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Results for “Brain Injuries”

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PubMed2000

Recovery of intellectual ability following traumatic brain injury in childhood: impact of injury severity and age at injury.

Traumatic brain injury (TBI) may have a profound impact on a child's ongoing development. Various risk factors have been found to predict outcome, but considerable variability remains unexplained. This study used a prospective, longitudinal design to examine the relationship between recovery, injury severity, age at injury and pre-injury ability. 124 children were divided according to (1) age at injury: 'young' (3-7 years) 'old' (8-12) and (2) injury severity (mild, moderate, severe). Children were evaluated acutely (T1) and at 12 months post-injury (T2), using standardized intellectual measures (IQ). Results showed a relationship between greater injury severity and poorer IQ. Age at injury was not predictive of outcome for children with mild/moderate TBI. For severe TBI, younger age at injury led to minimal recovery in IQ, while recovery from later injury was similar to that for adults. Findings suggest that children sustaining severe TBI in early childhood may be particularly at risk for residual problems post-injury.

Adaptation, Psychological↗

PubMed1988

Spinal cord injury and concomitant traumatic brain injury. Results of a longitudinal investigation.

One-hundred fifty persons with traumatic onset spinal cord injury (SCI) were administered a comprehensive neuropsychologic test battery an average of 7 weeks after SCI, and 67 were retested using the same battery an average of 38 weeks after initial testing. It was hypothesized that if traumatic brain injury were a significant sequela of SCI, retesting would reveal evidence of cognitive recovery over time and would further enable a clearer separation of preinjury cognitive capacity from the effects of injury. Significant improvement in test performance occurred across time to the degree and in a pattern similar to that noted in persons who have sustained mild to moderate traumatic brain injury. Hypothesized relationships between level and extent of SCI, etiology of injury and presence/absence of loss of consciousness and neuropsychologic test scores were not observed. Implications for the rehabilitation process are discussed.

Brain Injuries↗

PubMed2005

Alteration in brain natriuretic peptide (BNP) plasma concentration following severe traumatic brain injury.

BACKGROUND: Brain natriuretic peptide (BNP) is a potent natriuretic and vasodilator factor which, by its systemic effects, can decrease cerebral blood flow (CBF). In aneurysmal subarchnoid hemorrhage (aSAH), BNP plasma concentrations were found to be associated with hyponatremia and were progressively elevated in patients who eventually developed delayed ischemic deficit secondary to vasospasm. The purpose of the present study was to evaluate trends in BNP plasma concentrations during the acute phase following severe (traumatic brain injury) TBI. METHODS: BNP plasma concentration was evaluated in 30 patients with severe isolated head injury (GCS<8 on admission) in four time periods after the injury (period 1: days 1-2; period 2: days 4-5; period 3: days 7-8; period 4: days 10-11). All patients were monitored for ICP during the first week after the injury. FINDINGS: The initial BNP plasma concentrations (42+/-36.9 pg/ml) were 7.3 fold (p<0.01) higher in TBI patients as compared to the control group (5.78+/-1.90 pg/ml). BNP plasma concentrations were progressively elevated through days 7-8 after the injury in patients with diffused SAH as compared to patients with mild or no SAH (p<0.001) and in patients with elevated ICP as compared to patients without elevated ICP (p<0.001). Furthermore, trends in BNP plasma concentrations were significantly and positively associated with poor outcome. INTERPRETATION: BNP plasma concentrations are elevated shortly after head injury and are continuously elevated during the acute phase in patients with more extensive SAH and in those with elevated ICP, and correlate with poor outcomes. Further studies should be undertaken to evaluate the role of BNP in TBI pathophysiology.

Adolescent↗

PubMed2002

Motor skill and mobility recovery outcomes of children and youth with traumatic brain injury.

Traumatic brain injury (TBI) is a major cause of disability in children. Along with other neurological clinical sequelae, children often exhibit motor skill impairment and limitations in functional mobility following TBI. The purpose of this annotated bibliography is to: (1) familiarize therapists with the literature available regarding motor skill and mobility recovery outcomes for children and adolescents with TBI; (2) assist therapists in the selection of motor skill and mobility outcome assessments for use in clinical practice; and (3) provide therapists with comparisons of outcomes for external benchmarking. A number of reports document motor and mobility recovery outcomes as well as recovery in other domains. Studies vary, however, in design, sample size, number and type of outcome assessments used, time since injury at assessment(s), and the consideration of correlating factors such as age at time of injury and injury severity. Further research is needed to describe clinical, satisfaction and resource utilization outcomes, determine outcome predictors, and provide evidence for therapeutic intervention effectiveness.

Brain Injuries↗

PubMed1998

What happens after brain injury?

