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PubMed2003

The current status and problems of rehabilitation for TBI (traumatic brain injury) patients in Japan.

Recently, traumatic brain injury (TBI) is one of the major topics of rehabilitation medicine. In the USA, a nationwide research project has already been underway since 1987. However, interest in the rehabilitation of TBI patients became a matter of concern in Japan from the 1990s. TBI patients do not only have physical impairments, but also impairments of higher cortical functions such as cognitive impairment and abnormal behavior, so both physical and cognitive rehabilitation are very important for TBI patients. The purpose of this paper is to report on the current status of and problems with TBI rehabilitation in Japan, and also to introduce a new TBI evaluation system that we originally developed in Japan.

Brain Injuries↗

PubMedDate not supplied

Hyponatremia-associated cognitive impairment in traumatic brain injury.

The case of a traumatic brain injury (TBI) patient with dramatic cognitive deterioration in the absence of medical aetiology other than simultaneous decline in serum sodium led to an investigation of the association between declines in sodium levels and cognitive status. In a population of 50 persons undergoing TBI rehabilitation, 12 (24%) had relative (3 mEq/L) decreases in serum sodium while five (10%) experienced absolute hyponatremia (136 mEq/L). Correlation with cognitive status was significant when the absolute hyponatremia group was compared with those whose sodium levels remained above 136 mEq/L. A case-matched study of the relative hyponatremia group yielded no significant association between sodium-level decreases and cognitive status. These data support previous conclusions indicating wide variation in individual responses to changes in serum sodium. The threshold for significant effects of hyponatremia may be higher in patients with TBI than in populations studied previously.

Bicycling↗

PubMed1994

After traumatic brain injury: a discussion of consequences.

Traumatic brain injury is followed by many changes in cognition, emotion, social interaction and functioning, and communication. These changes may range from severe to subtle. They create complex difficulties for the individual and his or her network of support. Presented here is a review of the literature on the changes and their impact. The review comprises Part I, on brain injury and its effects, and Part II, on social interaction research.

Adolescent↗

PubMed1995

A profile of outcome: 2 years after traumatic brain injury.

A group of 175 traumatic brain injury (TBI) patients who had undergone intensive rehabilitation at Bethesda Hospital attended a follow-up interview 2 years after injury. The majority of patients had suffered severe TBI. Outcome was documented in ten areas: medical/physical, mobility, activities of daily living (ADLs) accommodation, marital status, leisure and recreation, employment/study, communication, cognition and behaviour. Whilst most patients were physically independent and competent in personal and domestic activities of daily living, a third of the group were still reliant on assistance with community skills and transport, and more than half of those who previously had a job, were not working at 2 years post-injury. Around two-thirds of the sample reported cognitive, behavioural and emotional changes. There is clearly a need for ongoing community-based support and assistance in dealing with practical difficulties and psychological problems as they are experienced after return to the community.

Activities of Daily Living↗

PubMed2005

Effect of atorvastatin on spatial memory, neuronal survival, and vascular density in female rats after traumatic brain injury.

OBJECT: Atorvastatin administered after traumatic brain injury (TBI) induced by controlled cortical impact promotes functional improvement in male rats. Note, however, that parallel studies have not been performed in female rats. Therefore, the authors tested the effect of atorvastatin on TBI in female rats. METHODS: Atorvastatin (1 mg/kg/day) was orally administered for 7 consecutive days in female Wistar rats starting I day after TBI; control animals received saline. Modified neurological severity scores, the corner turn test, and the Morris water maze test were used to evaluate functional response to treatment. Rats were killed on Day 15 post-TBI, and brain tissue samples were processed for immunohistochemical staining. Atorvastatin administration after brain injury significantly promoted the restoration of spatial memory but did not reduce sensorimotor functional deficits. Treatment of TBI with atorvastatin increased neuronal survival in the CA3 region and the lesion boundary zone and prevented the loss of neuronal processes of damaged neurons in the hippocampal CA3 region but not in the lesion boundary zone on Day 15 after TBI. The protective effect of atorvastatin on the injured neurons perhaps is mediated by increasing the density of vessels in the lesion boundary zone and the hippocampus after TBI. CONCLUSIONS: . These data indicate that atorvastatin is beneficial in the treatment of TBI in female rats, although the effect may differ between sexes.

