Diffuse Axonal Injury Research Articles

Biomechanical comparison of four isometric prosthetic ligament repair techniques for tarsal medial collateral ligament injury.

To compare the stability, ultimate strength, and isometry of 4 prosthetic ligament repairs for canine tarsal medial collateral ligament injury. 24 cadaveric canine distal hind limbs with induced medial tarsal instability were randomly divided into 4 groups. Simulated medial shearing injury of the collateral and medial malleolus were repaired using 1 of 4 isometric suture techniques: bone tunnels with nylon suture (TN), ultrahigh-molecular-weight polyethylene (UHMWPE) suture (TU), tibial bone anchor with nylon suture (AN), or talar bone anchor with UHMWPE suture (AU). Each repair was evaluated for medial stability before and after cyclic range of motion. 3 of 4 repair configurations allowed string potentiometer isometry data collection during cyclic range of motion. Each construct was subsequently tested to failure; the strength and failure mode were recorded. All repair groups showed statistically increased laxity compared to intact ligament. There was no difference in joint laxity between repair techniques. Cyclic range-of-motion testing did not increase joint laxity at any tested joint angle. Strength to failure was no different between repair groups. Isometry was achieved in the TU and TN groups. All 4 techniques improved medial stability compared to that medial collateral ligament injury; however, no technique returned stability to the tarsal of the intact ligament. All 4 techniques maintained stability after range-of-motion testing. Isometric placement of the prosthetic suture was achievable. The constructs did not provide sufficient resistance to physiologic valgus stress. Isometric placement of a prosthetic ligament is possible; secondary stabilization appears necessary to support the repair postoperatively.

Assessing Mild Traumatic Brain Injury-Associated Blood–Brain Barrier (BBB) Damage and Restoration Using Late-Phase Perfusion Analysis by 3D ASL MRI: Implications for Predicting Progressive Brain Injury in a Focused Review

Mild traumatic brain injury (mTBI) is a common occurrence around the world, associated with a variety of blunt force and torsion injuries affecting all age groups. Most never reach medical attention, and the identification of acute injury and later clearance to return to usual activities is relegated to clinical evaluation—particularly in sports injuries. Advanced structural imaging is rarely performed due to the usual absence of associated acute anatomic/hemorrhagic changes. This review targets physiologic imaging techniques available to identify subtle blood–brain barrier dysfunction and white matter tract shear injury and their association with chronic traumatic encephalopathy. These techniques provide needed objective measures to assure recovery from injury in those patients with persistent cognitive/emotional symptoms and in the face of repetitive mTBI.

P18.42.B TAU AND AMYLOID BETA PATHOLOGY IN IDH-MUTANT GLIOMA

Abstract BACKGROUND With an aging population the incidence of brain tumors and neurodegenerative diseases is increasing. Although biological associations between glioma and Alzheimer’s disease (AD) have been suggested, the frequency of comorbidity is insufficiently defined. We here screen tumor-adjacent cortex of a representative cohort of patients with low grade glioma for AD neuropathological changes (ADNC) specifically for phosphorylated tau (pTau) and amyloid beta (Abeta) deposition, microglial activation, amyloid precursor protein (APP) expression, diffuse axonal injury, and cortical tumor cell infiltration. MATERIAL AND METHODS A total of 85 patients with astrocytoma, IDH mutant, CNS-WHO grade 2-3, (N=37, median age: 39) and oligodendroglioma, IDH mutant and 1p-19q co-deleted, CNS-WHO grades 2-3 (N=48 median age: 50) were included. 2µm sections were immunohistochemically stained for the markers b-A4, t-AT8, NeuN, APP and Iba1. Whole slide quantification was performed using Matlab and QuPath codes. For a subset of 15 patients, longitudinal samples were available for analysis of post-treatment effects. RESULTS The median cell density in the tumor-adjacent cortex was 1355/mm2 for astrocytoma and 1392/mm2 for oligodendroglioma, which was significantly higher than in non-tumor infiltrated cortex (median: 1030 cells/mm², p-value<0.0001). A total of 32 patients (38%) showed Abeta (14%, n=12/85) and/or pTau pathology (36%, n=31/85) in the tumor-adjacent cortex. No difference between astrocytoma and oligodendroglioma was reported. ADNC was mostly frequently observed in older patients but was also present in young individuals (median: 34 years, range: 17 to 77 years). pTau was significantly positively correlated with tumor cell infiltration (Kendall´s tau=0.13, p=0.002). Both Abeta and pTau deposits were frequently observed in the frontal cortex (30%, N=18/60). The tumor infiltration into the cortical regions was associated with neuronal loss (Kendall´s tau=-0.29, p<0.0001). Microglial activation depended on the degree of tumor infiltration (R=0.29), followed by increasing patient age (R=0.12). Diffuse axonal injury was associated with ADNC (Chi²=19.6, p<0.05). APP expression of tumor cells was highest in patients of old age (R=0.35). Longitudinal samples showed stable ANDC pathology in 15/15 subjects. CONCLUSION Our preliminary findings suggest presence of ADNC in roughly a third of patients with low-grade glioma, which increases with tumor cell infiltration into the cortex, microglial activation and patient age. Notably, isolated pTau pathology was more pronounced than Abeta pathology suggesting the acquisition of a secondary tauopathy.

