The use of hyperventilation in the acute management of severe traumatic brain injury. Brain Trauma Foundation.
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Brain Injuries↗
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Congenital and acquired brain injury. 1. Brain injury: epidemiology and pathophysiology.
UNLABELLED: This self-directed learning module highlights recent advances in the understanding of brain injury pathophysiology, epidemiology. severity scales, and treatment interventions to minimize brain injury in adults and children. It is part of the chapter on congenital and acquired brain injury in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. In this article, brain injury epidemiology is summarized, and differences in between brain injury in pediatric and elderly persons are highlighted. Underlying physiologic and chemical mechanisms for secondary brain injury are reviewed, along with strategies and research to minimize this injury. Contemporary understanding of the mechanisms and treatments of brain injury in preterm infants is also discussed. Classification of brain injury severity provides a way to stratify this heterogeneous group. OVERALL ARTICLE OBJECTIVE: (a) To summarize brain injury epidemiology and prevention strategies across the age spectrum, (b) to review the pathophysiology of pediatric and adult brain injury, and (c) to classify brain injury by severity scales.
Aged↗
Cultural variations in the understanding of traumatic brain injury and brain injury rehabilitation.
Little is known about how people from different cultures experience and understand traumatic brain injury (TBI) and the process of brain injury rehabilitation. The Brain Injury Rehabilitation Unit (BIRU) undertook a qualitative project to research cultural variations in the understanding of TBI and the rehabilitation process, interviewing 39 people with TBI and family members from Italian, Lebanese and Vietnamese backgrounds. The focus was on the reporting of sequelae of the TBI; valued qualities of service providers; barriers to effective communication; the role of the families in the rehabilitation process; and the experience of social stigma. Findings suggest there is a universal experience of TBI that transcends individual cultures. Study participants valued attentiveness, friendliness and guidance from rehabilitation staff. Family support was not always available to the person with TBI due to family conflict. Generally, people with TBI and family members valued the assistance of health interpreters facilitating their communication with rehabilitation staff. People with TBI from all three cultures experienced problems of stigma and social isolation. The findings have a number of implications for how brain injury rehabilitation staff can approach service provision to people from diverse cultural backgrounds.
Adaptation, Psychological↗
Congenital and acquired brain injury. 2. Brain injury rehabilitation: medical management.
UNLABELLED: This self-directed learning module focuses on the importance of developing comprehensive problem lists and treatment plans for the patient with acute brain injury. It is part of the chapter on Congenital and Acquired Brain Injury in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. This article focuses on general medical management, interpretation of brain injury severity, cranial nerve dysfunction, acute changes in neurologic function, and treatment of spasticity. OVERALL ARTICLE OBJECTIVE: To present guidelines for assessment, treatment, and management of the patient who has acute brain injury.
Brain Injuries↗
A neuropsychological comparison of psychotic disorder following traumatic brain injury, traumatic brain injury without psychotic disorder, and schizophrenia.
Neuropsychological functioning in individuals with psychotic disorder following traumatic brain injury (PDFTBI), traumatic brain injury without psychosis (TBIWP), and schizophrenia were compared against each other and to the means of normal subjects. It was predicted that the PDFTBI group would be similar to the schizophrenic group in patterns of deficits, but milder in severity. Compared to scores from a normal sample, the PDFTBI group scored significantly lower in intelligence, vocabulary, verbal memory, and executive functioning, while the schizophrenic group scored significantly lower in intelligence, working memory, verbal memory, visual spatial abilities, and executive functioning. No differences were found between normal subjects and the TBIWP group. Implications of our findings for the conceptualization of psychotic disorders are discussed.
Adult↗
Diagnostic criteria and differential diagnosis of mild traumatic brain injury.
Brain injury is classified clinically as severe, moderate or mild brain injury characteristics, including admission Glasgow coma score, duration of unconsciousness and post-traumatic amnesia and any focal neurological findings. Most traumatic brain injuries are classified as mild traumatic brain injury (MTBI). Headache, nausea and dizziness are frequent symptoms after MTBI and may continue for weeks to months after the trauma. MTBI may also be complicated by intracranial injuries. Experimental animal models and post-mortem studies have shown axonal damage and dysfunction in MTBI. This damage is mostly localized in the frontal lobes. Serum S-100 and NSE have been reported to be markers for the seventy of brain damage. In the literature, indications for radiodiagnostic evaluation following MTBI have been the subject of debate. Radiographs of the skull are used to exclude skull fractures, but are not useful for an evaluation of brain injury. Computed tomography of the brain seems to be the best way to exclude the development of relevant intracranial lesions. MTBI has a good clinical outcome, although a substantial group of patients develop post-concussional complaints (PCC). There is little information on the effectiveness of various methods suggested for reducing the frequency of PCC.
