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Effect of moderate hypothermia on systemic and internal jugular plasma IL-6 levels after traumatic brain injury in humans.

Moderate hypothermia may reduce subsequent neuronal damage after traumatic brain injury. Interleukin (IL)-6 may have a role in the pathogenesis of traumatic neuronal damage or repair. Using the enzyme-linked immunological sorbent assay (ELISA), we serially measured IL-6 levels in plasma obtained from the radial artery (systemic) and internal jugular vein (regional) in 13 cerebral trauma patients who underwent hypothermia of 32-33 degrees C ranged from 4-9 days postinjury and 10 head-injured patients who were maintained at normothermic levels (36-37 degrees C). In both patient populations, surface cooling was used since even in the normothermic group, cooling was needed to maintain patient temperature in the normothermic range. All patients were mechanically ventilated after injection of midazolam and vecuronium. The administration of these agents were continued until the end of the study. Hypothermia was typically maintained for four days, however, in some cases based upon CT findings and/or intra-cranial pressure change, the duration was prolonged. No significant differences were found between the two groups in age, gender and Glasgow Coma Scale upon admission. Further, no differences were found in terms of the classification of computed tomography findings or the occurrence of pupillary abnormalities on admission. The patients in this study had not sustained either abdominal or thoracic trauma. Before inducing hypothermia, IL-6 levels in the arterial and internal jugular venous blood exceeded the normal range. Specifically, the internal jugular plasma levels were significantly higher than those in the arterial plasma. While IL-6 levels in the normothermic group did not decrease even at 4 days postinjury, the plasma cytokine levels fell at both sites sharply after moderate hypothermia. The cytokine suppression found in the hypothermic group continued even after rewarming in these patients showing an improved clinical course, but not in those whose condition worsened. In addition to these changes in cytokine levels, the Glasgow Outcome Scale at 6 months postinjury was significantly higher in the hypothermic group than in the normothermia group. Based on the above, this clinical study with its small patient sample size suggests the need for further prospective randomized studies to examine the role of cytokine suppression in the beneficial effects of moderate hypothermia in patients with traumatic brain injury.

Adolescent↗

Influences of traumatic brain injury on the outcomes of delayed and repeated hemorrhages.

Effects of traumatic brain injury (fluid percussion) on outcomes of hemorrhage, either delayed (70.5 min after the injury) or repeated (0.5 min after injury, then followed by a delayed hemorrhage), were examined in 4 groups of 10 anesthetized rats. Comparisons were made for delayed hemorrhage following sham injury (A1) vs. injury (A2) and for repeated hemorrhage following sham injury (B1) vs. injury (B2). No significant differences were observed in MAP, Cl, HR, SVI, SVRI, and CVP between groups A1 and A2. Hemodynamic recovery was significantly better in B1 than B2 at 70 min after the initial hemorrhage. The respective values of MAP and Cl for the groups B1 and B2 at 70 min were 65 +/- 3 vs. 56 +/- 4 mmHg and 220 +/- 15 vs. 182 +/- 15 ml/min/kg. Brain trauma did not affect survival rate (90 vs. 100%) following delayed hemorrhage, but significantly worsened the outcome of repeated hemorrhage. The 130 min survival rates for groups B1 and B2 were 50% and 10% (P = 0.08), respectively; their survival curves were significantly different (P = 0.02). Our data indicate that brain trauma has greater impact on responses to immediate hemorrhage than delayed hemorrhage, suggesting that traumatic brain injury may have a time-dependent effect on the response to hemorrhage.

Animals↗

Brain-derived neurotrophic factor administration after traumatic brain injury in the rat does not protect against behavioral or histological deficits.

