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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↗

PubMed1998

Increased ornithine decarboxylase activity and protein level in the cortex following traumatic brain injury in rats.

There is increasing evidence that the elevated levels of polyamines play an important role in the secondary injury following traumatic brain injury (TBI). Ornithine decarboxylase (ODC) is the rate-limiting enzyme of polyamine biosynthesis. Presently, we measured the ODC protein levels by Western blot analysis in the cerebral cortex of rats sacrificed at 2 h, 6 h, 24 h, 72 h and 168 h after controlled cortical impact injury. TBI resulted in a significant increase in ODC protein levels (2.5 to 5.5 fold, P<0.05) and enzyme activity (13 to 21 fold, p<0.01) between 2 and 6 h after the injury. ODC protein levels and enzyme activity returned to normal, control levels by 72 h after the injury. Increased ODC protein and enzyme activity could contribute to vasogenic edema and the pathogenesis of neuronal dysfunction after TBI by stimulating the formation of polyamines.

Animals↗

PubMed2002

The effect of severe traumatic brain injury on the family.

BACKGROUND: The effects of traumatic brain injury on family dynamics and finances have not been extensively studied. We designed a 30-item survey to determine the effects of the injury on the child, parent(s), and siblings, and whether parents were retrospectively content with the decisions related to aggressiveness of care. METHODS: A questionnaire written on a sixth-grade reading level was mailed to 46 families of children who survived a traumatic brain injury resulting in an initial Glasgow Coma Scale score < or = 7. This is a descriptive study without statistical analysis. Human Studies Committee review and informed consent were obtained. RESULTS: Thirty-two of 46 (69.6%) surveys were completed by mail or telephone. Mean patient age at time of injury was 8.7 years, mean time since injury was 3 years, and mean Glasgow Coma Scale score was 3.7. Approximately one third of children have disabilities related to education, socialization, and/or self-care skills; require multiple health care visits each month; and require prescription medications. Over one third of families were impacted in a moderate to profoundly negative way; 30% of families reported a deterioration in finances or loss of job; and 16% reported a worsening of adult relationships. In 13 of 32 cases, modification of current housing or new housing was required to facilitate home care. Siblings were adversely affected in approximately 16 of 28 families, exhibiting behavioral problems, increased fear, and withdrawal from the injured child. Only 1 of 32 families stated that they would have considered less aggressive treatment, even if it led to the child's death. CONCLUSION: Traumatic brain injury of a child had a negative impact on family dynamics and/or sibling behavior in more than one third of families. Despite this, most families would not limit or withdraw care if they could reconsider decisions regarding treatment. This information can be used to counsel families.

Adaptation, Psychological↗

PubMed2001

Traumatic brain injury and schizophrenia in members of schizophrenia and bipolar disorder pedigrees.

OBJECTIVE: Schizophrenia following a traumatic brain injury could be a phenocopy of genetic schizophrenia or the consequence of a gene-environment interaction. Alternatively, traumatic brain injury and schizophrenia could be spuriously associated if those who are predisposed to develop schizophrenia have greater amounts of trauma for other reasons. The authors investigated the relationship between traumatic brain injury and psychiatric diagnoses in a large group of subjects from families with at least two biologically related first-degree relatives with schizophrenia, schizoaffective disorder, or bipolar disorder. METHOD: The Diagnostic Interview for Genetic Studies was used to determine history of traumatic brain injury and diagnosis for 1,275 members of multiplex bipolar disorder pedigrees and 565 members of multiplex schizophrenia pedigrees. RESULTS: Rates of traumatic brain injury were significantly higher for those with a diagnosis of schizophrenia, bipolar disorder, and depression than for those with no mental illness. However, multivariate analysis of within-pedigree data showed that mental illness was related to traumatic brain injury only in the schizophrenia pedigrees. Independent of diagnoses, family members of those with schizophrenia were more likely to have had traumatic brain injury than were members of the bipolar disorder pedigrees. The members of the schizophrenia pedigrees also failed to show the gender difference for traumatic brain injury (more common in men than in women) that was expected and was present in the bipolar disorder pedigrees. Subjects with a schizophrenia diagnosis who were members of the bipolar disorder pedigrees (and thus had less genetic vulnerability to schizophrenia) were less likely to have had traumatic brain injury (4.5%) than were subjects with schizophrenia who were members of the schizophrenia pedigrees (and who had greater genetic vulnerability to schizophrenia) (19.6%). CONCLUSIONS: Members of the schizophrenia pedigrees, even those without a schizophrenia diagnosis, had greater exposure to traumatic brain injury compared to members of the bipolar disorder pedigrees. Within the schizophrenia pedigrees, traumatic brain injury was associated with a greater risk of schizophrenia, consistent with synergistic effects between genetic vulnerability for schizophrenia and traumatic brain injury. Posttraumatic-brain-injury schizophrenia in multiplex schizophrenia pedigrees does not appear to be a phenocopy of the genetic disorder.

