[Histological changes of the hypophysis in traumatic brain injuries and in brain tumors].
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Brain Diseases↗
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Results for “Brain Injuries”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
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[Experimental and clinical studies on brain injury and energy-rich phosphate compounds. I. Brain injury and ATP content in the brain].
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Adenine Nucleotides↗
Mechanisms of perinatal brain injury.
Perinatal brain injury is associated with pathological conditions caused by pathogenetic mechanisms that remain unclear. Brain lesions can result not only from brain injury but may also originate during fetal growth. Fetal encephalopathy includes 4 groups of causes: maternal, fetal, placental and idiopathic. Hypoxic-ischemic lesions (periventricular leucomalacia and subcortical leucomalacia) and hemorrhage lesions (germinal hemorrhage) are discussed.
Brain Diseases↗
Magnetic resonance spectroscopy detects brain injury and predicts cognitive functioning in children with brain injuries.
Proton magnetic resonance spectroscopy (1H-MRS) and neuropsychological assessment were utilized in a longitudinal investigation of traumatic brain injury (TBI) in children. A spectroscopic imaging protocol was implemented, and neurometabolite ratios of NAA/Cre and Cho/Cre were calculated for anterior and posterior halves of a supraventricular slab of brain tissue. NAA/Cre was reduced and Cho/Cre increased in TBI patients as compared to controls, for both brain regions. Each ratio predicted aspects of neuropsychological performance, though the specific relationships varied somewhat by region and function. Anterior NAA/Cre increased and anterior Cho/Cre decreased from 3 to 21 weeks post-injury, suggesting neurometabolic recovery.
Adolescent↗
Biocompatibility of methylcellulose-based constructs designed for intracerebral gelation following experimental traumatic brain injury.
Tissue engineering in the post-injury brain represents a promising option for cellular replacement and rescue, providing a cell scaffold for either transplanted or resident cells. We have characterized the use of methylcellulose (MC) as a scaffolding material, whose concentration and solvent were varied to manipulate its physical properties. MC solutions were produced to exhibit low viscosity at 23 degrees C and form a soft gel at 37 degrees C, thereby making MC attractive for minimally invasive procedures in vivo. Degradation and swelling studies in vitro demonstrated a small amount of initial polymer erosion followed by relative polymer stability over the 2-week period tested as well as increased hydrogel mass due to solvent uptake. Concentrations up to 8% did not elicit cell death in primary rat astrocytes or neurons at 1 or 7 days. Acellular 2% MC (30 microl) was microinjected into the brains of rats 1 week after cortical impact injury (velocity = 3 m/s, depth = 2 mm) and examined at 2 days (n = 8; n = 3, vehicle injected) and 2 weeks (n = 5; n = 3, vehicle injected). The presence of MC did not alter the size of the injury cavity or change the patterns of gliosis as compared to injured, vehicle-injected rats (detected using antibodies against GFAP and ED1). Collectively, these data indicate that MC is well suited as a biocompatible injectable scaffold for the repair of defects in the brain.
Animals↗
Cerebrospinal fluid enzymes in acute brain injury. 1. Dynamics of changes in CSF enzyme activity after acute experimental brain injury.
Changes in CSF enzyme activity were studied after brain trauma for their prognostic value. Raised values of CPK and HBDH were demonstrated in the CSF of patients with severe brain injuries. Standardised cold lesions of the brain were induced in cats. The activities of the enzymes CPK, HBDH, LDH, GOT, GPT, and pseudocholinesterase were studied at half hour intervals in the cerebrospinal fluid and at hourly intervals in the serum. A statistically highly significant increase of all enzymes studied developed in the CSF. The greatest changes occurred within four hours of freezing. Large increases could occur in half an hour. Isoenzyme studies demonstrated that CPK and LDH were of cerebral origin. No consistently significant changes could be shown in the serum enzyme activity. It is concluded that after brain injuries, enzymes are released into the extracellular fluid of the brain and transported to the CSF. The limited value of a single enzyme estimation is emphasised. The results described seem to provide indirect evidence for transependymal flow of extracellular fluid in brain oedema.
Alanine Transaminase↗
Dual diagnoses: the person with a spinal cord injury and a concomitant brain injury.
Spinal cord injury (SCI) alone is a devastating event that often results in physical disability. When the SCI is combined with a brain injury, the degree of disability can be magnified and the patient's rehabilitation becomes further complicated. It is not unusual for the head injury to be overlooked or undetected during the emergent and acute phases of treatment. The brain injury may first appear when the client demonstrates an inability or resistance to carry out functional activities appropriate to his/her level of injury. Cognitive deficits can limit or complicate the client's ability to adapt to his/her physical limitations, learn compensatory skills, and achieve the maximal level of independence. These patients require a wide base of physical, psychological, educational, and medical support. Because they are at a high risk for developing complications, they will require lifelong interventions and involvement from an interdisciplinary team to provide a safety net. The following article examines the patient with dual diagnoses of SCI and brain injury. A comprehensive review of commonly encountered problematic scenarios and interventions is presented.
