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PubMedDate not supplied

[Traumatic brain injury in paediatrics. Our results].

INTRODUCTION: 75% of all children admitted to hospital with traumatic injuries involve traumatic brain injuries (TBI), 70% of the deaths occur within the first 48 hours and mortality fluctuates between 20 and 35%. It is estimated that every year 600,000 consultations are made for this reason, 300 out of every 100,000 children suffer a TBI and about 250,000 cases involve hospitalisation. PATIENTS AND METHODS: A descriptive observational study was carried out of all the patients of paediatric age who attended our Casualty Department in the period between January and December 2001, and had suffered a TBI in any of its clinical variations. The Glasgow coma scale (GCS) was used to classify cases according to their seriousness and results were defined by employing the Glasgow results scale (GRS). RESULTS: A survey of 339 cases with TBI was performed, of which 329 (97%) were mild, eight (2.4%) moderate and two (0.6%) were serious. Of the first, 122 (36%) required hospitalisation and the remaining 217 (64%) were given ambulatory treatment (all of them had mild TBI). Complementary examinations carried out were simple head X rays in 117 (95.9%). CAT (computerised axial tomography) scans were only performed in three cases (2.5%). Only two (1.8%) deaths occurred in our series and there were no cases of disability, according to the GRS. CONCLUSIONS: Mild TBI was the common event in our series. Application of treatment systems that are suited to the conditions in each medical centre helps to reduce the number of hospital admissions for mild TBI.

Adolescent↗
PubMed1991

Traumatic brain injury rehabilitation.

Improved survival from severe traumatic brain injury has prompted the development of dedicated rehabilitation programs. Ideally, rehabilitation should begin during acute care in order to prevent later complications. Medically stable patients should be referred from acute care to acute rehabilitation programs for evaluation and then treatment or transfer as appropriate. Dedicated brain injury rehabilitation programs follow a method in which treatment is adapted to the major physical and cognitive impairments at each stage of recovery. Specialized treatment protocols have been developed for unconscious or agitated patients, partly on the basis of advances in neuropharmacology. Because of the long recovery course after severe brain injury, many patients are appropriate for postacute rehabilitation programs directed at community reentry, including return to work. Newer program models for patients with traumatic brain injuries, especially programs using cognitive rehabilitation techniques, are controversial because of inadequate research support and uncertain cost-effectiveness.

Brain Damage, Chronic↗
PubMed2002

Long-term employment outcomes in a rural area following traumatic brain injury.

One of the major sequelae following traumatic brain injury is a change in employment status. This poses significant challenges for rehabilitation services. Several studies have investigated the longer-term outcome after traumatic brain injury. Longer-term outcome in an economically disadvantaged rural environment with limited rehabilitation services has not been studied extensively. A group of individuals (n = 65) who sustained a traumatic brain injury were compared regarding pre- and post-employment status. The moderate and severely injured sub-groups showed a significant change in employment status. Ideally rehabilitation programs should target re-employment as an outcome. Limited employment opportunities in rural areas may make this more difficult to achieve.

Adult↗
PubMed2001

Abnormal cerebral blood volume in regions of contused and normal appearing brain following traumatic brain injury using perfusion magnetic resonance imaging.

Following traumatic brain injury, there may be secondary alterations in cerebrovascular parameters leading to ischemia and further cellular damage. To assess possible subacute hemodynamic disturbances following traumatic brain injury, we used conventional and perfusion magnetic resonance imaging (MRI) in 18 patients, on average 10 days following injury. Six of the 18 patients had focal contusions or edema visible on conventional MRI. These six patients had a significantly reduced normalized regional cerebral blood volume (rCBV) in the regions of focal pathology compared to equivalent areas in control subjects (patients 0.47 +/- 0.20 [means +/- SD], controls 1.02 +/- 0.11, p < 0.001). In addition, four of these six patients had an increased rCBV (outside control range) in the region of normal appearing brain immediately surrounding the contusion. These six patients were more significantly injured and had a worse clinical outcome compared to the remaining patients (p = 0.004,p = 0.03, respectively). There were five patients who had a region of reduced rCBV (outside control range) in a quadrant of normal appearing white matter, away from any visible abnormality, who were not more significantly injured than the remaining patients but went on to have a significantly poorer clinical outcome (p = 0.27, p = 0.01, respectively). Traumatic brain injury is a heterogeneous insult causing a variety of pathology, not all of which is visible using conventional imaging methods. The current study has shown that regions of both normal appearing and contused brain may have an abnormal rCBV and that alterations in rCBV may play a role in determining the clinical outcome of patients.

