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BACKGROUND: Traumatic brain injury is a kind of injury caused by external violence on the head. Its danger is not limited to life rescue in the early stage of the disease. Moreover, the subsequent inflammatory reaction and the change in its oxidative stress level will cause secondary myocardial injury. The purpose of this study is to explore the myocardial protective effect of ozone autohemotherapy (OA) in the progression of acute traumatic brain injury (TBI). METHODS: Forty patients with acute TBI were recruited and divided into The treatment group (Group OA, n = 18) and the Control group (Group C, n = 19). Patients in Group OA received OA before surgery and on the 1st and 2nd postoperative days, while patients in Group C underwent autologous blood transfusion. Venous blood was collected from all patients before (T0) and after 7 days (T1) days of surgery for measurement of cardiac troponin T (cTnT) and amino-terminal pro-B-type natriuretic peptide (NT-proBNP). At T0 and T1, transthoracic cardiac ultrasound was performed to measure left ventricular ejection fraction (LVEF), tricuspid annular plane systolic excursion (TAPSE), and venous blood was sampled to determine the contents of superoxide dismutase (SOD) and malondialdehyde (MDA). NIH Stroke Scale (NIHSS) and Glasgow Coma Scale (GCS) scores were calculated, and other clinical indexes were recorded. RESULTS: (1) The levels of cTnT at T1 were significantly higher as compared with that at T0 in both groups (p < 0.01). Compared with Group C, a remarkable decline in the content of NT-proBNP was found in Group OA at T1 (p = 0.021). (2) The LVEF (p = 0.002) and serum SOD (p = 0.015) at T1 were significantly increased in Group OA as compared with those in Group C. (3) The length of Intensive Care Unit and hospitalization time for patients in Group OA was distinctly shorter than that for patients in Group C (p = 0.021, p = 0.015, respectively). CONCLUSION: Perioperative OA treatment can alleviate the secondary myocardial injury during the disease course of TBI, which might be associated with its myocardial protective effect against oxidative stress. TRIAL REGISTRATION: This study was approved by the Ethical Committee of Changzhou NO.2 People's Hospital. The protocol was registered prospectively with the Chinese Clinical Trial Registry (ChiCTR2000029612) on February 02, 2020.

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BACKGROUND: This study tested whether phloretin (a brain-edema inhibitors) would augment therapeutic impact of human-derived platelet-rich plasma (hPRP) on attenuating brain-hemorrhagic volume (BHV) and preserving the neurologic function in rodent following acute traumatic brain damage (TBD). METHODS: Rats (n=40) were separated into group-1 (sham-control), group-2 (TBD), group-3 [TBD + phloretin (80mg/kg/dose by intra-peritoneal administration at 30min and days 2/3 followed-by TBD), group-4 (TBD + PRP/80µL by left intra-carotid-artery injection at 3h after TBD) and group-5 (TBD + phloretin + hPRP) and cerebral tissues were harvested by day 28 after TBD. RESULTS: The brain MRI at day 28 revealed that the BHV was lowest in group 1, highest in group 2 and significantly lower in group 5 than in groups 3/4, but it was similar between groups 3/4, whereas neurological function displayed a opposite pattern of BHV among the groups (all p&amp;amp;lt;0.0001). By 72h, the protein levels of upstream (HGMB1/TLR-2/TLR-4/MyD88/Mal/TRAM/ TRIF/TRAF6/IKK-α/IKK-ß/p-NF-κB) and downstream (IL-1ß/TNF-α/iNOS) inflammation signalings, apoptosis (caspase3/PARP) and fibrosis (Smad3/TGF-ß) biomarkers and flow cytometric assessment of inflammation cells (CD11b/c+//Ly6G+/PMO+) and early (AN-V+/PI-)/late (AN-V+/PI+) mononuclear-cell apoptosis displayed a similar manner of BHV among the groups (all p&amp;amp;lt;0.0001). Cell number of inflammatory (CD68+/MMP9+) and brain-swelling/myelin-damaged (AQP4+/ GFAP+) mediators revealed a similar way, whereas the neuronal-myelin (Doublecortin+/NeuN/nestin) mediators exhibited an inverse manner of BHV among the groups (all p&amp;amp;lt;0.0001). CONCLUSION: Combination of phloretin and hPRP regimen was better than just one treatment to offer synergic benefits for protecting the brain against TBD.

