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PubMedDate not supplied

Long-term multi-dimensional outcome following isolated traumatic brain injuries and traumatic brain injuries associated with multiple trauma.

We retrospectively investigated long-term, multi-dimensional quality-of-life outcomes in 68 male patients who suffered pure head injuries and 63 male head-injured patients with associated multiple trauma. Results indicated that patients sustaining associated multiple trauma were significantly younger and more deeply comatose on admission. Trends were found to suggest that patients sustaining associated multiple trauma also remain in coma longer, and experience more difficulties in social interaction and overall psychosocial functioning, but less difficulties in mobility compared with pure-head-injured patients. These findings should be taken into account in the evaluation of results of treatment as well as in the planning and allocation of resources for head-injured patients.

Activities of Daily Living↗
PubMed2004

A proposed injury threshold for mild traumatic brain injury.

Traumatic brain injuries constitute a significant portion of injury resulting from automotive collisions, motorcycle crashes, and sports collisions. Brain injuries not only represent a serious trauma for those involved but also place an enormous burden on society, often exacting a heavy economical, social, and emotional price. Development of intervention strategies to prevent or minimize these injuries requires a complete understanding of injury mechanisms, response and tolerance level. In this study, an attempt is made to delineate actual injury causation and establish a meaningful injury criterion through the use of the actual field accident data. Twenty-four head-to-head field collisions that occurred in professional football games were duplicated using a validated finite element human head model. The injury predictors and injury levels were analyzed based on resulting brain tissue responses and were correlated with the site and occurrence of mild traumatic brain injury (MTBI). Predictions indicated that the shear stress around the brainstem region could be an injury predictor for concussion. Statistical analyses were performed to establish the new brain injury tolerance level.

Acceleration↗
PubMed1999

An intrathecal bolus of cyclosporin A before injury preserves mitochondrial integrity and attenuates axonal disruption in traumatic brain injury.

Traumatic brain injury evokes multiple axonal pathologies that contribute to the ultimate disconnection of injured axons. In severe traumatic brain injury, the axolemma is perturbed focally, presumably allowing for the influx of Ca2+ and initiation of Ca2+ -sensitive, proaxotomy processes. Mitochondria in foci of axolemmal failure may act as Ca2+ sinks that sequester Ca2+ to preserve low cytoplasmic calcium concentrations. This Ca2+ load within mitochondria, however, may cause colloid osmotic swelling and loss of function by a Ca2+ -induced opening of the permeability transition pore. Local failure of mitochondria, in turn, can decrease production of high-energy phosphates necessary to maintain membrane pumps and restore ionic balance in foci of axolemmal permeability change. The authors evaluated the ability of the permeability transition pore inhibitor cyclosporin A (CsA) to prevent mitochondrial swelling in injured axonal segments demonstrating altered axolemmal permeability after impact acceleration injury in rat. At the electron microscopic level, statistically fewer abnormal mitochondria were seen in traumatically injured axons from CsA-pretreated injured animals. Further, this mitochondrial protection translated into axonal protection in a second group of injured rats, whose brains were reacted with antibodies against amyloid precursor protein, a known marker of injured axons. Pretreatment with CsA significantly reduced the number of axons undergoing delayed axotomy, as evidenced by a decrease in the density of amyloid precursor protein-immunoreactive axons. Collectively, these studies demonstrate that CsA protects both mitochondria and the related axonal shaft, suggesting that this agent may be of therapeutic use in traumatic brain injury.

Amyloid beta-Protein Precursor↗
PubMed2005

Elevated lactate as an early marker of brain injury in inflicted traumatic brain injury.