Brain-derived neurotrophic factor has been shown to be neuroprotective in models of excitotoxicity, axotomy and cerebral ischemia. The present study evaluated the therapeutic potential of brain-derived neurotrophic factor following traumatic brain injury in the rat. Male Sprague-Dawley rats (N=99) were anesthetized and subjected to lateral fluid percussion brain injury of moderate severity (2.4-2.8 atm) or sham injury. Four hours after injury, the animals were reanesthetized, an indwelling, intraparenchymal cannula was implanted, and infusion of brain-derived neurotrophic factor or phosphate-buffered saline vehicle was initiated from a mini-osmotic pump and continued for two weeks. In Study 1 (N=48), vehicle or 12 microg/day of brain-derived neurotrophic factor was infused into the dorsal hippocampus. In Study 2 (N=51), vehicle or brain-derived neurotrophic factor at a high (12 microg/day) or low dose (1.2 microg/day) was infused into the injured parietal cortex. All animals were evaluated for neurological motor function at two days, one week and two weeks post-injury. Cognitive function (learning and memory) was assessed at two weeks post-injury using a Morris Water Maze. At two weeks post-injury, neuronal loss in the hippocampal CA3 and dentate hilus and in the injured cortex was evaluated. In Study 2, neuronal loss was also quantified in the thalamic medial geniculate nucleus. All of the above outcome measures demonstrated significant deleterious effects of brain injury (P<0.05 compared to sham). However, post-traumatic brain-derived neurotrophic factor infusion did not significantly affect neuromotor function, learning, memory or neuronal loss in the hippocampus, cortex or thalamus when compared to vehicle infusion in brain-injured animals, regardless of the infusion site or infusion dose (P>0.05 for each). In contrast to previous studies of axotomy, ischemia and excitotoxicity, our data indicate that brain-derived neurotrophic factor is not protective against behavioral or histological deficits caused by experimental traumatic brain injury using the delayed, post-traumatic infusion protocol examined in these studies.

Animals↗

Norepinephrine and traumatic brain injury: a possible role in post-traumatic edema.

Unilateral cerebral contusion is associated with an early (30 min) increase in norepinephrine (NE) turnover followed by a later (6-24 h) depression of turnover which is bilateral and widespread throughout the brain. Blockade of NE function during the first few hours after traumatic brain injury (TBI) impedes subsequent recovery of function without enlarging the size of the lesion. The current studies were carried out to characterize further the timing of the switch from increased to decreased NE turnover and to investigate the pathogenesis of the delayed recovery of function associated with blocking NE function. Adult male rats had unilateral somatosensory cortex contusions made with a 5 mm diameter impact piston. They were killed after 2 h and their brains analyzed for NE turnover by HPLC with electrochemical detection. In general, NE turnover (the ratio of 3-methoxy-4-hyroxyphenylglycol to NE levels) had returned to sham-lesion control levels in most brain regions by 2 h after either left or right sided contusions. The only exceptions were a persistent 87% increase at the lesion site after right-sided contusions and 22% and 32% increases in the contralateral cerebellum after right- and left-sided contusions, respectively. Blockade of alpha1-adrenoceptors by treatment with prazosin (3 mg/ kg, i.p.) 30 min prior to TBI produced edema in the striatum and hippocampus at 24 h which was not seen saline-treated rats nor in rats where NE reuptake was blocked with desmethylimipramine (DMI; 10 mg/kg, i.p.). DMI increased edema at the lesion site at 24 h, however. These data suggest that the early increase in NE release following unilateral cerebral contusion is protective and that this may act to stabilize the blood-brain barrier in areas adjacent to the injury site. Drugs that interfere with this enhanced noradrenergic function might enhance the damage caused by TBI.

3,4-Dihydroxyphenylacetic Acid↗

Therapeutic effects of environmental enrichment on cognitive function and tissue integrity following severe traumatic brain injury in rats.

