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PubMed1995

Pharmacologic therapy for traumatic brain injury: experimental approaches.

An important feature of traumatic brain injury is that much of the ultimate damage appears to occur in a delayed or secondary fashion. Although the exact timing of these secondary sequelae has yet to be elucidated, recent experimental evidence suggests that an extended window of opportunity exists during which various forms of therapy appear to be efficacious. Moreover, new therapies have been developed which can be targeted at distinct pathophysiologic aspects of brain trauma. This article summarizes recent efforts to define secondary mechanisms of brain trauma and review the development of therapeutic strategies for reversing these deleterious events.

Animals↗

PubMed1997

Apoptosis-suppressor gene bcl-2 expression after traumatic brain injury in rats.

Neuronal death after experimental traumatic brain injury (TBI) has features of both apoptosis and necrosis. Neurons in the peritrauma cortex, hippocampus, and dentate gyrus are particularly vulnerable. The apoptosis-suppressor gene bcl-2 is induced in brain after ischemia and epilepsy-induced injury and may serve to regulate neuronal death. We studied expression of bcl-2 mRNA and protein after experimental TBI in rats. To determine whether bcl-2 protein expression occurred in cells with evidence of apoptosis, triple-labeling studies were performed using (1) antibody against bcl-2, (2) bis-benzimide dye to examine gross nuclear morphology, and (3) terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick-end labeling (TUNEL) to assess for DNA fragmentation. At 6 and 24 hr, bcl-2 mRNA was induced in ipsilateral peritrauma cortex, hippocampus, and dentate gyrus. By 72 hr the increase in bcl-2 mRNA was detected only in cortex. bcl-2 protein was induced at 8, 24, 72, and 168 hr in ipsilateral cortex and hippocampus. Cells expressing bcl-2 protein included neurons in the peritrauma cortex, hippocampus, hilus, and dentate gyrus. The gross nuclear morphology of neurons expressing bcl-2 appeared normal. Furthermore, biochemical evidence of DNA fragmentation, in a pattern characteristic of either apoptosis or necrosis, was seldom seen in neurons expressing bcl-2 protein (bcl-2 colocalized with TUNEL in 0-2% of TUNEL-positive cells observed). These data suggest that bcl-2 may play an important role in the regulation of neuronal death after TBI, and they support a role for bcl-2 as an inducible neuroprotective gene.

Animals↗

PubMed2005

Lesional accumulation of P2X4 receptor+ monocytes following experimental traumatic brain injury.

P2X4 receptor (P2X4R) is an ATP-gated ion channel. ATP is an important messenger in traumatic brain injury. Here, we report expression of P2X4R in rat traumatic brain injury with focus on the early phase, most amenable to therapy. Accumulation of P2X4R+ cells was observed as early as 6 h after injury and continued to increase 4 days post-injury at the lesion and remote areas. Double staining revealed that most P2X4R+ cells co-expressed ED-1, a marker for reactive microglia/macrophages, but not nestin or W3/13. Our data suggest that P2X4R expression defines a subtype of activated microglia/macrophages involved in the early processes following traumatic brain injury.

Animals↗

PubMed2000

Traumatic brain injury as a risk factor for Alzheimer's disease: a review.

Accumulating epidemiological evidence implicates traumatic brain injury as a pathogenic agent in the development of Alzheimer's disease (AD). Considering the increase in the prevalence of both traumatic brain injury and AD in recent times, the possibility that brain trauma may provoke the early development of AD has important implications for health service planning, preventative efforts, and medico-legal compensation settlements. This paper evaluates the plausibility of the proposed link between traumatic brain injury and AD, largely by way of exploring a theoretical perspective advanced by Satz (1993) and considering recent contributions from the epidemiological, neuropathological, and biochemical literature that are pertinent to this issue. The literature reviewed provides sufficient support and empirical vindication to give credence to the proposed association between these two neuropsychological entities at the statistical, theoretical, and biological level.

Age of Onset↗

PubMed1991

Delayed presentation of a carotid-cavernous sinus fistula in a patient with traumatic brain injury.