Adult↗
PubMed1992

Cognitive deficits following traumatic brain injury produced by controlled cortical impact.

Traumatic brain injury produces significant cognitive deficits in humans. This experiment used a controlled cortical impact model of experimental brain injury to examine the effects of brain injury on spatial learning and memory using the Morris water maze task. Rats (n = 8) were injured at a moderate level of cortical impact injury (6 m/sec, 1.5-2.0 mm deformation). Eight additional rats served as a sham-injured control group. Morris water maze performance was assessed on days 11-15 and 30-34 following injury. Results revealed that brain-injured rats exhibited significant deficits (p less than 0.05) in maze performance at both testing intervals. Since the Morris water maze task is particularly sensitive to hippocampal dysfunction, the results of the present experiment support the hypothesis that the hippocampus is preferentially vulnerable to damage following traumatic brain injury. These results demonstrate that controlled cortical impact brain injury produces enduring cognitive deficits analogous to those observed after human brain injury.

Animals↗
PubMed1993

Excitatory amino acids in cerebrospinal fluid following traumatic brain injury in humans.

Evidence from models of traumatic brain injury implicates excitotoxicity as an integral process in the ultimate neuronal damage that follows. Concentrations of the excitatory amino acid glutamate were serially measured in the cerebrospinal fluid (CSF) of patients with traumatic brain injuries and in control patients for comparison. The purpose of the study was to determine whether glutamate concentrations were significantly elevated following traumatic brain injury and, if so, whether they were elevated in a time frame that would allow the use of antagonist therapy. Cerebrospinal fluid was sampled fresh from ventricular drains every 12 hours and analyzed using high-performance liquid chromatography for the excitatory amino acids. The peak concentrations of glutamate in the CSF of the 12 brain-injured patients ranged from 14 to 474 microM and were significantly higher than those in the three control patients, 4.9 to 17 microM (Mann-Whitney U-test, p < 0.02). Glutamate concentrations in five of the eight patients who were still being sampled on Day 3 were beyond the control group range. The implication of this study is that severely head-injured patients are exposed to high concentrations of a neurotoxic amino acid for days following injury and thus may benefit from antagonist intervention.

Adolescent↗
PubMed1996

Association between injury indices and outcome after severe traumatic brain injury in children.

OBJECTIVES: (1) To determine whether indices of traumatic brain injury (TBI) in children are associated with outcome at hospital discharge and 5 to 7 years later; (2) to describe persisting disabilities. DESIGN: Retrospective, uncontrolled study of a cohort of children with severe, nonpenetrating TBI. SETTING: Consecutive admissions to a level 1 trauma center over 2 years. SUBJECTS: Seventy-five children younger than 17 years old were previously studied to identify predictors of disability at acute care discharge. Thirty-three of the 50 survivors (66%) were enrolled. MAIN OUTCOME MEASURES: A database of variables abstracted from medical records was available from the previous study. Subjects were surveyed about premorbid problems, school, employment, and current function, and school records were reviewed. Using all information, a Glasgow Outcome Scale (GOS) score was assigned 5 to 7 years after TBI. Associations between database variables and GOS score at discharge and follow-up were examined using nonparametric analyses. The odds ratio for good recovery was calculated for all significant associations. RESULTS: Late GOS was good recovery for 27%, moderate disability for 55%, and severe disability for 18%. Discharge GOS scores were related (p < or = .01) to the head Abbreviated Injury Scale score, Injury Severity Scale score, Glasgow Coma Scale (GCS) score measured in the field and at 6, 24, and 72 hours, the length of coma, and initial discharge site. Late GOS scores were related (p < or = .01) to the same variables except the field and 6-hour GCS scores, as well as pupillary responses in the field and the discharge GOS. At follow-up, 64% were independent in mobility, 70% in self-care, and 24% in cognitive items on the Functional Independence Measure. Seventy percent of children received special education services. Employment histories were poor. Most subjects were not receiving neurological or rehabilitation follow-up. CONCLUSIONS: Early and late outcome after severe TBI are related to variables measured at and after injury. Subjects had long-term educational and vocational problems but often did not utilize the medical model of neurorehabilitation.

