Prognosis Of Traumatic Brain Injury Research Articles

Gamma frequency entrainment rescues cognitive impairment by decreasing postsynaptic transmission after traumatic brain injury.

The relationship between oscillatory activity in hippocampus and cognitive impairment in traumatic brain injury (TBI) remains unclear. Although TBI decreases gamma oscillations and 40 Hz light flicker improves TBI prognosis, the effects and mechanism of rhythmic flicker on TBI remain unclear. In this study, we aimed to explore whether light flicker could reverse cognitive deficits, and further explore its potential mechanisms in TBI mouse model. The Morris water maze test (MWM), step-down test (SDT), and novel object recognition test (NOR) were applied to evaluate the cognitive ability. The local field potential (LFP) recording was applied to measure low gamma reduction of CA1 in hippocampus after TBI. And electrophysiological experiments were applied to explore effects of the gamma frequency entrainment on long-term potentiation (LTP), postsynaptic transmission, and intrinsic excitability of CA1 pyramidal cells (PCs) in TBI mice. Immunofluorescence staining and western blotting were applied to explore the effects of 40 Hz light flicker on the expression of PSD95 in hippocampus of TBI mice. We found that 40 Hz light flicker restored low gamma reduction of CA1 in hippocampus after TBI. And 40 Hz, but not random or 80 Hz light flicker, reversed cognitive impairment after TBI in behavioral tests. Moreover, 40 Hz light flicker improved N-methyl-D-aspartate (NMDA) receptor-dependent LTP (LTPNMDAR ) and L-type voltage-gated calcium channel-dependent LTP (LTPL-VGCC ) after TBI treatment. And gamma frequency entrainment decreased excitatory postsynaptic currents (EPSCs) of CA1 PCs in TBI mice. Our results have illustrated that 40 Hz light flicker could decrease intrinsic excitability of PCs after TBI treatment in mice. Furthermore, 40 Hz light flicker decreased the expression of PSD95 in hippocampus of TBI mice. These results demonstrated that 40 Hz light flicker rescues cognitive impairment by decreasing postsynaptic transmission in PCs after TBI treatment in mice.

Prognosis and Outcome of Severe Traumatic Brain Injury Following Decompressive Craniectomy- A Single Center Study

Prognosis and Outcome of Severe Traumatic Brain Injury Following Decompressive Craniectomy- A Single Center Study

Colloidal gold-based immunochromatographic biosensor for quantitative detection of S100B in serum samples.

Traumatic brain injury has become a serious public health problem. Timely detection, diagnosis and treatment of brain injury are closely related to the prognosis of patients, so identification of highly sensitive and specific biochemical markers of brain injury has important clinical value. Currently, the most studied and most promising marker is the protein S100B. In this study, a rapid quantitative biosensor for S100B was established using colloidal gold labeling and double antibody (8C10-6B8) sandwich immunochromatography. The biosensor was capable of quantifying S100B within 15 min, and showed no cross-reactivity with S100A, NSE, GFAP, or PGP9.5. The detection limit was determined to be 4.6 pg mL-1 with a linear range of 0.01-2 ng mL-1. Recovery experiments also indicated that the method had an acceptable accuracy. Moreover, the quantitative colloidal gold assay correlated well with the results of a chemiluminescence immunoassay when testing 40 clinical serum samples. Our developed colloidal gold quantitative immunochromatographic biosensor is a rapid, sensitive, specific and accurate method for the detection of S100B protein in serum, which is useful in the clinic for early diagnosis, as well as assessment of disease progression and prognosis of traumatic brain injury.

Retracted: Analysis of Clinical Characteristics and Prognosis of Traumatic Brain Injury in Papua New Guinea.

[This retracts the article DOI: 10.1155/2021/4948664.].

