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PubMed2000

Peripheral plasma amino acid abnormalities in rehabilitation patients with severe brain injury.

OBJECTIVE: Acute severe brain injury causes an increased mobilization of amino acids from tissue. The plasma amino acid profile of patients undergoing rehabilitation after brain injury is unknown. This study was aimed at delineating the plasma amino acid profile of rehabilitation patients with brain injury. DESIGN: Peripheral plasma aminogram, lactate, pyruvate, glycerol, ketone body, and carnitine concentrations were determined in 11 patients with brain injury (34.6+/-15 years old, 60+/-16.8 days after injury) and in 8 controls. Resting energy expenditure and nitrogen balance were also determined. RESULTS: (1) All essential amino acids and about 50% of nonessential amino acids were significantly lower in brain injury patients than in controls (p < .05). (2) Plasma amino acids were lower irrespective of either energy and protein intake or nitrogen balance. (3) Total carnitine concentration and esterified/free carnitine ratio were higher in brain injury patients than in controls (p < .05). CONCLUSIONS: Rehabilitation patients with brain injury may have an important reduction of their plasma aminogram. Muscle tissue depletion and the persistence of a hypercatabolic state caused by subclinical infections, pressure sores, and immobility may contribute to this reduction.

Adolescent↗
PubMedDate not supplied

[Functional outcome at discharge of patients with severe traumatic brain injury admitted to a brain damage unit].

INTRODUCTION: Severe traumatic brain injuries (TBI) are linked to high morbidity and mortality rates and have important individual and social costs, not only because of the high incidence of deaths they cause but also owing to the large number of individuals who are left with some kind of disability. AIMS: The purpose of this study was to analyse the epidemiological, clinical, functional and rehabilitational aspects of patients with severe TBI admitted to a brain damage unit for neurorehabilitation therapy with special emphasis on the functional outcome at discharge. PATIENTS AND METHODS: We carried out a descriptive study of patients suffering from TBI admitted to the Brain Damage Unit of the Institut Guttmann hospital between January 2000 and June 2002. We analysed epidemiological (age, sex, cause of the TBI), clinical (aetiology, initial Glasgow Coma Scale --GCS--, motor deficit, type of injury, duration of post-traumatic amnesia), functional (Glasgow Outcome Scale --GOS--, Level of Cognitive Functioning Scale --LCFS-- and Disability Rating Scale --DRS--) variables, in addition to patients' destination on discharge. RESULTS: Of a total of 174 hospitalised patients, 88.52% were cases of serious TBI, 80% of which involved males, with a mean age of 29.72 years (standard deviation: 12.63), and an average of 99.28 days' hospitalisation (standard deviation: 60.72). Road accidents were the chief cause of the TBI (78%). The most frequent neurological injuries were parenchymatous (68.05%), followed by subarachnoid haemorrhages (40.58%). 87.58% of the patients presented TBI-related complications. Functional improvement at discharge was statistically significant (p < 0.001) as regards the GOS, LCFS and DSR scales, and 87.5% of the patients were able to reintegrate into their home life. CONCLUSIONS: Despite the severity of the sequelae left by serious TBI, the functional outcome at discharge, associated with the high rate of reintegration into home life, justifies admission of these patients to a brain damage unit for neurorehabilitation therapy.

Adolescent↗
PubMed1998

Partner relationships, functioning, mood and global quality of life in persons with spinal cord injury and traumatic brain injury.

The aim of this study was to assess and compare spinal cord injured (SCI) and traumatic brain injured (TBI) persons and people from the general population concerning partner relationships, functioning, mood and global quality of life. One hundred and sixty seven SCI persons, 92 TBI persons and 264 controls participated in the study. The median age was: SCI persons 33 years (range 19 to 79 years), TBI persons 40 years (range 20 to 70 years), and controls 31 years (range 19 to 79 years). Age at injury ranged among SCI persons from 14 to 76 years (Md 28 years), and among TBI persons from 16 to 56 years (Md 32 years). Half of the SCI group (51%), 58% of the TBI group and 59% of the controls had a stable partner relationship at the time of the investigation. Many of these SCI and TBI relationships (38% and 55% respectively) were established after injury. Both SCI and TBI persons showed significantly more depressive feelings compared with the controls. Perceived quality of life (global QL rating) was significantly lower in the SCI group compared with the controls, whereas the ratings of TBI persons and controls did not differ significantly. SCI and TBI persons did not differ significantly in level of education, perceived quality of life or distress. In all three groups, global quality-of-life ratings were significantly lower among single persons compared to those with a partner relationship. It was concluded that both SCI and TBI appear to affect overall quality of life and mental well-being negatively. The number of partner relationships contracted after injury among both SCI and TBI persons indicates, however, that the injury is not a major barrier to establishing close partner relationships. Being in good spirits, that is, lack of depressive feelings has a profound impact on the perception of a high quality of life in all three groups. For the SCI and TBI persons, a high level of physical and social independence were further positive determinants of a perceived high quality of life.

