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PubMed1997

Pediatric traumatic brain injury.

Pediatric traumatic brain injury is a challenge to critical care practitioners. The prevention of secondary injury is key to improving morbidity and mortality outcomes. Interventions are targeted at maintaining adequate cerebral blood flow and minimizing oxygen consumption by the brain. The anticipation and prevention of systemic complications are also of vital importance. The impact that nursing judgment has on outcomes is notable. Pediatric traumatic brain injury is described, current treatments and issues are discussed, and an overview of outcomes related to morbidity are presented.

Brain Injuries↗
PubMed1999

An intrathecal bolus of cyclosporin A before injury preserves mitochondrial integrity and attenuates axonal disruption in traumatic brain injury.

Traumatic brain injury evokes multiple axonal pathologies that contribute to the ultimate disconnection of injured axons. In severe traumatic brain injury, the axolemma is perturbed focally, presumably allowing for the influx of Ca2+ and initiation of Ca2+ -sensitive, proaxotomy processes. Mitochondria in foci of axolemmal failure may act as Ca2+ sinks that sequester Ca2+ to preserve low cytoplasmic calcium concentrations. This Ca2+ load within mitochondria, however, may cause colloid osmotic swelling and loss of function by a Ca2+ -induced opening of the permeability transition pore. Local failure of mitochondria, in turn, can decrease production of high-energy phosphates necessary to maintain membrane pumps and restore ionic balance in foci of axolemmal permeability change. The authors evaluated the ability of the permeability transition pore inhibitor cyclosporin A (CsA) to prevent mitochondrial swelling in injured axonal segments demonstrating altered axolemmal permeability after impact acceleration injury in rat. At the electron microscopic level, statistically fewer abnormal mitochondria were seen in traumatically injured axons from CsA-pretreated injured animals. Further, this mitochondrial protection translated into axonal protection in a second group of injured rats, whose brains were reacted with antibodies against amyloid precursor protein, a known marker of injured axons. Pretreatment with CsA significantly reduced the number of axons undergoing delayed axotomy, as evidenced by a decrease in the density of amyloid precursor protein-immunoreactive axons. Collectively, these studies demonstrate that CsA protects both mitochondria and the related axonal shaft, suggesting that this agent may be of therapeutic use in traumatic brain injury.

Amyloid beta-Protein Precursor↗
PubMed2001

Increased expression of neuronal glucose transporter 3 but not glial glucose transporter 1 following severe diffuse traumatic brain injury in rats.

Traumatic brain injury results in an increased brain energy demand that is associated with profound changes in brain glycolysis and energy metabolism. Increased glycolysis must be met by increasing glucose supply that, in brain, is primarily mediated by two members of the facilitative glucose transporter family, Glut1 and Glut3. Glut1 is expressed in endothelial cells of the blood-brain barrier (BBB) and also in glia, while Glut3 is the primary glucose transporter expressed in neurons. However, few studies have investigated the changes in glucose transporter expression following traumatic brain injury, and in particular, the neuronal and glial glucose transporter responses to injury. This study has therefore focussed on investigating the expression of the glial specific 45-kDa isoform of Glut1 and neuronal specific Glut3 following severe diffuse traumatic brain injury in rats. Following impact-acceleration injury, Glut3 expression was found to increase by at least 300% as early as 4 h after induction of injury and remained elevated for at least 48 h postinjury. The increase in Glut3 expression was clearly evident in both the cerebral cortex and cerebellum. In contrast, expression of the glial specific 45-kDa isoform of Glut1 did not significantly change in either the cerebral cortex or cerebellum following traumatic injury. We conclude that increased glucose uptake after traumatic brain injury is primarily accounted for by increased neuronal Glut 3 glucose transporter expression and that this increased expression after trauma is part of a neuronal stress response that may be involved in increasing neuronal glycolysis and associated energy metabolism to fuel repair processes.

Animals↗
PubMed1994

The effect of hypertonic resuscitation on pial arteriolar tone after brain injury and shock.