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There is currently no efficacious intervention for preventing post-traumatic epilepsy (PTE). Preclinical studies support the potential use of anticholinergics for this condition. The purpose of this study was to evaluate the effects of biperiden as an intervention for preventing PTE. A randomized, double-blinded clinical trial was conducted at HC/FMUSP between 2018-2022. Adults with acute traumatic brain injury (TBI) were randomly assigned to receive biperiden or placebo, for 10 days. The primary outcome was the incidence of PTE while the secondary outcomes included the frequency of seizures, the frequency of any adverse events and mortality after 24 months. The study was powered at a planned enrolment of 132 patients. The trial began in January 2018 and was halted by researchers on March 2020 (and terminated in December 2022) in the face of the global COVID-19 pandemic. Overall, 123 participants were randomized and 112 contributed with data for modified mITT analysis, being that 61 (49.5%) participants completed the 24-month follow-up consult. Data analysis indicated lack of evidence of biperiden for either, the incidence of post-traumatic epilepsy (2.6, 95%CI, 0.65-10.57; p = 0.170) or the mortality rate (1.57, 95%CI, 0.73-3.38; p = 0.248). The frequency of late post-traumatic seizures was higher for biperiden group (2.03, 95%CI = 0.912-3.1597; p <0.001). The present study suggests that there was insufficient evidence regarding the effect of biperiden in preventing PTE after TBI, which underpins the need for larger studies. Clinical trial registration: ClinicalTrials.gov, identifier: NCT01048138.

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Traumatic brain injury (TBI) stands as a significant contributor to traumatic death and disability worldwide. In recent years, researchers have identified biomarkers to gauge useful outcomes in TBI patients. However, the enigma of timely sample collection to measure the biomarkers remains a controversial point in the case of TBI, unlike other degenerative diseases like Alzheimer's disease and Parkinson's disease, where we can collect the sample at any point in time. The purpose of this study is to evaluate the sensitivity of biomarkers in TBI concerning time of injury by analyzing recent available data on biomarkers in the medical literature. A total of 2,256 studies were initially retrieved from the search engine. After an initial screening, only 1,750 unique articles remained. After excluding review articles, animal studies, meta-analysis, and studies with children (screened by title and abstract), 30 kinds of literature were found relevant to search the required variables. Further 16 studies were excluded due to the nonavailability of complete variables or data. Finally, 14 studies remained and were included in the analysis. This study has analyzed the four most commonly described biomarkers for TBI in the literature: glial fibrillary acidic protein (GFAP), S100 calcium-binding protein B, ubiquitin carboxy-terminal hydrolase L1, and Tau. According to this statistical analysis, all biomarkers included in the study have shown their serum levels after trauma. So, all these biomarkers can be used for further study in the outcome prediction and diagnosis of TBI patients. The meta-analysis suggests that the best biomarker for TBI is Tau in cases where sample collection is done within 24 hours, while GFAP is the best biomarker to be studied for TBI if sample collection is done 24 hours after trauma.

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The focus of this article is on the acute management of traumatic brain injury. The article focuses on the classification of traumatic brain injury, general acute management of traumatic brain injury, the role of the physiatrist on this team, and lastly, behavioral and family considerations in the acute care setting. The article includes a focus on physiologic systems, strategies for the management of various aspects of brain injury, and consideration of factors associated with the continuum of care. Overall, the article reviews this critical period of brain injury recovery and provides a primer for the physiatrist.