Activities of Daily Living↗
PubMed1999

Regional changes in the expression of neurotrophic factors and their receptors following acute traumatic brain injury in the adult rat brain.

We have analyzed the effect of severe traumatic brain injury (TBI) on the levels of mRNA expression of neurotrophic factors (NTFs): brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), ciliary neurotrophic factor (CNTF) and their respective receptors: trkB, trkA and CNTFRalpha. The expression was examined in the region of the lesion as well as a region remote from the lesion at 12, 24, and 36 h following the injury. Our data suggest that after the brain injury, the expression of NGF and BDNF mRNAs were early, transiently and significantly upregulated while that of CNTF was a slow and less amplified response in both areas of the brain. We also found that trkA mRNA expression was only upregulated significantly in the remote area; trkB mRNA showed no significant change in either area except an upregulation at 12 h in the remote area. CNTFRalpha was downregulated significantly by 24-36 h in the lesion area and by 24 h in the remote area. These changes suggest that TBI regulates the expression of NTFs and their receptors. These alterations in expression may be involved in modulating the neuronal response after brain injury.

Age Factors↗
PubMed2005

Functional plasticity or vulnerability after early brain injury?

CONTEXT: Traumatic brain injury (TBI) is a common, acquired, childhood disability that may be used as a model to understand more completely the impact of early brain injury on both brain structure and day-to-day function. Contrary to previously held views of the "plasticity" of the young brain, recent research suggests that such early insults may have a profound impact on development. To date, these suggestions remain largely untested. OBJECTIVES: To plot changes in cognitive abilities after childhood TBI over the 30 months after injury and to examine the impact of age at injury on cognitive outcomes. DESIGN: Prospective longitudinal study. SETTING: Royal Children's Hospital, Victoria, Australia. MAIN OUTCOME MEASURES: Global intellectual ability, verbal and nonverbal skills, attention, and processing speed. PARTICIPANTS: A total of 122 children admitted to the hospital with a diagnosis of TBI were divided according to injury age, ie, young (age: 3-7 years) or old (age: 8-12 years), and injury severity (mild, moderate, or severe) and were evaluated acutely and at 12 and 30 months after injury. An additional sample of children injured before 3 years of age (n = 27) was compared with these groups with respect to global intellectual ability only. RESULTS: A clear relationship was documented between injury severity and cognitive performance. For children who sustained severe injury, younger age at injury was associated with minimal, if any, recovery after injury, but better outcomes were observed after severe TBI among older children. Age at injury was not predictive of outcomes for children with mild or moderate TBI, although infants (age: 0-2.11 years) with moderate TBI showed poorer outcomes than did older children with injury of similar severity. CONCLUSIONS: Findings support a "double-hazard" model for severe and early brain insults and add to the ongoing debate regarding cerebral plasticity, suggesting that, contrary to traditional views, young children who sustain severe TBI in early childhood or moderate or severe TBI in infancy may be particularly vulnerable to significant residual cognitive impairment. From a clinical perspective, results indicate that long-term follow-up monitoring and management should be targeted to this high-risk group.

Brain Injuries↗
PubMed2006

Regionally distinct patterns of calpain activation and traumatic axonal injury following contusive brain injury in immature rats.