Acute brain injury followed by hemorrhagic shock (HEM) causes prohibitive mortality in trauma patients because these combined events lead to low cerebral blood flow (CBF) and cerebral oxygen delivery (co2del). Proper treatment therefore requires rapid correction of cerebral perfusion deficits. Previous studies have shown that hypertonic crystalloid resuscitation significantly improves CBF and co2del in a model of brain injury and HEM when compared to lactated Ringer's (LR) solution. The mechanism or mechanisms for this advantage, however, are not well understood. We hypothesized that hypertonic fluid resuscitation would reduce pial arteriolar tone after brain injury and HEM resulting in an increase in CBF when compared to LR resuscitation. We measured cerebral and systemic variables in a porcine model of focal cryogenic brain injury and hemorrhagic shock over a 5-hour period. Swine were randomized to receive either hypertonic sodium lactate (HSL) or LR fluid resuscitation. The HSL resuscitation produced a significant and sustained elevation in cerebral perfusion pressure and pial arteriole diameter (p < 0.05), and a sustained elevation in CBF after brain injury and HEM when compared with LR. These data suggest that hypertonic fluid resuscitation following brain injury and HEM improves CBF, at least in part, by causing vasodilation of cerebral resistance vessels.

Animals↗
PubMed1984

The contribution of brain injury to the overall injury severity of brain-injured patients.

Several recent population-based studies of the incidence of head injury have identified cases by screening hospitalized patients. This method assumes a close relationship between severity of head injury and overall injury severity, since it is the latter that determines hospital admission. Thus, a patient whose overall injury severity is high will be admitted to the hospital regardless of the degree of his head injury. Similarly, since a patient's outcome status after treatment depends on his response to all his injuries, studies of the prognosis of various types of head injury also assume a close relationship between head injury severity and overall injury severity. The present study examines the relationship between brain injury severity and overall injury severity in a series of hospitalized head-injured patients with evidence of actual or probable brain trauma. Among these patients, brain injury severity was closely related to overall injury severity. Head injury severity and head and neck injury severity were also closely related to overall injury severity. For all other body regions, injury severity was not closely related to overall injury severity in this group of patients.

Adolescent↗
PubMed1986

Incidence, severity, and external causes of pediatric brain injury.

The number of fatal brain injuries and hospital admissions for brain injuries in children up to 15 years old in San Diego County, California, were ascertained from emergency room and hospital records, coroners' reports, death certificates, and nursing home and extended-care records for 1981. The annual brain-injury rate per 100 000 children was 185 (235 for boys and 132 for girls). The major causes of pediatric brain injury were falls (35%), recreational activities (29%), and motor vehicle crashes (24%). The case-fatality ratio was six deaths per 100 injured children. Of those children admitted to a hospital alive, 88% had a mild brain injury and 44% had no evidence of loss of consciousness. Two thirds of children with mild brain injuries and one third of those with serious brain injuries were transported to a hospital in private nonemergency vehicles.

Accidents, Traffic↗
PubMed1996

Cobalt-55 positron emission tomography in traumatic brain injury: a pilot study.

Traumatic brain injury is usually assessed with the Glasgow coma scale (GCS), CT, or MRI. After such injury, the injured brain tissue is characterised by calcium mediated neuronal damage and inflammation. Positron emission tomography with the isotope cobalt-55 (Co-PET) as a calcium tracer enables imaging of affected tissue in traumatic brain injury. The aim was to determine whether additional information can be gained by Co-PET in the diagnosis of moderate traumatic brain injury and to assess any prognostic value of Co-PET. Five patients with recent moderately severe traumatic brain injury were studied. CT was performed on the day of admission, EEG within one week, and MRI and Co-PET within four weeks of injury. Clinical assessment included neurological examination, GCS, neuropsychological testing, and Glasgow outcome scale (GOS) after one year. Co-PET showed focal uptake that extended beyond the morphological abnormalities shown by MRI and CT, in brain regions that were actually diagnosed with EEG. Thus Co-PET is potentially useful for diagnostic localisation of both structural and functional abnormalities in moderate traumatic brain injury.

Brain Injuries↗
PubMed2005

Cognitive appraisal accuracy moderates the relationship between injury severity and psychosocial outcomes in traumatic brain injury.