Postinjury environmental enrichment (EE) has been shown to alter functional and anatomical outcomes in a number of injury paradigms, including traumatic brain injury (TBI). The question of whether EE alters functional outcome following TBI in a model which produces overt histopathological consequences has not been addressed. We investigated this question using the severe, parasagittal fluid percussion injury (FPI) model. Rats (n = 7 per group, enriched and standard for behavior; n = 15 per group for histology) underwent severe (2.2-2.6 atm) FPI, with sham-operated rats (n = 7 per group, enriched and standard for behavior; n = 6 enriched, n = 3 standard for histology) serving as controls. Animals were allowed to recover for 11 days either in standard single housing or together (injured and sham) in an enriched environment consisting of a 92 x 61 x 77-cm ferret cage filled with various stimulatory objects. Consistent with earlier reports, injured animals recovering in the enriched environment showed significantly (P < 0.05) shorter latencies to find the platform in a Morris Water Maze task versus injured/standard animals on day 12 post-TBI. However, both injured groups showed significant deficits versus sham groups (P < 0.05). There were no differences between the sham/enriched and sham/standard groups. No significant group differences in swim speed were observed. At 14 days post-TBI, enriched animals had approximately twofold smaller lesion areas in regions of the cerebral cortex posterior to the injury epicenter (-4.5, -5.8, -6.8 mm relative to bregma; P < 0.05) compared to injured/standard animals. In addition, overall lesion volume for the entire injured cortical hemisphere was significantly smaller in animals recovering in the enriched environment. These results indicate that noninvasive environmental stimulation is beneficial in attenuating cognitive deficits and preserving tissue integrity in a TBI model which causes cerebral contusion and cell death.

Animals↗

The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury.

Cognitive impairments are among the most common neuropsychiatric sequelae of traumatic brain injury at all levels of severity. Cerebral cholinergic neurons and their ascending projections are particularly vulnerable to acute and chronic traumatically mediated dysfunction. In light of the important role of acetylcholine in arousal, attention, memory, and other aspects of cognition, cerebral cholinergic systems contribute to and may also be a target for pharmacologic remediation among individuals with post-traumatic cognitive impairments. This article will review the evidence in support of this hypothesis. Evidence of relatively selective damage to cholinergic injury, the development of persistent anticholinergic sensitivity, and the effects of cholinergic augmentation on memory performance are presented first. Thereafter, neuropathologic, electrophysiologic, and pharmacologic evidence of cholinergic dysfunction after traumatic brain injury in humans is reviewed. Finally, future directions for investigation of the cholinergic hypothesis and possible clinical applications of this information are discussed.

Acetylcholine↗

Ultrastructural changes in tracheobronchial epithelia following experimental traumatic brain injury in rats: protective effect of erythropoietin.

BACKGROUND: We aimed to demonstrate the time dependent ultrastructural changes in tracheobronchial epithelia after traumatic brain injury. And also, protective effect of erythropoietin was demonstrated. METHODS: We used 56 Wistar-Albino female rats weighing 170 to 200 g. The rats were allocated into 7 groups. First group was the control. The second underwent craniotomy without trauma. The third, fourth, and fifth groups were respectively 2-, 8-, and 24-hour trauma groups. The sixth and seventh groups were respectively treatment (erythropoietin, 1,000 IU/kg) and vehicle (0, 4 ml/rat) groups. Weight-drop method was used for achieving head trauma. Samples were obtained from both trachea and main bronchi. Modified electron microscopic scoring model was used to reveal the ultrastructural changes in both trauma and treatment groups. RESULTS: There was no statistical difference between control and sham groups (p >0.05). Scores of all trauma groups were significantly different from the controls (p <0.05). Trauma produced obvious gradual damage on ultrastructure of the tracheobronchial epithelia. Erythropoietin decreased tracheobronchial scores after traumatic brain injury in significant levels. Erythropoietin attenuated ultrastructural scores for each organelle in significant levels (p <0.05 for each organelle). CONCLUSIONS: The data suggested that ultrastructural damage is obvious at 2 hours deteriorating with time. Erythropoietin protects epithelia against damage after traumatic brain injury. Pharmaceutical lung preservation may help gaining efficacious donor lungs in brain death. But, further time dependent experiments are needed to determine the liability of the donor lung after traumatic brain injury. This fact is to be known for achieving higher graft survival rates.

Animals↗

Use of advanced neuroimaging techniques in the evaluation of pediatric traumatic brain injury.