Carotid-cavernous sinus fistulas are rare complications of traumatic brain injury, facial trauma and postorthognathic surgery. A high level of clinical suspicion is necessary, particularly for patients who are unable to communicate, to establish the diagnosis. A case of delayed presentation of a carotid-cavernous sinus fistula after traumatic brain injury is presented. This case illustrates that early recognition of this disorder is crucial to prevent significant morbidity.

Adult↗

PubMed2005

Long-term medical care utilization and costs among traumatic brain injury survivors.

OBJECTIVE: To examine billing patterns and predictors of healthcare utilization and costs associated with traumatic brain injury. DESIGN: Retrospective cohort study of healthcare billings for 63 survivors of traumatic brain injury, over a 19-mo period, using a state-sponsored Medicaid program. The relationship of indicators of injury severity and disability to billings and payments was investigated. Mean age at time of injury was 33 yrs. Mean highest Glasgow Coma Scale rating immediately after brain injury was 8. RESULTS: A total of 795,635 US dollars was billed to Medicaid for 3,950 services and medications used. A total of 281,897 US dollars was paid for these billings out of the Medicaid account studied. Billings were used for statistical analyses, as they were considered the most stable indicator of cost. Motor deficits at discharge from inpatient rehabilitation (FIM motor score) showed inverse relationships to total billings (rho = -0.42, P < 0.001), subcategories of billings reflecting equipment and supplies (rho = -.26, P = 0.020), and outpatient billings (rho = -0.27, P = 0.015). Change in FIM motor scores during inpatient rehabilitation was inversely associated with billings (rho = -0.40). Change in FIM motor scores provided unique information in predicting utilization after accounting for demographic characteristics and severity of injury. CONCLUSIONS: Motor disability and improvement during inpatient rehabilitation were significant predictors of billings after traumatic brain injury. Initial severity of brain injury was not a significant factor in utilization.

Adolescent↗

PubMed2003

Inhibition of neuronal nitric oxide synthase-mediated activation of poly(ADP-ribose) polymerase in traumatic brain injury: neuroprotection by 3-aminobenzamide.

Focal traumatic injury to the cerebral cortex is associated with early activation of the neuronal isoform of nitric oxide synthase (nNOS), where high concentrations of nitric oxide-derived free radicals elicit extensive DNA damage. Subsequent activation of the nuclear repair enzyme poly(ADP-ribose) polymerase (PARP) causes a severe energy deficit leading to the ultimate demise of affected neurons. Little is known about the temporal relationship of nNOS and PARP activation and the neuroprotective efficacy of their selective blockade in traumatic brain injury. To determine the relationship of nNOS and PARP activation, brain injury was induced by cryogenic lesion to the somatosensory cortex applying a pre-cooled cylinder after trephination for 6 s to the intact dura mater. Pre-treatment with 3-bromo-7-nitroindazole (BrNI; 25 mg/kg, i.p.), and pre- or combined pre- and post-treatment with 3-aminobenzamide (AB; 10 mg/kg (i.c.v.) or 10 mg/kg/h (i.p.)) were used to inhibit nNOS and PARP, respectively. Cold lesion-induced changes in the somatosensory cortex and neuroprotection by BrNI and AB were determined using immunocytochemistry and immunodot-blot for detection of poly(ADP-ribose; PAR), the end-product of PARP activation, and the triphenyltetrazolium-chloride assay to assess lesion volume. PAR immunoreactivity reached its peak 30 min post-lesion and was followed by gradual reduction of PAR immunolabeling. BrNI pre-treatment significantly decreased the lesion-induced PAR concentration in damaged cerebral cortex. Pre-treatment by i.c.v. infusion of AB markedly diminished cortical PAR immunoreactivity and significantly reduced the lesion volume 24 h post-injury. In contrast, i.p. AB treatment remained largely ineffective. In conclusion, our data indicate early activation of PARP after cold lesion that is, at least in part, related to nNOS induction and supports the relevance of nNOS and/or PARP inhibition to therapeutic approaches of traumatic brain injury.