Adult↗

PubMed1999

Secondary neurologic injury resulting from nonhypotensive hemorrhage combined with mild traumatic brain injury.

Although the emergency physician often treats patients with multiple injuries, there are relatively few clinically relevant models that mimic these situations. To describe the changes after a hemorrhagic insult superimposed on traumatic brain injury (TBI), anesthetized and ventilated juvenile pigs were assigned to 35% hemorrhage (35H), TBI (via fluid percussion); TBI + 35H, and TBI + 40H (40% hemorrhage). Animals were resuscitated with shed blood and crystalloid. Hemodynamic, metabolic, behavioral, and histologic parameters were assessed for 48 h. In TBI, mean arterial pressure (MAP) was not significantly different from baseline. For TBI + 40H, MAP fell by 60% (p < 0.05). This was corrected with resuscitation. Interestingly, TBI + 35H did not show a fall in MAP, while in 35H, MAP was reduced similarly to the TBI + 40H group. ICP was elevated only initially in the TBI group. In TBI + 40H and TBI + 35H, ICP increased markedly with resuscitation, remaining elevated for 60 min. ICP remained at baseline with 35 H. Hemorrhagic focal cerebal contusions at the gray-white interface were observed in 3/5 of TBI + 40H and 5/7 of TBI + 35H. Despite the presence of subarachnoid hemorrhage (SAH) in all the animals in the TBI alone group, none of these animals demonstrated grossly discernible intraparenchymal injury. There was no evidence of intracranial injury in the 35H group. Only in animals receiving a secondary insult of hemorrhage following the primary TBI were cerebral contusions found. These experiments demonstrate the evolution of cerebral contusions as a form of secondary neurologic injury following resuscitation from traumatic brain injury and hemorrhage, even in the absence of significant blood pressure changes.

Animals↗

PubMed2003

Moderate hypothermia may be detrimental after traumatic brain injury in fentanyl-anesthetized rats.