Sex-dependent temporal changes in astrocyte-vessel interactions following diffuse traumatic brain injury in rats.

Traumatic brain injury (TBI) is associated with diffuse axonal injury (DAI), a primary pathology linked to progressive neurodegeneration and neuroinflammation, including chronic astrogliosis, which influences long-term post-TBI recovery and morbidity. Sex-based differences in blood-brain barrier (BBB) permeability increases the risk of accelerated brain aging and early-onset neurodegeneration. However, few studies have evaluated chronic time course of astrocytic responses around cerebrovascular in the context of aging after TBI and sex dependence. We observed increased glial fibrillary acidic protein (GFAP)-labeled accessory processes branching near and connecting with GFAP-ensheathed cortical vessels, suggesting a critical nuance in astrocyte-vessel interactions after TBI. To quantify this observation, male and female Sprague Dawley rats (∼3months old, n = 5-6/group) underwent either sham surgery or midline fluid percussion injury. Using immunohistochemical analysis, we quantified GFAP-labeled astrocyte primary and accessory processes that contacted GFAP-ensheathed vessels in the somatosensory barrel cortex at 7, 56, and 168days post-injury (DPI). TBI significantly increased GFAP-positive primary processes at 7 DPI (P < 0.01) in both sexes. At 56 DPI, these vessel-process interactions remained significantly increased exclusively in males (P < 0.05). At 168 DPI, both sexes showed a significant reduction in vessel-process interactions compared to 7 DPI (P < 0.05); however, a modest but significant injury effect reemerged in females (P < 0.05). A similar sex-dependent pattern in the number of accessory processes provides novel evidence of long-term temporal changes in astrocyte-vessel interactions. TBI-induced changes in astrocyte-vessel interactions may indicate chronic BBB vulnerability and processes responsible for early onset vascular and neurodegenerative pathology.

Microglial process convergence onto injured axonal swellings, a human postmortem brain tissue study

Traumatic brain injury (TBI) affects millions globally, with a majority of TBI cases being classified as mild, in which diffuse pathologies prevail. Two of the pathological hallmarks of TBI are diffuse axonal injury (DAI) and microglial activation. While progress has been made investigating the breadth of TBI-induced axonal injury and microglial changes in rodents, the neuroinflammatory progression and interaction between microglia and injured axons in humans is less well understood. Our group previously investigated microglial process convergence (MPC), in which processes of non-phagocytic microglia directly contact injured proximal axonal swellings, in rats and micropigs acutely following TBI. These studies demonstrated that MPC occurred on injured axons in the micropig, but not in the rat, following diffuse TBI. While it has been shown that microglia co-exist and interact with injured axons in humans post-TBI, the occurrence of MPC has not been quantitatively measured in the human brain. Therefore, in the current study we sought to validate our pig findings in human postmortem tissue. We investigated MPC onto injured axonal swellings and intact myelinated fibers in cases from individuals with confirmed DAI and control human brain tissue using multiplex immunofluorescent histochemistry. We found an increase in MPC onto injured axonal swellings, consistent with our previous findings in micropigs, indicating that MPC is a clinically relevant phenomenon that warrants further investigation.