BACKGROUND: Traumatic brain injury is a major cause of disability and death in the pediatric population. The metabolic and neurochemical abnormalities that underlie traumatic brain injury remain poorly understood, but hypoxia-ischemic injury might play an important role. OBJECTIVE: This study evaluated children with inflicted traumatic brain injury using magnetic resonance spectroscopy (MRS). We postulated that children with hypoxic-ischemic injury indicated by elevated lactate in the acute phase of injury will have worse early neurological status and short-term clinical outcomes than those without lactate upon MRS. MATERIALS AND METHODS: This prospective study employed proton MRS to sample bilaterally the frontal lobes and the parasagittal cortex within the parietal and occipital lobes of 11 patients with inflicted traumatic brain injury who were undergoing a clinical MRI examination. Patients' measured clinical course while hospitalized included initial neurological evaluation, presence of seizure activity, need for admission to the pediatric intensive care unit (PICU), number of days hospitalized, presence of retinal hemorrhages and presence of bone fractures. Measurement of outcome was determined using the Pediatric Overall Performance Category Scale (POPCS; 1=good performance; 6=death). RESULTS: Four children demonstrated elevated lactate and diminished N-acetyl aspartate (a neuronal marker) within several regions, indicating global ischemic injury (lactate-positive global group). These four children all had seizure activity and abnormal initial neurological examinations and required admission to the PICU. The mean POPCS for this group was 3.25. In four other children, lactate was detected within at least one region, indicating a focal ischemic injury (lactate-positive focal group); two of these children had seizure activity, and two had an abnormal initial neurological examination. The mean POPCS score was 1.5 for this group. The remaining three children had no evidence of lactate upon MRS (lactate-negative group). These children did not have seizure activity, did not require admission to the PICU, nor did they have initial abnormal neurological examinations. The mean POPCS score was 1.3 for this group. SUMMARY: Patients with inflicted traumatic brain injury and evidence of hypoxic-ischemic injury as indicated by elevated lactate on MRS tend to have worse early neurological status and early outcome scores. Lactate levels as sampled by MRS might predict early clinical outcome in inflicted traumatic brain injury.

Aspartic Acid↗
PubMed2026

Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.

Traumatic brain injury (TBI) initiates a complex secondary injury cascade that significantly contributes to long-term neurological deficits, with post-translational modifications (PTMs) emerging as pivotal molecular regulators of this process. Unlike primary mechanical damage, secondary injury evolves over hours to years and involves intricate proteomic alterations that changes in gene expression alone cannot fully explain. PTMs-including phosphorylation, ubiquitination, acetylation, SUMOylation, glycosylation, and emerging modifications such as succinylation, lactylation, and nitrosylation-serve as dynamic molecular switches that fine-tune protein function, stability, localization, and interactions in response to TBI-induced stressors. These modifications play dual roles: they can either promote neuroprotection and recovery or drive pathological processes such as neuronal cell death (via apoptosis, necroptosis, and ferroptosis), neuroinflammation through glial activation and inflammasome signaling, blood-brain barrier disruption, mitochondrial dysfunction, and impaired synaptic plasticity. Critically, extensive crosstalk exists among different PTM pathways-such as the interplay between phosphorylation and ubiquitination in protein degradation or the competitive balance between acetylation and SUMOylation-that collectively shape cellular fate after injury. This nuanced regulatory network presents both challenges and opportunities for therapeutic intervention. Targeting PTM-related enzymes, including kinases, phosphatases, E3 ligases, and histone deacetylases, has shown promise in preclinical models, while novel strategies like Proteolysis-Targeting Chimeras (PROTACs) and repurposed drugs (e.g., metformin, resveratrol) offer innovative avenues for modulating the PTM landscape. Advances in high-throughput proteomics and mass spectrometry are enabling the mapping of TBI-specific PTM signatures across spatiotemporal phases, facilitating the identification of pro-survival versus pro-death modification thresholds. Despite hurdles in clinical translation-such as blood-brain barrier penetration and off-target effects-the growing understanding of PTM dynamics underscores their potential as both biomarkers and therapeutic targets. Future TBI management may thus rely on precision medicine approaches that integrate multi-PTM profiling to guide combination therapies aimed at tipping the balance toward neural repair and functional recovery.

Brain Injuries, Traumatic↗
PubMed2000

Opportunities for neuroprotection in traumatic brain injury.

Traumatic injury of the brain in man is normally followed by little or no recovery of function by the lesioned tissue. Neuroprotective strategies employed in the acute period after traumatic CNS injury attempt to use pharmacological tools to reduce the progressive secondary injury processes that follow after the initial lesion occurs to limit overall tissue damage. Results from experimental animal studies using a variety of drugs that modulate neurotransmitter function, scavenge free radicals, or interfere with cell death cascades point toward many new opportunities for pharmacological intervention in the acute and subacute period after traumatic brain injury.

Acute Disease↗
PubMed2002

Specific gap junctions enhance the neuronal vulnerability to brain traumatic injury.