Administration, Oral↗

PubMed2001

MR imaging, single-photon emission CT, and neurocognitive performance after mild traumatic brain injury.

BACKGROUND AND PURPOSE: Mild traumatic brain injury (mTBI) (Glasgow Coma Scale = 14-15) is a common neurologic disorder and a common cause of neurocognitive deficits in the young population. Most patients recover fully from mTBI, but 15% to 29% of patients have persistent neurocognitive problems. Although a partially organic origin is considered likely, little brain imaging evidence exists for this assumption. The aims of the present study were to establish the prevalence of posttraumatic lesions in mTBI patients on MR images and to assess the relation between these imaging findings and posttraumatic symptoms. Secondly, we explored the value of early posttraumatic single-photon emission CT (SPECT) for the evaluation of mTBI. METHODS: Twenty-one consecutive patients were included in the study. Patients underwent MR examination, technetium-99m hexamethylpropylene amine oxime SPECT, and neurocognitive assessment within 5 days after injury. Neurocognitive follow-up was conducted 2 and 6 months after injury, and MR imaging was repeated after 6 months. Lesion size and brain atrophy were measured on the MR studies. RESULTS: Twelve (57%) of 21 patients had abnormal MR findings, and 11 (61%) of 18 had abnormal SPECT findings. Patients with abnormal MR or SPECT findings had brain atrophy at follow-up. The mean neurocognitive performance of all subjects was within normal range. There was no difference in neurocognitive performance between patients with normal and abnormal MR findings. Patients with abnormal MR findings only showed significantly slower reaction times during a reaction-time task. Seven patients had persistent neurocognitive complaints and one patient met the criteria for a postconcussional syndrome. CONCLUSION: Brain lesions are common after mTBI; up to 77% of patients may have abnormal findings either on MR images or SPECT scans, and these lesions may lead to brain atrophy. The association between hypoperfusion seen on acute SPECT and brain atrophy after 6 months suggests the possibility of (secondary) ischemic brain damage. There is only a weak correlation between neuroimaging findings and neurocognitive outcome.

Adolescent↗

PubMed1987

The clinical significance of cerebral atrophy in traumatic brain injury.

The neuropsychological effects of traumatic brain injury (TBI) as they relate to the chronic neuropathological chang.es of cortical atrophy and ventricular enlargement are reviewed. Computerized tomography (CT) and magnetic resonance imaging (MRI) methods are excellent at detecting many of these changes and results from these diagnostic methods should be incorporated in the interpretation of neuropsychological outcome in TBI patients. Several Clinical guidelines are presented on the relationship between TBI induced atrophy and neurobehavioral outcome.

Journal Article↗

PubMed2005

The epidemiology of traumatic brain injury in Wisconsin, 2001.

PROBLEM: Traumatic brain injury (TBI) is a leading cause of death and disability in the United States. To implement more effective injury prevention and treatment programs, it is important to identify the regional impact, causes, risk factors, and trends of TBI. This report summarizes the public health impact of TBI in Wisconsin. METHODS: Data on fatal and non-fatal TBI injuries in Wisconsin in 2001 were obtained from 2 separate data sources: National Center for Vital Statistics and the Wisconsin Bureau for Health Information. Rates of fatal and nonfatal TBI were calculated using 2000 population estimates as denominators. RESULTS: There were 1059 TBI fatalities and 4006 living TBI-related hospital discharges in Wisconsin in 2001. The overall rate of TBI in Wisconsin for 2001 was 94.4 per 100,000 people. The number of fatal and nonfatal TBI related injuries was higher for males than females, at all ages, except nonfatal injuries in persons older than 65 years. Fatalities from TBI were highest in young adults and the elderly. CONCLUSIONS: TBI is a major cause of death and hospitalizations in Wisconsin. Male teens and young adults, and the elderly are high-risk groups for TBI. Preventive measures should be aimed at these high-risk groups.

Adolescent↗

PubMed2006

The influence of neuropsychological characteristics on the use of CI therapy with persons with traumatic brain injury.

The great prevalence of traumatic brain injury (TBI) and its high economic costs make reducing TBI-related disability a national health care priority. In our research laboratory, CI therapy has been found to significantly improve upper extremity function for persons with chronic TBI. The results have suggested that persons with TBI are less likely to adhere to critical components of the CI therapy protocol than participants with stroke in other studies. Treatment outcomes have also been more variable. Our findings suggest that some cognitive skills appear related to treatment outcome. In addition, cognitive and behavioral deficits, commonly seen with participants with TBI, challenge the delivery of the standard CI therapy protocol with some persons. We discuss the implications of these neuropsychological factors for CI therapy used for chronic TBI and propose further research to more thoroughly investigate these issues.