B - 21 11-Year Longitudinal Study of a Competitive Swimmer Following a Severe TBI

Abstract Objective Symptoms of severe traumatic brain injuries (TBIs) are oftentimes significant, long lasting, and treated by a variety of medications and therapies. Although exercise is known to be beneficial for brain health, the effects of substantial exercise on recovery following severe TBI (sTBI) in female athletes are undiscovered. Method This case study examines a 51-year-old woman who sustained a sTBI, involving multiple hemorrhagic contusions to the right cerebellum, inferior bilateral frontal lobes, anterior left temporal lobe, and diffuse axonal injury on 8/5/13 from a bicycle accident, resulting in a 13-day coma and cognitive impairment. She underwent 6 brain surgeries, an artificial skull implant and intensive therapies. Before the accident, she was a competitive swimmer and triathlon racer. Despite being told that she would never swim again, she resumed swimming on 09/1/14. She swims 6 days a week for 90-minutes a day, winning open water races. Results Examination from four neuropsychological assessments over 11 years provide substantial longitudinal data. Results revealed improvement over the 4 testing periods particularly on processing speed, verbal fluency, and Boston Naming Test with t-score differences ranging between 8 and 24. Additionally, she performed in the average range on General Abilities Index, NAB Mazes, and Trail Making Test across all four assessments. Conclusion This longitudinal case study provides evidence that extensive swimming is associated with cognitive recovery from sTBI in a female athlete and documents her return to high level exercise and competition. Evidence suggests that carefully tailored and monitored exercise programs can benefit long term cognitive following from sTBI.

B - 55 Diffusion Tensor Imaging Analysis of Former American Football Players Exposed to Repetitive Head Impacts

Abstract Objective Exposure to repetitive head impacts (RHI) has been linked to Chronic Traumatic Encephalopathy (CTE) and neuropathological alterations such as white matter shear injuries. In this study, we use diffusion-tensor imaging (DTI) to investigate in vivo white matter alterations among former American football players. We also investigate how age and factors associated with RHI exposure influence white matter integrity. Methods We analyzed data from the DIAGNOSE CTE Research Project, focusing on former American football players (n = 166). The measures included whole-brain Fractional Anisotropy (FA), reflecting water diffusion directionality in white matter, and FreeWater-corrected FA (FAt) accounting for extracellular free water, using FSL Tract-Based Spatial Statistics (TBSS). We performed linear regressions on FA and FAt with age, age of first exposure to football, and estimates of cumulative head impact index (CHII) scores of frequency, linear acceleration, and rotational force controlling for age, body mass index, race, education, and APOE e4 allele presence as covariates. Results Both FA (p &amp;lt; 0.00001) and FAt (p &amp;lt; 0.00001) decreased as age increased. Moreover, FA (p &amp;lt; 0.01) and FAt (p &amp;lt; 0.01) were significantly lower with an earlier age of first exposure to football. Finally, FAt decreased as CHII linear acceleration (p &amp;lt; 0.04) and rotational forces (p &amp;lt; 0.02) increased. Conclusion Our study reveals age-related declines in both FA and FAt and highlights that the duration and intensity of exposure to RHI have an impact on white matter microstructure later in life. Overall, these results underscore the impact of prolonged exposure to RHI on white matter microstructure.

Stretch triggers microtubule stabilization and MARCKS-dependent membrane incorporation in the shaft of embryonic axons

Neurons have a unique polarized nature that must adapt to environmental changes throughout their lifespan. During embryonic development, axon elongation is led by the growth cone,1 culminating in the formation of a presynaptic terminal. After synapses are formed, axons elongate in a growth cone-independent manner to accompany body growth while maintaining their ultrastructure and function.2,3,4,5,6 To further understand mechanical strains on the axon shaft, we developed a computer-controlled stretchable microfluidic platform compatible with multi-omics and live imaging. Our data show that sensory embryonic dorsal root ganglia (DRGs) neurons have high plasticity, with axon shaft microtubules decreasing polymerization rates, aligning with the direction of tension, and undergoing stabilization. Moreover, in embryonic DRGs, stretch triggers yes-associated protein (YAP) nuclear translocation, supporting its participation in the regulatory network that enables tension-driven axon growth. Other than cytoskeleton remodeling, stretch prompted MARCKS-dependent formation of plasmalemmal precursor vesicles (PPVs), resulting in new membrane incorporation throughout the axon shaft. In contrast, adolescent DRGs showed a less robust adaptation, with axonal microtubules being less responsive to stretch. Also, while adolescent DRGs were still amenable to strain-induced PPV formation at higher stretch rates, new membrane incorporation in the axon shaft failed to occur. In summary, we developed a new resource to study the biology of axon stretch growth. By unraveling cytoskeleton adaptation and membrane remodeling in the axon shaft of stretched neurons, we are moving forward in understanding axon growth.