Brain Injuries↗
Increased expression of aquaporin-4 in human traumatic brain injury and brain tumors.
OBJECTIVE: To characterize the expression of aquaporin-4 (AQP4), one of the aquaporins (AQPs), in human brain specimens from patients with traumatic brain injury or brain tumors. METHODS: Nineteen human brain specimens were obtained from the patients with traumatic brain injury, brain tumors, benign meningioma or early stage hemorrhagic stroke. MRI or CT imaging was used to assess brain edema. Hematoxylin and eosin staining were used to evaluate cell damage. Immunohistochemistry was used to detect the AQP4 expression. RESULTS: AQP4 expression was increased from 15 h to at least 8 d after injury. AQP4 immunoreactivity was strong around astrocytomas, ganglioglioma and metastatic adenocarcinoma. However, AQP4 immunoreactivity was only found in the centers of astrocytomas and ganglioglioma, but not in metastatic adenocarcinoma derived from lung. CONCLUSION: AQP4 expression increases in human brains after traumatic brain injury, within brain-derived tumors, and around brain tumors.
Adult↗
The molecular basis of brain injury and brain edema: the role of oxygen free radicals.
This review article outlines basic concepts and pathophysiological aspects of the chemistry of oxygen free radicals in all forms of brain injury and brain edema. Recent experimental studies have demonstrated that oxygen free radicals may be important mediators of brain injury and brain edema, and pharmacological antagonism of oxygen free radicals shows beneficial therapeutic results. A number of fundamental questions need to resolved, and advanced techniques for detecting oxygen free radicals will be needed. No clinical data are available, but oxygen free radical scavengers may possibly become a critical therapeutic modality for brain injury and brain edema.
Animals↗
Dual role of tumor necrosis factor alpha in brain injury.
Brain injury (ischemia, trauma) is among the leading cause of mortality and disability in the western world. It induces increased production of tumor necrosis factor (TNF alpha) by brain resident cells. There is conflicting evidence on the role of this response in the injured brain, showing its potential effect in both processes of repair and of damage. This review presents data from clinical and experimental studies on the stimulation of TNF alpha production in brain injury and on the deleterious consequence of this acute response. Its inhibition by pharmacologic agents, neutralizing antibodies or soluble receptors has protective effects. In contrast, there are reports (from in-vitro studies or knock-out mice) on the beneficial effects of TNF alpha. To reconcile these apparently conflicting reports, the exact timing and extent of TNF alpha activation must be taken into account, as well as the presence of other mediators such as reactive oxygen species. It is suggested that the appropriate context of mediators, at any given time after brain injury may well determine whether the effect of TNF alpha is protective or toxic.
Animals↗
Autonomic cardiovascular state after severe brain injury and brain death in children.
OBJECTIVE: To study and compare the autonomic cardiovascular state of children after severe brain injury and brain death. DESIGN: Prospective clinical study. SETTING: Pediatric ICU. PATIENTS: Pediatric patients suffering severe brain injury caused by trauma, anoxia, or hemorrhage. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: We analyzed cardiorespiratory parameters, heart rate power spectra, plasma catecholamine concentrations, and the response to the cold pressor test in nine brain-dead patients and compared the results with the test findings of 11 patients with severe brain injury. Low-frequency total heart rate power (p < .03), peak amplitude (p < .02), and plasma catecholamine concentrations (p < .001) were different with no overlap of values between groups. Cold pressor testing in patients with severe brain injury showed changes in respiratory rate and low-frequency heart rate power that were +/- 20% to 100% from baseline values; however, there were no measurable changes in brain-dead patients. CONCLUSIONS: Our results support the concept of a damaged sympathetic cardiovascular system in severe brain injury and complete interruption of the autonomic cardiovascular pathways in brain death. Since determination of brain death may be difficult, our findings have implications for corroborating brain death using autonomic cardiovascular testing.
Brain Death↗
Amelioration of hypoxemia by neuromuscular blockade following brain injury.