Emergency Management of Traumatic Brain Injuries Current Guideline and New Developments

Annually, traumatic brain injury keeps afflicting millions of individuals around the world. Traumatic brain injury may manifest in various forms from minor changes in consciousness to persistent comatoseness and death. The entirety of the brain is impacted by a diffused type of injury and edema in the most severe form of traumatic brain injury. Depending on the degree of the injury, there are many different treatment options, ranging from regular cognitive therapy sessions to invasive surgical procedures like bilateral decompressive craniectomies. Clinical practice guidelines have been developed to standardize assessment, discharge education, and referral of traumatic brain injury patients in order to achieve best practice management. Guidelines are described as propositions derived from research and used to direct clinicians and patients in making decisions about the highest degree of care and best practices in clinical practice. In order to minimise the risk of secondary brain injury and maximise the prognosis, early detection and therapy of severe traumatic brain injury are essential. The methodical evaluation and management of life-threatening situations that result from this is followed by invasive steps to control the airway, respiratory physiology, and hemodynamics, all with the main objective of maintaining a sufficient level of cerebral perfusion. Preventing secondary injury is the fundamental goal of early therapy of severe traumatic brain injury, specifically by preventing hypotension and hypoxia. The purpose of this research is to review the available information about the emergency management of traumatic brain injury current guideline and new developments

Diagnostic Competence of Creatine Kinase BB, in Mild Traumatic Brain Injury and its Prognostic Value.

Due to the very high and increasing prevalence, essential complications, and risk factors for psychiatric disorders, it is necessary to introduce screening tests for diagnosing and predicting mild traumatic brain injury (mTBI) prognosis. After completing the consent form and recording information and examination findings of patients with mild trauma, venous blood samples were taken from these patients. The samples were measured by observing the cold chain. After 3 months from mTBI, the post concussion symptoms questionnaire (PCSQ) and the short form 36 (SF-36) questionnaire for physical and mental evaluations were performed. Statistical tests analyzed the relationship between different variables and serum Creatine kinase BB (CKBB) levels. Statistic analyses showed no relation between CKBB level of serum and age, gender, level of consciousness, PCSQ, and SF 36 scale, and the interval between trauma and arrival to the hospital. Further, there is a significant correlation between CK-BB levels and intracranial damage based on Fisher's exact test. This study and following more significant considerations can introduce a serum-based biomarker panel that can accurately differentiate patients with complicated mTBI from those with uncomplicated.

The role of spectrin breakdown products in patients with traumatic brain injury: a systematic review and meta-analysis.

Spectrin Breakdown Products (SBDPs) accumulate in the brain after traumatic brain injury (TBI) and are expected to become a potentially promising biomarker of TBI. This systematic review and meta-analysis were undertaken to evaluate the role of SBDPs in the diagnosis and prognosis of TBI. We systematically searched the following databases up to 31 October 2022: Ovid MEDLINE, PubMed, EMBASE, Cochrane Library, and Web of Science Database, and studies were only included if they had sufficient data on SBDP concentrations in TBI patients. We calculated the standardized mean differences (SMDs) and 95% confidence intervals (CIs) for continuous outcomes and assessed the potential publication bias by using Egger's test and funnel plots. The statistical analysis was conducted by RevMan 5.4 and Stata 17. Of 1429 identified studies, 10 studies involving 417 participants were included in our systematic review and meta-analysis. The results demonstrated that serum and cerebrospinal fluid (CSF) SBDP concentrations were significantly increased in TBI compared to controls (SBDP120: SMD = 1.42, 95% CI = 0.71 ~ 2.12, P < 0.00001; SBDP145: SMD = 1.32, 95% CI = 0.78 ~ 1.86, P < 0.00001; SBDP150: SMD = 1.39, 95% CI = 0.97 ~ 1.80, P < 0.00001), and CSF SBDPs were significantly associated with poor functional outcomes (PFO) (SBDP145: SMD = 1.75, 95% CI = 1.37 ~ 2.13, P < 0.00001; SBDP150: SMD = 1.14, 95% CI = 0.75 ~ 1.52, P < 0.00001). In addition, CSF and serum SBDP145 are valuable in diagnosing TBI (AUC = 0.89, 95% CI = 0.80 ~ 0.99, P < 0.00001), and CSF SBDP145 also has diagnostic value for PFO (AUC = 0.80, 95% CI = 0.76 ~ 0.84,P < 0.00001). The limited evidence supports that the SBDPs can be employed as potential biomarkers for the diagnosis and prognosis of TBI.

