***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Mild traumatic brain injury ( mTBI ) secondary to blast exposure is the most common battlefield injury in Southwest Asia . There has been little prospect i ve work in the combat setting to test the efficacy of new counter measures . The goal of this study was to compare the efficacy of N-acetyl cysteine ( NAC ) versus placebo on the symptoms associated with blast exposure mTBI in a combat setting . Methods This study was a r and omized double blind , placebo-controlled study that was conducted on active duty service members at a forward deployed field hospital in Iraq . All symptomatic U.S. service members who were exposed to significant ordnance blast and who met the criteria for mTBI were offered participation in the study and 81 individuals agreed to participate . Individuals underwent a baseline evaluation and then were r and omly assigned to receive either N-acetyl cysteine ( NAC ) or placebo for seven days . Each subject was re-evaluated at 3 and 7 days . Outcome measures were the presence of the following sequelae of mTBI : dizziness , hearing loss , headache , memory loss , sleep disturbances , and neurocognitive dysfunction . The resolution of these symptoms seven days after the blast exposure was the main outcome measure in this study . Logistic regression on the outcome of ‘ no day 7 symptoms ’ indicated that NAC treatment was significantly better than placebo ( OR = 3.6 , p = 0.006 ) . Secondary analysis revealed subjects receiving NAC within 24 hours of blast had an 86 % chance of symptom resolution with no reported side effects versus 42 % for those seen early who received placebo . Conclusion This study , conducted in an active theatre of war , demonstrates that NAC , a safe pharmaceutical countermeasure , has beneficial effects on the severity and resolution of sequelae of blast induced mTBI . This is the first demonstration of an effective short term countermeasure for mTBI . Further work on long term outcomes and the potential use of NAC in civilian mTBI is warranted . Trial Registration Clinical Trials.gov BACKGROUND Traumatic brain injury is a major cause of death and disability . We sought to assess the safety and efficacy of dexanabinol , a synthetic cannabinoid analogue devoid of psychotropic activity , in severe traumatic brain injury . METHODS 861 patients with severe traumatic brain injury admitted to 86 specialist centres from 15 countries were included in a multi-centre , placebo-controlled , phase III trial . Patients were r and omised to receive a single intravenous 150 mg dose of dexanabinol or placebo within 6 h of injury . The primary outcome was the extended Glasgow outcome scale assessed at 6 months , with the point of dichotomisation into unfavourable versus favourable outcome differentiated by baseline prognostic risk . Prespecified subgroup analyses were defined by injury severity , recruitment rate , and time to dosing . Secondary analysis included control of intracranial pressure and quality of life . Analysis were prespecified in the protocol and the statistical analysis plan . This study is registered with Clinical Trials.gov , number NCT00129857 . FINDINGS 846 patients were included in the efficacy analysis . The extended Glasgow outcome scale at 6 months did not differ between groups ; 215 ( 50 % ) patients in the dexanabinol group and 214 ( 51 % ) patients in the placebo group had an unfavourable outcome ( odds ratio for a favourable response 1.04 ; 95 % CI 0.79 - 1.36 ) . Improvements in the control of intracranial pressure or quality of life were not recorded and subgroup analysis showed no indication of differential treatment effects . Dexanabinol was not associated with hepatic , renal , or cardiac toxic effects . INTERPRETATION Dexanabinol is safe , but is not efficacious in the treatment of traumatic brain injury OBJECTIVE To investigate whether supplementation with branched-chain amino acids ( BCAAs ) may improve recovery of patients with a posttraumatic vegetative or minimally conscious state . DESIGN Patients were r and omly assigned to 15 days of intravenous BCAA supplementation ( n=22 ; 19.6g/d ) or an isonitrogenous placebo ( n=19 ) . SETTING Tertiary care rehabilitation setting . PARTICIPANTS Patients ( N=41 ; 29 men , 12 women ; mean age , 49.5+/-21 y ) with a posttraumatic vegetative or minimally conscious state , 47+/-24 days after the index traumatic event . INTERVENTION Supplementation with BCAAs . MAIN OUTCOME MEASURE Disability Rating Scale ( DRS ) as log(10)DRS . RESULTS Fifteen days after admission to the rehabilitation department , the log(10)DRS score improved significantly only in patients who had received BCAAs ( log(10)DRS score , 1.365+/-0.08 to 1.294+/-0.05 ; P<.001 ) , while the log(10)DRS score in the placebo recipients remained virtually unchanged ( log(10)DRS score , 1.373+/-0.03 to 1.37+/-0.03 ; P not significant ) . The difference in improvement of log(10)DRS score between the 2 groups was highly significant ( P<.000 ) . Moreover , 68.2 % ( n=15 ) of treated patients achieved a log(10)DRS point score of .477 or higher ( 3 as geometric mean ) that allowed them to exit the vegetative or minimally conscious state . CONCLUSIONS Supplemented BCAAs may improve the recovery from a vegetative or minimally conscious state in patients with posttraumatic vegetative or minimally conscious state An accurate prognostic model is extremely important in severe traumatic brain injury ( TBI ) for both patient management and research . Clinical prediction models must be vali date d both internally and externally before they are considered widely applicable . Our aim is to independently externally vali date two prediction models , one developed by the Corticosteroid R and omization After Significant Head injury ( CRASH ) trial investigators , and the other from the International Mission for Prognosis and Analysis of Clinical Trials in Traumatic Brain Injury ( IMPACT ) group . We used a cohort of 300 patients with severe TBI ( Glasgow Coma Score [ GCS ] ≤8 ) consecutively admitted to the National Neuroscience Institute ( NNI ) , Singapore , between February 2006 and December 2009 . The CRASH models ( base and CT ) predict 14 day mortality and 6 month unfavorable outcome . The IMPACT models ( core , extended , and laboratory ) estimate 6 month mortality and unfavorable outcome . Validation was based on measures of discrimination and calibration . Discrimination was assessed using the area under the receiving operating characteristic curve ( AUC ) , and calibration was assessed using the Hosmer-Lemeshow ( H-L ) goodness-of-fit test and Cox calibration regression analysis . In the NNI data base , the overall observed 14 day mortality was 47.7 % , and the observed 6 month unfavorable outcome was 71.0 % . The CRASH base model and all three IMPACT models gave an underestimate of the observed values in our cohort when used to predict outcome . Using the CRASH CT model , the predicted 14 day mortality of 46.6 % approximated the observed outcome , whereas the predicted 6 month unfavorable outcome was an overestimate at 74.8 % . Overall , both the CRASH and IMPACT models  showed good discrimination , with AUCs ranging from 0.80 to 0.89 , and good overall calibration . We conclude that both the CRASH and IMPACT models satisfactorily predicted outcome in our patients with severe TBI BACKGROUND AND PURPOSE Enzogenol , a flavonoid-rich extract from Pinus radiata bark with antioxidant and anti-inflammatory properties has been shown to improve working memory in healthy adults . In traumatic brain injury ( TBI ) , oxidation and inflammation have been linked to poorer cognitive outcomes . Hence , this phase II , r and omized controlled trial investigated safety , compliance and efficacy of Enzogenol for improving cognitive functioning in people following mild TBI . METHODS Sixty adults , who sustained a mild TBI , 3 - 12 months prior to recruitment , and who were experiencing persistent cognitive difficulties [ Cognitive Failures Question naire ( CFQ ) score > 38 ] , were r and omized to receive Enzogenol ( 1000 mg/day ) or matching placebo for 6 weeks . Subsequently , all participants received Enzogenol for a further 6 weeks , followed by placebo for 4 weeks . Compliance , side-effects , cognitive failures , working and episodic memory , post-concussive symptoms and mood were assessed at baseline , 6 , 12 and 16 weeks . Simultaneous estimation of treatment effect and breakpoint was effected , with confidence intervals ( CIs ) obtained through a treatment-placebo balance-preserving bootstrap procedure . RESULTS Enzogenol was found to be safe and well tolerated . Trend and breakpoint analyses showed a significant reduction in cognitive failures after 6 weeks [ mean CFQ score , 95 % CI , Enzogenol versus placebo -6.9 ( -10.8 to -4.1 ) ] . Improvements in the frequency of self-reported cognitive failures were estimated to continue until week 11 before stabilizing . Other outcome measures showed some positive trends but no significant treatment effects . CONCLUSIONS Enzogenol supplementation is safe and well tolerated in people after mild TBI , and may improve cognitive functioning in this patient population . This study provides Class IIB evidence that Enzogenol is well tolerated and may reduce self-perceived cognitive failures in patients 3 - 12 months post-mild TBI 
    Output:
    
FINDINGS Critical evaluation of the six studies that met inclusion criteria suggests that antioxidant therapies such as amino acids , vitamins C and E , progesterone , N-acetylcysteine , and enzogenol may be safe and effective adjunctive therapies in adult patients with TBI .
Although certain limitations were found , the overall trend of using antioxidant therapies to improve the clinical outcomes of TBI was positive .
LINKING EVIDENCE TO ACTION By incorporating antioxidant therapies into practice , clinicians can help attenuate the oxidative posttraumatic brain damage and optimize patients ' recovery