OBJECTIVES: To determine whether transient, moderate hypothermia is beneficial after traumatic brain injury in fentanyl-anesthetized rats. DESIGN: Prospective, randomized study. SETTING: University-based animal research facility. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: All rats were intubated, mechanically ventilated, and anesthetized with fentanyl (10 microg/kg intravenous bolus and then 50 microg.kg(-1).hr(-1) infusion). Controlled cortical impact was performed to the left parietal cortex, followed immediately by 1 hr of either normothermia (brain temperature 37 +/- 0.5 degrees C) or hypothermia (brain temperature 32 +/- 0.5 degrees C). Hypothermic rats were rewarmed gradually over 1 hr. Fentanyl anesthesia and mechanical ventilation were continued in both groups until the end of rewarming (2 hrs after traumatic brain injury). MEASUREMENTS AND MAIN RESULTS: Histologic assessment performed 72 hrs after traumatic brain injury was the primary outcome variable. Secondary outcome variables were physiologic variables monitored during the first 2 hrs after traumatic brain injury and plasma catecholamine and serum fentanyl concentrations measured at the end of both hypothermia and rewarming (1 and 2 hrs after traumatic brain injury). Contusion volume was larger in hypothermic vs. normothermic rats (44.3 +/- 4.2 vs. 28.6 +/- 4.0 mm, p <.05), but hippocampal neuronal survival did not differ between groups. Physiologic variables did not differ between groups. Plasma dopamine and norepinephrine concentrations were increased at the end of hypothermia in hypothermic (vs. normothermic) rats (p <.05), indicating that hypothermia augmented the systemic stress response. Similarly, serum fentanyl concentrations were higher in hypothermic (vs. normothermic) rats at the end of both hypothermia and rewarming (p <.05), demonstrating that hypothermia reduced the clearance and/or metabolism of fentanyl. CONCLUSIONS: Moderate hypothermia was detrimental after experimental traumatic brain injury in fentanyl-anesthetized rats. Since treatment with hypothermia has provided reliable benefit in experimental traumatic brain injury with inhalational anesthetics, these results indicate that the choice of anesthesia/analgesia after traumatic brain injury may dramatically influence response to other therapeutic interventions, such as hypothermia. Given that narcotics commonly are administered to patients after severe traumatic brain injury, this study may have clinical implications.

Anesthesia, Intravenous↗

PubMed1995

Trends in death associated with traumatic brain injury, 1979 through 1992. Success and failure.

OBJECTIVE: To report updated national trends in traumatic brain injury deaths from 1979 through 1992. DESIGN: Retrospective analysis of Multiple Cause-of-Death Public Use Data Tapes from the National Center for Health Statistics. All deaths associated with traumatic brain injury were identified, the underlying causes of death were categorized, and the annual rates were calculated per 100,000 US residents. PATIENTS: Residents of the United States who died with traumatic brain injury from 1979 through 1992. RESULTS: An average of 52,000 US residents die each year with traumatic brain injuries. The brain injury-associated death rate declined 22% from 24.6 per 100,000 US residents in 1979 to 19.3 per 100,000 US residents in 1992. Firearm-related rates increased 13% from 1984 through 1992, undermining a 25% decline in motor vehicle-related rates for the same period. Firearms surpassed motor vehicles as the largest single cause of death associated with traumatic brain injury in 1990. CONCLUSIONS: These data highlight the success of efforts to prevent traumatic brain injury due to motor vehicles and failure to prevent such injuries due to firearms. The increasing importance of penetrating injury has important implications for research, treatment, and prevention of traumatic brain injury in the United States.

Accidental Falls↗

PubMed1987

Catecholamines predict outcome in traumatic brain injury.

Activation of the sympathetic nervous system attends traumatic brain injury, but the association of the severity of neurological impairment and recovery with the extent of sympathetic nervous system stimulation is poorly defined. In this study, plasma norepinephrine (NE), epinephrine (E), and dopamine (DA) levels were measured serially in 33 patients with traumatic brain injury and compared with the Glasgow Coma Score (GCS), which was obtained concurrently. A catecholamine gradient that reflected the extent of brain injury was demonstrated within 48 hours of the injury. In patients with a GCS of 3 to 4, NE and E levels increased four- to fivefold and the DA level increased threefold above normal (NE, 1686 +/- 416 pg/ml; E, 430 +/- 172 pg/ml; DA, 236 +/- 110 pg/ml), while patients with mild brain injury (GCS, greater than 11) had slightly elevated or normal levels. Patients with marked (GCS, 5 to 7) and moderate (GCS, 8 to 10) traumatic brain injuries had intermediate levels. The prognostic value of determining admission levels of NE was shown in patients with an admission GCS of 3 to 4 1 week after injury. Patients with severe and unchanging neurological impairment 1 week after injury had markedly elevated initial NE levels (2,176 +/- 531 pg/ml), whereas initial NE levels (544 +/- 89 pg/ml) were only mildly elevated in patients who improved to a GCS of greater than 11. These data indicate that markedly elevated NE levels predict outcome in patients with comparable neurological deficits. Thus levels of circulating catecholamines are excellent endogenous and readily quantifiable markers that appear to reflect the extent of brain injury and that may predict the likelihood of recovery.