Troponin I New Biomarker in Traumatic Brain Injury

Mortality in traumatic brain injury (TBI) is thought to be pathology in the heart-brain axis but its effect on the prognosis of traumatic brain injury remains unclear. Our study aimed to investigate the relationship between cardiac troponin I (cTnI) level and prognosis in TBI patients. Between January 2017 and May 2021, 480 patients diagnosed with TBI, who applied to the emergency department, were retrospectively included in this multicentric study. The databases of the hospitals were examined comprehensively and the demographic, clinical, laboratory, radiological, and therapeutic data and results of the patients were obtained. The severity of trauma and clinical status was evaluated with AIS, Injury Severity Score (ISS), ASA physical status, and Glasgow Coma Scale (GCS). The severity of the trauma was evaluated with the ISS. The modified Rankin Scale (mRS) and the Glasgow Outcome Scale (GOS) at discharge were used to evaluate in-hospital clinical outcomes. cTnI levels were classified into three categories: normal (< 0.05 ng/ml), mildly elevated (0.05–0.99 ng/ml), and severely elevated (≥ 1 ng/ml). The mean age of the patients was 41.7 and 75.4% of them were men. It was observed that mortality among patients over 65 years (13.9%) increased. High cTnI was detected in 284 (59.1%) patients. Although it was not statistically significant regarding the elevation of cTnI in patients under 65 years of age (P = 0.62), the difference was significant for cTnI in patients over 65 years of age (P < 0.001). The relationship between cTnI elevation was found to be statistically significant (P < 0.001) as the severity of the trauma increased and when severe additional traumas (thoracic, abdominal, or pelvic) occurred. A high cTnI level is associated with poor prognosis in TBI patients. cTnI measurement is a useful tool for early risk stratification and accelerated care; however, further prospective studies are needed.

Predictors of Early Outcome in Patients Admitted at the Emergency Department with Traumatic Brain Injury: a Retrospective Cross-Sectional Study

Aim: The purpose of this study was to determine the factors that help predict early mortality in patients in the emergency department that have suffered a severe traumatic brain injury. Study design: A retrospective cross-sectional study Place and duration: Chandka Medical College/ Civil Hospital Larkana. April 2018- March 2020 Methodology: Retrospective analysis was used to study 198 patients that were admitted to the emergency department due to severe traumatic brain injury. The radiological, clinical, basic demographical, and biological data were all recorded when the patient was first admitted and while they were staying in the emergency department. Results: The results showed that 42 patients died. According to the univariate analysis, the presence of low value of Glasgow coma scale, bilateral mydriasis, shock, the high value of injury severity score, and cardiac arrest played a major role in the deaths of such patients. Poor outcome was associated with cerebral hematoma, subdural hematoma, and meningeal hemorrhage. A link was seen between poor prognosis and cardiac arrest and cerebral hematoma. Conclusions: In our study, subdural hematoma, intracranial hematoma, and meningeal hemorrhage were associated with mortality. To improve the prognosis of severe traumatic brain injury, prehospital care has to be improved. Additionally, futile resuscitations should be avoided. It is also very important to take a CT scan of the head as urgently as possible to detect operable mass lesions. Keywords: traumatic brain injury, early outcome, emergency department

Effect of Red Cell Distribution Width on the Prognosis of Patients with Traumatic Brain Injury: A Retrospective Cohort Study

The link between red cell distribution width (RDW) and prognosis of traumatic brain injury (TBI) is controversial. Whether RDW can increase the prognostic value of established predictors remains unknown. This study aimed to provide supportive evidence for the prognostic value of RDW. Clinical data of 1488 patients with TBI were extracted from the Multiparameter Intelligent Monitoring in Intensive Care III database and classified into 2 groups: 1) one with RDW <14.5% (n= 1061) and 2) the other with RDW ≥14.5% (n= 427). Multivariable logistic regression models were used to estimate the relationship between RDW and outcomes. Stratified analyses and interactions were also performed. We compared the area under the receiver operating characteristic curve of the International Mission for Prognoses and Clinical Trial Design in TBI (IMPACT) core and extended models with and without RDW. After adjusting for confounding factors, RDW was an independent risk consideration for TBI prognoses; the odds ratios were 1.62 (95% confidence interval (CI): 1.05, 2.50) and 1.89 (95% CI: 1.35, 2.64) for hospital mortality and 6-month mortality, respectively. This association was crucial for patients with a Glasgow Coma Score of 3-12 (odds ratio, 2.79; 95% CI: 1.33, 5.87). For 6-month mortality, when RDW was added to the core and extended IMPACT models, the area under the receiver operating characteristic curve increased from 0.833 to 0.851 (P= 0.001) and from 0.842 to 0.855 (P= 0.002), respectively. Elevated RDW is an independent risk consideration for hospital and 6-month mortality rates. When RDW was added to the IMPACT core and extended models, it improved its predictive ability for 6-month mortality in patients with TBI.