Traumatic brain injury is one of the leading causes of injury and death among the young in the United States. Severity can range from the brief confusion of a football player who has had his "bell rung" to the complete loss of voluntary behavior seen in the vegetative state. In this article, Dr Goldberg reviews the rehabilitation process used to restore the fullest function possible within the limits of the patient's injury, with emphasis on innovative assessment and treatment techniques. He also describes an approach to evaluation of minimally conscious patients that can be used to detect and confirm the presence of active cognition.

Brain Concussion↗

PubMed2002

Trajectories of cognitive recovery following a minor brain injury.

Minor brain injury (MBI) is the most frequently diagnosed head trauma in the United States, with treatment costing more than $1.5 billion annually and many patients incapacitated for months following injury. The purpose of this study was to characterize the brain function disruptions associated with MBI and to determine the time trajectory of recovery, using a theoretical model of attention. Distractibility, impulsivity, irritability, and impaired executive functioning were demonstrated in all participants during the 24 hr after injury. Twenty percent of participants continued to complain of distractibility, impulsivity, and/or irritability throughout the 30-day study. Loss of consciousness was shown to confound participants' healing trajectories. These results suggest that standard emergency room treatment following MBI is inadequate and should include discharge directives to reduce cognitive demands for at least 48 hr at a minimum, for 30 days or longer for those with loss of consciousness.

Adult↗

PubMed2005

N-acetylcysteine attenuates early induction of heme oxygenase-1 following traumatic brain injury.

Traumatic brain injury (TBI) results in a cascade of events that includes the production of reactive oxygen species. Heme oxygenase-1 (HO-1) is induced in glial cells following head trauma, suggestive of oxidative stress. We have studied the temporal and spatial effects of the antioxidant N-acetylcysteine (NAC) on HO-1 levels following lateral fluid-percussion injury by immunoblotting and immunohistochemistry. In the injured cerebral cortex, maximal HO-1 induction was seen 6 h post-TBI and was maintained for up to 24 h following the insult, while the ipsilateral hippocampus and thalamus showed marked induction at 24 h postinjury. In all three brain regions, little or no HO-1 immunoreactivity was observed on the contralateral side. Astrocytes exhibited positive immunoreactivity for HO-1 in the injured cerebral cortex, hippocampus, and thalamus, while some neurons and microglia were also immunoreactive in the injured cortex. The administration of NAC 5 min following TBI resulted in a marked reduction in this widespread induction of HO-1, concomitant with a decrease in the volume of injury in all three brain regions. Together, these findings indicate that HO-1 induction is related to both oxidative and injury characteristics of the affected tissue, suggesting that protein expression of this gene is a credible marker of oxidative damage in this model of TBI.

Acetylcysteine↗

PubMed2003

Protein accumulation in traumatic brain injury.

Traumatic brain injury (TBI) is one of the most devastating diseases in our society, accounting for a high percentage of mortality and disability. A major consequence of TBI is the rapid and long-term accumulation of proteins. This process largely reflects the interruption of axonal transport as a result of extensive axonal injury. Although many proteins are found accumulating after TBI, three have received particular attention; beta-amyloid precursor protein and its proteolytic products, amyloid-beta (Abeta) peptides, neurofilament proteins, and synuclein proteins. Massive coaccumulations of all of these proteins are found in damaged axons throughout the white matter after TBI. Additionally, these proteins form aggregates in other neuronal compartments and in brain parenchyma after brain trauma. Interestingly, TBI is also an epigenetic risk factor for developing neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. Here, the similarities and differences of these accumulations with pathologies of neurodegenerative diseases will be explored. In addition, the potential deleterious roles of protein accumulations on functional outcome and progressive neurodegeneration following TBI will be examined.

Amyloid beta-Peptides↗

PubMed2003

Combat hypoxia: the importance of airway management & oxygenation of the traumatic brain injury patient.

Brain injury, specifically TBI, is a common occurrence in our society, with devastating physical, emotional, social and economic costs. Injury not only occurs on initial impact, but also develops slowly over ensuing hours or days. TBI poses unique challenges and requires special care, especially with airway management and ventilatory treatment. Serial assessment, particularly of the GCS and pupillary changes, is vital in continuing to monitor patient status. All treatment associated with the TBI patient is aimed at restoring CPP and allowing oxygenated blood to reach injured brain tissues.

Accidents, Traffic↗

PubMed1990

Effect of THAM on brain oedema in experimental brain injury.