Adolescent↗

PubMed2026

Risk Factors for Long-Term Health-Related Quality-of-Life and Mental Health Outcomes in Traumatic Brain Injury: A Systematic Review and Meta-Analysis.

Traumatic brain injury (TBI) often leads to long-term disability, including persistent mental health issues and lower health-related quality of life (HRQoL). Early interventions can improve recovery, but because resources limit routine monitoring of all patients, trauma care remains largely symptom-driven. The combination of long-term disability and limited capacity for routine follow-up highlights the need for risk-stratified follow-up care and reliable evidence on early prognostic factors. However, the existing literature is sparse and methodologically heterogeneous, limiting the clinical applicability of findings. We therefore conducted a systematic review and meta-analysis to identify early risk factors for poorer long-term mental health and HRQoL outcomes. A systematic search of seven electronic databases identified studies of adult patients with TBI, with outcomes assessed at least 6 months postdischarge. Two authors independently screened the studies, assessed the risk of bias, and extracted the data. We pooled effect estimates using a random-effects meta-analysis and calculated 95% prediction intervals. A narrative synthesis was applied when meta-analysis was not feasible. The review was registered with PROSPERO (CRD42024576912) and reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Of the 8,104 articles screened, 64 studies met the inclusion criteria (n = 334,672). Most studies (58%) had a low risk of bias. Female sex, socioeconomic disadvantage, psychiatric history, assaultive-related injuries, and previous TBI were consistently associated with worse long-term outcomes. Across meta-analyses, assault-related injuries more than doubled the odds of post-traumatic stress disorder (odds ratio [OR] = 2.72; 95% confidence interval [CI]: 2.01-3.66, I2 = 0%). Higher odds were also observed among females (OR = 1.33; 95% CI: 1.11-1.59, I2 = 0%), individuals with prior TBI (OR = 1.56; 95% CI: 1.07-2.27, I2 = 0%), and those with psychiatric history (OR = 2.38; 95% CI: 1.83-3.10, I2 = 48%). We found that female sex (OR = 1.72; 95% CI: 1.38-2.16, I2 = 58%), prior TBI (OR = 1.52; 95% CI: 1.25-1.85, I2 = 0%), and psychiatric history (OR = 3.25; 95%CI: 1.86-5.69, I2 = 98%) were associated with higher odds of depression. Furthermore, higher pooled anxiety scores were observed in females and in individuals with a psychiatric history. The study identified several readily available factors present before or at discharge that are associated with poor long-term HRQoL and mental health outcomes. Leveraging these factors in follow-up protocols, prediction modeling, and clinical decision support systems may facilitate risk-stratified postdischarge care for TBI patients.

Humans↗

PubMed2005

Predicting depression following mild traumatic brain injury.

CONTEXT: Minimizing negative consequences of major depression following traumatic brain injury is an important public health objective. Identifying high-risk patients and referring them for treatment could reduce morbidity and loss of productivity. OBJECTIVE: To develop a model for early screening of patients at risk for major depressive episode at 3 months after traumatic brain injury. DESIGN: Prediction model using receiver operating characteristic curve. SETTING: Level I trauma center in a major metropolitan area. PARTICIPANTS: Prospective cohort of 129 adults with mild traumatic brain injury. MAIN OUTCOME MEASURES: Center for Epidemiologic Studies Depression Scale score and current major depressive episode module of the Structured Clinical Interview for the DSM-IV. RESULTS: A prediction model including higher 1-week Center for Epidemiologic Studies Depression Scale score, older age, and computed tomographic scans of intracranial lesions yielded 93% sensitivity and 62% specificity. CONCLUSION: This study supports the feasibility of identifying patients with mild traumatic brain injury who are at high risk for developing major depressive episode by 3 months' postinjury, which could facilitate selective referral for potential treatment and reduction of negative outcomes.