Slipped capital femoral epiphysis: emphasis on early recognition and potential pitfalls.

Slipped capital femoral epiphysis is a shearing injury through the growth plate of the proximal femur and is the most common hip disorder in adolescence. Delays in diagnosis persist across practice settings despite ongoing innovations in imaging. Recent insights into pathomechanics highlight the importance of femoral head surface morphology and rotational microinstability centered at the epiphyseal tubercle in causing early physeal changes, which can be detected on imaging prior to frank slip. Scrutiny of physeal morphology and comparison to the contralateral hip is critical at all stages of disease progression, and improper technique may result in undue diagnostic delay. Selective use of cross-sectional imaging can be helpful for troubleshooting equivocal early slips and can inform operative technique and adjuvant therapy candidacy in more severe cases. This review provides a comprehensive approach to imaging suspected slipped capital femoral epiphysis, with an emphasis on early detection and potential pitfalls.

Intranasal human-recombinant nerve growth factor administration improves cognitive functions in a child with severe traumatic brain injury.

Behavioral and neuropsychological functions are frequent long-term sequelae of severe traumatic brain injury (TBI). Neuropeptides, such as nerve growth factor (NGF), can enhance neurogenesis and improve cognitive functions after TBI, playing a pivotal role in neuroplasticity. A limited number of studies documented the safety and efficacy of intranasal NGF administration in children with severe TBI. A fourteen-year-old boy with a diffuse axonal injury secondary to severe TBI was treated with human-recombinant NGF administration. This patient underwent treatment with intranasal hr-NGF administration at a total dose of 50 gamma/kg, three times a day for seven consecutive days. The treatment schedule was performed for 4 cycles, at one month distance each. NGF administration improved radiologic functional assessment evaluated with positron emission tomography scan (PET) and single photon emission computed tomography (SPECT), with an important improvement in clinical conditions. Significant improvements were also observed, mainly in cognitive processes, memory, the planning of a communication strategy, execution skills, attention, and verbal expression. No side effects were reported. Additional studies are required to gain a deeper insight into this neurotrophin's neuroprotective function, but our findings reveal a potential efficacy of intranasal hr-NGF administration in enhancing cognitive and clinical outcomes among children with diffuse axonal injury after severe TBI.

Molecular and Functional Alterations in the Cerebral Microvasculature in an Optimized Mouse Model of Sepsis-Associated Cognitive Dysfunction.

Systemic inflammation has been implicated in the development and progression of neurodegenerative conditions such as cognitive impairment and dementia. Recent clinical studies indicate an association between sepsis, endothelial dysfunction, and cognitive decline. However, the investigations of the role and therapeutic potential of the cerebral microvasculature in sepsis-induced cognitive dysfunction have been limited by the lack of standardized experimental models for evaluating the alterations in the cerebral microvasculature and cognition induced by the systemic inflammatory response. Herein, we validated a mouse model of endotoxemia that recapitulates key pathophysiology related to sepsis-induced cognitive dysfunction, including the induction of an acute systemic hyperinflammatory response, blood-brain barrier (BBB) leakage, neurovascular inflammation, and memory impairment after recovery from the systemic inflammation. In the acute phase, we identified novel molecular (e.g., upregulation of plasmalemma vesicle-associated protein, PLVAP, a driver of endothelial permeability, and the procoagulant plasminogen activator inhibitor-1, PAI-1) and functional perturbations (i.e., albumin and small-molecule BBB leakage) in the cerebral microvasculature along with neuroinflammation. Remarkably, small-molecule BBB permeability, elevated levels of PAI-1, intra-/perivascular fibrin/fibrinogen deposition, and microglial activation persisted 1 month after recovery from sepsis. We also highlight molecular neuronal alterations of potential clinical relevance following systemic inflammation including changes in neurofilament phosphorylation and decreases in postsynaptic density protein 95 and brain-derived neurotrophic factor, suggesting diffuse axonal injury, synapse degeneration, and impaired neurotrophism. Our study serves as a standardized mouse model to support future mechanistic studies of sepsis-associated cognitive dysfunction and to identify novel endothelial therapeutic targets for this devastating condition.