Animals↗

PubMed2000

Service utilization following traumatic brain injury.

OBJECTIVES: To document service utilization by people with a traumatic brain injury at different times postinjury and to identify factors that predict service use. DESIGN: Cross-sectional study design. Four groups of subjects were randomly selected from a regional database, according to their time postinjury: 6-18 months; 2-4 years; 6-9 years; and 10-17 years. SUBJECTS: A total of 119 adults with a traumatic brain injury (TBI). SETTING: Hospital and community-based clients in Sydney, Australia. OUTCOME MEASURES: Glasgow Outcome Scale, Disability Rating Scale; Functional Independence Measure; Lidcombe Psychosocial Disability Scale; number, type, and frequency of services used in the previous 12 months. RESULTS: Subjects in all four groups used a variety of services. The mean number of services used was 4.2, and there was only a moderate decline in service use over time. The use of medical and allied health services remained high in all four groups. Severity of injury, physical and cognitive disability, and psychosocial disability were all predictors of service utilization. Psychosocial disability was strongly associated with ongoing service utilization. CONCLUSION: In this study, people with TBI used services well beyond the early stage of recovery. Psychosocial disability may be a better predictor of service use than physical and cognitive disability alone.

Activities of Daily Living↗

PubMed2005

Long-term outcome in severe traumatic brain injury is significantly influenced by brainstem involvement.

PRIMARY OBJECTIVE: To study the 1-year-outcome of 32 survivors of severe traumatic brain injury with respect to the impact of brainstem injury. RESEARCH DESIGN: Retrospective clinical study performed in a university hospital. METHODS AND PROCEDURES: Thirty-two 1-year-survivors (15 with brainstem injury present) of severe traumatic brain injury were investigated for neurological function, activities of daily living, need for care and professional ability. MAIN OUTCOMES AND RESULTS: Visual impairment, spasticity, co-ordination deficits and organic psychosis were more frequent in the group harbouring brainstem lesions. Professional ability was worse among these patients. CONCLUSION: Brainstem involvement in survivors of severe traumatic brain injury conveys a negative impact on long-term outcome.

Activities of Daily Living↗

PubMed2006

Early ventilation and outcome in patients with moderate to severe traumatic brain injury.

OBJECTIVES: An increase in mortality has been reported with early intubation in severe traumatic brain injury, possibly due to suboptimal ventilation. This analysis explores the impact of early ventilation on outcome in moderate to severe traumatic brain injury. DESIGN: Retrospective, registry-based analysis. SETTING: This study was conducted in a large county trauma system that includes urban, suburban, and rural jurisdictions. PATIENTS: Nonarrest trauma victims with a Head Abbreviated Injury Score of > or =3 were identified from our county trauma registry. INTERVENTIONS: Intubated patients were stratified into 5 mm Hg arrival PCO(2) increments. Logistic regression was used to calculate odds ratios for each increment, adjusting for age, gender, mechanism of injury, year of injury, preadmission Glasgow Coma Scale score, hypotension, Head Abbreviated Injury Score, Injury Severity Score, PO(2), and base deficit. Increments with the highest relative survival were used to define the optimal PCO(2) range. Outcomes for patients with arrival PCO(2) values inside and outside this optimal range were then explored for both intubated and nonintubated patients, adjusting for the same factors as defined previously. In addition, the independent outcome effect of hyperventilation and hypoventilation was assessed. MEASUREMENTS AND MAIN RESULTS: A total of 890 intubated and 2,914 nonintubated patients were included. Improved survival was observed for the arrival PCO(2) range 30-49 mm Hg. Patients with arrival PCO(2) values inside this optimal range had improved survival and a higher incidence of good outcomes. Conversely, there was no improvement in outcomes for patients within this optimal PCO(2) range for nonintubated patients after adjusting for all of the factors defined previously. Both hyperventilation and hypoventilation were associated with worse outcomes in intubated but not nonintubated patients. The proportion of arrival PCO(2) values within the optimal range was lower for intubated vs. nonintubated patients. CONCLUSIONS: Arrival hypercapnia and hypocapnia are common and associated with worse outcomes in intubated but not spontaneously breathing patients with traumatic brain injury.