Adolescent↗
PubMed2001

The effect of groups II and III metabotropic glutamate receptor activation on neuronal injury in a rodent model of traumatic brain injury.

OBJECTIVE: The role of metabotropic glutamate receptor activation after traumatic brain injury (TBI) is not well understood. In vitro studies suggest that activation of Groups II and III metabotropic glutamate receptors may provide some degree of neuroprotection and may be potential targets for the development of therapeutic strategies. Thus, we examined the effects of Group II and Group III selective agonists on neuronal degeneration after in vivo TBI. METHODS: Fifty male Sprague-Dawley rats were subjected to lateral fluid percussion brain injury immediately followed by an intracranial injection of 2-(2',3')-dicarboxycyclopropylglycine (DCG-IV) (Group II) or (R,S)-4-phosphonophenylglycine (Group III) in the CA2 and CA3 areas of the hippocampus. DCG-IV was injected at doses of 20 fmol, 100 fmol, and 500 fmol, and (R,S)-4-phosphonophenylglycine was injected at 8 nmol, 40 nmol, and 200 nmol. Vehicle injection control groups were used for comparison with each drug group. All animals were killed 24 hours after TBI was induced. Four 50-microm brain sections were obtained from each animal and stained for degenerating neurons with the fluorochrome Fluoro-Jade. Two independent, blinded investigators counted the number of degenerating (Fluoro-Jade-positive) neurons in the CA2 and CA3 areas of the hippocampus of each brain section. RESULTS: Compared with vehicle, the 500-fmol dose of DCG-IV significantly reduced the number of Fluoro-Jade-positive degenerating neurons (P < 0.001). Lower doses of DCG-IV were associated with a decreased but not statistically significant number of Fluoro-Jade-positive neurons. In contrast, (R,S)-4-phosphonophenylglycine had no significant effect on the number of degenerating neurons. CONCLUSION: Administration of selective Group II metabotropic glutamate receptor agonists protects neurons against in vivo TBI. These receptors may thus be a promising target for future neuroprotective drugs.

Animals↗
PubMed2026

Effect of ketofol versus Fentanyl-Midazolam sedation on neurological recovery in traumatic brain Injury: A randomised study.

Neurological recovery after traumatic brain injury (TBI) is multifactorial, and sedation is a cornerstone of neurocritical care because of its neuroprotective role. Although ketofol is widely used for anaesthesia, its effectiveness as a sedative regimen in the intensive care unit (ICU) has not been well studied. This preliminary exploratory double-blind, randomised study compared ketofol (KP) with fentanyl-midazolam (FM) sedation in adults with moderate-to-severe TBI. Sedation was administered for 72&#xa0;h and titrated to a Richmond Agitation-Sedation Scale (RASS) score&#xa0;&#x2264;&#xa0;&#xa0;-&#xa0;3. The primary outcome was the Extended Glasgow Outcome Scale (GOSE) at 30&#xa0;days. Secondary outcomes included GOSE at 90&#xa0;days, incidence of propofol infusion syndrome (PRIS), duration of mechanical ventilation, haemodynamic stability, and ICU and hospital length of stay. Of 120 enrolled patients, 111 were included in the final analysis (57 FM, 54 KP). Baseline characteristics, including injury severity and Marshall CT scores, were comparable. At 30&#xa0;days, good neurological recovery (GOSE 7-8) was more frequent in the KP group than the FM group (26% vs. 10.5%, p&#xa0;=&#xa0;0.03). At 90&#xa0;days, recovery remained higher with KP (44.4% vs. 33.3%), though the difference was not statistically significant (p&#xa0;=&#xa0;0.16). Multivariate analysis confirmed ketofol as an independent predictor of good recovery at 30&#xa0;days (adjusted OR 3.63, 95% CI 1.11-11.85, p&#xa0;=&#xa0;0.033). No PRIS occurred, and secondary outcomes were similar. Ketofol-based sedation was safe and may be associated with improved early neurological recovery compared with fentanyl-midazolam, with a favourable trend toward improved long-term neurological recovery.