Advanced neuroimaging techniques are now used to expand our knowledge of traumatic brain injury, and increasingly, they are being applied to children. This review will examine four of these methods as they apply to children who present acutely after injury. (1) Susceptibility weighted imaging is a 3-dimensional high-resolution magnetic resonance imaging technique that is more sensitive than conventional imaging in detecting hemorrhagic lesions that are often associated with diffuse axonal injury. (2) Magnetic resonance spectroscopy acquires metabolite information reflecting neuronal integrity and function from multiple brain regions and provides sensitive, noninvasive assessment of neurochemical alterations that offers early prognostic information regarding the outcome. (3) Diffusion weighted imaging is based on differences in diffusion of water molecules within the brain and has been shown to be very sensitive in the early detection of ischemic injury. It is now being used to study the direct effects of traumatic injury as well as those due to secondary ischemia. (4) Diffusion tensor imaging is a form of diffusion weighted imaging and allows better evaluation of white matter fiber tracts by taking advantage of the intrinsic directionality (anisotropy) of water diffusion in human brain. It has been shown to be useful in identifying white matter abnormalities after diffuse axonal injury when conventional imaging appears normal. An important aspect of these advanced methods is that they demonstrate that 'normal-appearing' brain in many instances is not normal, i.e. there is evidence of significant undetected injury that may underlie a child's clinical status. Availability and integration of these advanced imaging methods will lead to better treatment and change the standard of care for use of neuroimaging to evaluate children with traumatic brain injury.

Body Water↗

Executive functions after traumatic brain injury in children.

There is growing recognition that executive function, the superordinate, managerial capacity for directing more modular abilities, is frequently impaired by traumatic brain injury in children and mediates the neurobehavioral sequelae exhibited by these patients. This review encompasses the definition of specific executive functions, age-related changes in executive functions in typically developing children, and the effects of traumatic brain injury on executive functions. The neural substrate for executive functions is described, including relevant functional brain imaging studies that have implicated mediation by prefrontal and parietal cortex and their circuitry. The vulnerability of the neural substrate for executive function to the pathophysiology of traumatic brain injury is discussed, including focal lesions and diffuse axonal injury. Domains of executive functions covered in this review include the basic processes of working memory and inhibition and more complex processes such as decision making. Other domains of executive function, including motivation, self-regulation, and social cognition are discussed in terms of research methodology, clinical assessment, and findings in children with traumatic brain injury. Proposed approaches to the rehabilitation of executive functions are presented.

Brain Injuries↗

Concordance of patient and family report of neurobehavioral symptoms at 1 year after traumatic brain injury.

OBJECTIVE: To determine concordance between patient and family report of neurobehavioral symptoms and problems across 6 domains of function and 3 levels of injury severity at 1 year after traumatic brain injury (TBI). DESIGN: Prospective longitudinal design with follow-up between 10 and 14 months postinjury. SETTING: Seventeen Traumatic Brain Injury Model Systems centers. PARTICIPANTS: A total of 267 adults with primarily moderate and severe TBI who had completed self-ratings and whose neurobehavioral symptoms had also been rated by their significant others. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Neurobehavioral Functioning Inventory-Revised, a 70-item scale with subscales assessing frequency of symptoms in motor, somatic, memory and attention, depression, communication, and aggression domains. RESULTS: Twenty-three items showed significant differences or trends between the self- and other ratings; 18 of these were in the direction of the injured individual reporting less frequent problems. Differences were most pronounced on the depression, aggression, and memory and attention subscales. On the latter 2 subscales, patient-family concordance was higher for those with less severe injuries. However, severity effects were not clear cut. Analyses of selected rating patterns indicating clinically significant "underreporting" of symptoms revealed that these affected the depression, aggression, and memory and attention subscales more than the motor or somatic subscales. CONCLUSIONS: At 1 year post-TBI, concordance between self- and other report of neurobehavioral symptoms was moderately high overall, but varied by symptom domain. For persons with moderate and severe TBI, reports from significant others may be needed for a full picture of the range, severity, and clinical importance of the patient's emotional, behavioral, and cognitive difficulties.

Adolescent↗

Hospitalizations for critically ill children with traumatic brain injuries: a longitudinal analysis.