Adult↗

PubMed1998

Prevalence of traumatic brain injury in psychiatric and non-psychiatric subjects.

Traumatic brain injury (TBI) and its sequelae may impact the expression and treatment of psychiatric disorders. The prevalence of TBI in psychiatric patients is unknown and investigations in the general population are limited. This study examined the prevalence of TBI with loss of consciousness in mental health setting patients (n = 231), general hospital and university staff and students (n = 534) and non-psychiatric medical clinical patients (n = 59). The Traumatic Brain Injury Questionnaire was used to assess TBI. A greater percentage of psychiatric patients reported TBI than medical patients or staff and students. Traumatic brain injuries were typically mild--moderate, medical assistance was frequently sought and use of alcohol and drugs was reported in a minority of TBI incidents. Multiple injuries were most common in psychiatric patients. The percentage of medical patients and staff and students reporting TBI was similar to previous research. The greater percentage of psychiatric patients reporting TBI indicates the need to assess TBI in this population. The role of TBI in the emergence, expression and treatment outcome of psychiatric disorders and the risk factors that leave psychiatric patients vulnerable to TBI should be further examined.

Adult↗

PubMed1991

The effect of age on outcome following traumatic brain injury in rats.

Age of the patient is one of the most important predictors of outcome following human traumatic brain injury. This study employs the fluid-percussion model to investigate the effects of aging on outcome following traumatic brain injury in rats. The results revealed that there was an age-associated increase in mortality rate following both low (1.7 to 1.8 atm) and moderate (2.00 to 2.25 atm) levels of traumatic brain injury. Age-related changes in systemic physiological, neurological, and histopathological indexes of brain injury were also examined following a low level of traumatic brain injury. Traumatic brain injury produced equivalent acute hypertension and increased plasma glucose levels in both young adult and aging rats. Injury produced an acute increase in heart rate in the young adult rat group, while the heart rate decreased in the aged rats. At low levels of brain injury, no significant gross histopathological alterations were produced in either age group. Neurological outcome was assessed by measuring the duration of suppression of a number of nonpostural and postural reflexes and more complex somatomotor functions (righting, escape, head support). Except for head support, there was a significant age-related increase in the duration of the suppression of these reflexes following brain injury. These data demonstrate that aging is associated with an increased mortality rate and greater acute neurological deficits following traumatic brain injury. These data also demonstrate the usefulness of the fluid-percussion model for studying the mechanisms responsible for the age-related increase in vulnerability to brain injury.

Aging↗

PubMed1998

Brain injury as a result of violence: preliminary findings from the traumatic brain injury model systems.

OBJECTIVES: To identify possible risk factors that may predispose individuals to violent traumatic brain injury (TBI) and to determine the effect of etiology of injury on outcomes. STUDY DESIGN: Prospective, longitudinal multicenter study. SETTING: TBI Model Systems (TBIMS) located at Wayne State University/Rehabilitation Institute of Michigan, Detroit, MI; The Institute for Rehabilitation and Research, Houston, TX; Medical College of Virginia, Richmond, VA; and Santa Clara Valley Medical Center, San Jose, CA. SUBJECTS: Individuals treated in the four TBIMS programs between 3/89 and 9/96 who met the criteria for inclusion in the TBIMS National Database and for whom the etiology was known (n=812). MAIN OUTCOME MEASURES: Functional Independence Measure, Alcohol Quantity Frequency Variability Index, Community Integration Questionnaire. RESULTS: Individuals who incur violence-related TBI tend to be male, nonwhite, unmarried, living alone, less educated, and unemployed at time of injury. They tend to have less severe brain injuries and better motor function at the time of admission to inpatient rehabilitation. At 1 year postinjury, they score lower on community integration measures; however, no difference exists in functional status. Etiology of injury was found to only play a minor role in the prediction of social and productive integration at 1 year postinjury. CONCLUSIONS: Survivors of violent and nonviolent TBI have similar functional outcomes; however, they differ in preinjury and postinjury socio-economic characteristics, injury severity, and postinjury community integration. Socio-economic factors appear to play a large role in the risk for violent injury and in community integration following injury.

