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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↗
PubMed2002

Self-regulatory learning and generalization for people with brain injury.

PRIMARY OBJECTIVE: brain injury can result in the loss of previous learnt behaviours that affect an individual's daily functioning. The use of self-regulation helps the individual to relearn the lost behaviours by bringing him/her to self-conscious level through independent and reflective learning derived using a social cognitive perspective. The purpose of this paper is to report on clinical observations made with the use of self-regulation in people with brain injury during the relearning of lost functions. METHODS AND PROCEDURES: daily tasks were used to assess the relearning ability of the subjects pre- and post-programme. EXPERIMENTAL INTERVENTION: one-week self-regulatory training on five selected daily tasks. MAIN OUTCOMES AND RESULTS: these provisory observations would suggest that, with specific guidance for people with different needs, such as with impaired cognitive function and depression, self-regulation is effective in enhancing their relearning. CONCLUSION: Self-regulatory training is effective in enhancing the relearning of lost functions.

Aged↗
PubMed2006

Magnesium for acute traumatic brain injury.

BACKGROUND: Acute traumatic brain injury is a leading cause of death and disability in young adults. Magnesium had been considered as a potential therapeutic tool because of its activity on NMDA-receptors, calcium channels and neuron membranes. Animals studies have indicated a beneficial effect of magnesium on outcome after brain injury, but its efficacy in humans is unknown. OBJECTIVES: To quantify the effect of magnesium administration on mortality and morbidity in patients with acute traumatic brain injury. SEARCH STRATEGY: We searched the Cochrane Injuries Group's specialised register, Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, National Research Register, Current Controlled Trials, SIGLE, LILACS, Zetoc. The searches were conducted in July 2005. SELECTION CRITERIA: We included all randomized controlled trials comparing any magnesium salt with no magnesium or with placebo, in patients following acute traumatic brain injury. DATA COLLECTION AND ANALYSIS: Two authors independently screened search results and assessed the full texts of potentially relevant studies for inclusion. Data were extracted and methodological quality was examined. MAIN RESULTS: Three studies met the inclusion criteria, one of which is an ongoing study. Two studies were included in the analysis. No data on mortality were available. For Glasgow Outcome Score at six months the pooled WMD = 0.55 (95% CI -0.15 to 1.26), P = 0.12. AUTHORS' CONCLUSIONS: There is currently no evidence to support the use of magnesium salts in patients with acute traumatic brain injury.

Acute Disease↗
PubMed2002

Decompressive surgery in the treatment of traumatic brain injury.

According to European Brain Injury Consortium (EBIC) and American Brain Injury Consortium (ABIC) guidelines for severe head injuries, decompressive craniectomy is one therapeutic option for brain edema that does not respond to conventional therapeutic measures. As a result of the failure of all recently developed drugs to improve outcome in this patient group, decompressive craniectomy has experienced a revival during the last decade. Although class I studies of this subject are still lacking, there is strong evidence from prospective, uncontrolled trials that such an operation improves outcome in general and also has beneficial effects on various physiologic parameters that are known to be independent predictors for poor outcome. Whether this operation should be performed in a protocol-driven or in a prophylactic manner remains unclear. Decompressive craniectomy may, however, be the only method available in developing countries with limited ICU and monitoring resources. Prospectively controlled and randomized studies to definitively evaluate the effect of this old neurosurgical method on outcome in patients with traumatic brain injury (TBI) are forthcoming.

Brain Edema↗
PubMed1997

Effects of brain injury on college academic performance.

Brain injury, a leading cause of mortality, morbidity and disability in the United States, has serious consequences and substantial costs. Although previous studies have assessed a variety of outcomes subsequent to brain injury, documentation of performance prior to brain injury using a case-control approach has not been included; preinjury performance differences may confound the estimate of the effects of brain injury on performance. The primary objective of this study was to compare academic performance before and after brain injury in a population of university undergraduate students to determine the extent to which the academic career of the brain-injured person was altered from what would have been expected in the absence of such an injury. Cases included all undergraduate students in a major university, between the ages of 17 and 27, who incurred a brain injury requiring hospitalization between 1980 and 1984 (n = 99). Two comparison groups were used to determine whether changes in academic performance were specifically related to brain injuries or injuries in general: (1) injured controls, i.e. 121 students between the ages of 17 and 27 years, hospitalized for injuries other than to the central nervous system, and (2) uninjured academic controls, i.e. 198 students with out injuries requiring hospitalization during the study period, matched 2:1 to the brain-injured students by age, gender, and completed course credits categorized as < 90, > or = 90. Although there were no differences when the total groups, including both males and females, were compared, there was a significant pre- to postinjury decrease in the grade point average for female cases when compared to their uninjured academic controls (p < 0.02). This difference was related to the effects of brain injury, and not to the effects of injury in general. No such difference was observed for the males. There were also no differences when the total groups, including males and females, were compared relevant to return to school. However, a significantly higher proportion of the female cases, compared with their uninjured academic controls, did not return to school after their injury; similar findings were identified for the injured controls as well. Thus, these differences were not specific to brain injury but rather to injury in general. In spite of this observation, the difference between female cases who returned and those who did not return was associated with neurological deficits, especially upper left limb motor deficits, as the time of hospital discharge. The findings from this effort are suggestive of gender differences in the consequences of brain injury and serve as a basis for further studies to evaluate the magnitude of this problem.