Traumatic brain injury results in neuronal loss and associated neurological deficits. Although most research on the factors leading to trauma-induced damage focuses on synaptic or ionic mechanisms, the possible role of direct intercellular communication via gap junctions has remained unexplored. Gap junctions connect directly the cytoplasms of coupled cells; hence, they offer a way to propagate stress signals from cell to cell. We investigated the contribution of gap junctional communication (GJC) to cell death using an in vitro trauma model. The impact injury, induced by a weight dropped on the distal CA1 area of organotypic hippocampal slices, results in glutamate-dependent cell loss. The gap junctional blockers carbenoxolone and octanol decreased significantly post-traumatic cell death, measured by propidium iodide staining over a 72 hr period after the impact. Dye coupling in the pyramidal layers was enhanced immediately after the injury and decreased over the following 24 hr. To determine whether specific connexins were involved in the spread of trauma-induced cell death, we used organotypic slices from connexin43 (Cx43) knock-out mice, as well as acute knock-outs by incubation with antisense oligodeoxynucleotides. Simultaneous knockdown of two neuronal connexins resulted in significant neuroprotection. Slices from the null-mutant Cx43 mice, as well as the acute Cx43 knockdown, also showed decreased cell death after the impact. The gap junctional blockers alleviated the trauma-induced impairment of synaptic function as measured by electrophysiological field potential recordings. These results indicate that GJC enhances the cellular vulnerability to traumatic injury. Hence, specific gap junctions could be a novel target to reduce injury and secondary damage to the brain and maximize recovery from trauma.

Animals↗
PubMed2005

Administration of the immunophilin ligand FK506 differentially attenuates neurofilament compaction and impaired axonal transport in injured axons following diffuse traumatic brain injury.

Traumatic axonal injury (TAI) following traumatic brain injury (TBI) remains a clinical problem for which no effective treatment exists. TAI was thought to involve intraaxonal changes that universally led to impaired axonal transport (IAT), disconnection and axonal bulb formation. However, recent, immunocytochemical studies employing antibodies to amyloid precursor protein (APP), a marker of IAT and antibodies to neurofilament compaction (NFC), RM014, demonstrated that NFC typically occurs independent of IAT, indicating the existence of different populations of damaged axons. FK506 administration has been shown to attenuate IAT. However, in light of the above, the ability of FK506 to attenuate axonal damage demonstrating NFC requires evaluation. The current study explored the potential of FK506 to attenuate both populations of damaged axons. Rats were administered FK506 (3 mg/kg) or vehicle 30 min preinjury. Three hours post-TBI, tissue was prepared for the visualization of TAI using antibodies targeting IAT (APP) or NFC (RMO14) or a combined labeling strategy. Confirming previous reports, FK506 treatment reduced the number of axons demonstrating IAT in the CSpT, from 411 +/- 54.70 to 91.00 +/- 33.87 (P <or= 0.05) and in the ML from 78.62 +/- 16.87 to 41.00 +/- 5.80 (P <or= 0.05). FK506 treatment failed to reduce the number of axons demonstrating NFC in either the CSpT or ML. FK506's failure to attenuate NFC suggests that additional therapeutic agents may be necessary to blunt the full burden of TAI. Because FK506 targets IAT, calcineurin appears to be a major target for neuroprotection in damaged axons demonstrating IAT.

Amyloid beta-Protein Precursor↗
PubMed2005

Quantitative analysis of the relationship between intra- axonal neurofilament compaction and impaired axonal transport following diffuse traumatic brain injury.

Traumatic axonal injury (TAI) following traumatic brain injury (TBI) contributes to morbidity and mortality. TAI involves intra-axonal changes assumed to progress to impaired axonal transport (IAT), disconnection, and axonal bulb formation. Immunocytochemical studies employing antibodies to amyloid precursor protein (APP), a marker of IAT and RMO14, a marker of neurofilament compaction (NFC), have shown that TAI involves both NFC and IAT, with the suggestion that NFC leads to IAT. Recently, new data has suggested that NFC may occur independently of IAT. The objective of this study was to determine quantitatively the precise relationship between NFC and IAT. Following TBI, rats were studied at 30 min, 3 h, and 24 h. Using single-label immunocytochemistry employing the antibodies RM014, APP, or a combined labeling strategy targeting APP/RMO14 in aggregate, the immunoreactive (IR) profiles were counted in the corticospinal tract (CSpT) and medial lemniscus (ML). In the CSpT, the number of axons demonstrating RMO14-IR approximated the number of axons showing APP-IR, with the APP-IR population showing a significant increase over 24 h (p < 0.05). The sum of both single-label counts equaled the aggregate APP/RMO14 numbers, demonstrating little relationship between NFC and IAT. In the ML, 75% of fibers demonstrated a separation of APP-IR and NFC-IR; however, 25% of the ML fibers showed co-localization of APP-IR and RMO14. The results of these studies indicate that, in the majority of damaged axons, NFC is not associated with IAT. Our findings argue for the use of multiple markers when evaluating the extent of TAI or the efficacy of therapies targeting the treatment of TAI.