Adult↗

PubMed1998

Evidence for the involvement of corticotrophin-releasing hormone in the pathogenesis of traumatic brain injury.

The aim of this study was to investigate the role of the neuropeptide corticotrophin-releasing hormone (CRH) in neurodegeneration induced by traumatic brain injury, using a well characterized model of lateral fluid percussion injury in male, Sprague-Dawley rats. In the first series of experiments, CRH gene expression was assessed by in situ hybridization after traumatic brain injury. A bilateral increase in CRH mRNA in the paraventricular nucleus was observed in rats subjected to traumatic brain injury compared with sham-operated controls. A maximal (40%) increase in hybridization signal was detected 2 h after trauma compared with control rat brains. In addition, marked induction of CRH transcripts was found in the ipsilateral amygdala after trauma, but no increase was detected in the ipsilateral cortex around the area of damage. In a separate experiment, the effects of the CRH antagonist, D-Phe CRH(12-41) (25 microg total dose), or appropriate vehicle injected intracerebroventricularly, was tested on infarct volume caused by brain injury. Repeated intracerebroventricular injection of D-Phe CRH(12-41) significantly reduced, by 45%, the volume of cortical damage in injured rats compared with vehicle-treated, trauma animals. The rapid upregulation of CRH gene expression in the paraventricular nucleus and amygdala following lateral fluid percussion injury and the marked neuroprotection achieved by inhibiting CRH action suggest that CRH is involved directly in the pathogenesis of traumatic brain injury. This observation may have important implications for the development of novel therapeutic strategies for treating the neurological consequences of brain trauma and related conditions.

Animals↗

PubMed2005

[Rehabilitation results of persons with severe traumatic brain injury].

OBJECTIVE: There is a significant improvement in acute treatment and rehabilitation of patients with severe traumatic brain injury in the last 20 years. PURPOSE: Introduction of the rehabilitation result of patients with severe traumatic brain injury treated at Neurorehabilitation unit of the National Institute for Medical Rehabilitation. METHOD: Retrospective analysis of patients' data treated in the Neurorehabilitation unit 2002. year. RESULTS: Data of 53 patients from the 165 severe traumatic brain injured patients treated in 2002. year were complete enough for analysis. The mean age of the patients was 30.6 (8-65) years. The interval between the time of injury and admission was 53 (21-120) days. The majority of patients injured in vehicular accidents (42/53). The length of stay in rehabilitation unit was 41 (8-92) days, but 20 patients were readmitted for further therapy (1-6 times) in these cases the hospitalization was 70 (8-206) days. The functional status of these patients was scored with Barthel Index (0-100). At the time of admission the mean score was: 25, at the time of discharge 50, one year after injury: 75. Twenty-two patients were independent one year after injury in performing daily activities. 35 patients became ambulatory at the time of discharge. 45 patients were discharged to their home, 6 patients had to be send back to the acute ward for observation serious complication. CONCLUSION: Rehabilitation treatment of patients with severe traumatic brain injury is suggested in centers, where special team is available for the patients with multifunctional impairments. Nowadays, only one third of these patients are treated by rehabilitation centers in Hungary. Establishing new centers, development of the existing units, improvement the outpatient or community based rehabilitation facilities are suggested in order to improve the rehabilitation outcome of patients with severe traumatic brain injury.

Activities of Daily Living↗

PubMed2003

S-100beta protein-serum levels in healthy children and its association with outcome in pediatric traumatic brain injury.