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Background: Traumatic brain injuries involving the posterior fossa are rare and case reports indicate they often result in severe outcomes. We seek to describe characteristics and outcomes of traumatic posterior fossa injuries. Methods: We performed a planned secondary analysis of all patients with posterior fossa injuries enrolled in the NEXUS head computed tomography (CT) validation study dataset. The dataset includes prospectively collected data on all patients undergoing non-contrast cranial CT following blunt traumatic head injury from April 2006 to December 2015, at four emergency departments comprising community and university sites, as well as urban, suburban and rural settings in California (Antelope Valley Hospital, San Francisco General Hospital, UCLA Ronald Reagan Medical Center, UCSF Fresno Community Regional Medical Center). We classified each patient into one of three injury patterns: Type I-notable traumatic injuries primarily above the tentorium, with minimal posterior fossa involvement; Type II-notable traumatic injuries both above and within the posterior fossa; and Type III-notable traumatic injuries primarily within the posterior fossa. We extracted demographic data for each patient as well as physician assessments of the NEXUS head CT and Canadian Head CT rule clinical criteria, mechanisms of injury, patient outcomes, and the location and types of intracranial injuries sustained. Findings: Of 11,770 patients in the database, 184 (1.6%) had posterior fossa injuries on CT imaging. Mean age was 55.4 years (standard deviation 22.5 years, range 2-96 years); 131 (71.2%) were males. We identified 63 patients with Type I injuries, 87 with Type II injuries, and 34 Type III injuries. The most common mechanisms of injury were falls (41%), pedestrian vs automobile (15%), and motor vehicle collisions (13%). On presentation most patients had altered mental status (72%), abnormal behavior (53%), or a neurologic deficit (55%). The majority of individuals, 151 (82%), had clinically important injuries and 111 (60%) required neurosurgical intervention. The dispositions for the subjects included 52 deaths (28%), 49 (27%) patients discharged home, and 48 (26%) discharged to rehabilitation facilities. When compared to individuals with Type I and Type II injuries, patients with Type III injuries had lower mortality (6% vs 30% and 35%) and higher percentage of patients discharged home (60% vs 19% and 21%). Interpretation: Patients with Type I and II injury patterns (those that involve both the posterior fossa and supratentorium) experienced high mortality and disability. Patients with Type III injuries (isolated posterior fossa) had a better prognosis. Funding: None.

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BACKGROUND:It has been shown that in a mouse model of acute traumatic brain injury,the transcriptional and translational levels of silent information regulator 1(SIRT1)activated by drugs significantly elevates the expression of SIRT1 in brain tissue,reduces inflammatory and oxidative stress in brain tissue,and improves neurological function. OBJECTIVE:To investigate the mechanism of intraperitoneal injection of SRT1720,an activator of SIRT1,to alleviate acute traumatic brain injury in rats. METHODS:Ninety Sprague-Dawley rats were randomized into three groups(n=30 per group):a sham group(without modeling),a model group and an activator group.Animal models of acute traumatic brain injury were established in the latter two groups.At 6 hours after modeling,the sham,model and activator groups were injected intraperitoneally with dimethyl sulfoxide solution,methylsulfoxide solution and SRT1720 once a day for 28 days,respectively.The time points for sampling were set,and rats'neurological function,brain tissue water content,brain tissue oxidative stress and inflammatory response,brain tissue morphology,apoptosis and angiogenesis,and the protein expression of SIRT1 in brain tissue were detected and measured. RESULTS AND CONCLUSION:Compared with the sham group,the modified neurological deficit score,brain tissue water content and apoptosis rate of rats were increased in the model group at 7,14 and 28 days of injection(P<0.05);compared with the model group,the modified neurological deficit score,brain tissue water content and apoptosis rate of rats were decreased in the activator group(P<0.05).Compared with the sham group,the levels of reactive oxygen radicals and myeloperoxidase in the brain tissue were increased(P<0.05),the levels of malondialdehyde,tumor necrosis factor α and interleukin 6 in the serum were increased(P<0.05),and the levels of superoxide dismutase in the serum were decreased in the model group at 7,14 and 28 days of injection(P<0.05).Compared with the model group,the levels of reactive oxygen radicals and myeloperoxidase in the brain tissue were decreased(P<0.05),the levels of malondialdehyde,tumor necrosis factor α and interleukin 6 in the serum were decreased(P<0.05),and the levels of superoxide dismutase in the serum were increased in the activator group at 7,14 and 28 days of injection(P<0.05).Immunohistochemical staining at 7,14 and 28 days of injection showed that the number of new vessels in the brain tissue was higher in the model group than the sham group(P<0.05)as well as higher in the activator group than the model group(P<0.05).Western blot assay indicated that at 7,14 and 28 days of injection,the expression of SIRT1 protein in the brain tissue was lower in the model group than the sham group(P<0.05)and higher in the activator group than the model group(P<0.05).Hematoxylin-eosin staining showed that at 7,14 and 28 days of injection,the degree of brain injury in the activator group was less than that in the model group.To conclude,intraperitoneal injection of the SIRT1 signal activator SRT1720 can significantly reduce oxidative and inflammatory stress in the brain tissue,inhibit neuronal apoptosis,promote angiogenesis,and alleviate brain injury in rats with acute traumatic brain injury.