OBJECTIVE: This study examines the incidence, utilization of procedures, and outcomes for critically ill children hospitalized with traumatic brain injury over the period 1988-1999 to describe the benefits of improved treatment. DESIGN: Retrospective analysis of hospital discharges was conducted using data from the Health Care Cost and Utilization Project Nationwide Inpatient Sample that approximates a 20% sample of U.S. acute care hospitals. SETTING: Hospital inpatient stays from all types of U.S. community hospitals. PARTICIPANTS: The study sample included all children aged 0-21 with a primary or secondary ICD-9-CM diagnosis code for traumatic brain injury and a procedure code for either endotracheal intubation or mechanical ventilation. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Deaths occurring during hospitalization were used to calculate mortality rates. Use of intracranial pressure monitoring and surgical openings of the skull were investigated as markers for the aggressiveness of treatment. Patients were further classified by insurance status, household income, and hospital characteristics. Over the 12-yr study period, mortality rates decreased 8 percentage points whereas utilization of intracranial pressure monitoring increased by 11 percentage points. The trend toward more aggressive management of traumatic brain injury corresponded with improved hospital outcomes over time. Lack of insurance was associated with vastly worse outcomes. An estimated 6,437 children survived their traumatic brain injury hospitalization because of improved treatment, and 1,418 children died because of increased mortality risk associated with being uninsured. Improved treatment was valued at approximately dollar 17 billion, whereas acute care hospitalization costs increased by dollar 1.5 billion (in constant 2000 dollars). Increased mortality in uninsured children was associated with a dollar 3.76 billion loss in economic benefits. CONCLUSIONS: More aggressive management of pediatric traumatic brain injury appears to have contributed to reduced mortality rates over time and saved thousands of lives. Additional lives could be saved if mortality rates could be equalized between insured and uninsured children.

Adolescent↗

Effects of magnesium administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats.

In this study, we examined the effects of magnesium sulfate administration on brain edema and blood-brain barrier breakdown after experimental traumatic brain injury in rats. Seventy-one adult male Sprague-Dawley rats were anesthetized, and experimental closed head trauma was induced by allowing a 450-g weight to fall from a 2-m height onto a metallic disk fixed to the intact skull. Sixty-eight surviving rats were randomly assigned to receive an intraperitoneal bolus of either 750 micromol/kg magnesium sulfate (group 4; n = 30) or 1 mL of saline (group 2; n = 30) 30 minutes after induction of traumatic brain injury; 39 nontraumatized animals received saline (group 1; n = 21) or magnesium sulfate (group 3; n = 18) with an identical protocol of administration. Brain water content and brain tissue specific gravity, as indicators of brain edema, were measured 24 hours after traumatic brain injury. Blood-brain barrier integrity was evaluated quantitatively 24 hours after injury by spectrophotometric assay of Evans blue dye extravasations. In the magnesium-treated injured group, brain water content was significantly reduced (left hemisphere: group 2, 83.2 +/- 0.8; group 4, 78.4 +/- 0.7 [P <.05]; right hemisphere: group 2, 83.1 +/- 0.7; group 4, 78.4 +/- 0.5. [P <.05]) and brain tissue specific gravity was significantly increased (left hemisphere: group 2, 1.0391 +/- 0.0008; group 4, 1.0437 +/- 0.001 [P <.05]; right hemisphere, group 2, 1.0384 +/- 0.001; group 4, 1.0442 +/- 0.005 [P <.05]) compared with the saline-treated injured group. Evans blue dye content in the brain tissue was significantly decreased in the magnesium-treated injured group (left hemisphere: group 2, 0.0204 +/- 0.03; group 4, 0.0013 +/- 0.0002 [P <.05]; right hemisphere: group 2, 0.0064 +/- 0.0009; group 4, 0.0013 +/- 0.0003 [P <.05]) compared with the saline-treated injured group. The findings of the present study support that beneficial effects of magnesium sulfate exist after severe traumatic brain injury in rats. These results also indicate that a blood-brain barrier permeability defect occurs after this model of diffuse traumatic brain injury, and magnesium seems to attenuate this defect.