Autonomic Nervous System Diseases↗
The Pediatric Acquired Brain Injury Community Outreach Program (PABICOP) - an innovative comprehensive model of care for children and youth with an acquired brain injury.
The Pediatric Acquired Brain Injury Community Outreach Program - an innovative, comprehensive model of care for children and youth with an acquired brain injury is described. The background to the formation of the idea is delineated and the current function of the model given. Future directions are discussed. The program addresses the needs and issues of children and youth with an acquired brain injury and their families. Subsequent literature supports the concept of care that this program espouses.
Adolescent↗
Regional brain injury epidemiology as the basis for planning brain injury treatment.
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Brain Injuries↗
Brain injury as a result of violence: preliminary findings from the traumatic brain injury model systems.
OBJECTIVES: To identify possible risk factors that may predispose individuals to violent traumatic brain injury (TBI) and to determine the effect of etiology of injury on outcomes. STUDY DESIGN: Prospective, longitudinal multicenter study. SETTING: TBI Model Systems (TBIMS) located at Wayne State University/Rehabilitation Institute of Michigan, Detroit, MI; The Institute for Rehabilitation and Research, Houston, TX; Medical College of Virginia, Richmond, VA; and Santa Clara Valley Medical Center, San Jose, CA. SUBJECTS: Individuals treated in the four TBIMS programs between 3/89 and 9/96 who met the criteria for inclusion in the TBIMS National Database and for whom the etiology was known (n=812). MAIN OUTCOME MEASURES: Functional Independence Measure, Alcohol Quantity Frequency Variability Index, Community Integration Questionnaire. RESULTS: Individuals who incur violence-related TBI tend to be male, nonwhite, unmarried, living alone, less educated, and unemployed at time of injury. They tend to have less severe brain injuries and better motor function at the time of admission to inpatient rehabilitation. At 1 year postinjury, they score lower on community integration measures; however, no difference exists in functional status. Etiology of injury was found to only play a minor role in the prediction of social and productive integration at 1 year postinjury. CONCLUSIONS: Survivors of violent and nonviolent TBI have similar functional outcomes; however, they differ in preinjury and postinjury socio-economic characteristics, injury severity, and postinjury community integration. Socio-economic factors appear to play a large role in the risk for violent injury and in community integration following injury.
Activities of Daily Living↗
Viewing the functional consequences of traumatic brain injury by using brain SPECT.
High-resolution brain SPECT is increasingly benefiting from improved image processing software and multiple complementary display capabilities. This enables detailed functional mapping of the disturbances in relative perfusion occurring after TBI. The patient population consisted of 26 cases (ages 8-61 years)between 3 months and 6 years after traumatic brain injury.A very strong case can be made for the routine use of Brain SPECT in TBI. Indeed it can provide a detailed evaluation of multiple functional consequences after TBI and is thus capable of supplementing the clinical evaluation and tailoring the therapeutic strategies needed. In so doing it also provides significant additional information beyond that available from MRI/CT. The critical factor for Brain SPECT's clinical relevance is a carefully designed technical protocol, including displays which should enable a comprehensive description of the patterns found, in a user friendly mode.
Adolescent↗
Neuroanatomic correlates of CVLT-C performance following pediatric traumatic brain injury.
Traumatic brain injury (TBI) frequently results in memory problems, and the degree of memory impairment is related to injury severity and is commonly associated with lesions in frontal and temporal brain areas. This study examined the relationship among injury severity, brain lesions, and memory in children with moderate to severe TBI using Donders' (1999) 5-factor model of performance on the California Verbal Learning Test-Children's Version (CVLT-C). Seventy-six children underwent magnetic resonance imaging (MRI) scans 3 months post-TBI and testing 1 year post-TBI. Results showed injury severity (Glasgow Coma Scale) was not predictive of performance on 4 of the 5 factors. Volume of frontal and/or temporal brain lesions was significantly predictive of performance on 3 of the 5 factors. Unexpectedly, lesion volume outside these areas (extra-frontotemporal) was predictive of performance on all 5 factors. In contrast, Verbal IQ at 1 year was most strongly associated with preinjury factors (socioeconomic status and special education involvement), although extra-frontotemporal lesions also contributed to the variability in this measure. Results suggest that in children with moderate to severe TBI, extra-frontal/temporal lesions are predictive of memory outcome 1 year postinjury above and beyond initial severity or frontal/temporal contusions. This finding may relate to widespread diffuse axonal injury, which potentially disconnects brain circuits mediating memory following moderate to severe TBI.
Adolescent↗
Is being plastic fantastic? Mechanisms of altered plasticity after developmental traumatic brain injury.
Traumatic brain injury (TBI) is predominantly a clinical problem of young persons, resulting in chronic cognitive and behavioral deficits. Specifically, the physiological response to a diffuse biomechanical injury in a maturing brain can clearly alter normal neuroplasticity. To properly evaluate and investigate developmental TBI requires an understanding of normal principles of cerebral maturation, as well as a consideration of experience-dependent changes. Changes in neuroplasticity may occur through many age-specific processes, and our understanding of these responses at a basic neuroscience level is only beginning. In this article, we will particularly discuss mechanisms of TBI-induced altered developmental plasticity such as altered neurotransmission, distinct molecular responses, cell death, perturbations in neuronal connectivity, experience-dependent 'good plasticity' enhancements and chronic 'bad plasticity' sequelae. From this summary, we can conclude that 'young is not always better' and that the developing brain manifests several crucial vulnerabilities to TBI.