Relationship Between Brain CT Scan Findings, Consciousness Levels, and Outcomes in Brain Trauma Patients: A Cross-Sectional Study

Background: Trauma is the fourth leading cause of mortality worldwide. The Glasgow Coma Scale (GCS) is a crucial tool for evaluating the consciousness levels of trauma patients, serving as a diagnostic instrument for assessing injury severity and the condition of brain trauma patients. Additionally, Computed Tomography (CT) Scans are the most practical and accurate imaging modality for diagnosing the types and locations of lesions in cases of brain trauma in the emergency department. The study was designed to explore the correlation between pathological findings in Brain CT scans and the consciousness levels of brain trauma patients, as assessed by the GCS. Methods: This cross-sectional descriptive-analytical study investigated 200 brain trauma patients admitted to the emergency department of Khatam Al-Anbia Hospital in Zahedan. Upon arrival, an emergency medicine specialist recorded the patients’ consciousness levels based on the GCS criteria. After performing a CT scan and determining the type and location of the lesion, a radiologist, emergency medicine, and neurosurgery specialists determined the continuation of the treatment process. Subsequently, patients requiring admission to the neurosurgery department or intensive care unit were monitored. The final patient status (deceased/survivor) was tracked at the end of the treatment period and added to the checklist. Following data coding and entry into the computer, descriptive statistics, including mean, standard deviation, and confidence intervals, were used for evaluation. Additionally, the Chi-square and independent t-tests, along with SPSS 22, were employed to examine the relationship between consciousness levels and CT scan results. Results: Three out of 200 patients were excluded from the study due to transfers to other medical facilities during treatment. The mean age of the remaining patients was 27.94 ± 11.25. Results showed that 67.5% of all patients survived, while 32.4% succumbed to injuries. The initial GCS score was 14-15 for 83 patients (42.1%), 9-13 for 69 patients (35%), and 3-8 for 45 patients (22.8%). Brain CT scans of trauma patients predominantly revealed subdural hematomas in 48 patients (24.3%). In the examination of the relationship between the mechanism of brain trauma and mortality, 75% of patients involved in falls and 65.5% in accidents survived, while all patients who experienced other causes of trauma survived. Ultimately, no significant difference was observed between the mechanism of brain trauma and patient mortality (p=0.318). Furthermore, all patients with a GCS score of 14-15 (100%), 85.6% with a GCS score of 9-13, and 35.5% with a GCS score of 3-8 survived. A significant relationship between initial consciousness levels and mortality rates in the emergency department was evident (p=0.001). Statistical analysis indicated that 66.7% of patients with subdural hematomas, 75% with epidural hematomas, 81% with cerebral contusions, 35.3% with intracerebral hemorrhages (ICH), and 92.3% with diffuse axonal injuries (DAI) ultimately survived, signifying a significant relationship between CT scan results and mortality rates (p=0.01). Moreover, the highest mortality rate was observed in patients with ICH, with a frequency of 64.7%. Conclusions: Simultaneously evaluating consciousness levels using the GCS, along with considering the type of pathology identified in CT scans of brain trauma patients admitted to the emergency department, significantly aids in determining patient mortality rates. Promptly initiating the patient’s treatment process can lead to reduced complications from brain trauma and, in some cases, decreased mortality.

Embedded finite element modeling of the mechanics of brain axonal fiber tracts under head impact conditions

Investigating and understanding the biomechanical kinematics and kinetics of human brain axonal fibers during head impact process is crucial to study the mechanisms of Traumatic Axonal Injury (TAI). Such a study may require the explicit incorporation of brain fiber tracts into the host brain in order to distinguish the mechanical states of axonal fibers and brain tissue. Herein we extend our previously developed human head model by using an embedded element method to include fiber tracts reconstructed from diffusion tensor images in a host brain with the purpose of numerically tracking the deformation state of axonal fiber tracts during a head impact simulation. The updated model is validated by comparing its prediction of intracranial pressures with experimental data, followed by a thorough study of the effects of element types used for fiber tracts and the stiffness ratios of fiber to host brain. The validated model is also used to predict and visualize the damaged region of fiber tracts during the head impact process based on different injury criteria. The model is promising in tracking the state of fiber tracts and can add more objective functions such as axonal fiber deformation if used in the future design optimization of head protective equipment such as a football helmet.

Complementary therapy with Chinese aromatic herbs to promote awakening in a comatose patient: A case report.

