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PubMed2004

Benefits of early enteral nutrition with glutamine and probiotics in brain injury patients.

Brain injury patients have higher energy and protein expenditures and are prone to infections. The aim of the present study was to evaluate the results of early enteral feeding with glutamine and probiotics in brain injury patients. Twenty-three brain injury patients (Glasgow score between 5-12 and therapeutic intervention scoring system>20) were studied. Three patients were excluded to leave 20 remaining patients. Patients were randomized to receive either an early enteral diet (control group, n=10) or the same formula with glutamine and probiotics added (study group, n=10) for a minimum of 5 days (range, 5-14 days). The diets were isocaloric and isonitrogenous [35 kcal.kg(-1).day(-1) (where 1 kcal approximately 4.184 kJ) and 1.5 g of protein.kg(-1).day(-1)]. Main outcome measures were the incidence of infection, the length of stay in the intensive care unit and the number of days requiring mechanical ventilation. The two groups were homogeneous in gender, age, nutritional status and severity of trauma. There was no mortality during the study period. The infection rate was higher in controls (100%) when compared with the study group (50%; P=0.03) and the median (range) number of infections per patient was significantly greater (P<0.01) in the control group [3 (1-5)] compared with the study group [1 (0-3)]. Both the critical care unit stay [22 (7-57) compared with 10 (5-20) days; P<0.01; median (range)] and days of mechanical ventilation [14 (3-53) compared with 7 (1-15) days; P=0.04; median (range)] were higher in the patients in the control group than in the study group. We conclude that the enteral formula containing glutamine and probiotics decreased the infection rate and shortened the stay in the intensive care unit of brain injury patients.

Adult↗

PubMed2001

Current concepts: diffuse axonal injury-associated traumatic brain injury.

OBJECTIVES: To review the probable physical, physiologic mechanisms that result in the medical and neuropsychologic complications of diffuse axonal injury (DAI)-associated traumatic brain injury (TBI). DATA SOURCES: Various materials were accessed: MEDLINE, textbooks, scientific presentations, and current ongoing research that has been recently reported. STUDY SELECTION: Included were scientific studies involving TBI, particularly direct injury to the axons and glia of the central nervous system (CNS) in both in vitro and in vivo models. These studies include pathologic findings in humans as well as the medical complications and behavioral outcomes of DAI. Studies that addressed animal models of DAI as well as cellular and/or tissue models of neuronal injury were emphasized. The review also covered work on the physical properties of materials involved in the transmission of energy associated with prolonged acceleration-deceleration injuries. DATA EXTRACTION: Studies were selected with regard to those that addressed the mechanism of TBI associated with DAI and direct injury to the axon within the CNS. The material was generally the emphasis of the article and was extracted by multiple observers. Studies that correlate the above findings with the clinical picture of DAI were included. DATA SYNTHESIS: Concepts were developed by the authors based on the current scientific findings and theories of DAI. The synthesis of these concepts involves expertise in physical science, basic science concepts of cellular injury to the CNS, acute medical indicators of DAI, neuropsychologic indicators of DAI, and rehabilitation outcomes from TBI. CONCLUSIONS: The term DAI is a misnomer. It is not a diffuse injury to the whole brain, rather it is predominant in discrete regions of the brain following high-speed, long-duration deceleration injuries. DAI is a consistent feature of TBI from transportation-related injuries as well as some sports injuries. The pathology of DAI in humans is characterized histologically by widespread damage to the axons of the brainstem, parasagittal white matter of the cerebral cortex, corpus callosum, and the gray-white matter junctions of the cerebral cortex. Computed tomography and magnetic resonance imaging scans taken initially after injury are often normal. The deformation of the brain due to plastic flow of the neural structures associated with DAI explains the micropathologic findings, radiologic findings, and medical and neuropsychologic complications from this type of injury mechanism. There is evidence that the types of cellular injury in TBI (DAI, anoxic, contusion, hemorrhagic, perfusion-reperfusion) should be differentiated, as all may involve different receptors and biochemical pathways that impact recovery. These differing mechanisms of cellular injury involving specific biochemical pathways and locations of injury may, in part, explain the lack of success in drug trials to ameliorate TBI.

Animals↗

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↗

PubMed2001

Establishing minimum recommended standards for post-acute brain injury rehabilitation.

