part, to edema-induced blood vessel compression. Enoxaparin, a low-molecular weight heparin, which is efficacious in models of myocardial and brain ischemia was studied in lateral fluid percussion-induced TBI in rats. Enoxaparin was administered 2 h post-TBI at 0.5 mg/kg i.v. followed by 4 x 0.5, 4 x 1, or 4 x 2 mg/kg s.c. over 30 h. Brain edema was measured in the hippocampus, temporal cortex and parietal cortex. Edema was reduced by enoxaparin (0.5 + 4 x 0.5 mg/kg) in the hippocampus (-53%, p = 0.07) and the parietal cortex (-39%, ns). At 0.5 + 4 x 1 mg/kg edema was reduced in the hippocampus (-63%, p < 0.05) and the parietal cortex (-47%, p = 0.06). At 0.5 + 4 x 2 mg/kg, the reduction was more important in the hippocampus (-69%, p < 0.01) and in the parietal cortex (-50%, p < 0.05). No reduction was seen in the temporal cortex. The lesion size was reduced by enoxaparin at 0.5 + 4 x 1 mg/kg (-50%, p < 0.05), and at 0.5 + 4 x 2 mg/kg (-35%, ns). The neurological deficit evaluated with a 9-point scale was also improved with enoxaparin at 0.5 + 4 x 1 mg/kg 1 week post-TBI (p < 0.05). The cognitive impairment evaluated with a Lashley maze task was improved with enoxaparin (0.5 + 4 x 1 mg/kg) from 48 h (p < 0.05) to 2 weeks post-TBI (p < 0.01). Our results demonstrate for the first time that enoxaparin significantly reduces the brain contusion and edema, and improves the functional outcomes induced by a TBI. Therefore, enoxaparin could be a candidate drug to treat acute brain-injured patients.

Animals↗

PubMed2004

Proton MR spectroscopy detected glutamate/glutamine is increased in children with traumatic brain injury.

Adults with traumatic brain injury (TBI) have been shown by invasive methods to have increased levels of the excitatory neurotransmitter glutamate. It is unclear whether glutamate release contributes to primary or secondary injury and whether its protracted elevation is predictive of a poor outcome. Preliminary studies at our institution in adults found that early increases in magnetic resonance spectroscopy (MRS)-detected glutamate/glutamine (Glx) were associated with poor outcomes. We therefore studied 38 children (mean age, 11 years; range, 1.6-17 years) who had TBI with quantitative short-echo time (STEAM, TE = 20 msec) proton MRS, a mean of 7 +/- 4 (range, 1-17) days after injury in order to determine if their occipital or parietal Glx levels correlated with the severity of injury or outcome. Occipital Glx was significantly increased in children with TBI compared to controls (13.5 +/- 2.4 vs. 10.7 +/- 1.8; p = 0.002), but there was no difference between children with good compared to poor outcomes as determined by the Pediatric Cerebral Performance Category Scale score at 6-12 months after injury. We also did not find a correlation between the amount of Glx and the initial Glasgow Coma Scale score, duration of coma, nor with changes in spectral metabolites, including N-acetyl aspartate, choline, and myoinositol. In part, this may have occurred because, in this study, most patients with poor outcomes were studied later than patients with good outcomes, potentially beyond the time frame for peak elevation of Glx after injury. Additional early and late studies of patients with varying degrees of injury are required to assess the importance to the pathophysiology of TBI of this excitatory neurotransmitter.

Adolescent↗

PubMed2006

Lasting neuroendocrine-immune effects of traumatic brain injury in rats.