Progress in research on the role of clinical nutrition in treating traumatic brain injury affecting the neurovascular unit.

The neurovascular unit (NVU) is composed of neurons, glial cells, and blood vessels. NVU dysfunction involves the processes of neuroinflammation, and microcirculatory disturbances, as well as neuronal injury after traumatic brain injury (TBI). Traditional anti-inflammatory drugs have limited efficacy in improving the prognosis of TBI. Thus, treatments that target NVU dysfunction may provide a breakthrough. A large number of clinical studies have shown that the nutritional status of patients with TBI was closely related to their conditions and prognoses. Nutrient complexes and complementary therapies for the treatment of TBI are therefore being implemented in many preclinical studies. Importantly, the mechanism of action for this treatment may be related to repair of NVU dysfunction by ensuring adequate omega-3 fatty acids, curcumin, resveratrol, apigenin, vitamins, and minerals. These nutritional supplements hold promise for translation to clinical therapy. In addition, dietary habits also play an important role in the rehabilitation of TBI. Poor dietary habits may worsen the pathology and prognosis of TBI. Adjusting dietary habits, especially with a ketogenic diet, may improve outcomes in patients with TBI. This article discusses the impact of clinical nutrition on NVU dysfunction after TBI, focusing on nutritional complexes and dietary habits.

Surface-fill H2S-releasing silk fibroin hydrogel for brain repair through the repression of neuronal pyroptosis

Traumatic brain injury (TBI) remains the major cause of disability and mortality worldwide due to the persistent neuroinflammation and neuronal death induced by TBI. Among them, pyroptosis, a specific type of programmed cell death (PCD) triggered by inflammatory signals, plays a significant part in the pathological process after TBI. Inhibition of neuroinflammation and pyroptosis is considered a possible strategy for the treatment of TBI. In our previous study, exogenous hydrogen sulfide(H2S) exerted a neuroprotective effect after TBI. Here, we developed a surface-fill H2S-releasing silk fibroin (SF) hydrogel (H2S@SF hydrogel) to achieve small-dose local administration and avoid volatile and toxic side effects. We used a controlled cortical impact (CCI) to establish a mild TBI model in mice to examine the effect of H2S@SF hydrogel on TBI-induced pyroptosis. We found that H2S@SF hydrogel inhibited the expression of H2S synthase in neurons after TBI and significantly inhibited TBI-induced neuronal pyroptosis. In addition, immunofluorescence staining results showed that the necroptosis protein receptor-interacting serine/threonine-protein kinase 1 (RIPK1) partially colocalized with the pyroptosis protein Gasdermin D (GSDMD) in the same cells. H2S@SF hydrogel can also inhibit the expression of the necroptosis protein. Moreover, H2S@SF hydrogel also alleviates brain edema and the degree of neurodegeneration in the acute phase of TBI. The neuroprotective effect of H2S@SF hydrogel was further confirmed by wire-grip test, open field test, Morris water maze, beam balance test, radial arm maze, tail suspension, and forced swimming test. Lastly, we also measured spared tissue volume, reactive astrocytes and activated microglia to demonstrate H2S@SF hydrogel impacts on long-term prognosis in TBI. Our study provides a new theoretical basis for the treatment of H2S after TBI and the clinical application of H2S@SF hydrogel. Statement of significanceSilk fibroin (SF) hydrogel controls the release of hydrogen sulfide (H2S) to inhibit neuronal pyroptosis and neuroinflammation in injured brain tissue. In this study, we synthesized a surface-fill H2S-releasing silk fibroin hydrogel, which could slowly release H2S to reshape the homeostasis of endogenous H2S in injured neurons and inhibit neuronal pyroptosis in a mouse model of traumatic brain injury. Meanwhile, H2S@SF hydrogel could alleviate brain edema and the degree of neurodegeneration, improve motor dysfunction, anxious behavior and memory impairment caused by TBI, reduce tissue loss and ameliorate neuroinflammation. Our study provides a new theoretical basis for the treatment of H2S after TBI and the clinical application of H2S@SF hydrogel.