Brain injury has been commonly associated with respiratory failure and uncontrolled skeletal muscle activity. In the present study, neuromuscular (NM) blockade induced by injection of succinylcholine hydrochloride was used to block uncontrolled muscle contractions in dogs with brain injury caused by rapid elevation of intracranial pressure (ICP). Decerebrate posturing, a decrease in value (mean +/- SEM) of arterial oxygen tension (Pa02) of 26 +/- 1 torr, and an increase in arterial carbon dioxide tension (PaCO2) of 11 +/- 1 torr occurred in the dogs, which were supported by mechanical ventilation. The arterial hypoxemia developed independently of the decerebration; however, dogs that demonstrated decerebrate posturing exhibited significantly larger decreases in Pa02 than dogs that did not (P less than 0.01). NM blockade ameliorated the effects of elevated ICP on the arterial blood gases; i.e., the amount of hypoxemia in decerebrate dogs was significantly less in dogs subjected to NM blockade than in dogs not subjected to NM blockade. It is concluded that uncontrolled skeletal muscle activity that exacerbates arterial hypoxemia associated with brain injury is ameliorated by use of NM blockade as a therapeutic adjunct to mechanical ventilation.
Animals↗
Gene expression profile changes are commonly modulated across models and species after traumatic brain injury.
Brain trauma is a major cause of morbidity and mortality, both in adult and pediatric populations. Much of the functional deficit derives from delayed cell death resulting from induction of neurotoxic factors that overwhelm endogenous neuroprotective responses. To identify the potential molecular mechanisms underlying such delayed responses, we compared gene expression patterns using high-density oligonucleotide arrays at 4, 8, 24, and 72 h after moderate levels of lateral fluid percussion-induced brain injury in rats and lateral controlled cortical impact injury in mice (a total of 47 profiles). Expression of 82 genes in 12 functional categories was significantly changed in both species after trauma. The largest number of gene expression changes were found in the functional groups related to inflammation (17%), transcription regulation (16%), and cell adhesion/extracellular matrix (15%). Fifty percent of genes similarly altered across models had not been previously implicated in traumatic brain injury. Of particular interest were expression changes in genes linked to neurodegeneration, such as ATF3 and lysosomal membrane glycoprotein 2, and to neuroprotection including lipocortin 1, calponin 3, gelsolin, Id-1, and p45 NF-E2. Gene expression profiling across species and models may help identify candidate molecular pathways induced by brain injury, some of which may provide novel targets for therapeutic intervention.
Animals↗
Brain imaging and behavioral outcome in traumatic brain injury.
Brain imaging studies have become an essential diagnostic assessment procedure in evaluating the effects of traumatic brain injury (TBI). Such imaging studies provide a wealth of information about structural and functional deficits following TBI. But how pathologic changes identified by brain imaging methods relate to neurobehavioral outcome is not as well known. Thus, the focus of this article is on brain imaging findings and outcome following TBI. The article starts with an overview of current research dealing with the cellular pathology associated with TBI. Understanding the cellular elements of pathology permits extrapolation to what is observed with brain imaging. Next, this article reviews the relationship of brain imaging findings to underlying pathology and how that pathology relates to neurobehavioral outcome. The brain imaging techniques of magnetic resonance imaging, computerized tomography, and single photon emission computed tomography are reviewed. Various image analysis procedures, and how such findings relate to neuropsychological testing, are discussed. The importance of brain imaging in evaluating neurobehavioral deficits following brain injury is stressed.
Adolescent↗
Signal transduction and neurosurvival in experimental models of brain injury.
Brain injury and neurodegenerative disease are linked by their primary pathological consequence-death of neurons. Current approaches for the treatment of neurodegeneration are limited. In this review, we discuss animal models of human brain injury and molecular biological data that have been obtained from their analysis. In particular, signal transduction pathways that are associated with neurosurvival following injury to the brain are presented and discussed.
Animals↗
Modulation of IL-1 beta gene expression by lipid peroxidation inhibition after kainic acid-induced rat brain injury.