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Purpose: In order to evaluate the neuroprotective effect of low-intensity pulsed ultrasound (LIPUS) for acute traumatic brain injury (TBI), we studied the potential of apparent diffusion coefficient (ADC) values and ADC-derived first-order features regarding this problem. Methods: Forty-five male Sprague Dawley rats (sham group: 15, TBI group: 15, LIPUS treated: 15) were enrolled and underwent magnetic resonance imaging. Scanning layers were acquired using a multi-shot readout segmentation of long variable echo trains (RESOLVE) to decrease distortion. The ultrasound transducer was applied to the designated region in the injured cortical areas using a conical collimator and was filled with an ultrasound coupling gel. Regions of interest were manually delineated in the center of the damaged cortex on the diffusion weighted images (b = 800 s/mm2) layer by layer for the TBI and LIPUS treated groups using the open-source software ITK-SNAP. Before analysis and modeling, the features were normalized using a z-score method, and a logistic regression model with a backward filtering method was employed to perform the modeling. The entire process was completed using the R language. Results: During the observation time, the ADC values ipsilateral to the trauma in the TBI and LIPUS groups increased rapidly up to 24 h. After statistical analysis, the 10th percentile, 90th percentile, mean, skewness, and uniformity demonstrated a significant difference among three groups. The receiver operating characteristic curve (ROC) analysis shows that the combined LR model exhibited the highest area under the curve value (AUC: 0.96). Conclusion: The combined LR model of first-order features based on the ADC map can acquire a higher diagnostic performance than each feature only in evaluating the neuroprotective effect of LIPUS for TBI. Models based on first-order features may have potential value in predicting the therapeutic effect of LIPUS in clinical practice in the future.

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OBJECTIVE: Dizziness is common in patients with acute traumatic brain injury (aTBI). However, patients are not always managed by the ward team but instead are referred to a visiting vestibular neurology team or referred for outpatient follow-up. We aimed to ascertain whether training trauma ward therapists to manage a common form of post-traumatic dizziness (Benign paroxysmal positional vertigo [BPPV]) reduced referrals to a visiting vestibular neurology team. DESIGN: Referrals of patients with aTBI with complaints of dizziness to the visiting vestibular neurology team were audited from the Major Trauma Centre at Imperial College Healthcare NHS Foundation Trust, London, UK. Ward therapists subsequently received training on management of BPPV. Referrals to the vestibular neurology service were re-audited. Therapist confidence in assessing and treating BPPV was also assessed pre and post-training. RESULTS: Pre-training, referral rate to the visiting vestibular neurology service was eight patients per month. Following training, referrals to the vestibular neurology service reduced by 35%. Therapist confidence improved significantly following training. CONCLUSIONS: Training trauma ward therapists to manage BPPV reduced referrals to a visiting vestibular neurology service. Further research is necessary to assess implications for service and patient level parameters, such as length of stay and time to discharge.

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OBJECTIVES: Systematically review the medical literature for the impact of beta-blockers on mortality and functional capacity in patients who suffered severe traumatic brain injury. DATA SOURCES: The search included MEDLINE, EMBASE, and Ovid Evidence-Based Medicine, clinical trial registries, and bibliographies. STUDY SELECTION: All articles that reported outcome in TBI patients treated with beta-blockers. DATA EXTRACTION: Publication year, number of patients, outcome and follow-up. We performed a meta-analysis for each variable for which there were sufficient data to estimate mean differences. DATA SYNTHESIS: 12 studies were included, which involved retrospectively and prospectively collected data on 14,057 patients. The treatment with beta-blockers was associated with a reduction in mortality in patients who were treated with beta-blockers compared to the control group (OR 0.40, 95% CI 0.30-0.54p = <0.00001), with acceptable heterogeneity between studies (I2 = 65% p = 0.00008). Beta-blocker therapy decreases the risk of negative neurological and functional outcomes (OR 0.59, 95% CI 0.38-0.92 p = <0.00001), a very high statistical heterogeneity between the included studies (I2 = 80% p = 0.00004), being able to influence the results. An increase in favorable neurological and functional outcomes is shown (OR 1.19, 95% CI 1.07-1.31 p = 0.001) with acceptable heterogeneity (I2 = 52% p = 0.08). CONCLUSIONS: The beta-blockers therapy is associated with significantly improves outcome in patients with TBI. Treatment with beta-blockers in patients with TBI is a promising frontier in neurotrauma. ABBREVIATIONS: CI: confidence interval; BB: Beta-Blockers; OR = odds ratio; TBI: Traumatic Brain Injury SD: Standard deviation; SNS: Sympathetic nervous system.