Animals↗

The role of injury severity in neurobehavioral outcome 3 months after traumatic brain injury.

OBJECTIVE/BACKGROUND: To assess neurobehavioral outcome using the Neurobehavioral Rating Scale-Revised (NRS-R), an instrument with established specificity and validity in Traumatic Brain Injury (TBI) in a sample including the full spectrum of TBI severity 3 months after injury. METHOD: A cohort group of 102 subjects with mild TBI, 41 with moderate TBI, and 139 with severe TBI, from multiple academic trauma centers, were assessed using the NRS-R and the Glasgow Outcome Scale. RESULTS: Principal components analysis of the NRS-R resulted in a 3-factor model: (1) Cognitive, (2) Emotional, and (3) Hyperarousal. At 3 months, subjects with severe TBI show greater difficulties in cognitive and hyperarousal, but not emotional domains, than those with mild to moderate TBI. More than one third of subjects in all injury severity groups showed evidence of anxiety, depression, irritability, mental fatigability, and memory dysfunction. Scores on the NRS-R were related to outcome on the Glasgow Outcome Scale. CONCLUSIONS: Three months after injury, subjects with severe TBI have more dysfunction in cognitive and behavioral (but not emotional) domains than those with mild-to-moderate TBI. The NRS-R is a useful tool for assessing the full spectrum of neurobehavioral dysfunction at all ranges of TBI severity.

Adult↗

Cell death mechanisms following traumatic brain injury.

Neuronal and glial cell death and traumatic axonal injury contribute to the overall pathology of traumatic brain injury (TBI) in both humans and animals. In both head-injured humans and following experimental brain injury, dying neural cells exhibit either an apoptotic or a necrotic morphology. Apoptotic and necrotic neurons have been identified within contusions in the acute post-traumatic period, and in regions remote from the site of impact in the days and weeks after trauma, while degenerating oligodendrocytes and astrocytes have been observed within injured white matter tracts. We review and compare the regional and temporal patterns of apoptotic and necrotic cell death following TBI and the possible mechanisms underlying trauma-induced cell death. While excitatory amino acids, increases in intracellular calcium and free radicals can all cause cells to undergo apoptosis, in vitro studies have determined that neural cells can undergo apoptosis via many other pathways. It is generally accepted that a shift in the balance between pro- and anti-apoptotic protein factors towards the expression of proteins that promote death may be one mechanism underlying apoptotic cell death. The effect of TBI on cellular expression of survival promoting-proteins such as Bcl-2, Bcl-xL, and extracellular signal-regulated kinases, and death-inducing proteins such as Bax, c-Jun N-terminal kinase, tumor-suppressor gene, p53, and the calpain and caspase families of proteases are reviewed. In light of pharmacologic strategies that have been devised to reduce the extent of apoptotic cell death in animal models of TBI, our review also considers whether apoptosis may serve a protective role in the injured brain. Together, these observations suggest that cell death mechanisms may be representative of a continuum between apoptotic and necrotic pathways.

Animals↗

Traumatic Brain Injury Collaborative Planning Group: a protocol for community intervention.

OBJECTIVE: The Traumatic Brain Injury Collaborative Planning Group was formed in December 1992 to address service gaps and better use agencies and their programs to meet the specialized needs of individuals with traumatic brain injury (TBI). SETTING: The group meetings served as the interagency link between service providers for comprehensive planning and problem solving. OUTCOME MEASURES: This article focuses on the three main tasks of this group: (1) interagency case planning among participating agencies; (2) provision of training and networking opportunities for service providers working with this population; (3) development of creative funding mechanisms for community education and support services to assist individuals to live and work in the community. METHODS: The methods used to organize the collaborative, direct it toward the three main tasks, and maintain it without any agency funding are outlined. RESULTS: Data collected about the 21 persons served in the past 3 years is provided, and protocol forms are shared. CONCLUSION: This model of collaboration throughout a countywide area has been used as a basis for similar development in several other states.