Adult↗

PubMedDate not supplied

Neuropsychiatric sequelae of traumatic brain injury.

The authors review the psychiatric disturbances associated with traumatic brain injury. They highlight the close link between traumatic brain injury and psychiatry and provide an overview of the epidemiology, risk factors, classification, and mechanisms of traumatic brain injury. They describe various neuropsychiatric sequelae, and the respective treatments are outlined with emphasis on a multidisciplinary approach.

Brain Injuries↗

PubMed1998

A population-based study of seizures after traumatic brain injuries.

BACKGROUND: The risk of seizures is increased after traumatic brain injury, but the extent and duration of the increase in risk are unknown. The purpose of this study was to identify the characteristics of brain injuries that are associated with the development of seizures. METHODS: We identified 4541 children and adults with traumatic brain injury (characterized by loss of consciousness, post-traumatic amnesia, or skull fracture) in Olmsted County, Minnesota, during the period from 1935 through 1984. Injuries were classified as mild (loss of consciousness or amnesia lasting less than 30 minutes), moderate (loss of consciousness for 30 minutes to 24 hours or a skull fracture), or severe (loss of consciousness or amnesia for more than 24 hours, subdural hematoma, or brain contusion). We compared the incidence of new unprovoked seizures in this cohort with population rates, using standardized incidence ratios and Cox proportional-hazards analysis. RESULTS: The overall standardized incidence ratio was 3.1 (95 percent confidence interval, 2.5 to 3.8). The standardized incidence ratio was 1.5 (95 percent confidence interval, 1.0 to 2.2) after mild injuries but with no increase over the expected number after five years, 2.9 (95 percent confidence interval, 1.9 to 4.1) after moderate injuries, and 17.0 (95 percent confidence interval, 12.3 to 23.6) after severe injuries. In the multivariate analysis, significant risk factors for later seizures were brain contusion with subdural hematoma, skull fracture, loss of consciousness or amnesia for more than one day, and an age of 65 years or older. CONCLUSIONS: The increased risk of seizures after traumatic brain injury varies greatly according to the severity of the injury and the time since the injury.

Adolescent↗

PubMed2005

Gender associations with cerebrospinal fluid glutamate and lactate/pyruvate levels after severe traumatic brain injury.

OBJECTIVE: Female sex hormones appear to be neuroprotective after traumatic brain injury by attenuating multiple mechanisms of secondary insult, including excitotoxicity and ischemia. The purpose of this study was to evaluate associations between gender and cerebrospinal fluid glutamate and lactate/pyruvate production and the role of hypothermia with gender in attenuating these markers. DESIGN: Prospectively collected data were analyzed for adult patients with severe traumatic brain injury. Gender comparisons for cerebrospinal fluid glutamate and lactate/pyruvate production were determined using ventricular samples obtained over the first 48 hrs postinjury. SETTING: University-based level I trauma center. PATIENTS: There were 123 patients, male n = 93 and female n = 30 (n = 686 cerebrospinal fluid samples), with severe traumatic brain injury (Glasgow Coma Scale score < or =8). INTERVENTIONS: A portion of these patients were part of a randomized controlled trial evaluating the effect of (48 hrs) therapeutic hypothermia after severe traumatic brain injury. The remainder received hypothermia (24 hrs) if they met clinical care criteria. Patients were cooled to 32-33 degrees C (within approximately 8 hrs) for either 24 or 48 hrs and then were rewarmed or remained normothermic. MEASUREMENTS AND MAIN RESULTS: Regression analyses using generalized estimating equations for repeated measures showed significant increases in cerebrospinal fluid glutamate production for males compared with females (p = .0023) and a significant interaction between glutamate concentration, gender, and time (p = .0035) by 24 hrs postinjury. Females had lower lactate/pyruvate ratios than males (p = .0006), and there was a significant interaction between lactate/pyruvate, gender, and time (p = .0045) throughout the first 48 hrs postinjury. Hypothermia attenuated glutamate levels, particularly for males, over the time course studied. CONCLUSIONS: These data suggest significant gender differences with glutamate and lactate/pyruvate production after severe traumatic brain injury. Gender- and hormone-mediated differences in central nervous system pathophysiology should be considered with clinical trials in traumatic brain injury.