OBJECTIVE: To describe normal serum levels of S-100beta in healthy children and determine whether serum S-100beta levels after traumatic brain injury are associated with outcome. DESIGN: Prospective cohort study. SETTING: Urban, tertiary care, children's teaching hospital. PATIENTS: A total of 136 healthy children and 27 children with traumatic brain injury. METHODS: Serum S-100beta levels were measured in 136 healthy children. A total of 27 children with traumatic brain injury had S-100beta levels collected within 12 hrs of injury. Other indices of severity of injury measured were admission Glasgow Coma Scale score, and Pediatric Risk of Mortality score at 24 hrs (PRISM 24). Outcome was measured by the Pediatric Cerebral Performance Category (PCPC) score at hospital discharge and 6 months postinjury or at death. MEASUREMENTS AND MAIN RESULTS: S-100beta levels in healthy children had a mean of 0.3 microg/L (90% confidence interval, 0.03-1.47) and inversely correlated with age, (r = -.32, p <.001). In children with traumatic brain injury, 6-month postinjury outcome inversely correlated with Glasgow Coma Scale score (r = -.47, p =.01) and correlated with PRISM 24 score (r =.83, p <.001) and S-100beta levels (r =.75, p <.001). Six months postinjury, comparing good outcome (PCPC < or = 3, n = 20) vs. poor outcome (PCPC > or = 4, n = 7), median admission Glasgow Coma Scale scores were 8 (range, 3-15) and 3 (range, 3-7, p =.01), median PRISM 24 scores were 7 (range, 0-19) and 30 (range, 18-35, p <.001), and median S-100beta levels were 0.85 microg/L (range, 0.08-4.8 microg/L) and 3.6 microg/L (range, 1.4-20 microg/L, p <.001), respectively. A serum S-100beta level of > or =2.0 microg/L is associated with poor outcome, with a sensitivity of 86% and a specificity of 95%. The area under the receiver operating curve for S-100beta was 0.94 (+/-0.05). CONCLUSIONS: Serum S-100beta levels in healthy children have a moderate inverse correlation with age. After traumatic brain injury in children, the acute assessment of serum S-100beta levels seems to be associated with outcome.

Biomarkers↗

PubMed1998

Characteristics of impaired awareness after traumatic brain injury.

Impaired awareness of the effects of brain injury is a commonly observed and poorly understood finding in traumatic brain injury survivors. Nonetheless, impaired awareness has been identified as a major factor in determining outcome for traumatic brain injury survivors. Review of previous studies of impaired awareness in this patient population revealed a number of preliminary findings regarding the nature of this phenomenon. The present paper presents the results of 2 new studies with a total of 111 traumatic brain injury patients conducted to bring further clarity to this area. Findings confirmed and extended many results of previous investigations. Specific findings included patient overestimation of functioning as compared to family member ratings, patient report of greater physical than nonphysical impairment, greater patient-family agreement on specific ratings of patient functioning than on general ratings, greater agreement of family and clinician ratings of patient functioning with each other than with patient self-ratings, and partial disagreement of different methods of measuring impaired awareness.

Activities of Daily Living↗

PubMed2005

Severe traumatic brain injury in a large Canadian health region.

BACKGROUND: Although severe traumatic brain injury (sTBI) is a devastating condition with tremendous public health implications, the epidemiology of this disease has not previously been described in Canada. We sought to define the incidence, risk factors and outcome of patients suffering sTBI in a large Canadian region. METHODS: A population-based surveillance cohort design was utilized to identify all Calgary Heath Region residents who were victims of trauma with an injury severity score > or = 12. Subsequent application of a specific sTBI case definition defined the final cohort. RESULTS: The annual incidence of sTBI was 11.4 per 100,000 population. The incidence of sTBI was significantly higher for males as compared to females [17.1 vs. 5.9 per 100,000; relative risk (RR) = 2.91, 95% confidence interval; 2.17, 3.94; p<0.0001]. There was a striking increase in the annual age specific population incidence of sTBI observed among those older than 74 years of age. The relative risk among the highest risk group of elderly (>85 years) males as compared to the lowest risk female group (50-64 years) was 19.78 (95% CI; 6.27, 62.3; p<0.0001). One hundred and eight patients died prior to hospital discharge for a mortality rate of 5.1 per 100,000 per year. CONCLUSIONS: Severe traumatic brain injury is common among residents of the Calgary Health Region and is associated with a high mortality rate. Males and the elderly are at the highest risk for acquiring sTBI and may represent target groups for preventive efforts.