Brain injury was induced by intraperitoneal administration of kainic acid (KA, 10 mg/kg). Animals were randomized to receive either IRFI 042 (20 mg/kg i.p.), a lipid peroxidation inhibitor, or its vehicle (NaCl 0.9% DMSO 10% 1 ml/kg i.p.) 30 min before KA administration. A first set of animals was sacrificed 6 h after KA injection to measure malondialdehyde (MDA) content, glutathione-reduced (GSH) levels and the mRNA for interleukin-1beta (IL-1beta) in the cortex and in the hippocampus. A second set of animals was sacrificed 48 h after KA administration for histological analysis. All animals were observed for monitoring the behavioral sequelae and for evaluating latency of convulsions. Sham brain injury rats were used as controls. Intraperitoneal administration of IRFI 042 significantly decreased brain MDA (cortex: KA + vehicle = 0.285 +/- 0.04 nmol/mg protein; KA + IRFI 042 = 0.156 +/- 0.02 nmol/mg protein, P < 0.005; hippocampus: KA + vehicle = 0.350 +/- 0.03 nmol/mg protein; KA + IRFI 042 = 0.17 +/- 0.04 nmol/mg protein, P < 0.005), prevented the brain loss of GSH in both cortex (KA + vehicle = 7.81 +/- 1 micromol/g protein; KA + IRFI 042 = 12.1 +/- 1 micromol/g protein; P < 0.005) and hippocampus (KA + vehicle = 5 +/- 0.8 micromol/g protein; KA + IRFI 042 = 9.4 +/- 1.8 micromol/g protein; P < 0.005), reduced both brain IL-1beta mRNA expression and oedema, and increased latency of convulsions. Histological analysis showed a reduction of cell damage in IRFI 042-treated samples. The present data indicate that lipid peroxidation inhibition reduces IL-1beta gene expression and protects against kainic acid-induced brain damage.
Animals↗
Self awareness: effects of feedback and review on verbal self reports and remembering following brain injury.
Brain injury may produce impairments in self awareness. The magnitude of impairment is often determined by comparing patient self reports with self reports of others (report-report) or with patient performance (report-performance). This paper presents data on the pattern of a self-awareness deficit in memory functioning exhibited by a brain injury survivor 5 years post-injury. The effects of practice and feedback on reporting-recall differences was examined using single case methodology. Several prospective and retrospective self reports were obtained, to allow an examination of reporting about past or future recall. Results showed that recall improved and the magnitude of report-recall differences were reduced with practice and feedback.
Adult↗
Brain potentials associated with movement in traumatic brain injury.
Brain potentials may be used to assess the functional abnormalities that underlie impairments of movement. The purpose of this article is to illustrate the usefulness of examining these potentials. In addition to an overview of the topic, the article includes a report of a study demonstrating that there were differences between the brain potentials of five patients with traumatic brain injury and those of four healthy control subjects. All five patients were in the postacute phase of hemiplegia. Slow cortical potentials associated with simple goal-directed forearm and finger movements were recorded from frontal and parietal electrodes. Two seconds of movement-related electroencephalographic activity (movement-related potential) were recorded. The patients showed reduced brain potentials for movements associated with their paretic limb and, to a lesser extent, reduced brain potentials for movements associated with their nonparetic limb. The waveforms obtained from the patients were unusual, with uncharacteristic cross-cortical movement-related potential correlations associated with specific electrode configurations, as well as with specific movement conditions. Brain potentials associated with the fore-period interval of a simple reaction time paradigm were later recorded in two of the patients with traumatic brain injury and in a control subject to help determine the functional significance of the relative positivity apparent in their movement-related potential data. This preliminary study indicates that electroencephalographic potentials obtained during the preparation for and execution of movement can provide information regarding the basis for motor dysfunction.
Adolescent↗
Changes in concentration of cerebrospinal fluid components in patients with traumatic brain injury.
Brain injury, like other central nervous system pathologies, causes changes in the composition of the cerebrospinal fluid (CSF). In this study, changes in the concentration of small molecules of the CSF, which are in the minimal micromolar concentration, were observed and monitored using high-resolution proton (NMR) spectroscopy. Twenty-two patients with isolated traumatic brain injuries (TBI) and 15 patients making up the control group were recruited for the study. CSF samples were collected by lumbar puncture from the lumbar subarachnoid space in the patients just before commencement of therapy and on the first, third, seventh and fourteenth days of therapy at the ICU. Forty-four signals of the NMR spectra and NO concentration of the CSF samples were analyzed. The analysis shows that the amino acid and organic acid concentrations change during the therapy and mostly are higher than in the control group. Significant differences in concentration of the analyzed CSF components between the TBI patients and the control group have been noted. The rate of the lactate to pyruvate conversion increased because the L/P ratio showed no significant differences between the TBI group and the control group, while the concentrations of both components were significantly higher in the TBI patients than in the control group. Citrulline, arginine and nitric oxide concentrations were the focus of the analysis. Citrulline concentration changes overlapped NO changes from 0 until 3rd day of therapy, while for the remaining days of observation the NO concentration stabilized at the control level, whereas citrulline concentration significantly decreased.
Adult↗