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Gender may be related with the outcome of patients with acute traumatic brain injury (TBI). We explored the effect of gender on the outcome of 7145 patients with acute TBI. There was no statistical difference between male and female sex in the causes of trauma, age, Glasgow Coma Scale score, computed tomgraphy findings, and surgical management. The mortality of 7145 patients with acute TBI in males and females was 7.48% and 7.22%, respectively, with the corresponding unfavorable outcomes of 16.05% and 17.23%, respectively (p > 0.05 in both cases). The mortality of 1626 patients with severe TBI in males and females was 19.68% and 20.72%, respectively, with the corresponding unfavorable outcomes of 46.96% and 48.85%, respectively (p > 0.05 in both cases). Our data suggest that sex does not play a role in the outcome of patients with acute TBI.

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An 82-year-old female suffered from head trauma, and developed acute consciousness disturbance 6 days after the event. Head CT showed the acute subdural hematoma in the left temporooccipital area and the patient underwent emergency hematoma evacuation and decompression. However, her consciousness disturbance became worse after surgery. Intermittent large negative infraslow shifts (lasting longer than 40 seconds) were recorded in the right posterior quadrant by scalp EEG with TC of 2 sec, that was defined as cortical spreading depolarizations (CSDs). Clinically consciousness disturbance sustained poor until 1 month after surgery in spite of treatment by anti-epileptic drugs. CSDs were observed on the right side where head injury most likely occurred. It may explain the sustained consciousness disturbance associated with significant prolonged ischemia. Once scalp EEG could record CSDs in this particular patient, the degree and its prognosis of traumatic head injury were estimated.

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BACKGROUND: Traumatic brain injury (TBI) has increased in rank among traumatic injuries worldwide. Traumatic brain injury is a serious obstacle given that its complex pathology represents a long-term process. Recently, systems biology strategies such as metabolomics to investigate the multifactorial nature of TBI have facilitated attempts to find biomarkers and probe molecular pathways for its diagnosis and therapy. METHODS: This study included a group of 20 rats with controlled cortical impact and a group of 20 sham rats. We utilized mNSS tests to investigate neurological metabolic impairments on day 1 and day 3. Furthermore, we applied metabolomics and bioinformatics to determine the metabolic perturbation caused by TBI during the acute period in the hippocampus tissue of controlled cortical impact (CCI) rats. Notably, TBI-protein-metabolite subnetworks identified from a database were assessed for associations between metabolites and TBI by the dysregulation of related enzymes and transporters. RESULTS: Our results identified 7 and 8 biomarkers on day 1 and day 3, respectively. Additionally, related pathway disorders showed effects on arginine and proline metabolism as well as taurine and hypotaurine metabolism on day 3 in acute TBI. Furthermore, according to metabolite-protein database searches, 25 metabolite-protein pairs were established as causally associated with TBI. Further, bioinformation indicated that these TBI-associated proteins mainly take part in 5'-nucleotidase activity and carboxylic acid transmembrane transport. In addition, interweaved networks were constructed to show that the development of TBI might be affected by metabolite-related proteins and their protein pathways. CONCLUSION: The overall results show that acute TBI is susceptible to metabolic disorders, and the joint metabolite-protein network analysis provides a favorable prediction of TBI pathogenesis mechanisms in the brain. The signatures in the hippocampus might be promising for the development of biomarkers and pathways relevant to acute TBI and could further guide testable predictions of the underlying mechanism of TBI.