Adolescent↗

Coping and emotional adjustment following traumatic brain injury.

OBJECTIVES: To examine the association between coping style and emotional adjustment following traumatic brain injury. PARTICIPANTS: Thirty three individuals who had sustained a traumatic brain injury (mean duration of posttraumatic amnesia = 32 days) between 1(1/2) months and almost 7 years previously. MEASURES: Coping Scale for Adults, Hospital Anxiety and Depression Scale, Rosenberg Self-Esteem Scale, State-Trait Anger Expression Inventory, and the Sickness Impact Profile. RESULTS: Approximately 50% of the sample reported clinically significant levels of anxiety and depression. Coping characterized by avoidance, worry, wishful thinking, self-blame, and using drugs and alcohol was associated with higher levels of anxiety, depression, and psychosocial dysfunction and lower levels of self-esteem. Coping characterized by actively working on the problem and using humor and enjoyable activities to manage stress was associated with higher self-esteem. Lower premorbid intelligence (measured via the National Adult Reading Test) and greater self-awareness (measured via the Self-Awareness of Deficits Interview) were associated with an increased rate of maladaptive coping. CONCLUSIONS: The strong association between the style of coping used to manage stress and emotional adjustment suggests the possibility that emotional adjustment might be improved by the facilitation of more adaptive coping styles. It is also possible that improving emotional adjustment may increase adaptive coping. The development and evaluation of interventions aimed at facilitating adaptive coping and decreasing emotional distress represent important and potentially fruitful contributions to enhancing long-term outcome following brain injury.

Adaptation, Psychological↗

Long-time outcome after transient transtentorial herniation in patients with traumatic brain injury.

BACKGROUND: This study investigates mortality and morbidity in patients with traumatic brain injury (TBI) who developed episode(s) of transtentorial herniation. The transtentorial herniation was defined as a deterioration of consciousness accompanied by uni- or bilateral pupil dilatation. METHODS: The medical records of all patients with traumatic brain injury admitted during 1999 to the Neuro- or General Intensive Care Units at Sahlgrenska University Hospital were analyzed, and patients with at least one episode of transtentoryal herniation were included. Information regarding patient age, gender, type of trauma, initial GCS, precipitating reason for herniation, uni-/bilateral pupil dilatation, treatment(s) and outcome after at least 6 months, assessed with the Glasgow Outcome Scale (GOS), was collected from medical records. RESULTS: The study included 27 patients, average age 44 years (range 6-81), with a male proportion of 81%. The majority of the patients were victims of traffic accidents and falls. The results demonstrated that 16/27(59%) of the patients had a favorable outcome (GOS 4/5), 4/27(15%) were severely disabled (GOS 3), none was vegetative (GOS 2) and 7/27(26%) died (GOS 1). When analyzing patient subgroups, best outcome was found in children where 3/4 (75%) had a GOS 4/5. CONCLUSION: Transtentorial herniation is a serious consequence of supratentorial edema/mass lesions in patients with TBI. However, with aggressive neurointensive care and neurosurgical treatments we found a 59% patient incidence of a favorable outcome.

Adolescent↗

Life satisfaction following spinal cord and traumatic brain injury: a comparative study.

The current study was designed to examine the predictive validity of several factors that are common to spinal cord injury (SCI) and traumatic brain injury (TBI) populations to overall life satisfaction. We examined several demographic and functional predictors (1) within each group separately and (2) using both groups while controlling for unique predictors within groups. Participants included 190 and 57 individuals with SCI and TBI, respectively. To minimize the influence of injury duration, we assessed life satisfaction at 1-year postinjury in both groups. Functional disability (Functional Impairment Measure [FIM]) was the only common predictor within groups. For the TBI group, marital status was also a significant predictor of life satisfaction. None of the other predictors examined was significant among the SCI group. After functional disability and marital status were controlled, overall life satisfaction did not differ between groups. Total explained variance in life satisfaction was low in both groups, 9% and 25% in the SCI and TBI groups, respectively. Future directions are discussed.

Activities of Daily Living↗