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Results for “Traumatic Brain Injuries”

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PubMed2002

Severe traumatic brain injury: some effects on family caregivers.

This study assesses the effects of severe traumatic brain injuries on family members and functioning-a topic of interest for those working with survivors and their families. This issue is receiving increased attention as recent findings suggest that family adjustment influences outcome for brain-injured persons. The Family Environment Scale and the Profile of Mood States were completed by 25 individuals who had a family member with a severe traumatic brain injury. These scales were also completed by a comparison group of 32 individuals who had no brain-injured family member. In terms of family functioning, the findings suggest that, when a family member suffers a severe traumatic brain injury, depression may be elevated, along with a decreased ability to express feelings, decreased time and energy for social and recreational activities, and increased control in comparison to families without a brain-injured member. While this might contribute to family isolation which could last for many years, the overall finding of the present study was that caregiver families were coping adequately.

Brain Injuries↗

PubMed2006

Agitation following traumatic brain injury: an Australian sample.

PURPOSE: Agitation following traumatic brain injury (TBI) is perceived to limit the achievement of rehabilitation goals. The aims of this study were: (1) To examine the nature and incidence of agitation during TBI rehabilitation in an Australian sample; and (2) To explore the relationship between agitation and functional outcomes after TBI. METHOD: Retrospective medical record review of 80 participants admitted for rehabilitation following TBI. Outcome data collected at discharge, 6 and 24 months post-discharge, included length of stay, duration of post-traumatic amnesia (PTA), community integration, functional independence and life satisfaction. RESULTS: Seventy per cent of patients demonstrated agitation during rehabilitation for an average of 32 days. Agitated patients experienced longer PTA duration, increased length of stay and reduced functional independence, specifically cognitive function, at discharge. These differences between agitated and non-agitated participants did not appear to persist and were not evident at follow-up 6 and 24 months post-discharge. Longer duration of agitation was associated with delayed PTA emergence, longer rehabilitation stay and reduced functional independence at discharge and follow-up. CONCLUSIONS: A large proportion of patients with TBI experience agitation. Presence of agitation seems to limit rehabilitation gains at discharge. Longer duration of agitation is associated with persisting limitations to functional independence.

Adult↗

PubMed2004

Neuroimaging correlates of anxiety after pediatric traumatic brain injury.

BACKGROUND: Anxiety disorders are common after traumatic brain injury (TBI). Data on the neural correlates of these conditions are lacking. This study examines the relationship between brain damage, particularly to the orbitofrontal cortex (OFC) and temporal lobe, and anxiety symptoms and disorders. METHODS: Ninety-five children and adolescents were followed for one year postinjury. Preinjury and one-year postinjury anxiety status were obtained from the parent. Magnetic resonance imaging was performed to evaluate brain lesions. The primary analysis used regression models to determine relationships between brain lesions and anxiety outcomes. As a secondary analysis, previously reported posttraumatic stress disorder (PTSD) data were reanalyzed using similar methods for purposes of comparison. RESULTS: The primary analysis showed that greater volume and number of OFC lesions correlated with decreased risk for anxiety, whereas lesions in other brain areas did not correlate with anxiety. Consistent with prior data, the secondary analysis showed an inverse correlation between OFC damage and PTSD; temporal lobe damage was positively correlated with PTSD. CONCLUSIONS: After pediatric TBI, greater damage to the OFC is associated with decreased risk for anxiety outcomes. Similar to adult data, these findings implicate OFC dysfunction in childhood anxiety. Temporal lobe damage did not correlate with anxiety, in contrast to the findings for PTSD.

Adolescent↗

PubMed2003

Inter-rater reliability and concurrent validity of step length and step width measurement after traumatic brain injury.

PURPOSE: To determine the inter-rater reliability and concurrent validity of step length and step width measurement after traumatic brain injury. METHOD: Twelve people with traumatic brain injury completed six comfortable and six fast paced walking trials over a 10 m distance. Step length and step width were measured by five observers using two procedures. First, using pens taped on the subjects' heels which marked the floor at each heel strike and a tape measure. Second, by videotaping the subjects' feet as they walked on a mat marked with 5 cm grids and using a computer program to digitize foot position and calculate step length and width. RESULTS: The inter-rater reliability of step length and width measurements was very high, with intraclass correlation coefficients between 0.94 and 1.00, for both procedures. Concurrent validity was excellent, with correlations between the procedures ranging from 0.93 to 1.00. However, attaching pens to the heels did cause a slight reduction in right step length and walking speed when walking at a fast or comfortable pace, respectively. CONCLUSIONS: Assessing step length and width using pens taped to the subjects' heels and a tape measure is a reliable and valid clinical measure after traumatic brain injury.