Brain injury is the biggest cause of disability for men under the age of 60 in the UK, and yet there are no nationally set minimum standards of care. This article describes the process undertaken by the South Thames Brain Injury Association (STBIRA) in setting out minimum standards for post-acute brain injury rehabilitation in inpatient facilities. These standards cover just one aspect of the patient's journey from coma to community. It is hoped that other groups will take up the challenge to set standards for other parts of the integrated care pathway, in order to ensure appropriate treatment for individuals with acquired brain injury.

Adult↗

PubMed2001

Are neuropsychiatric symptoms associated with evidence of right brain injury in referrals to a neuropsychiatric brain injury unit?

Studies suggest that neuropsychiatric symptoms are more common in patients with injury to the right side of the brain. However, most studies have examined patients with penetrating injuries because these allow more accurate localization of brain damage. This study investigates whether a similar association would be found in patients with non-penetrating brain injuries presenting to a neuropsychiatric unit. Over a 2 year period, 98 referrals were examined. Damage was localized using routine operation notes, EEG and neuroimaging. In total, 34 patients (35%) had a predominately right-sided injury, 33 (34%) had a left-sided injury and 31 (32%) had a diffuse or bilateral injury. Right-sided injuries were associated with hallucinations (p = 0.05), and left-sided injuries were associated with confabulation (p = 0.05) and lack of insight (p = 0.07). These results are consistent with findings from patients with penetrating head injuries. They suggest that evidence of the laterality of injury may be useful for planning the rehabilitation of patients seen in neuropsychiatric brain injury units.

Attention↗

PubMed1975

Respiration and acid-base balance of blood after diffuse experimental brain injury.

Diffuse brain injury in rabbits was caused by injecting olive oil and saline into one internal carotid artery. In this report, the fourth of a series, the effects of this experimental brain injury on respiration and acid-base balance of blood are analyzed. The animals that withstood the injury best were those that had a lower pre-traumatic pCO2; the animals that suffered a rise in intracranial pressure and succumbed to the injury quickly did so in spite of pronounced hyperventilation after the injury. Arterial pCO2 immediately before the injury was the only significant prognostic factor in this analysis. Respiratory rate only dropped immediately before respiratory arrest and death. The findings concerning pCO2 tally with results after experimental ligation of a cerebral artery, but less so with results after other types of experimental brain injury. This emphasizes again that conclusions drawn from one type of brain injury must not be extrapolated to other types.

Acid-Base Equilibrium↗

PubMed2001

Towards the development of brain injury specialists.

Brain injury presents a hugely complex, and sometimes daunting arena for the rehabilitation professional. With disruption to a person's core sense of self being almost the sine qua non of brain injury, rehabilitation can cover physical, psychological, social, philosophical and psychiatric realms. Those with brain injury can also be amongst the most vulnerable people in our society. Their rehabilitation has profound implications socio-politically, both in how we seek to understand disturbance in others, and also how we strive to ameliorate it. Whilst both theory and practice have grown exponentially over the last two decades, there is still no formal training or qualification within the brain injury rehabilitation field. This paper discusses the need for such formal training at both a theoretical and practical level not only for clinicians but also for front line staff, families and primary care services. The difficulties inherent in providing co-ordinated and structured training in such a complex area are discussed, and finally a model that attempts to meet user needs is outlined.

Brain Injuries↗

PubMed2004

Methodological issues and research recommendations for mild traumatic brain injury: the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury.

The WHO Collaborating Centre for Neurotrauma Task Force on Mild Traumatic Brain Injury performed a comprehensive search and critical review of the literature published between 1980 and 2002 to assemble the best evidence on the epidemiology, diagnosis, prognosis and treatment of mild traumatic brain injury. Of 743 relevant studies, 313 were accepted on scientific merit and comprise our best-evidence synthesis. The current literature on mild traumatic brain injury is of variable quality and we report the most common methodological flaws. We make recommendations for avoiding the shortcomings evident in much of the current literature and identify topic areas in urgent need of further research. This includes the need for large, well-designed studies to support evidence-based guidelines for emergency room triage of children with mild traumatic brain injury and to explore more fully the issue of prognosis after mild traumatic brain injury in the elderly population. We also advocate use of standard criteria for defining mild traumatic brain injury and propose a definition.

Adult↗

PubMedDate not supplied

Therapeutic hypothermia in traumatic brain injury.