Amyloid beta-Protein Precursor↗
PubMed2000

Calcium channel blockers for acute traumatic brain injury.

BACKGROUND: Acute traumatic brain injury is a major cause of death and disability. Calcium channel blockers have been used in an attempt to prevent cerebral vasospasm after injury, maintain blood flow to the brain and so prevent further damage. OBJECTIVES: To estimate the effects of calcium channel blockers in patients with acute traumatic brain injury and in a subgroup of brain injury patients with traumatic subarachnoid haemorrhage. SEARCH STRATEGY: Hand searching and electronic searching for randomized controlled trials available by October 1997. SELECTION CRITERIA: Randomized controlled trials in patients with all levels of severity of clinically diagnosed acute traumatic brain injury. DATA COLLECTION AND ANALYSIS: Two reviewers (JL and CG) independently assessed the identified studies for eligibility and extracted data from each study. Summary odds ratios were calculated using the Mantel-Haenszel method. MAIN RESULTS: Four RCTs were identified as eligible for inclusion in the systematic review. The effect of calcium channel blockers on the risk of death was reported in all RCTs. The pooled odds ratio for the four studies was 0.91 (95% confidence interval 0. 70 to 1.17). For the three RCTs that reported death and severe disability the pooled odds ratio was 0.85 (95% CI 0.68 to 1.07). In the two RCTs which reported the risk of death in a sub group of traumatic subarachnoid haemorrhage patients, the pooled odds ratio was 0.59 (95% CI 0.37 to 0.94). Three RCTs reported death and severe disability as an outcome in this subgroup, and the pooled odds ratio was 0.67 (95% CI 0.46 to 0.98). REVIEWER'S CONCLUSIONS: This systematic review of randomized controlled trials of calcium channel blockers in acute traumatic head injury patients shows that considerable uncertainty remains over their effects. The effect of nimodipine in a subgroup of brain injury patients with subarachnoid haemorrhage shows a beneficial effect, though the increase in adverse reactions suffered by the intervention group may mean that the drug is harmful for some patients.

Brain Injuries↗
PubMed2000

Mannitol for acute traumatic brain injury.

BACKGROUND: Mannitol is sometimes dramatically effective in reversing acute brain swelling, but its effectiveness in the on-going management of severe head injury remains open to question. There is evidence that in prolonged dosage mannitol may pass from the blood into the brain, where it might cause reverse osmotic shifts that increase intracranial pressure. OBJECTIVES: To assess the effects of different mannitol therapy regimens, of mannitol compared to other intracranial pressure (ICP) lowering agents, and to quantify the effectiveness of mannitol administration given at other stages following acute traumatic brain injury. SEARCH STRATEGY: The review drew on the search strategy for the Injuries Group as a whole. We checked reference lists of trials and review articles, and contacted authors of trials. SELECTION CRITERIA: Randomised trials of mannitol, in patients with acute traumatic brain injury of any severity. The comparison group could be placebo-controlled, no drug, different dose, or different drug. Trials where the intervention was started more than eight weeks after injury, and cross-over trials were excluded. DATA COLLECTION AND ANALYSIS: The reviewers independently rated quality of allocation concealment and extracted the data. Relative risks (RR) and 95% confidence intervals (CI) were calculated for each trial on an intention to treat basis. MAIN RESULTS: Overall there were few eligible trials. There were no trials comparing different doses, or type of administration. One trial compared ICP-directed therapy to 'standard care' (RR for death= 0.83; 95% CI 0.47;1.46). One trial compared mannitol to pentobarbital (RR for death = 0.85; 95% CI 0. 52;1.38). No trials compared mannitol to other ICP lowering agents. One trial tested the effectiveness of pre-hospital administration of mannitol against placebo (RR for death=1.59; 95% CI 0.44;5.79). REVIEWER'S CONCLUSIONS: There are insufficient data to recommend one form of mannitol infusion over another. Mannitol therapy for raised ICP may have a beneficial effect on mortality when compared to pentobarbital treatment. ICP-directed treatment shows a small beneficial effect compared to treatment directed by neurological signs and physiological indicators. There are insufficient data on the effectiveness of pre-hospital administration of mannitol to preclude either a harmful or a beneficial effect on mortality.

Brain Injuries↗
PubMed2005

Corticosteroids for acute traumatic brain injury.