Adolescent↗
PubMed1993

The association of leukocytes with secondary brain injury.

Shock increases mortality from brain injuries, but the mechanism is poorly understood. We hypothesized that brain injury followed by shock and resuscitation leads to a secondary reperfusion injury mediated in part by polymorphonuclear leukocytes (PMNs). To validate this hypothesis, we studied cerebral perfusion pressure (CPP), intracranial pressure (ICP), cerebral blood flow (CBF), cortical water content (CWC), and hemodynamic variables in a porcine model of focal cryogenic brain injury and hemorrhagic shock. Cerebral PMN accumulation (CPMN) in the injured and uninjured hemispheres was determined histologically from the total PMNs in five high-power fields (400x). Twenty-nine mature swine were randomized to four groups. Group 1, the control group, was instrumented only. Group 2 animals had a brain injury alone and were studied for 24 hours. Group 3 animals had a brain injury and hemorrhagic shock. Group 4 animals had hemorrhagic shock alone. Brain injury followed by shock caused a significantly greater ICP and a significantly lower CBF than brain injury or shock alone. There was no significant difference in CPP between groups after resuscitation. The CWC of the lesioned area was similar in both brain-injured groups but was significantly increased when compared with the controls and the shock-only group. The CWC of the nonlesioned hemisphere was higher in group 3 than in group 2. The CPMN in both hemispheres in group 3 was significantly greater than in either group 2 or group 4. There was a significant positive correlation between CPMN and both ICP and CWC, and a significant negative correlation between CPMN and CBF. These data suggest an association between CPMN accumulation and secondary brain injury.

Animals↗
PubMed1995

Enhanced vulnerability to secondary ischemic insults after experimental traumatic brain injury.

Both experimental traumatic brain injury and clinical traumatic brain injury appear to render the brain more vulnerable to a second ischemic insult. The mechanisms of enhanced vulnerability to subsequent ischemia appear to include a reduced ability to increase cerebral blood flow in response to hypotension, hypoxemia, or acute anemia and increased tissue sensitivity to ischemia. Although numerous mediators may be involved in increased tissue sensitivity, those that particularly merit investigation include oxygen free radicals, glutamate, arachidonate metabolites, calcium ions, and protein kinase C.

Animals↗
PubMed1999

Physiatric management of mild traumatic brain injury.

Mild traumatic brain injury (MTBI) is a common condition, afflicting as many as 1.5 million Americans yearly. Most individuals sustain MTBI as a result of motor vehicle collisions, but it may also occur as a result of falls, physical assault or sporting accidents. Problems related to MTBI include various pain syndromes, cognitive impairments, disorders of affect, cranial nerve dysfunction, and vertigo, arising from injury to the brain, head, or cervical spine. Symptoms are usually transient, although a small percentage of afflicted individuals develop long-lasting problems, often preventing them from leading productive lives. Recognition of these problems as arising from MTBI is difficult due to the frequent lack of abnormal findings on diagnostic tests and failure to identify a history of head trauma. The American Congress of Rehabilitation Medicine has defined MTBI, an important first step in identifying individuals who need treatment. Diagnosis is usually made by directed questions regarding trauma history and careful procurement and interpretation of appropriate tests. Once a diagnosis is made, proper care can be prescribed in order to lead patients toward more productive lives.

Brain Injuries↗
PubMed2005

Proton MR spectroscopic imaging depicts diffuse axonal injury in children with traumatic brain injury.