Traumatic brain injury is a leading cause of death by trauma in adults in the United States and a major contributor to permanent physical, emotional, and psychological disabilities. Therapeutic hypothermia, defined as cooling of the body to less than 36 degrees C, has been shown to decrease mortality and morbidity and improve long-term outcomes by protecting the brain from secondary brain injury. The most commonly seen benefits of hypothermic temperatures of 32 degrees C to 33 degrees C are a significant reduction in intracranial hypertension and improved cerebral perfusion and oxygenation. Although evidence to date is insufficient to recommend the routine use of therapeutic hypothermia outside of the research setting, therapeutic hypothermia is used in multiple healthcare facilities in the world. The following article will define hypothermia and provide critical information necessary to provide care for the critically ill patient under therapeutic hypothermia. It will define the processes of brain injury and how hypothermia is thought to counteract those to protect the brain. Also included is a review of 2 major randomized, controlled trials of hypothermia for traumatic brain injury that have been instrumental in establishing guidelines and directing further research.

Adult↗

PubMed1999

Expression of nestin after traumatic brain injury in rat brain.

We tested the hypothesis that traumatic brain injury upregulates expression of nestin, an embryonic cell intermediate filament protein. Brain from rats (n=24) subjected to controlled cortical impact injury and sham operated (n=3) and normal (n=3) rats were processed for dual label immunohistochemical study to identify cellular expression of nestin. Our results show that in normal noninjured animals, nestin is expressed slightly and localized only in a few endothelial and subventricular cells. In contrast, at 1-4 weeks postinjury nestin is strongly expressed in astrocytes and microglia. The expression of nestin in astrocytes and microglia after traumatic brain injury support the hypothesis that injured cerebral tissue expresses developmental proteins, and that these proteins may promote recovery after injury.

Animals↗

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↗

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↗

PubMed2000

Tissue tears in the white matter after lateral fluid percussion brain injury in the rat: relevance to human brain injury.

A characteristic feature of severe diffuse axonal injury in man is radiological evidence of the "shearing injury triad" represented by lesions, sometimes haemorrhagic, in the corpus callosum, deep white matter and the rostral brain stem. With the exception of studies carried out on the non-human primate, such lesions have not been replicated to date in the multiple and diverse rodent laboratory models of traumatic brain injury. The present report describes tissue tears in the white matter, particularly in the fimbria of Sprague-Dawley rats killed 12, 24, and 48 h and 7 days after lateral fluid percussion brain injury of moderate severity (2.1-2.4 atm). The lesions were most easily seen at 24 h when they appeared as foci of tissue rarefaction in which there were a few polymorphonuclear leucocytes. At the margins of these lesions, large amounts of accumulated amyloid precursor protein (APP) were found in axonal swellings and bulbs. By 1 week post-injury, there was macrophage infiltration with marked astrocytosis and early scar formation. This lesion is considered to be due to severe deformation of white matter and this is the first time that it has been identified reproducibly in a rodent model of head injury under controlled conditions.

Amyloid beta-Protein Precursor↗

PubMed2004

A proposed injury threshold for mild traumatic brain injury.

Traumatic brain injuries constitute a significant portion of injury resulting from automotive collisions, motorcycle crashes, and sports collisions. Brain injuries not only represent a serious trauma for those involved but also place an enormous burden on society, often exacting a heavy economical, social, and emotional price. Development of intervention strategies to prevent or minimize these injuries requires a complete understanding of injury mechanisms, response and tolerance level. In this study, an attempt is made to delineate actual injury causation and establish a meaningful injury criterion through the use of the actual field accident data. Twenty-four head-to-head field collisions that occurred in professional football games were duplicated using a validated finite element human head model. The injury predictors and injury levels were analyzed based on resulting brain tissue responses and were correlated with the site and occurrence of mild traumatic brain injury (MTBI). Predictions indicated that the shear stress around the brainstem region could be an injury predictor for concussion. Statistical analyses were performed to establish the new brain injury tolerance level.

Acceleration↗

PubMed1999

Regulation of pituitary adenylate cyclase activating polypeptide and its receptor type 1 after traumatic brain injury: comparison with brain-derived neurotrophic factor and the induction of neuronal cell death.