The metabolic brain acidosis after trauma has been thought to increase brain oedema and contribute to neurologic deterioration. Amelioration of the brain acidosis either by systemic buffering agents or by hyperventilation has been proposed as a method of treatment. The objective of this study was to explore brain oedema and the metabolic changes in brain that occur with the use of hyperventilation. Tromethamine and combination (THAM and hyperventilation) therapy in experimental fluid-percussion brain injury. Brain lactate, brain pH, inorganic phosphate (Pi) and ATP were measured by 1H and 31P magnetic resonance spectroscopy. Also Water content in brain tissue using the specific gravimetric technique were determined in 32 cats. Prolonged hyperventilation provided relative ischaemia in brain tissue and promoted more production of brain lactate, no recovery of PCr/Pi ratio, and no decrease in brain oedema. On the other hand the administration of THAM served to decrease production of brain lactate and brain oedema and promoted the recovery of cerebral energy dysfunction. THAM ameliorates the deleterious effects of hyperventilation by minimizing energy disturbance and also decreases brain oedema. We conclude that THAM may be effective in reducing brain tissue acidosis and helpful as a metabolic stabilizing agent following severe head injury.

Animals↗

PubMed2006

Evaluation of pharmacological treatment strategies in traumatic brain injury.

Traumatic brain injury (TBI) is a devastating disease, predominately affecting young people. Although the prognosis for TBI victims has improved in recent years, many survivors of TBI suffer from emotional, cognitive and motor disturbances and a decreased quality of life. In recent years, there has been a rapid increase in the number of pharmacological targets evaluated in clinically-relevant experimental TBI models, showing improved cognitive and motor outcome and decreased loss of brain tissue. Despite the completion of several recent clinical trials using compounds showing neuroprotection in preclinical studies, pharmaceutical treatment strategies with proven clinical benefit are still lacking. This paper reviews the preclinical pharmacological treatment studies evaluated to date in experimental models of TBI. Although human TBI is a complex and multifaceted disease, these studies provide encouraging translational data suggesting that pharmacological compounds, delivered in a clinically-relevant time window, may improve the outcome of TBI patients.

Animals↗

PubMed2004

Recent advances in the development of multifactorial therapies for the treatment of traumatic brain injury.

Traumatic brain injury (TBI) is one of the leading causes of death and disability in the industrialised world and remains a major health problem with serious socioeconomic consequences. So far, despite encouraging preclinical results, almost all neuroprotection trials have failed to show any significant efficacy in the treatment of clinical TBI. This may be due, in part, to the fact that most of the therapies investigated have targeted an individual injury factor. It is now recognised that TBI is a very heterogeneous type of injury that varies widely in its aetiology, clinical presentation, severity and pathophysiology. The pathophysiological sequelae of TBI are mediated by an interaction of acute and delayed molecular, biochemical and physiological events that are both complex and multifaceted. Accordingly, a successful TBI treatment may have to simultaneously attenuate many injury factors. Recent efforts in experimental TBI have, therefore, focused on the development of neuropharmacotherapies that target multiple injury factors and thus improve the likelihood of a successful outcome. This review will focus on three such novel compounds that are currently being assessed in clinical trials; progesterone, dexanabinol and dexamethasone, and provide an update on the progress of both magnesium and cyclosporin A.

Animals↗

PubMed2005

A review of the current management of severe traumatic brain injury.

Traumatic brain injury accounts for up to half of trauma related fatalities. This review describes current management practices including pre-hospital care, surgical interventions and various treatment modalities for intracranial hypertension. The lack of class I evidence for the majority of interventions is highlighted.

Brain↗

PubMed2004

Motor and cognitive function evaluation following experimental traumatic brain injury.

Traumatic brain injury (TBI) in humans may cause extensive sensorimotor and cognitive dysfunction. As a result, many TBI researchers are beginning to assess behavioral correlates of histologically determined damage in animal models. Although this is an important step in TBI research, there is a need for standardization between laboratories. The ability to reliably test treatments across laboratories and multiple injury models will close the gap between treatment success in the lab and success in the clinic. The goal of this review is to describe and evaluate the tests employed to assess functional outcome after TBI and to overview aspects of cognitive, sensory, and motor function that may be suitable targets for therapeutic intervention.

Animals↗

PubMed2006

Perivascular nerve damage in the cerebral circulation following traumatic brain injury.

Traumatic brain injury (TBI) causes cerebral vascular dysfunction. Most have assumed that it was the result of endothelial and/or smooth muscle alteration. No consideration, however, has been given to the possibility that the forces of injury may also damage the perivascular nerve network, thereby contributing to the observed abnormalities. To test this premise, we subjected rats to impact acceleration. At 6 h, 24 h and 7 days post-TBI, cerebral basal arteries were removed and processed with antibody targeting protein gene product 9.5 (PGP-9.5), with parallel assessments of 5-hydroxytryptamine (5-HT) accumulation in the perivascular nerves. Additionally, Fluoro-Jade was also used as a marker of axonal degeneration. The perivascular nerve network revealed no abnormality in sham animals. However, by 6 h post injury, Fluoro-Jade reactivity appeared in the perivascular regions, with the number of fibers increasing with time. By 24 h post injury, a significant reduction in the perivascular 5-HT accumulation occurred, together with a reduction in PGP-9.5 fiber staining. At 7 days, a recovery of the PGP-9.5 immunoreactivity occurred, however, it did not reach a control-like distribution. These studies suggest that neurogenic damage occurs following TBI and may be a contributor to some of the associated vascular abnormalities.