Humans↗
PubMed2002

Trauma to the pontomesencephalic brainstem-a major clue to the prognosis of severe traumatic brain injury.

The objective of this study was to assess the significance of an injury to the pontomesencephalic brainstem in severe traumatic brain injury [Glasgow coma score (GCS) below 8]. Forty victims of severe traumatic brain injury with and with out compounding pathologies almost equally distributed among both groups were studied. The outcome (mean follow-up, 11.3 months) was assessed by means of the Glasgow outcome score (GOS) and of the Disability rating scale (DRS). Injury of the brainstem was detected by electrophysiological investigation (evoked potentials, brainstem reflexes) and magnetic resonance imaging (MRI) carried out early after trauma. Statistical analysis (Wilcoxon signed rank test for matched pairs) revealed a significantly worse initial GCS (median 5 versus 6), GOS (median 3 versus 4), and DRS score (median 6 versus 2) for the group with brainstem lesions than for the group without such lesions. Moreover, there was a significant accumulation of lesions of the corpus callosum, the basal ganglia, and the (para-)hippocampal area detected by MRI in the brainstem lesion group. In addition, the finding of an abnormal cortical component of the median nerve evoked somatosensory potential was significantly more frequent in the patients with brainstem injury. Traumatic brainstem lesions diagnosed by MRI a nd/or electrophysiological investigation are associated with injury to other 'deeply' situated parts ofthe brain. The finding of a brainstem lesion influences to the outcome of patients after severe traumatic brain injury.

Adolescent↗
PubMed2005

Physiological thresholds for irreversible tissue damage in contusional regions following traumatic brain injury.

Cerebral ischaemia appears to be an important mechanism of secondary neuronal injury in traumatic brain injury (TBI) and is an important predictor of outcome. To date, the thresholds of cerebral blood flow (CBF) and cerebral oxygen utilization (CMRO(2)) for irreversible tissue damage used in TBI studies have been adopted from experimental and clinical ischaemic stroke studies. Identification of irreversibly damaged tissue in the acute phase following TBI could have considerable therapeutic and prognostic implications. However, it is questionable whether stroke thresholds are applicable to TBI. Therefore, the aim of this study was to determine physiological thresholds for the development of irreversible tissue damage in contusional and pericontusional regions in TBI, and to determine the ability of such thresholds to accurately differentiate irreversibly damaged tissue. This study involved 14 patients with structural abnormalities on late-stage MRI, all of whom had been studied with (15)O PET within 72 h of TBI. Lesion regions of interest (ROI) and non-lesion ROIs were constructed on late-stage MRIs and applied to co-registered PET maps of CBF, CMRO(2) and oxygen extraction fraction (OEF). From the entire population of voxels in non-lesion ROIs, we determined thresholds for the development of irreversible tissue damage as the lower limit of the 95% confidence interval for CBF, CMRO(2) and OEF. To test the ability of a physiological variable to differentiate lesion and non-lesion tissue, we constructed probability curves, demonstrating the ability of a physiological variable to predict lesion and non-lesion outcomes. The lower limits of the 95% confidence interval for CBF, CMRO(2) and OEF in non-lesion tissue were 15.0 ml/100 ml/min, 36.7 mumol/100 ml/min and 25.9% respectively. Voxels below these values were significantly more frequent in lesion tissue (all P < 0.005, Mann-Whitney U-test). However, a significant proportion of lesion voxels had values above these thresholds, so that definition of the full extent of irreversible tissue damage would not be possible based upon single physiological thresholds. We conclude that, in TBI, the threshold of CBF below which irreversible tissue damage consistently occurs differs from the classical CBF threshold for stroke (where similar methodology is used to define such thresholds). The CMRO(2) threshold is comparable to that reported in the stroke literature. At a voxel-based level, however (and in common with ischaemic stroke), the extent of irreversible tissue damage cannot be accurately predicted by early abnormalities of any single physiological variable.