Traumatic brain injury (TBI) is a principal cause of long-term physical, cognitive, behavioral, and social deficits in young adults, which frequently coexist with a high incidence of substance abuse disorders. However, few studies have examined the long-term effects of TBI on the neuroendocrine-immune system. TBI was induced in adult male rats under isoflurane anesthesia by cortical contusion injury with a pneumatic piston positioned stereotaxically over the left parietal cortex. Controls underwent sham surgery without injury. At 4 weeks post-injury, the plasma corticosterone response to 30-min restraint stress was significantly blunted in TBI rats compared to the sham controls. One week later, transmitters were implanted for continuous biotelemetric recording of body temperature and spontaneous locomotor activity. At 6 weeks post-injury, the febrile response to i.p. injection of the bacterial endotoxin, lipopolysaccharide (LPS; 50 microg/kg), was significantly lower in TBI than in sham rats. At 8 weeks, swimming in the forced swim test was significantly less in TBI than sham rats. At 9 weeks, rats were rendered ethanol (EtOH) dependent by feeding an EtOH-containing liquid diet for 14 days. Cosine rhythmometry analysis of circadian body temperature Midline Estimating Statistic of Rhythm (MESOR), amplitudes, and acrophases indicated differential effects of EtOH and withdrawal in the two groups. Light- and dark-phase activity analysis indicated that TBI rats were significantly more active than the sham group, and that EtOH and withdrawal differentially affected their activity. Given the extensive interactions of the neuroendocrine-immune systems, these results demonstrate that TBI produces lasting dysregulation amidst the central substrates for allostasis and circadian rhythmicity.

Alcohol-Related Disorders↗

PubMed1998

Pulmonary complications in traumatic brain injury.

Survivors of traumatic brain injury frequently develop respiratory complications that require specialized knowledge and management skills in both acute and postacute environments. This article discusses the pathophysiology of and treatment options for ventilatory failure, neurogenic pulmonary edema, and aspiration. Management of tracheostomies is also discussed, with particular attention paid to decision making regarding the removal of a tracheal appliance. Long-term tracheal complications are also outlined.

Brain Injuries↗

PubMed2026

Admission whole-blood transcriptomic characterization of a neutrophil-predominant systemic immune response in patients with acute traumatic brain injury.

BACKGROUND: Acute traumatic brain injury (TBI) is accompanied by systemic immune responses, but their whole-blood transcriptomic features at hospital arrival remain incompletely characterized. We aimed to characterize these features in patients with acute TBI compared with healthy controls. METHODS: In this single-center prospective observational study, we performed whole-blood RNA sequencing on hospital-arrival samples from 42 patients with acute TBI and 21 healthy controls. Analyses included differential expression (limma-voom; FDR < 0.05, |log2FC| > 0.7), functional enrichment, Ingenuity Pathway Analysis, CIBERSORTx LM22 deconvolution, and per-sample neutrophil degranulation signature scoring. RESULTS: Differential expression analysis identified 996 upregulated and 863 downregulated genes, with marked upregulation of inflammation-, innate immunity-, and neutrophil-related genes including DUSP1, HMGB2, MMP9, and S100A8. Canonical pathways with positive IPA z-scores included Neutrophil degranulation, Neutrophil Extracellular Trap Signaling Pathway, and Toll-like Receptor Signaling; upstream regulators included TNF, IL1B, IFNG, and STAT3. Deconvolution identified 7 of 22 differing subsets (q < 0.05), with relatively higher myeloid and lower lymphoid fractions in TBI. The Neutrophil degranulation signature score correlated with Injury Severity Score within TBI (Spearman ρ = +0.55; q < 0.001). CONCLUSIONS: Admission whole-blood transcriptomics characterized a neutrophil-predominant systemic transcriptional response in patients with acute TBI. This response was also evident among patients without major extracranial injury and was associated with total ISS. However, because the study lacked an appropriately matched non-TBI trauma comparator, the findings should be interpreted as a descriptive characterization of a systemic injury response accompanying TBI and do not establish a TBI-specific molecular signature or mechanism.

gene expression↗

PubMed1999

Nocturnal hormone secretion and the sleep EEG in patients several months after traumatic brain injury.

After severe traumatic brain injury (TBI), sleep disturbances and changes in hormone secretion are frequently observed. Similarly, in depression, abnormalities of sleep and neuroendocrine regulation are common. To test the hypothesis that the changes in brain-injured patients several months after injury are similar to those seen in patients with depression, the authors investigated simultaneously the sleep EEG and nocturnal hormone secretion in 13 young male nondepressed patients after TBI and 13 age-matched control subjects. The resulting data show a pattern of sleep-endocrine changes in patients after TBI, which has some similarities to that of patients with remitted depression.