Adult↗

PubMed2006

Monoaminergic agonists for acute traumatic brain injury.

BACKGROUND: Although there have been considerable gains in understanding the cascade of events that lead to secondary injury after traumatic brain injury (TBI), efforts to translate this understanding into new therapeutic, so-called neuroprotective approaches, have so far proven disappointing. As an alternative, there is growing interest in approaches to enhance brain repair after injury. Animal models suggest that agents enhancing monoaminergic (MA) transmission, particularly amphetamines, promote motor recovery from focal brain injury and it is proposed that this might represent a complementary means of therapeutic intervention in the later post-injury phase. OBJECTIVES: To evaluate the evidence that MAs improve final outcome after TBI. SEARCH STRATEGY: We searched CENTRAL (The Cochrane Library, Issue 2, 2005), the Cochrane Injuries Group's Specialised Register (to May 2005), MEDLINE (1966 to May 2005), EMBASE (1980 to May 2005) and the Science Citation Index (1992 to June 2005). We contacted researchers and authors of published and unpublished trials. Searches were updated in May 2005. SELECTION CRITERIA: Randomised controlled trials comparing the use of a MA (together with conventional non-pharmacological rehabilitative therapy) versus conventional non-pharmacological rehabilitative therapy alone. DATA COLLECTION AND ANALYSIS: Two authors independently screened records, extracted data and assessed trial quality. MAIN RESULTS: Although there is a limited clinical literature addressing this topic, none of the studies identified fully met inclusion criteria for this review. AUTHORS' CONCLUSIONS: At present there is insufficient evidence to support the routine use of MAs to promote recovery after TBI.

Acute Disease↗

PubMed2002

Acute systemic administration of interleukin-10 suppresses the beneficial effects of moderate hypothermia following traumatic brain injury in rats.

Traumatic injury to the central nervous system initiates inflammatory processes such as the synthesis of proinflammatory mediators that contribute to secondary tissue damage. Hence, administration of anti-inflammatory cytokines, such as interleukin-10 (IL-10) may be neuroprotective. Moderate hypothermia (30-32 degrees C) also decreases the pro-inflammatory response to traumatic brain injury (TBI). Thus, we hypothesized that the combination of IL-10 and hypothermia would provide synergistic neuroprotective effects after TBI. To test this hypothesis, fifty isoflurane-anesthetized rats underwent a controlled cortical impact (2.7 mm tissue deformation at 4 m/s) or sham injury and then were randomly assigned to one of five conditions (TBI/VEH Normothermia (37 degrees C), TBI/VEH Hypothermia (32 degrees C for 3 h), TBI/IL-10 Normothermia, TBI/IL-10 Hypothermia, and Sham/VEH Normothermia). Human IL-10 (5 microg) or VEH was administered (i.p.) 30 min after surgery. Function was assessed by established motor and cognitive tests on post-operative days 1-5 and 14-18, respectively. Cortical lesion volume and hippocampal CA(1)/CA(3) cell survival were quantified at 4 weeks. Brain sections from 15 additional rats were immunohistochemically assessed (MoAB RP-3) to determine neutrophil accumulation at 5 h after TBI. The administration of IL-10 after TBI produced an approximately 75% reduction in the number of RP-3-positive cells in both the normothermic and hypothermic groups vs. the normothermic vehicle-treated group (P<0.05), but did not improve functional outcome. In contrast, hypothermia alone enhanced both motor and cognitive function and increased CA(3) neuronal survival after TBI. Contrary to our hypothesis, systemic administration of IL-10 combined with hypothermia did not provide synergistic neuroprotective effects after TBI. Rather, IL-10 administration suppressed the beneficial effects produced by hypothermia alone after TBI. The mechanism(s) for the negative effects of IL-10 combined with hypothermia after TBI remain to be determined.

Animals↗

PubMedDate not supplied

Fever of unknown origin following traumatic brain injury.