Traumatic brain injury frequently leads to prolonged coma, posing significant medical management challenges. Complementary therapies, including traditional Chinese herbal medicine, have been investigated as potential interventions in comatose patients. Chinese aromatic herbs, such as Borneolum (Bingpian), Moschus (Shexiang), and Acori tatarinowii rhizoma (Shichangpu), have long been believed to be "resuscitation with aromatics" based on traditional Chinese medicines theory. A 16-year-old male was admitted to the intensive rehabilitation unit for further treatment due to prolonged coma and frequent seizures following traumatic brain injury. Western medicine diagnosed the patient as coma, diffuse axonal injury, and epilepsy. According to traditional Chinese medicine theory, the syndrome differentiation indicates a Yin-closed disease. According to the patient's condition, we use the Chinese aromatic herbs as a complementary therapy. Following a month-long administration, the patient's consciousness and electroencephalogram (EEG) background progressively improved. A 6-month follow-up demonstrated full arousal, though with ambulatory EEG revealing mild to moderate abnormality in the background. The addition of Chinese aromatic herbs appears to have a beneficial effect on the patient's consciousness and EEG background. This could be attributed to the herbs' inherent pharmacological properties, as well as their potential to enhance the permeability of the blood-brain barrier to other drugs. This makes them a promising option for complementary therapy.

Microglial process convergence onto injured axonal swellings, a human postmortem brain tissue study.

Traumatic brain injury (TBI) affects millions globally, with a majority of TBI cases being classified as mild, in which diffuse pathologies prevail. Two of the pathological hallmarks of TBI are diffuse axonal injury and microglial activation. While progress has been made investigating the breadth of TBI-induced axonal injury and microglial changes in rodents, the neuroinflammatory progression and interaction between microglia and injured axons following brain injury in humans is less well understood. Our group previously investigated microglial process convergence (MPC), in which processes of non-phagocytic microglia directly contact injured proximal axonal segments, in rats and micropigs acutely following TBI. These studies demonstrated that MPC occurred on injured axons in the micropig, but not in the rat, following diffuse TBI. While it has been shown that microglia co-exist and interact with injured axons in humans post-TBI, the occurrence of MPC has not been quantitatively measured in the human brain. Therefore, in the current study we sought to validate our pig findings in human postmortem tissue. We investigated MPC onto injured axonal swellings and intact myelinated fibers in cases from individuals that sustained a TBI and control human brain tissue using multiplex immunofluorescent histochemistry. We found an increase in MPC onto injured axonal swellings, consistent with our previous findings in micropigs, indicating that MPC is a clinically relevant phenomenon that warrants further investigation.

MRI and Clinical Variables for Prediction of Outcomes After Pediatric Severe Traumatic Brain Injury

Traumatic brain injury (TBI) is a leading cause of death and disability in children, and predicting functional outcome after TBI is challenging. Magnetic resonance imaging (MRI) is frequently conducted after severe TBI; however, the predictive value of MRI remains uncertain. To identify early MRI measures that predict long-term outcome after severe TBI in children and to assess the added predictive value of MRI measures over well-validated clinical predictors. This preplanned prognostic study used data from the Approaches and Decisions in Acute Pediatric TBI (ADAPT) prospective observational comparative effectiveness study. The ADAPT study enrolled 1000 consecutive children (aged <18 years) with severe TBI between February 1, 2014, and September 30, 2017. Participants had a Glasgow Coma Scale (GCS) score of 8 or less and received intracranial pressure monitoring. Magnetic resonance imaging scans performed as part of standard clinical care within 30 days of injury were collected at 24 participating sites in the US, UK, and Australia. Summary imaging measures were correlated with the Glasgow Outcome Scale-Extended for Pediatrics (GOSE-Peds), and the predictive value of MRI measures was compared with the International Mission for Prognosis and Analysis of Clinical Trials in TBI (IMPACT) core clinical predictors. Data collection, image analysis, and data analyses were completed in July 2023. Pediatric severe TBI with an MRI scan performed as part of clinical care. All measures were selected a priori. Magnetic resonance imaging measures included contusion, ischemia, diffuse axonal injury, intracerebral hemorrhage, and brainstem injury. Clinical predictors included the IMPACT core measures (GCS motor score and pupil reactivity). All models adjusted for age and sex. Outcome measures included the GOSE-Peds score obtained at 3, 6, and 12 months after injury. This study included 233 children with severe TBI who were enrolled at participating sites and had an MRI scan and preselected clinical predictors available. Their median age was 6.9 (IQR, 3.0-13.3) years, and more than half of participants (134 [57.5%]) were male. In a multivariable model including MRI measures and IMPACT core clinical variables, contusion volume (odds ratio [OR], 1.13; 95% CI, 1.02-1.26), brain ischemia (OR, 2.11; 95% CI, 1.58-2.81), brainstem lesions (OR, 5.40; 95% CI, 1.90-15.35), and pupil reactivity were each independently associated with GOSE-Peds score. Adding MRI measures to the IMPACT clinical predictors significantly improved model fit and discrimination between favorable and unfavorable outcomes compared with IMPACT predictors alone (area under the receiver operating characteristic curve, 0.77; 95% CI, 0.72-0.85 vs 0.67; 95% CI, 0.61-0.76 for GOSE-Peds score >3 at 6 months after injury). In this prognostic study of children with severe TBI, the addition of MRI measures significantly improved outcome prediction over well-established and validated clinical predictors. Magnetic resonance imaging should be considered in children with severe TBI to inform prognosis and may also promote stratification of patients in future clinical trials.