OBJECTIVE: Traumatic brain injury (TBI) frequently results in significant changes in physical, cognitive and emotional status. Outcomes after TBI may be related to accurate appraisal of these changes. This study examined the relationship between cognitive appraisal accuracy and psychosocial outcomes in TBI survivors. METHODS: Participants were male and female TBI survivors (n=103) who were at least 6 months post-injury and a family member of each survivor. Appraisal accuracy was assessed using self- and observer-report measures of perceived cognitive difficulties. Family members also completed a measure of psychosocial function. Hierarchical regression techniques were used to determine whether cognitive appraisal accuracy accounted for a significant proportion of variance in psychosocial outcomes. RESULTS: Study findings indicated cognitive appraisal accuracy moderated the relationship between injury severity and aspects of psychosocial function. CONCLUSIONS: The results suggest that brain injury outcomes may be improved when an individual is able to accurately assess limitations.

Adult↗
PubMed2005

Heat shock protein modulation of KATP and KCa channel cerebrovasodilation after brain injury.

Fluid percussion brain injury (FPI) impairs pial artery dilation to activators of the ATP-sensitive (K(ATP)) and calcium-activated (K(Ca)) K(+) channels. This study investigated the role of heat shock protein (HSP) in the modulation of K(+) channel-induced pial artery dilation after FPI in newborn pigs equipped with a closed cranial window. Under nonbrain injury conditions, topical coadministration of exogenous HSP-27 (1 mug/ml) blunted dilation to cromakalim, CGRP, and NS-1619 (10(-8) and 10(-6) M; cromakalim and CGRP are K(ATP) agonists and NS-1619 is a K(Ca) agonist). In contrast, coadministration of exogenous HSP-70 (1 mug/ml) potentiated dilation to cromakalim, CGRP, and NS-1619. FPI increased the cerebrospinal fluid (CSF) concentration of HSP-27 from 0.051 +/- 0.012 to 0.113 +/- 0.035 ng/ml but decreased the CSF concentration of HSP-70 from 50.42 +/- 8.96 to 30.9 +/- 9.9 ng/ml at 1 h postinsult. Pretreatment with topical exogenous HSP-70 (1 mug/ml) before FPI fully blocked injury-induced impairment of cromakalim and CGRP dilation and partially blocked injury-induced impairment of dilation to NS-1619. These data indicate that HSP-27 and HSP-70 contribute to modulation of K(+) channel-induced pial artery dilation. These data suggest that HSP-70 is an endogenous protectant of which its actions may be unmasked and/or potentiated with exogenous administration before brain injury.

Animals↗
PubMed1993

Traumatic brain injury and chronic pain: differential types and rates by head injury severity.

Traumatic brain injury has been associated with many physical and neurobehavioral consequences, including pain problems. Documented most has been the presence of posttraumatic headaches that are associated with the postconcussion syndrome. This study therefore examined types and rates of chronic pain problems in patients seen in an outpatient brain injury rehabilitation program. A total of 104 patients were evaluated, 66 of whom were male and 38 female, and the average time postinjury was 26 months. Headaches were the most frequent chronic pain problem across both mild and the moderate/severe groups, although in the former, a significantly higher frequency was noted (89%) when compared against the latter group. The same relative rates were seen for chronic neck/shoulder, back, and other pain problems. The mild group also showed a higher frequency of concurrent pain problems, whereas in the moderate/severe group only one patient had more than one chronic pain problem. Results also showed that in the mild group neck/shoulder accompanied headaches 47% of the time, and back pain coexisted with headaches 44% of the time. These results underscore the high frequency of chronic pain problems in the mild head injury population and implicate the need for avoiding the mislabeling of symptoms such attentional deficits or psychological distress as attributable only to head injury sequelae in those with coexisting chronic pain. Early identification and intervention of pain syndromes in the mild head-injury population is also suggested.

Adolescent↗
PubMed1992

The primary care optometric evaluation of the traumatic brain injury patient.

Traumatic brain injury can cause an assortment of visual problems for the patient. These problems, unless resolved, can hinder a patient's rehabilitative progress. This article discusses the characteristic visual deficits found after traumatic brain injury. It also explains how minor modifications made to a routine comprehensive optometric examination can tailor an examination to the head trauma patient.

Brain Injuries↗
PubMed1996

Neurobehavioral sequelae of high voltage electrical injuries: comparison with traumatic brain injury.