The combination of arterial lactate level with GCS-pupils score to evaluate short term prognosis in traumatic brain injury: a retrospective study

BackgroundThe aim of the study was to determine whether the combination of Glasgow Coma Scale (GCS) and Pupil responses score (GCSP) with arterial lactate level would be an index to predict the short term prognosis in patients with traumatic brain injury (TBI).MethodsA retrospective study was performed enrolling all TBI patients admitted to intensive care unit (ICU) from 2019 to 2020. The demographics, clinical characteristics, and arterial lactate concentration were recorded. The GCSP and arterial blood analysis (ABG) with lactate was tested as soon as the patient was admitted to ICU. The Glasgow Outcome Scale (GOS) after discharge was regarded as the clinical outcome. A new index named GCSP-L was the combination of GCSP and lactate concentration. GCSP-L was the GCSP score (range 1-15) plus the lactate score (range 0-2). The lactate score was defined based on different lactate concentrations. If lactate was below 2 mmol/L, lactate score was 0, which above 5 mmol/L was 2 and between 2 and 5 mmol/L, the score was 1. As the range of GCSP was 1-15, the range of the GCSP-L was 1 to 17. The area under receiver operating characteristic curve (AUC) was calculated to evaluate the predictive ability of GCSP, lactate and GCSP-L. Statistical significance was set when p value < 0.05.ResultsA total of 192 TBI patients were included in the study. Based on GCSP, mild, moderate, and severe TBI were 13.02, 14.06 and 72.92%, respectively. There were 103 (53.65%) patients with the lactate concentration below 2 mmol/L (1.23 ± 0.37 mmol/l), 63 (32.81%) of the range from 2 to 5 (3.04 ± 2.43 mmol/l) and 26 (13.54%) were above 5 mmol/l (7.70 ± 2.43 mmol/l). The AUC was 0.866 (95% CI 0.827-0.904) for GCSP-L, 0.812 (95% CI 0.765-0.858) for GCSP and 0.629 (95% CI 0.570—0.0.688) for lactate. The AUC of GCSP-L was higher than the other two, GCSP and lactate alone.ConclusionsThe combination of GCSP and lactate concentration can be used to predict the short term prognosis in TBI patients.

The predictive role of systemic inflammation response index in the prognosis of traumatic brain injury: A propensity score matching study.

We aimed to evaluate the predictive power of systemic inflammation response index (SIRI), a novel biomarker, to predict all-cause mortality in patients with traumatic brain injury (TBI) in the intensive care unit (ICU). Clinical data were retrieved from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database. Kaplan-Meier (KM) methods and cox proportional hazard models were performed to examine the association between SIRI and all-cause mortality. The predictive power of SIRI was evaluated compared to other leukocyte-related indexes including neutrophils, lymphocytes, monocytes and white blood cells (WBC) by the Receiver Operating Characteristic (ROC)curve for 30-day mortality. In addition, propensity score matching (PSM) was conducted to reduce confounding. A total of 350 TBI patients were enrolled overall in our study. The optimal cutoff point of SIRI was determined at 11.24 × 109/L. After 1:1 PSM, 66 matched pairs (132 patients) were generated. During the 30-day, in-hospital and 365-day follow-up periods, patients with low SIRI level were associated with improved survival (p < 0.05) compared with patients with high SIRI level. Cox regression analysis identified that higher SIRI values was an independent risk factor for all-cause mortality and results were stable on multiple subgroup analyses. Furthermore, ROC analysis indicated that the area under the curve of SIRI [0.6658 (95% Confidence Interval, 0.5630-0.7687)] was greater than that of neutrophils, monocytes, lymphocytes and WBC. The above results were also observed in the matched cohort. It was suggested that TBI patients with high SIRI level would suffer from a high risk of 30-day, in-hospital and 365-day mortality. SIRI is a promising inflammatory biomarker for predicting TBI patients' prognosis with relatively better predictive power than other single indicators related to peripheral differential leukocyte counts.