Impact-induced head injury in infants results in acute focal contusions and traumatic axonal injury (TAI) that are associated with chronic holohemispheric cortical and white matter atrophy and may contribute to poor outcome in brain-injured children less than 4 years of age. Contusive brain trauma in postnatal day (PND) 11 or PND 17 rat pups, ages neurologically equivalent to a human infant and toddler, respectively, leads to cortical tissue loss and white matter atrophy which are associated with cognitive deficits. In adult models of brain trauma and in brain-injured humans, acute and sustained activation of the calpain family of calcium-activated neutral proteases has been implicated in neuronal death and TAI. PND 11 or PND 17 rat pups were subjected to closed head injury over the left hemisphere using the controlled cortical impact device and sacrificed at 6 h, 24 h or 3 days. Hemorrhagic contusions and tissue tears in the cortex and white matter were visible at 6 h, and neuronal loss was evident by 3 days. Calpain activation was observed in cell soma and dendrites of injured neurons at 6 h, and in degenerating dendrites and atrophic neurons at 24 h after injury at both ages. Axonal accumulation of amyloid precursor protein, indicative of TAI, was observed in the corpus callosum and lateral aspects of the white matter below the site of impact, and in the thalamus in PND 11 rats only. Intra-axonal calpain activation was observed to a limited extent in the corpus callosum and subcortical white matter tracts in both brain-injured PND 11 and PND 17 rats. Collectively, these results provide evidence that calpain activation may participate in neuronal loss in the injured cortex, but may not contribute to the pathogenesis of TAI following contusive brain trauma in the immature rat.

Aging↗
PubMed2000

Spectrophotometric measurement of experimental brain injury.

Freshly sampled brain tissue exposed to 2,3,5-triphenyltetrazolium chloride (TTC) acquires a red color because mitochondrial enzymes reduce the colorless TTC to a red, water-insoluble formazan deposit. Pan-necrotic areas remain uncolored, which enables quantitation of experimental brain injury by optical scanning and image analysis of serial slices to determine the relative volume of red versus infarcted, non-stained, tissue. The accuracy of this method can be challenged, however, when infarction is accompanied by areas of partial, scattered injury where differences in coloration are difficult to see or quantify. We tested the feasibility of measuring scattered injury using a principle which underlies standard assays for in vitro cell survival, namely extracting deposited formazan with a solvent and measuring its level by spectrophotometry. Anesthetized, adult Sprague Dawley rats were subjected to 12 min of cerebral ischemia to produce selective, delayed neuronal death in hippocampus, striatum and cortex. Some rats also received 6 h of whole-body hypothermia treatment (31.5-32.5 degrees C) immediately after ischemia. Ischemia rats and non-operated controls were sacrificed 1 week later. Hippocampus and portions of cerebrum were incubated 90 min in a 2% TTC solution and then soaked in a measured volume of 50:50 ethanol and dimethylsulfoxide to extract the red formazan product. Spectrophotometric measurements of the extract showed a diminished formazan coloration (absorbance/g brain) in all samples from the untreated ischemia group compared to non-operated controls. This apparent brain injury was attenuated in the group of ischemia rats that received hypothermia treatment. We conclude that solvent extraction and spectrophotometric quantitation of formazan has potential utility as an objective way to index experimental brain injury even if this is diffuse in nature and not amenable to measurement by conventional image analysis techniques.

Animals↗
PubMed2004

The role of the helmet in the prevention of traumatic brain injuries.

Today, traumatic brain injuries (TBIs) exceed 1 million cases per year. Tens of thousands of people die and hundreds of thousands of people are hospitalized. The health care costs exceed US dollars 50 billion. The Centers for Disease Control and Prevention estimate that people with mild TBIs who are not hospitalized add another US dollars 17 billion to the total dollars spent on care. These high frequencies and costs place a high priority on programs and procedures to minimize the number of injuries and to reduce the severity of those that occur. One of these programs focuses on the protective devices worn by the people that work and play in environments where there is an identified risk of TBI. Because these environments cover a wide variety of activities, the design and effectiveness of these protective devices must be specific to the nature of the activity and the person they are designed to protect.

Accidents, Occupational↗
PubMed2003

Traumatic cerebral vascular injury: the effects of concussive brain injury on the cerebral vasculature.

