SEARCH · PubMed Health

Results for “Traumatic Brain Injuries”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

PubMed2006

Memory of the traumatic event as a risk factor for the development of PTSD: lessons from the study of traumatic brain injury.

Traumatic memories, and the mechanisms by which they operate, continue to occupy a central role in the scientific investigation of risk factors for the development of posttraumatic stress disorder (PTSD). However, empirically based studies are constrained by practical and ethical considerations and are limited to naturalistic models. Consequently, the paradigms most appropriate for the exploration of the relationship between traumatic memories and PTSD have been identified in conditions involving traumatic events where memories may be compromised. Indeed, traumatic brain injury, a condition that is commonly associated with memory impairment, has often been utilized as a naturally occurring model for the study of traumatic memory and its contribution to the development of PTSD. This article presents a critical review of these research efforts and discusses their theoretical and clinical implications.

Brain Injuries↗

PubMed2005

Effect of methylphenidate on ICU and hospital length of stay in patients with severe and moderate traumatic brain injury.

OBJECTIVE: Traumatic brain injury is one of the major causes of death and disability among young people. Methylphenidate, a neural stimulant and protective drug, which has been mainly used for childhood attention deficit/hyperactivity disorder, has shown some benefits in late psychosocial problems in patients with traumatic brain injury. Its effect on arousal and consciousness has been also revealed in the sub-acute phase of traumatic brain injury. We studied its effect on the acute phase of moderate and severe traumatic brain injury (TBI) in relation to the length of ICU and hospital admission. PATIENTS AND METHODS: Severely and moderately TBI patients (according to inclusion and exclusion criteria) were randomized to treatment and control groups. The treatment group received methylphenidate 0.3mg/kg per dose PO BID by the second day of admission until the time of discharge, and the control group received a placebo. Admission information and daily Glasgow Coma Scale (GCS) were recorded. Medical, surgical, and discharge plans for patients were determined by the attending physician, blinded to the study. RESULTS: Forty patients with severe TBI (GCS = 5-8) and 40 moderately TBI patients (GCS = 9-12) were randomly divided into treatment and control groups on the day of admission. In the severely TBI patients, both hospital and ICU length of stay, on average, were shorter in the treatment group compared with the control group. In the moderately TBI patients while ICU stay was shorter in the treatment group, there was no significant reduction of the period of hospitalization. CONCLUSION: There were no significant differences between the treatment and control groups in terms of age, sex, post resuscitation GCS, or brain CT scan findings, in either severely or moderately TBI patients. Methylphenidate was associated with reductions in ICU and hospital length of stay by 23% in severely TBI patients (P = 0.06 for ICU and P = 0.029 for hospital stay time). However, in the moderately TBI patients who received methylphenidate, there was 26% fall (P = 0.05) only in ICU length of stay.

Adolescent↗

PubMed2004

Hyperbaric oxygen therapy for the adjunctive treatment of traumatic brain injury.

BACKGROUND: Traumatic brain injury is common and presents a health problem with significant effect on quality of life. Hyperbaric oxygen therapy (HBOT) has been suggested to improve oxygen supply to the injured brain and, therefore, to reduce the volume of brain that will ultimately perish. It is postulated that the addition of HBOT to the standard intensive care regimen may result in a reduction in patient death and disability as a result of these additional brain-preserving effects. OBJECTIVES: To assess the benefits and harms of adjunctive HBOT for treating traumatic brain injury. SEARCH STRATEGY: We searched CENTRAL (The Cochrane Library Issue 4, 2003), MEDLINE (1966 - 2003), EMBASE (1974 - 2003), CINAHL (1982 - 2003), DORCTHIM (1996 - 2003), and reference lists of articles. Relevant journals were handsearched and researchers in the field were contacted. SELECTION CRITERIA: Randomised studies comparing the effect on traumatic brain injury of therapeutic regimens which include HBOT with those that exclude HBOT (with or without sham therapy). DATA COLLECTION AND ANALYSIS: Three reviewers independently evaluated the quality of the relevant trials using the validated Oxford-Scale (Jadad 1996) and extracted the data from the included trials. MAIN RESULTS: Four trials contributed to this review (382 patients, 199 receiving HBOT and 183 control). There was a trend towards, but no significant increase in, the chance of a favourable outcome when defined as full recovery, Glasgow outcome score 1 or 2, or return to normal activities of daily living (relative risk [RR] for good outcome with HBOT 1.94, 95% confidence interval [CI] 0.92 to 4.08, P=0.08). Pooled data from the three trials with 327 patients that reported mortality, showed a significant reduction in the risk of dying when HBOT was added to the treatment regimen (RR 0.69, 95% CI 0.54 to 0.88, P=0.003). Heterogeneity between studies was low (I(2) =0%), and sensitivity analysis for the allocation of dropouts did not affect that result. This analysis suggests we would have to treat seven patients to avoid one extra death (number needed to treat [NNT] 7, 95% CI 4 to 22). One trial suggested intracranial pressure was favourably lower in those patients receiving HBOT in whom myringotomies had been performed (WMD with myringotomy -8.2 mmHg, 95% CI -14.7 mmHg to -1.7 mmHg, P=0.01), while in two trials there was a reported incidence of 13% for significant pulmonary impairment in the group receiving HBOT versus 0% in the non-HBOT group (P=0.007). REVIEWERS' CONCLUSIONS: In people with traumatic brain injury, the addition of HBOT significantly reduced the risk of death but not of favourable clinical outcome. The routine application of HBOT to these patients cannot be justified from this review. In view of the modest number of patients, methodological shortcomings and poor reporting, this result should be interpreted cautiously, and an appropriately powered trial of high methodological rigour is justified to define those patients (if any) who can be expected to derive most benefit from HBOT.