BACKGROUND AND PURPOSE: Diffuse axonal injury (DAI) after traumatic brain injury (TBI) is important in patient assessment and prognosis, yet they are underestimated with conventional imaging techniques. We used MR spectroscopic imaging (MRSI) to detect DAI and determine whether metabolite ratios are accurate in predicting long-term outcomes and to examine regional differences in injury between children with TBI and control subjects. METHODS: Forty children with TBI underwent transverse proton MRSI through the level of the corpus callosum within 1-16 days after injury. T2-weighted, fluid-attenuated inversion recovery, and susceptibility-weighted MR imaging was used to identify voxels as normal-appearing or as nonhemorrhagic or hemorrhagic injury. Neurologic outcome was evaluated at 6-12 months after injury. Metabolite ratios for total (all voxels), normal-appearing, and hemorrhagic brain were compared and used in a logistic regression model to predict long-term outcome. Total and regional metabolite ratios were compared with control data. RESULTS: A significant decrease in N-acetylaspartate (NAA)/creatine (Cr) and increase in choline (Cho)/Cr (evidence of DAI) was observed in normal-appearing (P < .05) and visibly injured (hemorrhagic) brain (P < .001) compared with controls. In normal-appearing brain NAA/Cr decreased more in patients with poor outcomes (1.32 +/- 0.54) than in those with good outcomes (1.61 +/- 0.50, P = .01) or control subjects (1.86 +/- 0.1, P = .00). In visibly injured brains, ratios were similarly altered in all patients. In predicting outcomes, ratios from normal-appearing and visibly-injured brain were 85% and 67% accurate, respectively. CONCLUSION: MRSI can depict injury in brain that appears normal on imaging and is useful for predicting long-term outcomes.

Adolescent↗
PubMed1986

Brain injury improves survival of mice following brain ischemia.

Minor brain injury was inflicted with a small needle at 4 sites one week before the production of incomplete brain ischemia in the mouse. A bilateral carotid clamp was applied for 60 min under pentobarbital anesthesia, and the number of survivors at one week after the ischemic insult was compared with those in animals anesthetized only and those in a sham-operated group. The number of survivors in the brain-injured group was significantly higher than in the other two groups. The results suggest that anti-ischemic factors are released by the injured brain or that certain unknown protective mechanisms against ischemia become active following brain injury.

Anesthesia, General↗
PubMed2004

Effect of zolpidem on brain injury and diaschisis as detected by 99mTc HMPAO brain SPECT in humans.

The study investigates the effect of zolpidem (CAS 82626-48-0) on brain injuries and cerebellar diaschisis. Four patients with varied brain injuries, three of them with cerebellar diaschisis, were imaged by 99mTc HMPAO Brain SPECT before and after application of zolpidem. The baseline SPECT before zolpidem showed poor tracer uptake in brain injury areas and cerebellar diaschisis. After zolpidem, cerebral perfusion through brain injury areas improved substantially in three patients and the cerebellar diaschisis was reversed. Observations point to a GABA based phenomenon that occurs in brain injury and diaschisis that is reversible by zolpidem.

Adult↗
PubMed2001

Estrogen receptor alpha, not beta, is a critical link in estradiol-mediated protection against brain injury.

Estradiol protects against brain injury, neurodegeneration, and cognitive decline. Our previous work demonstrates that physiological levels of estradiol protect against stroke injury and that this protection may be mediated through receptor-dependent alterations of gene expression. In this report, we tested the hypothesis that estrogen receptors play a pivotal role in mediating neuroprotective actions of estradiol and dissected the potential biological roles of each estrogen receptor (ER) subtype, ER alpha and ER beta, in the injured brain. To investigate and delineate these mechanisms, we used ER alpha-knockout (ER alpha KO) and ER beta-knockout (ER beta KO) mice in an animal model of stroke. We performed our studies by using a controlled endocrine paradigm, because endogenous levels of estradiol differ dramatically among ER alpha KO, ER beta KO, and wild-type mice. We ovariectomized ER alpha KO, ER beta KO, and the respective wild-type mice and implanted them with capsules filled with oil (vehicle) or a dose of 17 beta-estradiol that produces physiological hormone levels in serum. One week later, mice underwent ischemia. Our results demonstrate that deletion of ER alpha completely abolishes the protective actions of estradiol in all regions of the brain; whereas the ability of estradiol to protect against brain injury is totally preserved in the absence of ER beta. Thus, our results clearly establish that the ER alpha subtype is a critical mechanistic link in mediating the protective effects of physiological levels of estradiol in brain injury. Our discovery that ER alpha mediates protection of the brain carries far-reaching implications for the selective targeting of ERs in the treatment and prevention of neural dysfunction associated with normal aging or brain injury.