Adult↗

PubMed1991

Passive P300 response in traumatic brain injury patients.

Severe traumatic brain injury (TBI) patients in a vegetative state were exposed to passive P300 (PP300) evoked potential tests under two conditions: two auditory tones (unimodality condition), and a flash and auditory tone (bimodality condition). A third non-P300 condition using a single repetitive auditory tone was also presented. Patients produced PP300 responses under all three conditions, even though the severity of their clinical condition did not allow them to respond to even simple commands. No peak latency differences were found. PP300 amplitude was significantly larger under the bimodality stimulus condition than either the unimodality or non-P300 condition. The PP300 amplitude under the unimodality condition, in turn, was larger than the P300-like response in the non-P300 condition. This replicates earlier findings with normal subjects. PP300 responses appear to be a tool that might find utility in evaluating TBI patients. Results raise questions about the neuropsychological/neurophysiological nature of the PP300 response.

Adolescent↗

PubMed2002

Epidemiology of traumatic brain injuries: Indian scenario.

Traumatic brain injuries (TBIs) are a leading cause of morbidity, mortality, disability and socioeconomic losses in India and other developing countries. Specific topics addressed in this paper include magnitude of the problem, causes, context of injury occurrence, risk factors, severity, outcome and impact of TBIs on rapidly transforming societies. It is estimated that nearly 1.5 to 2 million persons are injured and 1 million succumb to death every year in India. Road traffic injuries are the leading cause (60%) of TBIs followed by falls (20%-25%) and violence (10%). Alcohol involvement is known to be present among 15%-20% of TBIs at the time of injury. The rehabilitation needs of brain injured persons are significantly high and increasing from year to year. India and other developing countries face the major challenges of prevention, pre-hospital care and rehabilitation in their rapidly changing environments to reduce the burden of TBIs.

Accidental Falls↗

PubMed2005

Serum neuron-specific enolase as a predictor of short-term outcome in children with closed traumatic brain injury.

BACKGROUND: Closed traumatic brain injury (cTBI) is a significant cause of mortality and morbidity in children. The natural course and extent of recovery from cTBI in children are poorly understood. Neuron-specific enolase (NSE), an enzyme detected in serum following structural damage of neuronal brain cells, appears to be a good marker for intracranial injury. However, to the best of the authors' knowledge, the usefulness of NSE as a predictor of disability in children with cTBI has not been reported. OBJECTIVES: To examine the association between posttraumatic serum NSE level and short-term physical disability in children with cTBI. METHODS: This was a retrospective analysis of a prospectively enrolled cohort of children aged 0-18 years with isolated cTBI presenting to the emergency department (ED) within 24 hours of injury, and having a cranial computed tomography (CT) scan as part of the evaluation. The NSE level was obtained at the time of ED evaluation. Physical disability was measured using the Glasgow Outcome Scale (GOS). The GOS score was assigned retrospectively for enrolled patients by a single investigator blinded to NSE level. Patient outcomes were categorized as good (GOS = 5) or poor (GOS < 5). A single radiologist reviewed all cranial CT scans. RESULTS: Ninety eligible subjects with NSE levels were identified; 86 met the enrollment criteria. Seven subjects (8%) had poor outcome. There was a significant difference in NSE levels between the poor and good outcome groups, even within high-risk subgroups. The area under the curve (AUC) for NSE prediction of poor vs. good outcome was 0.83. A serum NSE level of 21.2 ng/dL was 86% sensitive and 74% specific in predicting poor outcome. CONCLUSIONS: It appears that the serum NSE level can be used as a predictor of global short-term physical disability in children following cTBI.

Adolescent↗

PubMed2001

Script knowledge after severe traumatic brain injury.