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Traumatic brain injury (TBI) is a public health problem worldwide. Secondary damage of brain injury begins within a few minutes after the trauma and can last a long time. It can be reversible, unlike primary injury. Therefore, therapeutic intervention can be used. The aims of this study were to assess the effects of minocycline on neurological function and serum S100B protein and neuron-specific enolase (NSE) levels in patients with moderate to severe TBI. Patients with acute onset of TBI and surgical evacuation of hematoma were randomized to receive either minocycline 100 mg orally twice daily or placebo for 7 days. The primary outcomes included changes in level of S100B and NSE at different time points during the trial. Additionally, changes in Glasgow coma scale (GCS) score were evaluated. The Glasgow Outcome Scale-Extended (GOS-E) score at 6 months after injury was assessed in discharge patients. Thirty four patients were randomized into the placebo (n = 20) and treatment (n = 14) groups. There was a marginal statistically significant differences in the normalized value of S100B between groups (p < 0.1). The reduction in serum NSE level from baseline to day 5 was statistically significant (p = 0.01) in minocycline group while it was not significantly decrease in placebo group (p = 0.2). Also, GCS improvement over time within the minocycline group was significant (p = 0.04) while was not significant in placebo group (p = 0.11). The GOS-E scores were not significantly different between minocycline and placebo group. Based on this study, it seems that the use of minocycline may be effective in acute TBI.

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OBJECTIVE： To evaluate the efficacy and safety of progesterone in the treatment of acute traumatic brain injury systematically， and to provide reference for clinical use. METHODS： Retrieved from Cochrane library， ClinicalTrials， Web of Science， PubMed， Embase， CBM， CNKI and Wanfang database， randomized controlled trial （RCTs） about progesterone （trial group） versus placebo or blank control （control group） in the treatment of acute traumatic brain injury were collected. After literature screening， data extraction and quality evaluation by risk bias evalution tool of Cochrane systematic evaluator manual 5.1.0， Meta-analysis was performed by using Rev Man 5.3 statistical software. RESULTS： A total of 10 RCTs were included， involving 2 652 patients. Results of Meta-analysis showed that there was no statistical significance in mortality[RR＝0.77，95％CI（0.56，1.07），P＝0.12]， the incidence of septicemia [RR＝1.11，95％CI（0.77，1.60），P＝0.59] or elevated liver enzymes[RR＝1.30，95％CI（0.68，2.50），P＝0.43]. The number of patients with favorable neurological outcome[RR＝1.23，95％CI（1.05，1.43），P＝0.008] in trial group was significantly more than control group. Results of subgroup analysis of mortality showed that there was no statistical significance in the mortality of patient’s GCS≤8 [RR＝0.79，95％CI（0.57，1.10），P＝0.16]， that of patient’s GCS≤12[RR＝0.69，95％CI（0.23，2.10），P＝0.52] or that of patient’s GCS ranging from 9 to 12 [RR＝0.78，95％CI（0.26，2.35），P＝0.65] between 2 groups. Results of subgroup analysis of neurological outcome showed that there was no statistical significance in the number of favorable neurological outcome of patient’s GCS≤8 [RR＝1.18， 95％CI（0.98，1.43），P＝0.09]， the number of favorable outcome of patient’s GCS≤12[RR＝1.15，95％CI（0.87，1.51），P＝0.32] and the number of favorable neurological outcome of patient’s GCS ranging from 9 to 12[RR＝2.07，95％CI（0.24，17.71），P＝0.51]. CONCLUSIONS： Progesterone can improve the prognosis of neurological function in patients with acute traumatic brain injury with good safety but cannot reduce mortality.

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Xuefu Zhuyu Decoction (XFZY), an important traditional Chinese herbal formula, has been reported effective on traumatic brain injury (TBI) in rats. However, its cerebral protection mechanism has not been clarified at the metabolic level. This work aims to explore the global metabolic characteristics of XFZY in rats during the acute phase of TBI on days 1 and 3. A plasma metabolomics method based on gas chromatography-mass spectrometry coupled with univariate analysis and multivariate statistical analysis was performed in three groups (Sham, Vehicle, XFZY). Then, a pathway analysis using MetaboAnalyst 3.0 was performed to illustrate the pathways of therapeutic action of XFZY in TBI. XFZY treatment attenuates neurological dysfunction and cortical lesion volume post-injury on day 3, and reverses the plasma metabolite abnormalities (glutamic acid, lactic acid, 3-hydroxybutyric acid, and ribitol, etc.). These differential metabolites are mainly involved in D-glutamine and D-glutamate metabolism, alanine, aspartate and glutamate metabolism, and inositol phosphate metabolism. Our study reveals potential biomarkers and metabolic networks of acute TBI and neuroprotection effects of XFZY, and shows this metabolomics approach with MetaboAnalyst would be a feasible way to systematically study therapeutic effects of XFZY on TBI.