Activities of Daily Living↗

PubMed2005

Traumatic brain injury and hemorrhagic hypotension suppress neuroprotective gene expression in injured hippocampal neurons.

BACKGROUND: After traumatic brain injury, memory dysfunction is due in part to damage to the hippocampus. To study the molecular mechanisms of this selective vulnerability, the authors used laser capture microdissection of neurons stained with Fluoro-Jade to directly compare gene expression in injured (Fluoro-Jade-positive) and adjacent uninjured (Fluoro-Jade-negative) rat hippocampal neurons after traumatic brain injury and traumatic brain injury plus hemorrhagic hypotension. METHODS: Twelve isoflurane-anesthetized Sprague-Dawley rats underwent moderate (2.0 atm) fluid percussion traumatic brain injury followed by either normotension or hemorrhagic hypotension. Animals were killed 24 h after injury. Frozen brain sections were double stained with 1% cresyl violet and 0.001% Fluoro-Jade. RNA from 10 Fluoro-Jade-positive neurons and 10 Fluoro-Jade-negative neurons, obtained from the hippocampal CA1, CA3, and dentate gyrus subfields using laser capture microdissection, was linearly amplified and analyzed by quantitative ribonuclease protection assay for nine neuroprotective and apoptosis-related genes. RESULTS: In injured CA3 neurons, expression of the neuroprotective genes glutathione peroxidase 1, heme oxygenase 1, and brain-derived neurotrophic factor was significantly decreased compared with that of adjacent uninjured neurons. Superimposition of hemorrhagic hypotension was associated with down-regulation of neuroprotective genes in both injured and uninjured neurons of all subregions. Expression of apoptosis-related genes did not vary between injured and uninjured neurons, with or without superimposed hemorrhage. CONCLUSIONS: The authors show, in the first direct comparison of messenger RNA levels in injured and uninjured hippocampal neurons, that injured neurons express lower levels of neuroprotective genes than adjacent uninjured neurons.

Animals↗

PubMed2002

Mitogen-activated protein kinase inhibition in traumatic brain injury: in vitro and in vivo effects.

The authors provide the first in vitro and in vivo evidence that perturbations in mitogen-activated protein kinase (MAPK) signal-transduction pathways are involved in the pathophysiology of traumatic brain injury. In primary rat cortical cultures, mechanical trauma induced a rapid and selective phosphorylation of the extracellular signal-regulated kinase (ERK) and p38 kinase, whereas there was no detectable change in the c-jun N-terminal kinase (JNK) pathway. Treatment with PD98059, which inhibits MAPK/ERK 1/2, the upstream activator of ERK, significantly increased cell survival in vitro. The p38 kinase and JNK inhibitor SB203580 had no protective effect. Similar results were obtained in vivo using a controlled cortical impact model of traumatic injury in mouse brain. Rapid and selective upregulation occurred in ERK and p38 pathways with no detectable changes in JNK. Confocal immunohistochemistry showed that phospho-ERK colocalized with the neuronal nuclei marker but not the astrocytic marker glial fibrillary acidic protein. Inhibition of the ERK pathway with PD98059 resulted in a significant reduction of cortical lesion volumes 7 days after trauma. The p38 kinase and JNK inhibitor SB203580 had no detectable beneficial effect. These data indicate that critical perturbations in MAPK pathways mediate cerebral damage after acute injury, and further suggest that ERK is a novel therapeutic target in traumatic brain injury.

Animals↗

PubMed2001

Posttraumatic hypothermia is neuroprotective in a model of traumatic brain injury complicated by a secondary hypoxic insult.