Adult↗

PubMed2004

Effect of methylphenidate on vital signs and adverse effects in adults with traumatic brain injury.

OBJECTIVE: To study methylphenidate's adverse effects and impact on vital signs within the adult traumatic brain injury population. DESIGN: Thirty-five adults with traumatic brain injury enrolled in a double-blind, placebo-controlled, 6-wk crossover study of methylphenidate, given in a dose of 0.3 mg/kg/dose, twice a day. Vital signs were taken by trained clinicians and research assistants. Participants filled out weekly questionnaires pertaining to the adverse effects. RESULTS: Poor appetite was the only adverse effect related to methylphenidate. Other adverse effects commonly associated with methylphenidate, such as insomnia, rapid heart rate, and anxiety, were not found to be significantly related to the medication. The average rise in mean arterial pressure on methylphenidate was 2.5 mm. Methylphenidate showed a stronger impact on pulse, with an average increase of 7 beats/min. Baseline vital signs did not predict the degree of increase on methylphenidate. CONCLUSION: Methylphenidate appears to be safe for the adult population with traumatic brain injury. However, because a few individuals experienced significant changes in vital signs and adverse effects, all patients should be monitored.

Adult↗

PubMed2005

A prospective, population-based, follow-up study of mild traumatic brain injury in children.

OBJECTIVE: Outline the annual incidence of mild traumatic brain injury in children, aged 0-17 years, using the American Congress of Rehabilitation Medicine classification and record the presence of new symptoms up to six months after injury. SETTINGS AND METHODS: The study population comprised all the children in the age group of 0-17 years (a total of 40,984) in an administrative district in south-western Sweden. All the individuals registered in the Brain Injury Register, during the periods 1 January to 30 June 1999 and 1 April to 30 September 2000, fulfilling the inclusion criteria defined by American Congress of Rehabilitation Medicine, were included. New symptoms occurring three to six months after the injury were recorded using a mailed 21-item questionnaire. RESULTS: 192 children fulfilled the criteria, yielding an annual incidence of 468/100,000 (95% CI 402-535/100,000). Boys accounted for 57 per cent and fall injuries accounted for 61 per cent of the external causes. New symptoms were reported by 24 per cent of those who answered the questionnaire. CONCLUSION: This study revealed that the annual incidence of mild traumatic brain injury in children was almost as high as that among adults in the same area and population.

Adolescent↗

PubMed2006

Outcome after surgical decompression of severe traumatic brain injury.

One of the factors that affects outcome following severe traumatic brain injury is development and progression of cerebral oedema with associated increase in intracranial pressure (ICP). Uncontrolled elevations of ICP may compromise energy metabolism of the injured brain and lead to secondary injury, affecting neurological outcome of the patient. Decompressive craniectomy has been used for over a century as a treatment of refractory brain swelling in a variety of neurological conditions. However, conclusive evidence of whether it has a beneficial or adverse affect on outcome is lacking. This article reviews the existing evidence on the role of decompressive craniectomy in management of patients with traumatic brain injury and stresses the need for randomised controlled trials.

Brain Injuries↗

PubMed2006

The potential role of mitochondria in pediatric traumatic brain injury.

Mitochondria play a central role in cerebral energy metabolism, intracellular calcium homeostasis and reactive oxygen species generation and detoxification. Following traumatic brain injury (TBI), the degree of mitochondrial injury or dysfunction can be an important determinant of cell survival or death. Literature would suggest that brain mitochondria from the developing brain are very different from those from mature animals. Therefore, aspects of developmental differences in the mitochondrial response to TBI can make the immature brain more vulnerable to traumatic injury. This review will focus on four main areas of secondary injury after pediatric TBI, including excitotoxicity, oxidative stress, alterations in energy metabolism and cell death pathways. Specifically, we will describe what is known about developmental differences in mitochondrial function in these areas, in both the normal, physiologic state and the pathologic state after pediatric TBI. The ability to identify and target aspects of mitochondrial dysfunction could lead to novel neuroprotective therapies for infants and children after severe TBI.

Aging↗

PubMed1999

Ankylosed hips caused by heterotopic ossification after traumatic brain injury: a difficult problem.