Eighteen survivors of high voltage electrical injuries (HVEI) underwent neuropsychological evaluation in the acute, short-term or long-term epochs Deficits in verbal learning and delayed recall of verbal information were present across various epochs No other cognitive performances were in the impaired range for the HVEI group, although many individual patients also had compromised attention Depression, anxiety and irritability were widespread among HVEI patients, especially beyond the acute period Extreme irritability was accompanied by assaultive behavior in several patients The neurobehavioral effects of HVEI were very similar to those of a closely matched traumatic brain injury (TBI) control group in each epoch The only significant difference between the groups was less successful immediate visual retention by TBI patients in the long-term epoch.

Journal Article↗
PubMed2006

Current controversies in the management of patients with severe traumatic brain injury.

BACKGROUND: Traumatic brain injury is a major cause of mortality and morbidity, particularly among young men. The efficacy and safety of most of the interventions used in the management of patients with traumatic brain injury remain unproven. Examples include the 'cerebral perfusion pressure-targeted' and 'volume-targeted' management strategies for optimizing cerebrovascular haemodynamics and specific interventions, such as hyperventilation, osmotherapy, cerebrospinal fluid drainage, barbiturates, decompressive craniectomy, therapeutic hypothermia, normobaric hyperoxia and hyperbaric oxygen therapy. METHODS: A review of the literature was performed to examine the evidence base behind each intervention. RESULTS: There is no class I evidence to support the routine use of any of the therapies examined. CONCLUSION: Well-designed, large, randomized controlled trials are needed to determine therapies that are safe and effective from those that are ineffective or harmful.

Barbiturates↗
PubMed1999

Inflicted traumatic brain injury: relationship of developmental outcome to severity of injury.

Inflicted traumatic brain injury (TBI) is a frequent consequence of physical child abuse in infants and children. Twenty-eight children who were 2-42 months of age when hospitalized for moderate to severe TBI were enrolled in a prospective, longitudinal study of neurobehavioral outcome following acquired brain injury. Relative to a comparison group, the children with inflicted TBI had significant deficits in cognitive, motor and behavioral domains when assessed with the Bayley Scales of Infant Development-II 1 and 3 months after the injury. Nearly half of the injured children showed persisting deficits in attention/arousal, emotional regulation and motor coordination. Greater injury severity, as indicated by lower coma scale scores, longer periods of unconsciousness and the presence of edema/cerebral infarctions was associated with poorer outcomes in all domains.

Battered Child Syndrome↗
PubMed2006

Early morphologic and spectroscopic magnetic resonance in severe traumatic brain injuries can detect "invisible brain stem damage" and predict "vegetative states".

A precise evaluation of the brain damage in the first days of severe traumatic brain injured (TBI) patients is still uncertain despite numerous available cerebral evaluation methods and imaging. In 5-10% of severe TBI patients, clinicians remain concerned with prolonged coma and long-term marked cognitive impairment unexplained by normal morphological T2 star, flair, and diffusion magnetic resonance imaging (MRI). For this reason, we prospectively assessed the potential value of magnetic resonance spectroscopy (MRS) of the brain stem to evaluate the functionality of the consciousness areas. Forty consecutive patients with severe TBI were included. Single voxel proton MRS of the brain stem and morphological MRI of the whole brain were performed at day 17.5 +/- 6.4. Disability Rating Scale and Glasgow Outcome Scale (GOS) were evaluated at 18 months posttrauma. MRS appeared to be a reliable tool in the exploration of brainstem metabolism in TBI. Three different spectra were observed (normal, cholinergic reaction, or neuronal damage) allowing an evaluation of functional damage. MRS disturbances were not correlated with anatomical MRI lesions suggesting that the two techniques are strongly complementarity. In two GOS 2 vegetative patients with normal morphological MRI, MRS detected severe functional damage of the brainstem (NAA/Cr < 1.50) that was described as "invisible brain stem damage." MRI and MRS taken separately could not distinguish patients GOS 3 (n = 7) from GOS 1-2 (n = 11) and GOS 4-5 (n = 20). However, a principal component analysis of combined MRI and MRS data enabled a clear-cut separation between GOS 1-2, GOS 3, and GOS 4-5 patients with no overlap between groups. This study showed that combined MRI and MRS provide a reliable evaluation of patients presenting in deep coma, specially when there are insufficient MRI lesions of the consciousness pathways to explain their status. In the first few days post-trauma metabolic (brainstem spectroscopy) and morphological (T2 star and Flair) MRI studies can predict the long-term neurological outcome, especially the persistent vegetative states and minimally conscious state.