BACKGROUND: Traumatic brain injury is a leading cause of death and disability. Corticosteroids have been widely used in treating people with traumatic brain injury. OBJECTIVES: To quantify the effectiveness and safety of corticosteroids in the treatment of acute traumatic brain injury. SEARCH STRATEGY: Electronic sources: MEDLINE, EMBASE, Cochrane Library and specialised database searches. Additional hand searching and contact with trialists. Date of the most recent search October 2004. SELECTION CRITERIA: All randomised controlled trials of corticosteroid use in acute traumatic brain injury with adequate or unclear allocation concealment. DATA COLLECTION AND ANALYSIS: Quality of allocation concealment was scored. Data on numbers of participants randomised, numbers lost to follow up, length of follow up, case fatality rates, disablement, infections and gastrointestinal bleeds were extracted independently and checked. MAIN RESULTS: We identified 20 trials with 12303 randomised participants. The effect of corticosteroids on the risk of death was reported in 17 included trials. Due to significant heterogeneity we did not calculate a pooled estimate of the risk of death. The largest trial, with about 80% of all randomised participants, found a significant increase in the risk ratio of death with steroids 1.18 (1.09 to 1.27). For the nine trials that reported death or severe disability, the pooled relative risk was 1.01 (0.91 to 1.11), although this does not yet contain data from the largest trial. For infections the pooled risk ratio from five trials was 1.03 (0.99 to 1.07) and for the ten trials reporting gastrointestinal bleeding 1.23 (0.91 to 1.67). AUTHORS' CONCLUSIONS: In the absence of a meta-analysis, we feel most weight should be placed on the result of the largest trial. The increase in mortality with steroids in this trial suggest that steroids should no longer be routinely used in people with traumatic head injury.

Brain Injuries↗
PubMed2005

Myelinated and unmyelinated axons of the corpus callosum differ in vulnerability and functional recovery following traumatic brain injury.

Traumatic axonal injury (TAI), a common feature of traumatic brain injury, is associated with postinjury morbidity and mortality. However, TAI is not uniformly expressed in all axonal populations, with fiber caliber and anatomical location influencing specific TAI pathology. To study differential axonal vulnerability to brain injury, axonal excitability and integrity were assessed in the corpus callosum following fluid percussion injury in the rat. In brain slice electrophysiological recordings, compound action potentials (CAPs) were evoked in the corpus callosum, and injury effects were quantified separately for CAP waveform components generated by myelinated axons (N1 wave) and by unmyelinated axons (N2 wave). Ultrastructural analyses were also conducted of TAI-induced morphological changes in these axonal populations. The two populations of axons differed in response to brain injury, and in their functional recovery, during the first week postinjury. Amplitudes of N1 and N2 were significantly depressed at 3 h, 1 day, and 3 days survival. N1 amplitudes exhibited a recovery to control levels by 7 days postinjury. In contrast, N2 amplitudes were persistently suppressed through 7 days postinjury. Strength-duration properties of evoked CAPs further differentiated the effects of injury in these axonal populations, with N2 exhibiting an elevated strength-duration time constant postinjury. Ultrastructural observations revealed degeneration of myelinated axons consistent with diffuse injury sequelae, as well as previously undocumented pathology within the unmyelinated fiber population. Collectively, these findings demonstrate differential vulnerabilities of axons to brain injury and suggest that damage to unmyelinated fibers may play a significant role in morbidity associated with brain injury.

Action Potentials↗
PubMed2004

Impaired axonal transport and altered axolemmal permeability occur in distinct populations of damaged axons following traumatic brain injury.