BACKGROUND: Heterotopic ossifications develop around major joints after severe traumatic brain injury and decrease the range of motion of the joints. METHODS: From 1982 to 1994, we operated on 22 ankylosed hips caused by heterotopic ossifications after traumatic brain injury. Our 15 patients had been hospitalized in the intensive care unit for a period of 8 to 57 days. Their preoperative neurologic status was evaluated precisely. Special interest was given also to the accurate estimation of the extent and location of the ectopic bone by using x-rays and computed tomography, as well as to the maturity of the bone by using Tc99 bone scan and measurements of serum alkaline phosphatase levels. Intraoperatively, we resected as much ectopic bone as was needed to achieve functional range of motion in the hip. Postoperatively, all the patients were administered 100 mg of indomethacin (suppository) per day for a month, antibiotics, and anticoagulants. They were also exposed to 1,000 cGy of radiation in two equal doses. RESULTS: We achieved a least functional range of motion in 15 of 22 hips. Of the seven hips with poor results, six cases were attributable to the uncontrolled neurologic syndrome and only one poor result was attributable to severe heterotopic ossification recurrence. Wound complications did occur. CONCLUSION: Ankylosed hips caused by heterotopic ossifications after traumatic brain injury are a difficult problem to manage. Accurate evaluation of the preoperative neurologic status is essential for the desired final outcome and the treatment options.

Adult↗

PubMed1999

[Animal experiment of the ketamine effects on traumatic brain injury resulting from impact maxillofacial injury].

OBJECTIVE: To test the effects of ketamine (KET) on traumatic brain injury resulting from impact maxillofacial injury. METHODS: The rat models with middle serious traumatic brain injury were obtained by falling impaction at maxillofacial region of the rats, then the animals were treated with KET in the early stage, and the alteration of the neural function in those rats was observed at the same time. RESULTS: There was obvious difference between the rats in the KET-treating groups and the control group. It took about 2 days fewer than that of the control group for rats in the KET-treating group to recover. CONCLUSION: KET can shorten the recovery time of rats with brain injury resulting from impact maxillofacial injury.

Animals↗

PubMed1998

Glutamate antagonism during secondary deafferentation enhances cognition and axo-dendritic integrity after traumatic brain injury.

The combination of central fluid percussion traumatic brain injury (TBI) followed 24 h later by a bilateral entorhinal cortical deafferentation (BEC) produces profound cognitive morbidity. We recently showed that MK-801 given prior to TBI in this insult improved spatial memory for up to 15 days. In the present study we examine whether MK-801 treatment of the BEC component in the combined insult model affects cognitive recovery. Two strategies for drug treatment were tested. Fifteen minutes prior to the BEC lesion in the combined insult, rats were given i.p. doses of either 3 mg/kg (acute group) or 1 mg/kg (chronic group) MK-801. The acute group received no further injections, whereas the chronic group received 1 mg/kg MK-801 i.p. twice a day for 2 days post-BEC lesion. Two additional groups of animals received BEC lesion alone and either acute or chronic MK-801 treatment identical with the combined insult cases. Each group was then assessed for spatial memory deficits with the Morris water maze at days 11-15 and 60-64 postinjury. Both acute and chronic MK-801 treatment in the combined insult group significantly reduced spatial memory deficits at 15 days postinjury relative to untreated injured cases (P < .01). This reduction appeared more robust at 15 days and persisted for up to 64 days in the chronically treated group (P < .05). By contrast, neither acute nor chronic MK-801 treatment affected memory performance with the BEC insult alone. Immunocytochemical localization of parvalbumin showed that chronic administration of MK-801 in the combined insult cases attenuated the injury-induced dendritic atrophy of inhibitory neurons in the dentate gyrus and area CA1. Synaptophysin immunobinding revealed that chronic MK-801 treatment of the BEC component of the combined insult normalized the distribution of presynaptic terminals within the dentate gyrus. These results suggest that cognitive deficits produced by head trauma involving both neuroexcitation and deafferentation can be attenuated with chronic application of glutamatergic antagonists during the period of deafferentation injury and that this attenuation is correlated with axo-dendritic integrity.

Afferent Pathways↗

PubMed2005

Impaired self-awareness after moderately severe to severe traumatic brain injury.