Severe diffuse traumatic brain injury (TBI) may impair the performance of daily-life complex activities. The aim of the present study was to assess whether these difficulties are related to a representational impairment of action knowledge. Two tasks requiring the manipulation of scripts were used. The first (script reconstitution) required subjects to sort cards describing actions belonging to 4 different scripts, presented in a random order. The second (script generation) required subjects to generate actions belonging to a given script. The results showed that TBI patients had preserved access to goal representation and action knowledge. However, they demonstrated (1) significant impairments when they had to deal with simultaneous competing sources of information and (2) a lack of inhibitory control on routine overlearned skills. Patients' performance was significantly correlated with behavioral modifications in everyday life. These data suggest that action impairment in severe TBI patients cannot be attributed to an impairment of action knowledge per se. As previously suggested by Schwartz et al., a restriction of limited-capacity processing resources may account for the observed deficits.

Activities of Daily Living↗

PubMed2003

Correlation of regional metabolic rates of glucose with glasgow coma scale after traumatic brain injury.

UNLABELLED: After traumatic brain injury (TBI), subcortical white matter damage may induce a functional disconnection leading to a dissociation of regional cerebral metabolic rate of glucose (CMRglc) between the cerebral cortex and deeper brain regions. Therefore, thalamic and brain stem CMRglc may have a closer correlation than does the cerebral cortex with depth of coma after TBI. METHODS: Eleven adult healthy volunteers and 23 adult patients with TBI (median initial Glasgow Coma Scale score [GCSini], 8) underwent (18)F-FDG PET within 5 d after injury. The CMRglc of cortical areas (remote from hemorrhagic lesions), striatum, thalamus, brain stem, cerebellar cortex, and whole brain was compared with severity of injury and the level of consciousness evaluated using GCSini and the Glasgow Coma Scale score at the time of PET (GCSpet). RESULTS: The regional CMRglc of the brain stem is relatively unaffected by the TBI. Compared with healthy volunteers, TBI patients exhibited significantly depressed CMRglc in the striatum (3.9 +/- 1.3 vs. 5.1 +/- 0.9 mg/100 g/min, P < 0.05) and thalamus (3.1 +/- 1.0 vs. 4.3 +/- 0.9 mg/100 g/min, P < 0.05). CMRglc levels were not statistically lower in the cerebellum (2.9 +/- 0.8 vs. 3.5 +/- 0.8 mg/100 g/min, P = NS) and brain stem (2.5 +/- 0.5 vs. 2.6 +/- 0.5 mg/100 g/min, P = NS). However, compared between comatose and noncomatose patients, CMRglc values in the thalamus (2.7 +/- 0.7 vs. 3.6 +/- 1.2 mg/100 g/min, P < 0.05), brain stem (2.2 +/- 0.4 vs. 2.8 +/- 0.5 mg/100 g/min, P < 0.01), and cerebellar cortex (2.6 +/- 0.5 vs. 3.4 +/- 1.0 mg/100 g/min, P < 0.05) were significantly lower in comatose patients. When individual values of regional CMRglc were plotted against posttraumatic level of consciousness, CMRglc values for the thalamus, brain stem, and cerebellum significantly correlated with the level of consciousness at the time of PET (r = 0.58, P < 0.01; r = 0.66, P < 0.01; r = 0.64, P < 0.01, respectively). CT or MRI findings were normal for the analyzed structures except for 3 patients with diffuse axonal injury of the brain stem. The presence of shear injury was associated with poor GCSini (P < 0.05.) but was not related to GCSpet and brain stem CMRglc. CONCLUSION: A PET investigation using (18)F FDG demonstrated a significant difference in glucose metabolism in the thalamus, brain stem, and cerebellum between comatose and noncomatose patients acutely after TBI. The metabolic rate of glucose in these regions significantly correlated with the level of consciousness at the time of PET.

Adolescent↗

PubMed1996

Treatment efficacy: cognitive-communicative disorders resulting from traumatic brain injury in adults.