Traumatic axonal injury (TAI) evolves within minutes to hours following traumatic brain injury (TBI). Previous studies have identified axolemmal disruption and impaired axonal transport (AxT) as key mechanisms in the evolution of TAI. While initially hypothesized that axolemmal disruption culminates in impaired AxT, previous studies employed single-label methodologies that did not allow for a full determination of the spatial-temporal relationships of these two events. To explore directly the relationship between impaired AxT and altered axolemmal permeability, the current investigation employed 40, 10, and 3 kDa fluorescently conjugated dextrans as markers of axolemmal integrity, with antibodies targeting the anterogradely transported amyloid precursor protein (APP) utilized as a marker of impaired AxT. Rats underwent impact acceleration TBI and were intrathecally administered 40 kDa, 40 + 10 kDa or 40 + 3 kDa fluorescently tagged dextrans, with brains subsequently prepared for APP immunofluorescence. Brainstem corticospinal tracts (CSpT), medial lemnisci (ML), and medial longitudinal fasciculi were examined for evidence of TAI. APP and all dextrans consistently localized to distinct classes of TAI. Dextrans were noted as early as 5 min following injury within axonal segments demonstrating an irregular/tortuous appearance, and were seen within thin and elongate/vacuolated axons by 30 min-6 h following injury. APP, first noted within swollen axons at 30 min following injury, was found within progressively swollen axons that showed no dextran colocalization within 3 h of injury. However, by 6 h, dextrans colocalized in disconnected axonal bulbs. At this time-point, dextrans also persisted within single-labeled, highly vacuolated/thin, and elongate axons. These studies confirm that axolemmal disruption and impaired AxT occur as distinct non-related events early in the pathogenesis of TAI. Further, these studies provide evidence that the process of impaired axonal transport and subsequent axonal disconnection leads to delayed axolemmal instability, rather than proceeding as a consequence of initial axolemmal failure. This finding underscores the need of multiple approaches to fully assess the axonal response to TBI.

Amyloid beta-Protein Precursor↗
PubMed1998

Interleukin-10 improves outcome and alters proinflammatory cytokine expression after experimental traumatic brain injury.

Traumatic injury to the central nervous system initiates inflammatory processes that are implicated in secondary tissue damage. These processes include the synthesis of proinflammatory cytokines, leukocyte extravasation, vasogenic edema, and blood-brain barrier breakdown. Interleukin-10 (IL-10), a cytokine with antiinflammatory properties, negatively modulates proinflammatory cascades at multiple levels. We examined the hypothesis that IL-10 treatment can improve outcome in a clinically relevant model of traumatic brain injury (TBI). IL-10 was administered via different routes and dosing schedules in a lateral fluid-percussion model of TBI in rats. Intravenous administration of IL-10 (100 micrograms) at 30 min before and 1 h after TBI improved neurological recovery and significantly reduced TNF expression in the traumatized cortex at 4 h after injury. Such treatment was associated with lower IL-1 expression in the injured hippocampus, and to a lesser extent, in the injured cortex. Subcutaneous IL-10 administration (100 micrograms) at 10 min, 1, 3, 6, 9, and 12 h after TBI also enhanced neurological recovery. In contrast, intracerebroventricular administration of IL-10 (1 or 6 micrograms) at 15 min, 2, 4, 6, and 8 h after TBI was not beneficial. These results indicate that IL-10 treatment improves outcome after TBI and suggest that this improvement may relate, in part, to reductions in proinflammatory cytokine synthesis.

Animals↗
PubMed2000

Corticosteroids for acute traumatic brain injury.

BACKGROUND: Traumatic brain injury is a leading cause of death and disability. Corticosteroids have been widely used in treating people with traumatic brain injury. OBJECTIVES: To quantify the effectiveness and safety of corticosteroids in the treatment of acute traumatic brain injury. SEARCH STRATEGY: Electronic sources: MEDLINE, EMBASE, Cochrane Library and specialised database searches. Additional hand searching and contact with trialists. Date of the most recent search June 1999. SELECTION CRITERIA: All randomized controlled trials of corticosteroid use in acute traumatic brain injury with adequate or unclear allocation concealment. DATA COLLECTION AND ANALYSIS: Quality of allocation concealment was scored. Data on numbers of participants randomized, numbers lost to follow up, length of follow up, case fatality rates, disablement, infections and gastrointestinal bleeds were extracted independently and checked. MAIN RESULTS: We identified 19 trials with 2295 randomized participants. The effect of corticosteroids on the risk of death was reported in 16 included trials. The pooled relative risk for the 16 trials was 0.96 (95% confidence interval 0.85 to 1. 08). Pooled risk difference was 1.3% (5.2% to 2.5% more). For the nine trials that reported death or severe disability, the pooled relative risk was 1.01 (0.91 to 1.11). For infections the pooled relative risk was 0.94 (0.76 to 1.16) and for the nine trials reporting gastrointestinal bleeding 1.11 (0.54 to 2.26). Using only those trials with the best quality of allocation concealment, the pooled relative risk estimate for death became closer to unity. REVIEWER'S CONCLUSIONS: Neither moderate benefits nor moderate harmful effects of steroids can be excluded. The widely practicable nature of the drugs and the importance of the health problem suggest that large simple trials are feasible, and worthwhile, to establish whether there are any benefits from corticosteroids in this situation.

Brain Injuries↗