Animals↗

PubMed2005

Synaptogenesis in the hippocampal CA1 field following traumatic brain injury.

Traumatic brain injury (TBI) results in both acute and chronic disruption of cognitive ability that may be mediated through a disruption of hippocampal circuitry. Experimental models of TBI have demonstrated that cortical contusion injuries can result in the loss of specific neurons in the CA3 subfield of the ipsilateral hippocampus, resulting in partial loss of afferents to the CA1 subfield. Numerous studies have documented the ability of the central nervous system to compensate for deafferentation by initiating a plasticity response capable of restoring lost synaptic contacts. The present study was designed to examine the time course of loss and replacement of synaptic contacts in stratum radiatum dendritic field of CA1. Young adult rats were subjected to a lateral cortical contusion injury and assayed for total synaptic numbers using unbiased stereology coupled with transmission electron microscopy. Injured animals demonstrated a 60% loss of synapses in CA1 at 2 days post-injury, followed by a reinnervation process that was apparent as early as 10 days post-injury. By 60 days post-injury, total synaptic numbers had approached pre-injury levels but were still significantly lower. Some animals were behaviorally tested for spatial memory in a Morris Water Maze at 15 and 30 days post-injury. While there was some improvement in spatial memory, injured animals continued to demonstrate a significant deficit in acquisition. These results show that the hippocampus ipsilateral to the cortical contusion is capable of a significant plasticity response but that synapse replacement in this area does not necessarily result in significant improvement in spatial learning.

Animals↗

PubMed2004

Occurrence of pituitary dysfunction following traumatic brain injury.

Traumatic brain injury (TBI) may be associated with impairment of pituitary hormone secretion, which may contribute to long-term physical, cognitive, and psychological disability. We studied the occurrence and risk factors of pituitary dysfunction, including growth hormone deficiency (GHD) in 50 patients (mean age 37.6 +/- 2.4 years; 40 males, age 20-60 years; 10 females, age 23-87 years) with TBI over 5 years. Cranial or facial fractures were documented in 12 patients, and neurosurgery was performed in 14. According to the Glasgow Coma Scale (GCS), 16 patients had suffered from mild, 7 moderate, and 27 severe TBI. Glasgow Outcome Scale (GOS) indicated severe disability in 5, moderate disability in 11, and good recovery in 34 cases. Basal pituitary hormone evaluation, performed once at times variable from 12 to 64 months after TBI, showed hypogonadotrophic hypogonadism in 7 (14%), central hypothyroidism in 5 (10%), low prolactin (PRL) levels in 4 (8%), and high PRL levels in 4 (8%) cases. All subjects had normal corticotrophic and posterior pituitary function. Seven patients showed low insulin-like growth factor-I (IGF-I) levels for age and sex. Results of GHRH plus arginine testing indicated partial GHD in 10 (20%) and severe GHD in 4 (8%) cases. Patients with GHD were older (p <0.05) than patients with normal GH secretion. Magnetic resonance imaging demonstrated pituitary abnormalities in 2 patients; altogether pituitary dysfunction was observed in 27 (54%) patients. Six patients (12%) showed a combination of multiple abnormalities. Occurrence of pituitary dysfunction was 37.5%, 57.1%, and 59.3% in the patients with mild, moderate, and severe TBI, respectively. GCS scores were significantly (p <0.02) lower in patients with pituitary dysfunction compared to those with normal pituitary function (8.3 +/- 0.5 vs. 10.2 +/- 0.6). No relationship was detected between pituitary dysfunction and years since TBI, type of injury, and outcome from TBI. In conclusion, subjects with a history of TBI frequently develop pituitary dysfunction, especially GHD. Therefore, evaluation of pituitary hormone secretion, including GH, should be included in the long-term follow-up of all TBI patients so that adequate hormone replacement therapy may be administered.

Adult↗

PubMed2003

Neurologic aspects of traumatic brain injury.

Traumatic brain injury is a common neurologic condition that can have a significant emotional and financial burden. Neurologic injury is classified on the basis of initial clinical status by the Glasgow Coma Scale, and also by the type and location of head injury. Complications in the management of these patients are reviewed, ranging from intracranial pressure management and stroke to post-traumatic epilepsy. In addition, predictive prognostic variables that can be used to predict outcome based on a patient's presentation at the time of a head trauma are discussed. Finally, interventions such as induced hypothermia that can be undertaken to try to optimize outcome, are discussed along with current data in support of or against such techniques.

Brain Injuries↗