Animals↗
PubMed2002

Intermediate and long-term outcome in traumatic brain injury is not influenced by additional multiple organ injury.

BACKGROUND: This investigation aims at evaluating the influence of additional multiple organ injury in traumatic brain injury on the outcome in terms of the ability to perform the activities of daily life, of the need of care, and of job ability. METHODS: 62 victims (male to female ratio 4 : 1; age range 15-68 years) of traumatic brain injury were studied. Group 1 (n = 24) consisted of patients who suffered from traumatic brain injury with additional multiple organ injury, group 2 (n = 38) comprised patients with isolated brain injury. Outcome was assessed at 6 and 12 months after trauma by means of different rehabilitation scores. RESULTS: After 6 as well as after 12 months, the majority of both groups were independent in the activities of daily living. Furthermore, no differences were observed concerning the need of care. Job ability was almost equal for both groups. CONCLUSION: Additional multiple organ injury does not pertain to prognosis of traumatic brain injury.

Activities of Daily Living↗
PubMedDate not supplied

Classification of the spectrum of mild traumatic brain injury.

Mild traumatic brain injury (TBI) is a very common injury, resulting in immediate and possible long-term symptoms. The accurate and consistent definition of mild TBI is important in the initial and rehabilitation management of the injury, and in research concerning mild TBI. A definition of mild TBI has been developed by the Head Injury Interdisciplinary Special Interest Group of the American Congress of Rehabilitation Medicine. Within the spectrum of injury severity in mild TBI there are several classification systems, primarily used in management of acute mild TBI, that breakdown mild TBI into grades of injury severity. These are based upon the presence or absence of mental status changes, amnesia, loss of consciousness, anatomical lesion or neurological deficit.

Athletic Injuries↗
PubMed2002

Pre-injury status and adaptation following traumatic brain injury.

There are an estimated two million traumatic brain injuries (TBI) each year in the US. Behavioural and psychosocial sequelae are the most disabling consequences of TBI, but relatively little empirical data exist that identify factors underlying the variability in patient outcomes. There is an increasing appreciation that pre-injury coping liabilities are likely to contribute to persistent disability and that outcome reflects the combined effects of pre-morbid, injury-related, and post-injury factors. Despite this, most outcome studies focus on the effects of injury-related and post-injury variables. The present study evaluated outcome in 45 adults who suffered a moderate or severe TBI at least 2 years earlier. It was hypothesized that severity of pre-morbid psychiatric and substance abuse problems and less social support following brain injury would be associated with poorer post-injury adaptation as measured by employment status, independent living status, and neurobehavioural symptomatology. The authors found that pre-injury psychiatric and substance abuse histories predicted employment status and that pre-injury substance abuse predicted independent living status. Social support following TBI predicted significant other's assessment of the patients' neurobehavioural status. None of the independent variables were found to predict patient assessment of his or her own neurobehavioural functioning. These findings support the premise that pre-morbid coping liabilities are related to the degree of post-injury disability.

Activities of Daily Living↗
PubMed2006

Impaired fibrinolysis and traumatic brain injury in mice.

Traumatic brain injury (TBI) has been associated with intravascular coagulation, which may be a result of thromboplastin released following brain injury. Clots thus formed are lysed by plasmin, which is activated by tissue-type and urokinase-type plasminogen activators (uPA). To evaluate the association between traumatic intravascular coagulation and post-traumatic outcome, uPA knockout (uPA-/-) transgenic mice (n=12) or wild-type littermates (WT; n=12) were anesthetized and subjected to controlled cortical impact (CCI) brain injury. A second group of uPA-/- (n=12) and WT mice (n=12) were subjected to sham injury. Motor function was assessed over 2 weeks using the composite neuroscore test and cognition (learning) was assessed with the Morris Water Maze (MWM) at 2 weeks post-injury, whereupon the animals were sacrificed for cortical lesion volume analysis. Motor function was significantly worse in the brain-injured uPA-/- mice when compared to brain-injured WT mice at 48 h (p<0.05) and one week post-injury (p<0.05). These differences resolved by 2 weeks post-injury. There was no significant difference in post-injury cognitive function between uPA-/- mice and WT mice. However, at 2 weeks post-injury, the brain-injured uPA-/- had a significantly larger volume of cortical tissue loss than their WT counterparts (p<0.05). These results demonstrate that the absence of uPA in mice aggravates acute motor deficit and exacerbates cortical tissue loss following CCI brain injury, and suggests a neuroprotective role of the fibrinolytic process following TBI.

Animals↗