Fever is a common complication of a traumatic brain injury, occurring during both the acute-care phase and the rehabilitation phase of recovery. The aetiology of fever in this population may remain obscure because of the presence of cognitive confusion associated with post-traumatic amnesia interfering with history taking and the difficult physical examination. We present a case where recovery from a traumatic brain injury was complicated by a fever of unknown origin that proved to be secondary to lateral sinus thrombophlebitis. This case emphasises the importance of a thorough knowledge of the differential diagnosis for fever that is unique to the traumatic brain injury population.

Adult↗

PubMed2001

Excitatory amino acid concentrations in ventricular cerebrospinal fluid after severe traumatic brain injury in infants and children: the role of child abuse.

BACKGROUND: Excitotoxicity is an important mechanism in secondary neuronal injury after traumatic brain injury (TBI). Excitatory amino acids (EAAs) are increased in cerebrospinal fluid (CSF) in adults after TBI; however, studies in pediatric head trauma are lacking. We hypothesized that CSF glutamate, aspartate, and glycine would be increased after TBI in children and that these increases would be associated with age, child abuse, poor outcome, and cerebral ischemia. METHODS: EAAs were measured in 66 CSF samples from 18 children after severe TBI. Control samples were obtained from 19 children who received lumbar punctures to rule out meningitis. RESULTS: Peak and mean CSF glycine and peak CSF glutamate levels were increased versus control values. Subgroups of patients with TBI were compared by using univariate regression analysis. Massive increases in CSF glutamate were found in children <4 years old and in child abuse victims. Increased CSF glutamate and glycine were associated with poor outcome. A trend toward an association between high glutamate concentration and ischemic blood flow was observed. CONCLUSIONS: CSF EAAs are increased in infants and children with severe TBI. Young age and child abuse were associated with extremely high CSF glutamate concentrations after TBI. A possible role for excitotoxicity after pediatric TBI is supported.

Adolescent↗

PubMed2000

The rehabilitation of attention in individuals with mild traumatic brain injury, using the APT-II programme.

Traumatic brain injury (TBI) is a prevalent cause of cognitive impairments and dysfunctions and affects over 2 million individuals each year. Mild traumatic brain injury (MTBI) is generally defined by a brief loss of consciousness, and post-traumatic amnesia that lasts for less than 24 hours. One region of the brain that is likely affected in patients with MTBI is the pre-frontal cortex. This region mediates several functions, including those required for adequate attention. Three individuals, diagnosed with MTBI and difficulties with attention, volunteered to participate in the study. Individuals were presented with 10 weeks of cognitive retraining with the Attention Process Training-II (APT-II) programme, followed by 6 or 7 weeks of educational and applicational programmes. Cognitive tests were administered both pre- and post-training to assess the effectiveness of the programme. Analysis of the results showed that the APT-II programme improved attention and performance speed in each of the three individuals. In addition, any rehabilitated cognitive skills remained stable in each individual in the absence of the rehabilitation programme for at least 6 weeks.

Adult↗

PubMedDate not supplied

Update of neuropathology and neurological recovery after traumatic brain injury.

This review focuses on the potential for traumatic brain injury to evoke both focal and diffuse changes within the brain parenchyma, while considering the cellular constituents involved and the subcellular perturbations that contribute to their dysfunction. New insight is provided on the pathobiology of traumatically induced cell body injury and diffuse axonal damage. The consequences of axonal damage in terms of subsequent deafferentation and any potential retrograde cell death and atrophy are addressed. The regional and global metabolic sequelae are also considered. This detailed presentation of the neuropathological consequences of traumatic brain injury is used to set the stage for better appreciating the neurological recovery occurring after traumatic injury. Although the pathological and clinical effects of focal and diffuse damage are usually intermingled, the different clinical manifestations of recovery patterns associated with focal versus diffuse injuries are presented. The recognizable patterns of recovery, involving unconsciousness, posttraumatic confusion/amnesia, and postconfusional restoration, that typically occur across the full spectrum of diffuse injury are described, recognizing that the patient's long-term recovery may involve more idiosyncratic combinations of dysfunction. The review highlights the relationship of focal lesions to localizing syndromes that may be embedded in the evolving natural history of diffuse pathology. It is noted that injuries with primarily focal pathology do not necessarily follow a comparable pattern of recovery with distinct phases. Potential linkages of these recovery patterns to the known neuropathological sequelae of injury and various reparative mechanisms are considered and it is proposed that potential biological markers and newer imaging technologies will better define these linkages.

Brain Injuries↗