Adult↗
PubMed1986

Oxygen radicals in brain injury.

Experimental fluid percussion brain injury in anesthetized cats causes vascular injury characterized by sustained arteriolar dilation, abnormal reactivity to vasoconstrictor and vasodilator interventions, focal endothelial lesions, and reduction of the oxygen consumption of the vessel wall. These abnormalities are minimized or completely inhibited by pretreatment with cyclooxygenase inhibitors or with oxygen radical scavengers. They were therefore ascribed to oxygen radicals generated in the course of accelerated arachidonate metabolism via cyclooxygenase. Following this type of brain injury, there is an increase in the activity of phospholipase c in the brain and a transient increase in brain concentration of prostaglandins. Superoxide anion radical was detected in the extracellular space of the brain both immediately following brain injury as well as one hour afterwards as the superoxide dismutase inhibitable portion of nitroblue tetrazolium reduction. The sustained dilation and abnormal reactivity of cerebral arterioles following brain injury were also reversed by superoxide dismutase and catalase applied on the brain surface 30 minutes after injury. These results suggest that treatment with oxygen radical scavengers might be effective in inhibiting or reversing some of the effects of brain injury, even though the intervention with the therapeutic agents occurs sometime after the injury has taken place.

Animals↗
PubMed2003

[Huperzine A attenuates cognitive deficits and brain injury after hypoxia-ischemic brain damage in neonatal rats].

OBJECTIVE: To investigate the protective effects of Huperzine A, a potent acetylcholinesterase inhibitor, against the hypoxic ischemic brain damage (HIBD) of the cognitive and morphology in the neonatal rats. METHODS: Postnatal 7 days old rats were given vehicle or Huperzine A (0.05 mg/kg or 0.1 mg/kg, i.p.) following HIBD (unilateral carotid artery ligation followed by hypoxia) or sham operation, and then tested the learning ability and memory in the Morris water maze (MWM) from 36 to 40 postnatal days. The performance in MWM (escape latency, probe time) were recorded to evaluate the learning and memory dysfunction. At the end of MWM trials, the rats were decapitated and their brains were histologically analyzed. The tissue loss in different brain regions including striatum, cortex, and hippocampus were analyzed by image analysis system. The CA(1) subfield neurons numbers were counted to evaluate the brain damage. The acetylcholinesterase histochemistry staining was used to determine the activity of acetylcholinesterase in different brain regions. RESULTS: Compared with sham-operated group, HIBD rats with the vehicle treatment displayed significant tissue losses in the hippocampus (including CA(1) neurons), cortex, and striatum, as well as severe spatial memory deficits (escape latency: 44 s vs 30 s, P < 0.05, probe time: 14 s vs 40 s, P < 0.01). Huperzine A treatment (0.1 mg/kg) resulted in significant protection against both HI-induced brain tissue losses and spatial memory impairments (mean escape latency: 34 s vs 44 s, P < 0.05, probe time: 35 s vs 14 s,P < 0.01). However, Huperzine A treatment (0.05 mg/kg) did not show any significant improvement of spatial memory impairments (mean escape latency: 45 s vs 44 s, P > 0.05, probe time: 17 s vs 14 s, P > 0.05), but moderate to severe brain tissue losses. There was a pronounced reduction of CA(1) neuron density in ipsilateral hemisphere of vehicle-treated group and 0.05 mg/kg Huperzine A group compared with contralateral hemisphere or ipsilateral hemisphere of sham-operated group and 0.1 mg/kg Huperzine A group (72 vs 232, P < 0.01, 72 vs 229, P < 0.01, respectively). There was a close linear correlation between the CA(1) neurons cell number and the mean escape latency for 5 d acquisition trials (r = 0.777, P < 0.01). CONCLUSION: The unilateral HI brain injury in a neonatal rat model was associated with cognitive deficits, and that Huperzine A treatment may be protective against both brain injury and spatial memory impairment. Huperzine A showed a therapeutic potential for the treatment of hypoxic-ischemic encephalopathy (HIE) caused by the perinatal asphyxia.

Acetylcholinesterase↗