In terms of human suffering, medical expenses, and lost productivity, head injury is one of the major health care problems in the United States, and inadequate cerebral blood flow is an important contributor to mortality and morbidity after traumatic brain injury. Despite the importance of cerebral vascular dysfunction in the pathophysiology of traumatic brain injury, the effects of trauma on the cerebral circulation have been less well studied than the effects of trauma on the brain. Recent research has led to a better understanding of the physiologic, cellular, and molecular components and causes of traumatic cerebral vascular injury. A more thorough understanding of the direct and indirect effects of trauma on the cerebral vasculature will lead to improvements in current treatments of brain trauma as well as to the development of novel and, hopefully, more effective therapeutic strategies.

Animals↗
PubMed2002

[Changes of dynorphinA1-13 on the treatment of hypoxic-ischemic brain injury by the brain-derived neurotrophic factor in neonatal rats].

OBJECTIVE: To explore changes and role of dynorphinA(1 - 13) on the experimental treatment of hypoxic-ischemic brain injury (HIBI) by intracerebral transplantation of genetically modified myoblasts expressing and secreting brain-derived neurotrophic factor (BDNF) in neonatal rats. METHODS: Seven-day-old Sprague-Dawley rats were randomly divided into HIBI + BDNF group (A), HIBI + BDNF + U50, 488H group (B), HIBI group (C) and sham-operated group (D). Pups were intracerebroparenchymally transplanted with either genetically modified myoblasts producing and secreting BDNF (A, B) or their parent cells (C) at 0.8 microl (4 x 10(4)/microl) followed by a cerebroventricular microinjection of opioid kappa receptor agonist U50, 488H (0.5 microg, B) or vehicles (A, C) shortly after HIBI undergone by a permanent ligation of left common carotid artery followed by a 2.5 h inhalation of humidified 8%O(2) + 92%N(2) at 37 degrees C. Water contents of the brain, levels of malondiadehye (MDA) and cell apoptosis were investigated 1 d after the procedure. Contents of dynorphinA(1 - 13)-like immunoreactivity (ir-DynA(1 - 13)) at the left and right cortex and hippocampus were tested by radioimmunoassay 0, 1, 3 d postinjury. RESULTS: Levels of ir-DynA(1 - 13) in left cortex were markedly increased in group A, B or C when compared to group D different times after the procedure and markedly decreased in group A or B vs group C 1, 3 d after the procedure. Levels of ir-DynA(1 - 13) in left hippocampus were also markedly increased in group A, B and C (0 d), B, C (1 d) and C (3 d) when compared to group D and markedly decreased in group A (1 d) and B (3 d) vs group C, respectively. Water contents, MDA levels and percentage of cell apoptosis were significantly higher in group A, B or C than those in group D and these parameters were obviously lowered in group A compared to group C in the left brain 1 d after the procedure. There were no significant differences of water contents and levels of MDA between group B and C but significantly lowered percentage of cell apoptosis in group B was seen when compared to group C in the left brain. CONCLUSION: It is suggested that dynorphinA(1 - 13) participates in the pathophysiological process of HIBI. One of the pathways of the beneficial effects of intracerebral transplantation of genetically modified myoblasts producing BDNF on HIBI lies on the inhibition of the function of dynorphin A(1 - 13) through the binding of kappa opioid receptor.

Animals↗
PubMed2000

Multidimensional telecare strategies for rural residents with brain injury.

Rural residents with brain injury have difficulty in accessing care from qualified psychologists for consequent cognitive, emotional and behavioural symptoms. We examined high-quality videoconferencing to enhance care for persons with brain injury in three areas: cognitive assessment, psychotherapy and rural mental health training. The assessment study evaluated 52 outpatients seen for diagnostic visits over videoconferencing, and compared their experiences with those of 52 age- and diagnosis-matched controls seen in person. Persons seen via telemedicine were more likely than controls to want to repeat their experience and more satisfied than were the neuropsychologists who examined them. In the psychotherapy study, neurorehabilitation patients were seen via videoconferencing for therapy related to brain injury or stroke. Persons receiving psychotherapy were less likely than persons receiving assessment services to want to repeat their experience. In the training study, 39 rural mental health providers were trained via videoconferencing, and trainees demonstrated significant improvement on tests of knowledge about brain injury. Trainees formed a network of mental health provider referrals for persons with brain injury in a wide geographic area. Given adequate training and ongoing support, rural clinicians can treat many brain-injury adjustment issues locally, reserving specialist consultation for emergency or complex problems.