OBJECTIVE: Human traumatic brain injury frequently results in secondary complications, including hypoxia. In previous studies, we have reported that posttraumatic hypothermia is neuroprotective and that secondary hypoxia exacerbates histopathologic outcome after fluid-percussion brain injury. The purpose of this study was to assess the therapeutic effects of mild (33 degrees C) hypothermia after fluid-percussion injury combined with secondary hypoxia. In addition, the importance of the rewarming period on histopathologic outcome was investigated. DESIGN: Prospective experimental study in rats. SETTING: Experimental laboratory in a university teaching hospital. INTERVENTION: Intubated, anesthetized rats underwent normothermic parasagittal fluid-percussion brain injury (1.8-2.1 atmospheres) followed by either 30 mins of normoxia (n = 6) or hypoxic (n = 6) gas levels and by 4 hrs of normothermia (37 degrees C). In hypothermic rats, brain temperature was reduced immediately after the 30-min hypoxic insult and maintained for 4 hrs. After hypothermia, brain temperature was either rapidly (n = 6) or slowly (n = 5) increased to normothermic levels. Rats were killed 3 days after traumatic brain injury, and contusion volumes were quantitatively assessed. MEASUREMENTS AND MAIN RESULTS: As previously shown, posttraumatic hypoxia significantly increased contusion volume compared with traumatic brain injury-normoxic animals (p <.02). Importantly, although posttraumatic hypothermia followed by rapid rewarming (15 mins) failed to decrease contusion volume, those animals undergoing a slow rewarming period (120 mins) demonstrated significantly (p <.03) reduced contusion volumes, compared with hypoxic normothermic rats. CONCLUSIONS: These data emphasize the beneficial effects of posttraumatic hypothermia in a traumatic brain injury model complicated by secondary hypoxia and stress the importance of the rewarming period in this therapeutic intervention.

Analysis of Variance↗

PubMed2006

Finding the person behind the pain: chronic pain management in a patient with traumatic brain injury.

Chronic pain is common after a traumatic brain injury. Cognitive impairment post injury may be a consequence of the brain injury alone, or in combination with pain, clinical depression, and psychological and emotional factors. We present a case of a severely cognitively impaired person post-traumatic brain injury, whose behavior included social withdrawal, irritability, and agitation around direct care--which was unresponsive to psychotropic intervention or care delivery strategies. The introduction of an opioid made a significant improvement in the cognition and quality of life of the individual. This case suggests that clinicians should consider a trial of opioid analgesics in individuals with brain injury who have significant cognitive impairment in association with other behaviors suggestive of depression and pain.

Analgesics, Opioid↗

PubMed2005

Clinical elements that predict outcome after traumatic brain injury: a prospective multicenter recursive partitioning (decision-tree) analysis.

Traumatic brain injury (TBI) often presents clinicians with a complex combination of clinical elements that can confound treatment and make outcome prediction challenging. Predictive models have commonly used acute physiological variables and gross clinical measures to predict mortality and basic outcome endpoints. The primary goal of this study was to consider all clinical elements available concerning a survivor of TBI admitted for inpatient rehabilitation, and identify those factors that predict disability, need for supervision, and productive activity one year after injury. The Traumatic Brain Injury Model Systems (TBIMS) database was used for decision tree analysis using recursive partitioning (n = 3463). Outcome measures included the Functional Independence Measure(), the Disability Rating Scale, the Supervision Rating Scale, and a measure of productive activity. Predictor variables included all physical examination elements, measures of injury severity (initial Glasgow Coma Scale score, duration of post-traumatic amnesia [PTA], length of coma, CT scan pathology), gender, age, and years of education. The duration of PTA, age, and most elements of the physical examination were predictive of early disability. The duration of PTA alone was selected to predict late disability and independent living. The duration of PTA, age, sitting balance, and limb strength were selected to predict productive activity at 1 year. The duration of PTA was the best predictor of outcome selected in this model for all endpoints and elements of the physical examination provided additional predictive value. Valid and reliable measures of PTA and physical impairment after TBI are important for accurate outcome prediction.

Activities of Daily Living↗