Patients with moderately severe to severe traumatic brain injury (TBI) can demonstrate disturbances in self-awareness several months or years after injury. Patients may underreport cognitive and behavioral difficulties, which are the true residuals of their brain injury. Increasingly, research indicates that the residuals of these disturbances in consciousness greatly affect the process and outcome of rehabilitation. A recent model for conceptualizing disturbances of self-awareness after various forms of brain injury is reviewed.

Awareness↗

PubMed1995

Differential modulation of carbachol and trans-ACPD-stimulated phosphoinositide turnover following traumatic brain injury.

In the fluid percussion model of traumatic brain injury (TBI), we examined muscarinic and metabotropic glutamate receptor-stimulated polyphosphoinositide (PPI) turnover in rat hippocampus. Moderate injury was obtained by displacement and deformation of the brain within the closed cranial cavity using a fluid percussion device. Carbachol and (+/-)-1-Aminocyclopentane-trans-1,3-dicarboxylic acid (trans-ACPD)-stimulated PPI hydrolysis was assayed in hippocampus from injured and sham-injured controls at both 1 hour and 15 days following injury. At 1 hour after TBI, the response to carbachol was enhanced in injured rats by up to 200% but the response to trans-ACPD was diminished by as much as 28%. By contrast, at 15 days after TBI, the response to carbachol was enhanced by 25% and the response to trans-ACPD was enhanced by 73%. The ionotropic glutamate agonists N-methyl-D-aspartate (NMDA), and alpha-amino-3 hydroxy-5-methyl-4-isoxazolepropionate (AMPA), did not increase PPI hydrolysis in either sham or injured rats and injury did not alter basal hydrolysis. Thus, hippocampal muscarinic and metabotropic receptors linked to phospholipase C are differentially altered by TBI.

Animals↗

PubMed2005

Epidemiology of traumatic brain injury and subarachnoid hemorrhage.

Incidence rates of traumatic brain injury are high in both industrialized and non-industrialized countries and have been estimated variously to be between 150-250 cases per 100,000 population per year. The estimated incidence rates for subarachnoid hemorrhage (SAH) are between 10 to 25 cases per 100,000 population per year. Seasonal variation in the occurrence of subarachnoid hemorrhage has been reported in studies from different countries, with significant seasonal variations and peak periods for aneurysmal SAH differing widely. A differential racial distribution for SAH has been found as well as a higher mortality rate for women than for men. The cognitive and behavioral consequences of TBI and SAH are significant and affect the quality of life of patients and their families. Recent publications have informed of hypopituitary deficits in patients sustaining TBI or SAH. It is not clear whether the cognitive deficits found in these patients are due to the consequences of the brain injury itself or are related to the hypopituitary deficits. There is a need for research distinguishing the differential cognitive and behavioral effects of the brain injury and the endocrinological deficits in these patients, and for developing adequate treatment.

Brain Injuries↗

PubMed2002

Emotional Disturbances Following Traumatic Brain Injury.

Mood disturbances are common sequelae of traumatic brain injury (TBI), but the scientific database for such disorders is very limited in descriptive, prognostic, and treatment data. Post-TBI symptoms often cross diagnostic boundaries and include cognitive loss, amotivation, psychosis, mood, changes, or other domains. The treating physician must be mindful that clear diagnostic boundaries may not exist. Premorbid level of functioning commonly affects post-TBI level of functioning. When setting treatment goals, this must be considered. Patients who had lower levels of psychosocial functioning before the injury may not fare as well afterwards. Treatment of post-TBI mood symptoms should proceed after a full diagnostic work-up including imaging and electroencephalographic (EEG) studies, neuropsychologic testing, and physical and laboratory examinations. Once the diagnostic picture is established, treatment should then proceed with a multidisciplinary team (physician, social worker, neuropsychologist, and others). For the medications, consider both target symptoms and side effects; start medications with low doses and raise slowly, give full therapeutic trials before switching or adding second agents, avoid benzodiazepines if possible, limit anticholinergic or antidopaminergic agents, and avoid providing large quantities of lethal medications. When starting medications for the treatment of mood disorders following TBI, several general principles of treatment in this population should be considered, including: balancing treatment of target symptoms with the potential for adverse effects; making use of side effects to treat comorbid problems when present (ie, relatively antidepressant for depression and marked insomnia); using a "start low, go slow" approach; continuing dose escalation to full therapeutic levels (ie, completing therapeutic trials) before switching or adding augmenting agents; avoiding agents with predictable and functionally important adverse effects (ie, benzodiazepines, strongly anticholinergic or antidopaminergic agents); and avoiding prescription of large and potentially lethal quantities of medications.