Adolescent↗
PubMed2006

The experience of surviving traumatic brain injury.

AIM: This paper reports a study describing the experience of surviving traumatic brain injury as narrated by individuals 1 year after injury. BACKGROUND: The experience of surviving traumatic brain injury is an individual and invisible experience. Healing and resolution of grief is still problematic for many years after injury. This experience includes those with severe injury. There is limited literature focusing on the survivor. METHODOLOGY: Sixty people with hospital admission diagnoses of traumatic brain injury were interviewed 1 year after injury using the Extended Glasgow Outcome Score questionnaire. Survivors then described their experiences of recovery. Data were collected through unstructured in-depth interviews, transcribed from audio-tapes and analysed into references. Qualitative content analysis was used to compile their frequencies from recurring themes. FINDINGS: Sixty survivors with a median age of 35 years were enrolled in the study, with 100% follow-up. Twelve per cent returned to full preinjury functioning, 35% had residual psychosocial and physical sequelae, 38% had significant restrictions in lifestyle and work capacity, and 15% were unable to care for themselves throughout the 24-hour period. The common narratives were classified into five categories: 'regret and grief within self'; 'insensitivity of health professionals'; 'invisibility of self'; 'stranded self'; and 'recovery in self'. These self-narratives reflected renewed ways to view the self, which were conceptualized to be intact 'in spite of' or to be worthwhile 'because of' the traumatic brain injury. CONCLUSIONS: Self-narratives could be a worthwhile focus of psychological intervention by substituting positive narratives for negative ones, demonstrating hope and a positive outlook on life in order to enhance self-reflection and improve mental health. They can assist people to minimize, avoid or overcome devaluation and, as such, provide a basis for considerable nursing rehabilitation practice, even in those with severe injury.

Adolescent↗
PubMedDate not supplied

[Autonomic dysfunction in children with traumatic brain injury].

INTRODUCTION: Autonomic dysfunction syndrome following traumatic brain injury is a situation involving adrenergic hyperactivity produced by the lack of control over the autonomous nervous system at a central level. The difficulties involved in its therapeutic management make it even more important. CASE REPORTS: We report the cases of a boy and a girl aged 6 and 12 years, respectively, who had suffered a severe traumatic brain injury with important brain damage that included diencephalic and mesencephalic compromise and areas of diffuse axonal injury. From the acute phase onwards, they presented episodes of hypertension, tachycardia, excessive sweating and spasticity in the form of attacks that initially led to a differential diagnosis between sepsis, opiate and/or benzodiazepine withdrawal syndrome and epilepsy. The length of time spent in coma was very long and the attacks went on throughout the awakening phase almost until the moment they were discharged from hospital, despite trying different treatments. In our cases, orally administered baclofen and midazolam seemed to be the most effective. CONCLUSIONS: Autonomic dysfunction is difficult to manage. There are no standardised treatments and speculation continues with regard to its true promoter. We might think that the central injury is the cause of the process and that the autonomic dysfunction increases the secondary lesion and contributes to the functional worsening. If we take into account that the survival rate of the children is high despite the severity of the injuries and although the dysautonomia can be self-limiting with time, we believe that its treatment is essential if the ultimate aim is to minimise the sequelae.

Autonomic Nervous System Diseases↗
PubMed2003

Introduction: the Traumatic Brain Injury Model Systems of Care.