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For a significant percentage of subjects, with chronic traumatic brain injury (TBI), who report persisting cognitive impairment and functional loss, the diagnosis is often impeded by the fact that routine neuroimaging often does not reveal any abnormalities. In this paper, we used diffusion tensor imaging (DTI) to investigate the apparently normal white matter (as assessed by routine magnetic resonance imaging) in the brains of 19 subjects with sub-acute (9) and chronic (10) TBI. We also assessed memory, executive function, and visual-motor coordination in these subjects. Using a voxel-wise approach, we investigated if parameters of diffusion were significantly different between TBI subjects and 17 healthy controls (HC), who were demographically matched to the TBI group. We also investigated if changes in DTI parameters were associated with neuropsychological performance in either group. Our results indicate significantly increased mean and axial diffusivity (MD and AD, respectively) values in widespread brain locations in TBI subjects, while controlling for age, sex, and time since injury. HC performed significantly better than the TBI subjects on tests of memory and executive function, indicating the persisting functional loss in chronic TBI. We found no correlation between diffusion parameters and performance on test of executive function in either group. We found negative correlation between FA and composite memory scores, and positive correlation between RD and visuomotor coordination test scores, in various tracts in both groups. Our study suggests that changes in MD and AD can indicate persisting micro-structure abnormalities in normal-appearing white matter in the brains of subjects with chronic TBI. Our results also suggest that FA in major white matter tracts is correlated with memory in health and in disease, alike; larger and longitudinal studies are needed to discern potential differences in these correlations in the two groups.

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AIM: The present study was carried out to examine this hypothesis that administration of selenium can prevent the development of injuries by brain trauma and thus can modulate patients' functional recovery and also improve posttraumatic outcome. MATERIALS AND METHODS: This double-blinded controlled trial was carried out on 113 patients who were hospitalized following traumatic brain injury (TBI) with Glasgow Coma Scale score of 4-12 that were randomly assigned to receive selenium within 8 h after injury plus standard treatment group or routine standard treatment alone as the control. The primary endpoint was to assess patients' functional recovery at 2 months after the injury based on extended Glasgow Outcome Scale score (GOS-E). Secondary outcomes included the changes in Full Outline of Unresponsiveness score (FOUR) score, Sequential Organ Failure Assessment (SOFA) score, and acute physiology and chronic health evaluation (APACHE) III score, side effects of selenium, length of Intensive Care Unit (ICU) stay, and length of hospital stay. RESULTS: There was no difference in the length of ICU and hospital stay, the trend of the change in FOUR and SOFA scores within 15 days of first interventions, and the mean APACHE III score on the 1st and 15th days between the two groups. Mortality was 15.8% in selenium group and 19.6% in control group with no between-group difference. No difference was revealed between the two groups in appropriate outcome according to GOS-E score at 60 ± 10 days and also 30 ± 5 days according to the severity of TBI. CONCLUSION: This human trial study could not demonstrate beneficial effects of intravenous infusion of selenium in the improvement of outcomes in patients with acute TBI.

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αII-spectrin breakdown products are regarded as potential biomarkers for traumatic brain injury (TBI). The aim of the present study was to further evaluate these biomarkers by assessing their clinical utility in predicting the severity of injury and clinical outcome of patients with TBI. Eligible patients with acute TBI (n=17), defined by a Glasgow Coma Scale (GCS) score of ≤8, were enrolled. Ventricular cerebrospinal fluid (CSF) was sampled from each patient at 24, 72 and 120 h following TBI. An immunoblot assay was used to determine the concentrations of SBDPs in the CSF samples. The concentrations of SBDPs combined with the GCS score at 24 h after injury and the Glasgow Outcome Score (GOS) at 30 days after injury were compared and analyzed. The levels of SBDPs in CSF were markedly increased following acute TBI in comparison with those in the control group. In the early period after TBI, the levels of SBDPs were closely associated with GCS score. Comparisons of the SBDP levels with the severity of injury revealed significant differences between patients with the most severe brain injury and patients with severe brain injury in the first 24 h post-injury (P<0.05). The levels and dynamic changes of SBDPs in CSF exhibited a close association with GOS at 30 days after injury. The levels of SBDPs differed significantly between patients grouped according to prognosis (P<0.05). These results suggest that in the early period after TBI, the levels and dynamic changes of SBDPs in CSF can be useful in the prediction of the severity of injury and clinical outcome of patients.