Brain Injuries↗
PubMed1998

Neuropsychological, psychosocial and vocational correlates of the Glasgow Outcome Scale at 6 months post-injury: a study of moderate to severe traumatic brain injury patients.

Traumatic brain injury (TBI) subjects at Glasgow Outcome Scale levels 3 (severe disability), 4 (moderate disability), 5 (good recovery), and an other-injury control group (OIC) were compared in terms of neuropsychological, psychosocial, and vocational functioning 6 months after injury. Subjects were a sample of 100 patients with a moderate to severe traumatic brain injury (TBI) and a matched sample of 30 other-injury control subjects (OIC) enrolled in the UCLA Brain Injury Research Center study of TBI outcome. Overall, the results showed a systematic decrease in mean neuropsychological test performance as a function of increasing GOS severity, as well as an increased prevalence of symptoms of depression and lower ratings on measures assessing employability and capacity for self care. TBI patients in the 'severe' and 'moderate disability' groups were distinctly inferior to the 'good recovery' and 'OIC' groups, who were quite similar to each other in terms of cognitive, psychosocial, and vocational outcomes. The results demonstrate overall support for the predictive and concurrent validity of the GOS 6 months post injury. Despite these results, which strengthen the utility and appeal of the GOS for multicentre studies, concerns still remain regarding GOS category 4 (moderate disability), which was shown to lack sufficient discriminability in this study.

Activities of Daily Living↗
PubMed2000

Aminosteroids for acute traumatic brain injury.

BACKGROUND: Traumatic brain injury is a leading cause of premature death and disability. Post-traumatic membrane lipid peroxidation has been proposed as one mechanism leading to secondary brain damage following head injury. Aminosteroids have been shown to inhibit lipid peroxidation in laboratory animals and have the potential to improve outcome following head injury. OBJECTIVES: To quantify the effectiveness and safety of aminosteroids in the treatment of acute traumatic brain injury. SEARCH STRATEGY: We searched the Cochrane Injuries Group trials register, The Cochrane Controlled Trials Register, MEDLINE and EMBASE. We contacted experts in the field and the company that manufactures tirilazad. SELECTION CRITERIA: We sought to identify all randomised controlled trials of aminosteroids versus placebo in the treatment of acute traumatic brain injury. Studies using a quasi random form of allocation, such as alternation, were excluded from the review. DATA COLLECTION AND ANALYSIS: One reviewer examined the electronic search results for reports of possibly relevant trials for retrieval in full. Two reviewers (IR and PA) applied the selection criteria independently to the trial report, with no disagreement. MAIN RESULTS: Two randomised controlled trials have examined the effect of the aminosteroid tirilazad mesylate on death and disability following head injury. To date, only the results of one of these trials are available for analysis. The risk of death in patients treated with tirilazad was almost identical to those given placebo RR=1.05 (95% confidence interval 0.86 to 1.29). The risk of death and severe disability in patients treated with tirilazad was again almost identical to those given placebo RR=1.07 (95% confidence interval 0.93 to 1.23). REVIEWER'S CONCLUSIONS: There is no evidence to support the routine use of aminosteroids in the management of traumatic head injury. On the basis of the existing evidence from randomised trials of aminosteroids in head injury it is not possible to refute the possibility of moderate but potentially clinically important benefits or harms. A further randomised controlled trial of tirilazad mesylate with 1156 participants has been completed, the results of which should become available in the near future.

Brain Injuries↗
PubMed1997

Efficacy of postacute brain injury rehabilitation for patients with primary malignant brain tumors.