Adolescent↗

PubMed2002

Novel therapies in development for the treatment of traumatic brain injury.

In industrialised countries, the mean per capita incidence of traumatic brain injury (TBI) that results in a hospital presentation is 250 per 100,000. In Europe and North America alone, this translates to > 2 million TBI presentations annually. Approximately 25% of these presentations are admitted for hospitalisation. Despite the significance of these figures, there is no single interventional pharmacotherapy that has shown efficacy in the treatment of clinical TBI. This lack of efficacy in clinical trials may be due, in part, to the inherent heterogeneity of the traumatic brain injury population. However, it is the multifactorial nature of secondary injury that also poses a major hurdle, particularly for those therapies that have been designed to specifically target an individual injury factor. It is now becoming increasingly recognised that any successful TBI therapy may have to simultaneously affect multiple injury factors, somewhat analogous to other broad spectrum interventions. Recent efforts in experimental TBI have therefore focussed on developing novel pharmacotherapies that may affect multiple injury factors and thus improve the likelihood of a successful outcome. While a number of interventions are noteworthy in this regard, this review will focus on three novel compounds that show particular promise: magnesium, substance P antagonists and cyclosporin A.

Animals↗

PubMed2001

N-Acetylaspartate reduction as a measure of injury severity and mitochondrial dysfunction following diffuse traumatic brain injury.

N-Acetylaspartate (NAA) is considered a neuron-specific metabolite and its reduction a marker of neuronal loss. The objective of this study was to evaluate the time course of NAA changes in varying grades of traumatic brain injury (TBI), in concert with the disturbance of energy metabolites (ATP). Since NAA is synthesized by the mitochondria, it was hypothesized that changes in NAA would follow ATP. The impact acceleration model was used to produce three grades of TBI. Sprague-Dawley rats were divided into the following four groups: sham control (n = 12); moderate TBI (n = 36); severe TBI (n = 36); and severe TBI coupled with hypoxia-hypotension (n = 16). Animals were sacrificed at different time points ranging from 1 min to 120 h postinjury, and the brain was processed for high-performance liquid chromatography (HPLC) analysis of NAA and ATP. After moderate TBI, NAA reduced gradually by 35% at 6 h and 46% at 15 h, accompanied by a 57% and 45% reduction in ATP. A spontaneous recovery of NAA to 86% of baseline at 120 h was paralleled by a restoration in ATP. In severe TBI, NAA fell suddenly and did not recover, showing critical reduction (60%) at 48 h. ATP was reduced by 70% and also did not recover. Maximum NAA and ATP decrease occurred with secondary insult (80% and 90%, respectively, at 48 h). These data show that, at 48 h post diffuse TBI, reduction of NAA is graded according to the severity of insult. NAA recovers if the degree of injury is moderate and not accompanied by secondary insult. The highly similar time course and correlation between NAA and ATP supports the notion that NAA reduction is related to energetic impairment.

Adenosine Triphosphate↗

PubMed2006

Self-awareness after acquired and traumatic brain injury.

Self-awareness deficits are common after acquired and (traumatic) brain injury (ABI), particularly in social behaviour, yet the underlying cognitive and neuroanatomical structures supporting social self-awareness are not fully understood. This paper reviews the current literature on prevalence, type and severity of self-awareness deficits in ABI. Neuropsychological and neuroanatomical models are reviewed and theoretical frameworks are examined. We summarise results of a case-control comparison of 20 ABI patients with and 20 ABI patients without behavioural disturbance. Our research found that lack of social self-awareness predicts behavioural disturbance in acquired and traumatic brain injury independent of cognitive and executive function. Theory of mind ability was related to self-awareness and a possible role for metacognition and affective processes in self-awareness is discussed to account for social self-awareness deficits.

Adult↗