Brain Injuries↗

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↗

PubMed2005

The membrane-associated progesterone-binding protein 25-Dx is expressed in brain regions involved in water homeostasis and is up-regulated after traumatic brain injury.

After traumatic brain injury, progesterone has important neuroprotective effects in the nervous system. There is better functional outcome and less oedema formation in pseudopregnant rat females (high levels of endogenous progesterone) than in males. In addition to intracellular progesterone receptors, membrane binding sites of the hormone such as 25-Dx may also be involved in neuroprotection. In the present study we investigated the distribution of the membrane-associated progesterone-binding protein 25-Dx in rat brain. Immunohistochemical analysis showed that 25-Dx is particularly abundant in the hypothalamic area, circumventricular organs, and ependymal cells of the lateral walls of the third and lateral ventricles. A strong signal was also detected in the meninges. Double immunofluorescence immunolabelling and confocal microscopy showed that 25-Dx is co-expressed with vasopressin in neurones of the paraventricular, supraoptic and retrochiasmatic nuclei. Levels of 25-Dx expression were higher in pseudopregnant females than in males. After traumatic brain injury, 25-Dx expression was up-regulated in neurones and induced in astrocytes, which play an important role in regulating water and ion homeostasis. The expression of 25-Dx in structures involved in CSF production (choroid plexus) and in osmoregulation (circumventricular organs, hypothalamus and meninges), and its up-regulation after brain damage, point to a novel and potentially important role of this progesterone-binding protein in the maintenance of water homeostasis after traumatic brain injury.

Animals↗

PubMed2002

Cytochrome c release and caspase activation after traumatic brain injury.

Experimental traumatic brain injury (TBI) results in a rapid and significant necrosis of cortical tissue at the site of injury. In the ensuing hours and days, secondary injury exacerbates the primary damage resulting in significant neurological dysfunction. The identification of cell death pathways that mediate this secondary traumatic injury have not been elucidated, however recent studies have implicated a role for apoptosis in the neuropathology of traumatic brain injury. The present study utilized a controlled cortical impact model of brain injury to assess the involvement of apoptotic pathways: release of cytochrome c from mitochondria and the activation of caspase-1- and caspase-3-like proteases in the injured cortex at 6, 12 and 24 h post-injury. Collectively, these results demonstrate cytochrome c release from mitochondria and its redistribution into the cytosol occurs in a time-dependent manner following TBI. The release of cytochrome c is accompanied by a time-dependent increase in caspase-3-like protease activity with no apparent increase in caspase-1-like activity. However, pretreatment with a general caspase inhibitor had no significant effect on the amount of cortical damage observed at 7 days post-injury. Our data suggest that several pro-apoptotic events occur following TBI, however the translocation of cytochrome c itself and/or other events upstream of caspase activation/inhibition may be sufficient to induce neuronal cell death.

Analysis of Variance↗

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↗

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↗

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↗

PubMed2001

Conducting statewide needs assessments for persons with traumatic brain injury.