BACKGROUND: Patients with primary malignant brain tumors (PMBT) often have neurobehavioral deficits due to the tumor, subsequent surgery, and therapies that interfere with their ability to live independently or work. Previous studies have shown that such patients generally have a progressive decline in functioning from diagnosis to death. Consequently, PMBT patients have not been considered good candidates for rehabilitation services. The current study is a preliminary, retrospective investigation of the effectiveness of postacute brain injury rehabilitation methods, originally developed for traumatic brain injury survivors, in a sample of patients with PMBT. METHODS: The subjects were 13 patients with a history of surgical resection of PMBT and subsequent radiation and chemotherapy. There were 8 males and 5 females with a mean age of 34.3 +/- 10.0 years and a mean educational level of 15.1 +/- 1.7 years. Mean time from tumor diagnosis to the commencement of rehabilitation was 75.4 +/- 87.9 months. All patients had cognitive deficits documented with neuropsychologic tests. Patients received an average of 2.6 +/- 1.9 months of postacute brain injury rehabilitation. RESULTS: Six patients had increased independence during the time from the start of rehabilitation to discharge, six were unchanged, and one patient had decreased independence. Eight patients had increased productivity during the same time period, four were unchanged, and one had decreased productivity. Treatment gains were maintained at follow-up 8.0 +/- 7.6 months after discharge. CONCLUSIONS: The results of the current study offer preliminary support for the effectiveness of postacute brain injury rehabilitation in the management of PMBT patients. Although additional investigation is needed, such treatment appears to be an attractive, relatively low cost option for these patients.

Adult↗
PubMed2004

Identification and characterization of heterogeneous neuronal injury and death in regions of diffuse brain injury: evidence for multiple independent injury phenotypes.

Diffuse brain injury (DBI) is a consequence of traumatic brain injury evoked via rapid acceleration-deceleration of the cranium, giving rise to subtle pathological changes appreciated best at the microscopic level. DBI is believed to be comprised by diffuse axonal injury and other forms of diffuse vascular change. The potential, however, that the same forces can also directly injure neuronal somata in vivo has not been considered. Recently, while investigating DBI-mediated perisomatic axonal injury, we identified scattered, rapid neuronal somatic necrosis occurring within the same domains. Moving on the premise that these cells sustained direct somatic injury as a result of DBI, we initiated the current study, in which rats were intracerebroventricularly infused with various high-molecular weight tracers (HMWTs) to identify injury-induced neuronal somatic plasmalemmal disruption. These studies revealed that DBI caused immediate, scattered neuronal somatic plasmalemmal injury to all of the extracellular HMWTs used. Through this approach, a spectrum of neuronal change was observed, ranging from rapid necrosis of the tracer-laden neurons to little or no pathological change at the light and electron microscopic level. Parallel double and triple studies using markers of neuronal degeneration, stress, and axonal injury identified additional injured neuronal phenotypes arising in close proximity to, but independent of, neurons demonstrating plasmalemmal disruption. These findings reveal that direct neuronal somatic injury is a component of DBI, and diffuse trauma elicits a heretofore-unrecognized multifaceted neuronal pathological change within the CNS, generating heterogeneous injury and reactive alteration within both axons and neuronal somata in the same domains.

Animals↗
PubMed1999

Determination and clinical significance of plasma levels of prostaglandins in patients with acute brain injury.

BACKGROUND: Models of brain injury in experimental animals have shown that the level of prostaglandins (PGs) is increased in damage brain tissue, and that PGs play an important role in secondary brain damage. Almost all previous studies of the relationship between PGs and brain injury have been carried out in animals. In the present study we show that the PGs change in humans with brain injury. METHODS: The plasma levels of thromboxane B2, 6-Keto-PGF2alpha, prostaglandin F2alpha, and prostaglandin E2 were measured by radioimmunoassay on the 1st, 3rd, 7th, and 14th days after brain injury. The same measurements were made on a control group of 26 healthy volunteers. RESULTS: The levels of all four PGs were elevated, most markedly in the first week, with levels remaining high in the second week in the severely injured. On the first day levels were, on average, three times those found in the controls, with a seven-fold rise in some of the severely injured patients. Dividing the patients into three groups according to outcome, it was found that if the PGs were markedly increased to begin with and remained high, death or permanent disability was likely. In the group with good outcome, the levels dropped steadily from the initial high levels. The T/K ratio was studied. It related closely to the severity of injury, being higher in more severe injuries and decreasing with recovery. In patients who did not recover, the ratio increased steadily to its highest value on the 7th day, and remained high at the 14th. CONCLUSION: Changes in PGs levels were closely related to the brain injury severity and its outcome, and there was a marked disturbance of the levels of PGs, which therefore appears to be an important indicator of secondary brain damage.

Acute Disease↗