Serum Acylcarnitine and Long-Term Functional Prognosis after Traumatic Brain Injury with Intracranial Injury: A Multi-Center Prospective Study.

Serum biomarkers have potential to help predict prognosis of traumatic brain injury (TBI). The objective of this study was to evaluate the association between serum acylcarnitine levels and functional outcomes at 1 month/6 months after injury for TBI patients with intracranial hemorrhage or diffuse axonal injury. This study is a multi-center prospective cohort study in which adult TBI patients with intracranial injury visiting the emergency departments (EDs) from December 2018 to June 2020 were enrolled. Serum acylcarnitine levels at the time of ED arrival were categorized into four groups: low (1.2-5.5 μmol/L), low-normal (5.6-10.0 μmol/L), high-normal (10.1-14.5 μmol/L), and high (1.4.6-56.6 μmol/L). The study outcome was set as poor functional recovery at 1 month/6 months after injury (Glasgow Outcome Scale score, 1-3). Multi-level logistic regression analyses were conducted to estimate association between serum acylcarnitine and functional outcomes. Among total of 549 patients, poor functional recovery at 1 month and 6 months after injury were observed in 29.1% (160/549) and 29.1% (158/543, follow-up loss n = 6). The odds for 1-month poor functional outcome increased in the high-normal and the high groups [adjusted odds ratios, AORs (95% confidence intervals, CIs): 1.56 (1.09-2.23) and 2.47 (1.63-3.75)], compared with the low-normal group) and also as a continuous variable [1.05 (1.03-1.07) for each 1 μmol/L]. Regarding 6-month mortality, the high group had significantly higher odds when compared with the low-normal group [AOR (95% CI): 2.16 (1.37-3.40)]. Higher serum acylcarnitine levels are associated with poor functional outcomes at 1 month/6 months after injury for TBI patients with intracranial injury.

Risk of pre-existing hyponatremia and mortality in patients with traumatic brain injury across age groups

Traumatic brain injurySodiumClinical outcomes.

Effect of Controlling Nutritional Status Score (CONUT) and Prognostic Nutritional Index (PNI) on patients after spinal tuberculosis surgery.

The controlling nutritional status (CONUT) score and prognostic nutrition index (PNI) are immune-nutritional biomarkers that are related to clinical prognosis. Previous studies have reported using them to predict the prognosis of traumatic brain injury, tumours and other diseases. The purpose of this study was to evaluate the relationship between the PNI and CONUT score and the one-year prognosis of patients with spinal tuberculosis (STB). In this study, the clinical characteristics of 97 patients with STB who underwent debridement and internal fixation at our institution between 2015 and 2020 were retrospectively analysed. According to the receiver operating characteristic (ROC) curve, patients were divided into two groups: a high CONUT group and a low CONUT group. Patients were also divided into a high PNI group and a low PNI group. One-year postoperative prognosis was evaluated by the clinical cure standard. Patients in the favourable group were younger and had a lower rate of pneumonia and urinary tract infection, higher PNI and lower CONUT score than those in the favourable group (P < 0.05). There was an obvious correlation between the PNI and CONUT score (r = − 0.884, P < 0.05). The areas under the curve (AUCs) of the CONUT score and PNI for predicting unfavourable prognosis were 0.888 (95% CI 0.808–0.943, P < 0.001) and 0.896 (95% CI 0.818–0.949, P < 0.001), respectively. The adjusted odds ratios (ORs) of the CONUT score and PNI for predicting unfavourable outcomes were 2.447 (95% CI 1.518–4.043, P < 0.001) and 0.689 (95% CI 0.563–0.843, P < 0.001), respectively. Higher CONUT scores and a lower PNI were associated with adverse outcomes in patients with spinal tuberculosis, and the CONUT score and PNI might be independent predictors of adverse outcomes of spinal tuberculosis postoperatively.