Aging↗
Disorders of Mood After Traumatic Brain Injury.
Traumatic brain injury (TBI) of any severity can result in broad and persisting biopsychosocial sequelae. Post-TBI sequelae impact, to varying degrees, a person's ability to function at home and work, leading to added emotional distress. It is in the context of these biological, interpersonal, and social disruptions that mood disorders can arise. Mood disorders after TBI occur at a greater frequency than in the general population, with estimates approaching 25% to 50% for major depression, 15% to 30% for dysthymia, and 9% for mania. Post-TBI depression and mania appear to embrace a symptom presentation that is similar to non-TBI depression and mania, and the symptoms can be discerned from other neurobehavioral symptoms. TBI-related brain damage consistently involves regions of the brain that are increasingly recognized as important in the regulation of mood, including the frontal cortex, basal ganglia, and temporal lobes. However, there is insufficient information to postulate a specific neuroanatomic model for post-TBI depression and mania. It is the variable nature of TBI-related brain injury, occurring in the context of other relevant factors that limit the ability to make accurate models to predict who will develop a post-TBI mood disorder.
Journal Article↗
Hippocampal head atrophy after traumatic brain injury.
Traumatic brain injury (TBI) causes hippocampal damage. The hippocampus can be macroscopically divided into the head, body and tail, which differ in terms of their sensitivity to excitability and also in terms of their cortical connections. We investigated whether damage also varies according to the hippocampal area involved, and studied the relationship of hippocampal reductions with memory performance. Twenty TBI patients and matched controls were examined. MRI measurements were performed separately for the hippocampal head, body and tail. Memory outcome was measured by Rey's auditory verbal learning test, Rey's complex figure test and a modified version of Warrington's facial recognition memory test. Group comparison showed that patients had bilateral hippocampal atrophy, mainly involving the hippocampal head. Moreover, TBI subjects showed verbal memory deficits which presented slight correlations with left hippocampal head atrophy.
Adolescent↗
Progesterone administration modulates AQP4 expression and edema after traumatic brain injury in male rats.
This study investigates whether progesterone administration regulates AQP4 and GFAP expression in rats with bilateral contusion injuries of the medial frontal cortex. Male rats were given 0 or 16 mg/kg injections of progesterone at 1, 6, 24, and 48 h post-injury. Brains were extracted at 24 h or 72 h post-injury and assayed for cerebral edema and AQP4 and GFAP expression using Western blot analysis. Progesterone treatments reduced brain water content significantly in the brain-injured groups. There was no significant change in AQP4 expression 24 h after progesterone treatment compared to lesion + vehicle animals. However, progesterone significantly reduced AQP4 expression at 72 h post-injury in the tissue bounded by the lateral ventricles and the peri-contusion areas compared to lesion+ vehicle rats, but increased AQP4 expression in the tissue surrounding the third ventricle. Also progesterone effects on GFAP expression varied according to brain region. Our results can be taken to show that the expression of AQP4 protein after TBI is time-dependent, region-specific, and possibly implicated in the formation and resolution of TBI-induced cerebral edema.
Analysis of Variance↗
Non-surgical intervention and cost for mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury.
We examined the evidence for non-surgical interventions and for economic costs for mild traumatic brain injury patients by a systematic search of the literature and a best-evidence synthesis. After screening 38,806 abstracts, we critically reviewed 45 articles on intervention and accepted 16 (36%). We reviewed 16 articles on economic costs and accepted 7 (44%). We found some evidence that early educational information can reduce long-term complaints and that this early intervention need not be intensive. Most cost studies were performed more than a decade ago. Indirect costs are probably higher than direct costs. Studies comparing costs for routine hospitalized observation vs the use of computerized tomography scan examination for selective hospital admission indicate that the latter policy reduces costs, but comparable clinical outcome of these policies has not been demonstrated. The sparse scientific literature in these areas reflects both conceptual confusion and limited knowledge of the natural history of mild traumatic brain injury.
Advisory Committees↗
Research, prevention, and quality assurance in traumatic brain injury: a public hospital perspective.
The following recommendations are made: increased Medicaid reimbursement for head injury patients to public hospitals that provide care to disproportionately large numbers of these unemployed, uninsured patients, develop comprehensive federal control legislation concerning gun control, develop violence prevention programs such as curricula to combine public health and criminal justice approach, develop trauma registry for neurologic injuries (brain and spinal cord), enforce the use of seat belts and cycle helmets, develop practice guidelines for traumatic brain-injured patients, continue research into the mechanisms and management of brain swelling, neuronal regrowth and transplantations, and other mechanisms to overcome neurologic deficits as well as continue research on post-traumatic syndrome, which results from minor head injuries yet causes significant morbidity and costs, and establish comprehensive rehabilitation and habilitation programs to include physical, cognitive, and behavioral approaches and support systems (eg, "halfway house").
Brain Injuries↗