Neurotrophic factors are known to promote neuronal survival during development and after acute brain injury. Recent data suggest that some neuropeptides also exhibit neurotrophic activities, as shown for the pituitary adenylate cyclase activating polypeptide, which increases the survival of various neuronal populations in culture. Employing in situ hybridization techniques, we have studied the regulation of messenger RNA for pituitary adenylate cyclase activating polypeptide and its receptor type 1 after a moderate traumatic brain injury to rat brain cortex. We have further compared their messenger RNA expression to that of brain-derived neurotrophic factor and to the amount of cell death occurring in the brain at various times after the brain injury. Levels of brain-derived neurotrophic factor messenger RNA increased rapidly within 2 h after trauma in cortex and hippocampus, and returned to control levels thereafter. The levels of messenger RNA for pituitary adenylate cyclase activating polypeptide also increased with time in the injured brains and reached maximal expression at 72 h, i.e. the end of the observation period. The alterations in pituitary adenylate cyclase activating polypeptide messenger RNA levels were particularly pronounced in the perifocal region and in the ipsilateral dentate gyrus of the brain injury. In contrast, the messenger RNA levels encoding pituitary adenylate cyclase activating polypeptide receptor type 1 first decreased after trauma and were then normalized in the dentate gyrus. There was a large increase in the number of cells labelled for DNA breaks at 12 h post-trauma, indicative of enhanced cell death. The number of labelled cells, however, decreased at later stages concomitant with an increase in the expression of pituitary adenylate cyclase activating polypeptide messenger RNA. Pituitary adenylate cyclase activating polypeptide rescued cortical neurons in cultures against ionomycin-induced cell death, supporting the concept of a neuroprotective effect for the peptide. These results demonstrate a differential regulation of messenger RNA for brain-derived neurotrophic factor and the pituitary adenylate cyclase activating polypeptide and its receptor after brain trauma. The data also suggest that pituitary adenylate cyclase activating polypeptide might have a beneficial effect in brain injury by counteracting neuronal cell death.

Animals↗

PubMed1998

Blood-free magnesium concentration declines following graded experimental traumatic brain injury.

Traumatic brain injury has been shown to result in a decrease in brain-free magnesium concentration that is associated with the development of neurologic motor deficits. Although these changes have been well characterized in the brain, changes in free magnesium homeostasis have not been characterized in other fluid compartments. The current experiments use ion selective electrodes to measure alterations in blood-free magnesium concentration following graded experimental brain injury in rats and to compare these changes with subsequent neurologic outcome. After severe impact-acceleration-induced injury, blood-free magnesium levels significantly declined (p < 0.05) by 25% and remained depressed for at least 4 days after injury. After moderate injury, the decline in blood-free magnesium was less than that observed in the severe injury group with respect to both degree of decline and duration of decline. The post-traumatic blood-free magnesium concentration correlated to observed motor deficits as assessed by rotarod evaluation (p < 0.001). We conclude that blood-free magnesium levels may be a prognostic indicator of outcome following severe traumatic brain injury.

Animals↗

PubMed1999

Traumatic brain injury.

Traumatic brain injury, caused by motor vehicle accidents, falls, assaults, or sports injuries affects approximately 7 million people each year. Early and rapid management of the initial brain injury and reduction in secondary insults can lead to improved outcomes. Nursing has an integral role in the care of the patient with traumatic brain injury and can have a positive impact on the outcome for the patient and the family. Types of injuries, treatment modalities, interdisciplinary management, and expected outcomes are discussed.

Algorithms↗

PubMed2000

[Model of diffuse axonal injury and focal brain injury in rats].

OBJECTIVE: To establish a rather ideal experimental brain injury model in rats, in which diffuse axonal injury(DAI) and focal brain contusion were made concurrently. METHODS: The pathophysiological changes were monitored, and the histological changes were observed under naked eye, microscope and electric microscope. RESULTS: 1. The mortality in the group suffering from DAI with focal contusion(Group A) was much higher than that in DAI(Group B) and sham group(Group C); 2. The time of post-injury primary coma in Group A [(5.19 +/- 0.49) h] was longer than that in Group B [(2.75 +/- 0.16) h] and Group C [(2.77 +/- 0.20) h] significantly(P < 0.01); 3. Immunohistological examination showed that the diffuse axonal injury could be seen in several parts of the brain(subcortical, corpus callosum and brainstem) in Group A; 4. We observed in Group A under electric microscope that the axons were swollen and degenerated fragmently, neurofilaments ranged disorderly and there was vacuolation. CONCLUSION: The model is cheap, simple and can be easily repeated. Furthermore it can be used to research the changes of pathophysiology, histology and moleculobiochemistry of head injury in human beings.

Animals↗