The Traumatic Brain Injury Act of 1996 (Public Law 104-166) gave new authority to the Health Resources and Services Administration (HRSA) in the United States Department of Health and Human Services (DHHS) to establish a grant program for states to assist in addressing the needs of persons with traumatic brain injury (TBI). The resulting State Demonstration Grant Program has made available two categories of grants: planning and implementation. Planning grants are awarded to assist states in building infrastructure through the development of four core components. One of the core components is a statewide needs and resource assessment encompassing the full spectrum of services, from initial acute treatment through rehabilitation and long-term community supports. In 1999, assessments completed in 11 states were subjected to a comparative analysis to identify trends across states and to extract salient issues for the State Demonstration Grant Program. This article summarizes the context of the HRSA-funded needs assessments and contrasts the methods of needs assessment utilized. Over-arching issues are discussed, including exemplary qualitative and quantitative methods, and the diversity of theoretical models employed in designing assessments and interpreting findings. Several limitations in approaches were also identified, including shortcomings of convenience samples for conducting mail surveys and the unlikely validity of using a needs and resource discrepancy approach to identify gaps in services.

Brain Injuries↗

PubMed2006

Apoptosis and functional changes of dipeptide transporter (PepT1) in the rat small intestine after traumatic brain injury.

BACKGROUND: Traumatic brain injury (TBI) can induce significant alterations of intestinal mucosal structure and barrier function. However, it has not been investigated whether, and to what degree, apoptosis and alterations of absorptive function in the intestinal mucosal epithelium occur after TBI. MATERIAL AND METHODS: Male Wistar rats were randomly divided into seven groups (five rats each group) including normal group, control group with sham operation, and TBI groups at hours 3, 12, 24, and 72, and on day 7. Parietal brain contusion was adopted using weight-dropping method. Intestinal mucosal structure was examined using histomorphmetric study and electron microscopy, and apoptosis was detected by TUNEL method. An everted sleeve of intestine was securely incubated in Kreb's solution with radioactive dipeptide ((3)H-Gly-Sar, 10 microCi/mL) to measure the uptake and transport of PepT1 of small intestinal epithelial cells. RESULTS: The villous height, crypt depth and surface area were significantly decreased at 24 h after TBI, and further declined to the degree of mucosal atrophy on day 7 after TBI. Apoptotic changes of condensed nuclei in epithelial cells and fractured, distorted, and sparse microvilli were found by electron microscopy. The number of apoptotic cells in the mucosal epithelium was significantly increased since 3 h after TBI, peaked at 72 h post-injury, then declined at 7 days, but was still higher than that of control. There was a highly negative relation between the apoptotic index and the villous height, the crypt depth, and villous surface area. Compared with that of normal and control rats, the transport and uptake of dipeptide was significantly increased at 3 h post-injury (P < 0.01), peaked at 12 h and declined a bit at 24 h post-injury, and returned to the level of normal and control rats at 72 h and 7 days. CONCLUSIONS: It is highly suggested that intestinal mucosa apoptosis plays an important role in the pathogenesis of acute gut damage after TBI. Intestinal PepT1 expression could be up-regulated after traumatic brain injury, and maintained the normal level under the condition of serious intestinal damage. Up-regulation of PepT1 may adaptively improve absorption of di- and tripeptides, independent of changes in the mucosal surface area.

Adaptation, Physiological↗

PubMed1999

Effects of dopaminergic combination therapy for frontal lobe dysfunction in traumatic brain injury rehabilitation.

Traumatic brain injury poses significant and diverse challenges to rehabilitation efforts. Neurobehavioural deficits represent a particularly difficult barrier to rehabilitative progress and societal reintegration. Early studies have identified dopaminergic drugs such as amantadine, bromocriptine and sinemet as potentially assistive in countering these deficits. To date, side effect profiles have been relatively benign, noted most frequently in small-scale case trials. The case of a 40-year-old patient with bilateral frontal traumatic brain injuries, and previous arteriovenous malformation (AVM) bleed with significant ataxia, dysarthria and neurobehavioural deficits is presented. This long range study demonstrates, through multiple varied dosing schedules, a trade off between the benefits and side effects of dopaminergic therapy, with implications for a larger brain injury population.

Accidental Falls↗

PubMed2005

The meaning of living with traumatic brain injury in people with moderate or severe traumatic brain injury.

A traumatic brain injury (TBI) extensively affects the injured person's daily life. Research based on the perspectives of people with TBI can increase understanding of the challenges they face and the possibility of supporting them in managing their lives. The aim of this study was to elucidate the meaning of living with TBI as narrated by the people with moderate or severe TBI. The data were collected by means of qualitative research interviews with 12 participants who had lived with TBI for 4-13 years. A phenomenological hermeneutic method was used to interpret the transcribed interviews. The study showed that people with TBI had lost their way and struggled to achieve a new normalcy. Losing one's way included experiences of waking up to unknown, missing relationships and experiencing the body as an enemy. Participants' struggles to attain a new normalcy included searching for an explanation, recovering the self, wishing to be met with respect, and finding a new way of living. Living with TBI seems to mean living with a perpetually altered body that changed the whole life and caused deep suffering, where feelings of shame and dignity competed with each other. Participants seem to be quite alone in their suffering and need more support from healthcare professionals.