Journal Article↗

PubMed2006

Expression of antiapoptotic survivin and aven genes in rat heart tissue after traumatic brain injury.

We have recently shown that experimental traumatic brain injury (TBI) results in ultrastructural damage in heart tissue. The aim of this study was to determine the two antiapoptotic signals "survivin" and "aven" in rat heart tissue following TBI, and comparing the effects of erythropoietin (EPO) and methylprednisolone (MPS). Thirty-six Wistar-Albino female rats weighing 190 to 230 g were randomly allocated into six groups: group 1 underwent head trauma with no treatment; group 2 and group 3, head trauma and intraperitoneally delivered EPO (1000 IU/kg) and MPS (30 mg/kg), respectively; group 4 (vehicle), head trauma and intraperitoneal albumin (0.4 mL/rat); groups 5 and 6, control and sham-operated groups, respectively. Three-hundred g-cm impact trauma was produced by the method of weight-drop. Real-time quantitative polymerase chain reactions were used to estimate survivin and aven gene expression at the total RNA level. Both survivin and aven were higher among the treatment than the trauma group (P = .0006, .0001 and P = .0038, .0033, respectively). Comparing survivin and aven between EPO and MPS treatment groups showed no significance (P = .3027, .2171, respectively). Also, both survivin and aven were significantly higher among the treatment than the vehicle, the control, or the sham-operated groups. These findings suggested that both EPO and MPS may play important roles in the expression of antiapoptotic survivin and aven genes in heart tissue after TBI.

Adaptor Proteins, Signal Transducing↗

PubMed1997

Histological markers of neuronal, axonal and astrocytic changes after lateral rigid impact traumatic brain injury.

The model of lateral, rigid impact traumatic brain injury is widely used but remains relatively poorly characterized by comparison with fluid percussion injury models. Thus, whilst the gross morphological changes that occur over the short- and long-term post-injury have been described, more subtle measures of neuronal injury and activation, and markers of axonal and glial reactions have not been investigated, complicating interpretation of data from this model. To address this issue, a variety of neurohistological markers were examined in adult male rats which had been subjected to open brain, lateral rigid impact injury. A piston device was unilaterally driven 3.0 mm into the somatosensory cortex at a speed of 3.2 m/s. Neuronal activation evidenced by Fos-like immunoreactivity showed a complex pattern at 3 h after injury which appeared to be related both to proximity to the impact site and cortical efferent connectivity. At 24 h after injury, acid fuchsin staining demonstrated dying neurons in the margin of the injury and in ipsilateral hippocampus and dorsal thalamus. Injured cells identified by heat-shock protein immunoreactivity showed a similar distribution. Axonal injury demonstrated with 68 kDa neurofilament immunoreactivity was more widely distributed. Less axonal damage was found with increasing distance from the injury site. At 7 days post-injury, glial fibrillary acidic protein immunoreactive astrocytes were prolific in the ipsilateral thalamus, hippocampus and striatum and throughout the injured cortex. In general, controlled, lateral rigid impact injury provides a more focused injury than is seen with lateral fluid percussion which may have implications for the behavioral deficits seen in this injury model.

Animals↗

PubMed2000

Frequency and duration of inattentive behavior after traumatic brain injury: effects of distraction, task, and practice.

Traumatic brain injury (TBI) is associated with impairments of attention, most typically measured through tests of information processing, or by subjective symptom endorsement by patients, families, and clinicians. We have previously shown increased rates of off-task behavior among patients with TBI versus controls as defined by videotaped records of independent work in distracting environments. In this research, we report on a more detailed method of coding such videotaped records which allows measurement of the precise number of off-task behaviors, their durations, and their relationship to distracting events. Using this method, we studied 20 patients with recent moderate-to-severe TBI and 20 demographically comparable controls as they performed independent work tasks while being subjected to controlled distracting events. This research confirms that patients are markedly less attentive than controls both in the presence of distractions and in their absence, that distractions have an influence on off-task behavior in both groups, and that the disruptive impact of distractors wanes relatively quickly for controls but not for patients. The duration of distraction produced by various classes of distracting events appeared similar for patients and controls, although the power to detect differences in behavioral duration between groups was limited. The pattern of inattentiveness among patients showed minimal relationship to measures of injury severity within this sample.

Adolescent↗