The Traumatic Brain Injury Model Systems of Care (TBIMS) is a program that has been funded by the National Institute on Disability and Rehabilitation Research (US Department of Education) since 1987. The program is a collaborative effort of rehabilitation centers across the United States to further knowledge about the natural history of recovery and outcomes over the life course of individuals with traumatic brain injury, as well as to provide comprehensive services across the continuum of care and to foster innovative research programs. This introduction describes the underlying principles of the TBIMS program and the research initiatives carried out in the 1997/1998-2002 funding cycle.

Brain Injuries↗
PubMed2006

Novel differential neuroproteomics analysis of traumatic brain injury in rats.

Approximately two million traumatic brain injury (TBI) incidents occur annually in the United States, yet there are no specific therapeutic treatments. The absence of brain injury diagnostic endpoints was identified as a significant roadblock to TBI therapeutic development. To this end, our laboratory has studied mechanisms of cellular injury for biomarker discovery and possible therapeutic strategies. In this study, pooled naïve and injured cortical samples (48 h postinjury; rat controlled cortical impact model) were processed and analyzed using a differential neuroproteomics platform. Protein separation was performed using combined cation/anion exchange chromatography-PAGE. Differential proteins were then trypsinized and analyzed with reversed-phase LC-MSMS for protein identification and quantitative confirmation. The results included 59 differential protein components of which 21 decreased and 38 increased in abundance after TBI. Proteins with decreased abundance included collapsin response mediator protein 2 (CRMP-2), glyceraldehyde-3-phosphate dehydrogenase, microtubule-associated proteins MAP2A/2B, and hexokinase. Conversely C-reactive protein, transferrin, and breakdown products of CRMP-2, synaptotagmin, and alphaII-spectrin were found to be elevated after TBI. Differential changes in the above mentioned proteins were confirmed by quantitative immunoblotting. Results from this work provide insight into mechanisms of traumatic brain injury and yield putative biochemical markers to potentially facilitate patient management by monitoring the severity, progression, and treatment of injury.

Animals↗
PubMed1996

Inattentive behavior after traumatic brain injury.

Clinicians and families report that traumatic brain injury results in a variety of attention deficits. Numerous laboratory studies have documented slowing of information processing, alteration in event-related potentials, or difficulty attending to specific relevant task dimensions in the presence of redundant information. However, little is known about how these information processing abnormalities relate to observable behaviors in daily living or work environments, which presumably form the basis for clinicians' and families' reports. We developed a quantitative assessment of behavioral inattentiveness in both quiet and distracting environments, and demonstrated excellent interrater reliability. Using this assessment, we have studied 20 patients with recent traumatic brain injury and 20 demographically comparable control subjects. We have confirmed marked differences in behavioral attentiveness between patients and controls in both distracting and nondistracting environments.

Activities of Daily Living↗
PubMed1999

Functional anatomy of neuropsychological deficits after severe traumatic brain injury.

BACKGROUND: Neurobehavioral disorders after severe traumatic brain injury (TBI) are poorly correlated with focal lesions detected by structural neuroimaging techniques such as CT scan or MRI. OBJECTIVE: To explore the relationships between regional cerebral glucose metabolism at rest, as measured by PET, and neurobehavioral status after severe TBI at the subacute stage. METHODS: Thirteen patients without focal structural lesion on MRI were studied. Neuropsychological assessment included tests of memory, attention and speed of information processing, and executive functions, and a global neurobehavioral assessment. Regional cerebral glucose metabolism at rest was measured with (18F)-fluorodeoxyglucose and PET. RESULTS: A close link was found between cognitive and behavioral disorders and decreased cortical metabolism in prefrontal and cingulate cortex. Tests of memory and executive functions significantly correlated with regional metabolism in the mesial and lateral prefrontal cortex and the cingulate gyrus. Behavioral disorders correlated significantly with mesial prefrontal and cingulate metabolisms. CONCLUSION: These results suggest a predominant role of prefrontal and cingulate dysfunction in cognitive and behavioral disorders of patients with severe traumatic brain injury, even in the absence of focal structural lesion of the brain. Further cognitive functional activation research using PET or functional MRI might help clarify the relative contributions of both areas to dysfunction.

Adolescent↗