Traumatic brain injuries (TBI) may result in a broad array of cognitive-communicative impairments. Cognitive-communicative impairments are the result of deficits in linguistic and nonlinguistic cognitive functions. The speech-language pathologist functions as a member of the multidisciplinary team of professionals that collaboratively assess and treat individuals with TBI. The role of the speech-language pathologist includes assessment of all aspects of communication, as well as the communicative implications of cognitive deficits, and swallowing; treatment planning and programming, as determined by the individual's stage of recovery; client and family training/counseling; and interdisciplinary consultation. The effectiveness of speech and language intervention for specific cognitive deficits (e.g., attention, memory, executive functions) as well as general issues of social-skills training and early intervention are illustrated by scientific and clinical evidence from group-treatment and single-subject studies as well as case studies.

Activities of Daily Living↗

PubMed2005

Diffuse axonal injury in mild traumatic brain injury: a diffusion tensor imaging study.

OBJECT: Diffuse axonal injury (DAI) is a major complication of traumatic brain injury (TBI) that leads to functional and psychological deficits. Although DAI is frequently underdiagnosed by conventional imaging modalities, it can be demonstrated using diffusion tensor imaging. The aim of this study was to assess the presence and extent of DAI in patients with mild TBI. METHODS: Forty-six patients with mild TBI and 29 healthy volunteers underwent a magnetic resonance (MR) imaging protocol including: dual-spin echo, fluid-attenuated inversion recovery, T2-weighted gradient echo, and diffusion tensor imaging sequences. In 20 of the patients, MR imaging was performed at a mean of 4.05 days after injury. In the remaining 26, MR imaging was performed at a mean of 5.7 years after injury. In each case, mean diffusivity and fractional anisotropy were measured using both whole-brain histograms and regions of interest analysis. No differences in any of the histogram-derived measures were found between patients and control volunteers. Compared with controls, a significant reduction of fractional anisotropy was observed in patients' corpus callosum, internal capsule, and centrum semiovale, and there were significant increases of mean diffusivity in the corpus callosum and internal capsule. Neither histogram-derived nor regional diffusion tensor imaging metrics differed between the two groups. CONCLUSIONS: Although mean diffusivity and fractional anisotropy abnormalities in these patients with TBI were too subtle to be detected with the whole-brain histogram analysis, they are present in brain areas that are frequent sites of DAI. Because diffusion tensor imaging changes are present at both early and late time points following injury, they may represent an early indicator and a prognostic measure of subsequent brain damage.

Adolescent↗

PubMed2006

Energy metabolic changes in the early post-injury period following traumatic brain injury in rats.

Impaired cerebral energy metabolism may be a major contributor to the secondary injury cascade that occurs following traumatic brain injury (TBI). To estimate the cortical energy metabolic state following mild and severe controlled cortical contusion (CCC) TBI in rats, ipsi-and contralateral cortical tissues were frozen in situ at 15 and 40 min post-injury and adenylate (ATP, ADP, AMP) levels were analyzed using high-performance liquid chromatography (HPLC) and the energy charge (EC) was calculated. At 15 min post-injury, mildly brain-injured animals showed a 43% decrease in cortical ATP levels and a 2.4-fold increase in AMP levels (P < 0.05), and there was a significant reduction of the ipsilateral cortical EC when compared to sham-injured animals (P < 0.05). At 40 min post-injury, the ipsilateral adenylate levels and EC had recovered to the values observed in the sham-injury group. In the severe CCC group, there was a 51% decrease in ipsilateral cortical ATP levels and a 5.3-fold increase in AMP levels with a significant reduction of cortical EC at 15 min post-injury (P < 0.05). At 40 min post-injury, a 2.6-fold ipsilateral increase in AMP levels and an 11% and 44% decrease in EC and ATP levels, respectively, remained (P < 0.05). A 37-38% reduction of the total adenylate pool was observed ipsilaterally in both CCC severity groups at the early time-point, and a 19% and 28% decrease remained in the mild and severe CCC groups, respectively, at 40 min post-injury. Significant contralateral ATP and EC changes were only observed in the severe CCC group at 40 min post-injury (P < 0.05). The energy-requiring secondary injury cascades that occur early post-injury do not challenge the brain tissue to the extent of ATP depletion and may provide a window of opportunity for therapeutic intervention.

Adenosine Monophosphate↗