Effect of Serum Osmolarity on Prognosis of Traumatic Brain Injury

Introduction: Road traffic accident has been a significant cause of mortality in today's fast paced world. Metabolic and intracranial parameters have affected the outcome of traumatic brain injury. Countless analysis on biomechanical injury and tissue damage has substantiated additional treatment strategies. Laboratory values have been less investigated to predict the outcome of brain injury.&#x0D; Aims: This study was done to find out the association between the serum osmolarity with severity of head injury and the outcome in traumatic brain injury.&#x0D; Methods: This study was conducted at Department of Neurosurgery, Nepalgunj Medical college, Kohalpur, Banke from July 2020 to June 2021. 106 patients were included in the study. Clinical profile of the patients and calculated plasma osmolarity were monitored daily.&#x0D; Results: 106 patients were enrolled with mean age of 39±18.6 and male study population being on the higher side. 62(58.49%) patients with Traumatic Brain Injury accounted for road traffic accident with mild head injury as the commonest presentation. In about 40.57% of the patients osmolarity ranged between 285 to 295 milliosmole/ litre with mean osmolarity of 290.99±10.60. There was no significant association between severity of head injury and serum osmolarity (p value=0.45).&#x0D; Conclusion: There is no association between the severity of head injury with serum osmolarity.

Neuroprotective effects of mild hypothermia against traumatic brain injury by the involvement of the Nrf2/ARE pathway.

BackgroundTraumatic brain injury (TBI) is the leading cause of death and disability worldwide. Mild hypothermia (32–35°C) has been found to show neuroprotective effects against TBI. However, the specific mechanism is still elusive. In the current study, we explored the relationship between oxidative damage after TBI and treatment with mild hypothermia as well as the underlying molecular mechanisms.MethodsWe used the closed cortex injury model to perform the brain injury and a temperature monitoring and control system to regulate the body temperature of mice after injury. Adult male C57BL/6 mice were adopted in this study and divided into four experimental groups. Tissue samples were harvested 24 h after injury.ResultsFirst, our results showed that treatment with mild hypothermia significantly improved neurobehavioral dysfunction and alleviated brain edema after TBI. Moreover, treatment with mild hypothermia enhanced the activity of the antioxidant enzymes superoxide dismutase and glutathione peroxidase and reduced the accumulation of lipid peroxidation malondialdehyde. Importantly, the expression and activation of the nuclear factor erythroid 2‐related factor 2‐antioxidant response element (Nrf2‐ARE) pathway were upregulated by mild hypothermia after TBI. Finally, treatment with hypothermia significantly decreased the cell apoptosis induced by TBI.ConclusionOur results showed that the protective effects of mild hypothermia after TBI may be achieved by the upregulation of the Nrf2‐ARE pathway and revealed Nrf2 as a potentially important target to improve the prognosis of TBI.

Correlation among the GCS Score, CT Scan Findings and Early Clinical Outcome of Traumatic Brain Injury- Study of Fifty Cases

Traumatic brain injury (TBI) is defined as an assault to the brain caused by an external physical force that may produce a state of diminished or altered consciousness and consequently, affecting cognitive abilities or physical function. According to the GCS, traumatic brain injuries are classified as mild, moderate or severe. Currently the imaging method of choice for the diagnosis and prognosis of TBI is CT scan. According to the disease profile in SBMCH about 30% patient is admitted in surgery ward in every admission due to traumatic injury. Out of them about 10% have traumatic head injury. The aim of the study was to evaluate an association among the GCS score, CT scan findings and clinical outcome of head injury. It is a prospective observational study at Sher-E-Bangla Medical college Hospital, Barisal. In this study 72% patients were with no CT scan findings (haemorrhagic / nonhaemorghagic). Rest of the patients had CT scan findings (intracerebral haemorrhage, extradural haematoma, subdural hematoma etc.). In severe TBI there was a significant increase in the incidence of CT findings, with a rate of 100% of abnormalities. In this study it was observed that, on admission patients with low GCS (severe TBI) deteriorate more in comparison to moderate and mild TBI on admission. This association is significant (p = .049). Patients in the severe TBI group (according to GCS) showed the highest mortality (2 out of 5). This association is also statistically significant (p = .002).