Adult↗

PubMed1992

Sequelae of minor traumatic brain injury.

Minor traumatic brain injury is the most common type of traumatic encephalopathy, with approximately 290,000 to 325,000 new cases occurring each year. Recent research has suggested that both anatomic factors (acceleration-deceleration injury, contusions) and neurotransmitter factors (cholinergic systems) may contribute to the pathologic sequelae. Symptoms may be broadly categorized as physical, behavioral/affective, cognitive and integrative. Patients with mild brain injury may demonstrate significant attention and information-processing impairments in the absence of apparent neurologic problems. Most symptoms abate within the first few months, but a sizable subgroup of patients remain symptomatic up to one year or more. Evidence suggests that patients whose symptoms persist are not simply "neurotic." Rehabilitation efforts should focus on proper evaluation, reassurance, education, support and monitoring of progress.

Animals↗

PubMed1995

Defining assessment parameters in dual injuries: spinal cord injury and traumatic brain injury.

Assessment parameters for muscle testing in the individual with a spinal cord injury (SCI) have been clearly defined by the American Spinal Injury Association (ASIA). However, the ASIA standard requires the individual's participation in reporting sensory information and he/she must be able to perform specific tasks to complete the examination. In an individual with a dual injury, a SCI and a traumatic brain injury (TBI), neurological assessment can be impeded by the individual's inability to participate in the exam. Assessment needs to incorporate both cognitive and physical parameters that will appropriately assess both injuries. This article reviews the assessment parameters for both spinal cord injury and traumatic brain injury and provides assessment guidelines for bedside evaluation of functional ability. In addition, a review of the biomechanics of injury will provide a model for understanding dual injury.

Biomechanical Phenomena↗

PubMed2001

Psychological distress and family burden following spinal cord injury: concurrent traumatic brain injury cannot be overlooked.

Although concurrent spinal cord injury (SCI) and traumatic brain injury (TBI) are recognized, there is little acknowledgement of SCI/TBI as a contributor to psychological distress and family burden. By mail-out questionnaire, we evaluated psychological distress and family burden in a married group (n = 12) with traumatic SCI who had not been identified as having concurrent TBI on referral to the Canadian Paraplegic Association. Both the person with SCI and the partner completed the Brief Symptom Inventory (BSI), the Adjective Checklist, and a Likert strain scale to measure the perception of the partner's strain. The partner also completed the Zarit Burden Interview. Despite screening criteria designed to selectively recruit individuals without TBI, seven individuals described post-traumatic amnesia (PTA) > or = 3 days. Subsequently, participants' reports were divided into two groups--"longer PTA" and "shorter PTA". On the Brief Symptom Inventory, the two SCI groups did not differ, but the partners of individuals with "longer PTA" had significantly elevated Global Severity Index scores compared to the other partners. The "longer PTA" partner group demonstrated more strain and more burden (as measured by the Likert strain scale and the Zarit Burden Interview). Given the size of the groups (n = 7, n = 5), these findings are presented to illustrate trends and to stimulate further research.

Adaptation, Psychological↗

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↗

PubMedDate not supplied

Deep venous thrombosis management following traumatic brain injury: a practice survey of the traumatic brain injury model systems.

OBJECTIVE: To determine national patterns of screening, prophylaxis, and treatment of deep venous thrombosis (DVT) following traumatic brain injury (TBI) within the Traumatic Brain Injury Model Systems (TBIMS). DESIGN: e-mail survey instrument. SETTING: Multicenter Regional TBIMS. RESULTS: Fifteen of the 16 rehabilitation centers within the TBIMS responded to the survey (94% response rate). Approximately half of these centers routinely screen to detect subclinical DVTs (56% venous duplex ultrasonography, 12% plasma D-dimer) on admission to inpatient rehabilitation. Fifty-six percent of respondents use anticoagulation prophylactically, while 69% use mechanical means for DVT prophylaxis. Eighty fatal pulmonary emboli were reported for TBI patients in 189 practice-years, corresponding to 0.42 fatalities per year of practice. CONCLUSIONS: No consensus exists regarding the optimal methods for screening, prevention, or treatment of DVT in TBI patients in the acute rehabilitation setting of the TBIMS. The number of fatal pulmonary emboli reported among these centers emphasizes the need to develop evidence-based clinical practice guidelines for the prevention and treatment of venous thromboembolism in this patient population.

Bed Rest↗