EVALUATION AND MANAGEMENT STRATEGIES FOR PATIENTS WITH BLUNT ABDOMINAL TRAUMA: A HOSPITAL-BASED STUDY

Introduction:Blunt trauma to the abdomen occurs due to forces that induce shearing, compression, or deceleration injuries, particularly affecting anatomical structures that are relatively immobile. The evaluation of abdominal injuries is challenging and often results in missed diagnoses due to the complexity of symptoms and the difficulty in identifying subtle signs of internal injury. Aims &amp; Objectives:To study the clinical presentation, evaluation, diagnostic investigations, and management strategies for various intra-abdominal organ injuries resulting from blunt trauma to the abdomen. Methods: - Following initial resuscitation and attainment of hemodynamic stability, all blunt abdominal trauma patients underwent meticulous clinical history-taking and comprehensive physical examination. Subsequent management decisions, whether operative or non-operative, were determined based on the integrated findings of clinical assessments and radiological evaluations. Results:Between August 2022 and August 2023, fifty (50) patients with blunt trauma to the abdomen were admitted to Basaveshwara Teaching and General Hospital, Kalaburagi. In this study, males predominated in the 21 to 30-year age group, which represented the most frequent demographic for abdominal blunt trauma. Traffic collisions were identified as the leading cause of abdominal blunt trauma. The spleen emerged as the organ most frequently affected. Of the patients, 28 underwent conservative management, while 22 required surgical intervention. Conclusion:In cases of blunt trauma to the abdomen, the early hours following injury are critically significant and represent a crucial window, often referred to as the golden period of trauma, associated with higher survival rates. Timely intervention andappropriate management during this phase have been shown to significantly decrease morbidity and mortality rates associated with blunt trauma abdomenandappropriate management during this phase have been shown to significantly decrease morbidity and mortality rates associated with blunt trauma abdomen.

Head injury mechanisms of the occupant under high-speed train rear-end collision

To improve the passive safety of high-speed trains, it is very important to understand the mechanism of head injury in high-speed train collisions. In this study, the head injury mechanisms of occupants in high-speed train rear-end collisions were investigated based on the occupant-seat coupling model, which included a dummy representing the Chinese 50th percentile adult male. The typical injury responses in terms of skull fractures, brain contusions, and diffuse axonal injury (DAI) were analyzed. Meanwhile, the influences of collision speed and seat parameters on head injury response were examined. The simulation results indicate that the skull fractures primarily occur at the skull base region due to excessive neck extension, while the brain contusions and DAI result from the relative displacement of different brain regions. The increase in collision speed will promote the probability of skull fracture, brain contusion, and DAI. Seat design modifications, such as reduced seat spacing, increased seat backrest angles, and selecting the appropriate cushion angle (76°) and friction coefficient (0.15), can effectively mitigate probably occupant's head injury.

Neurosurgical Management of Traumatic Brain Injury

The neurosurgical management of traumatic brain injury (TBI) plays a critical role in ensuring acute survival and mitigating secondary brain damage, which significantly impacts patients' quality of life. TBI is defined as an external force impacting the skull, leading to brain injuries and subsequent functional impairments. It is a leading cause of mortality and morbidity, particularly among young individuals. The initial clinical examination is crucial, with external signs like scalp injuries, hematomas, nasal fluid leakage, skull deformities, and neurological deficits providing important clues to injury patterns. Pupil examination is particularly critical, as mydriasis coupled with reduced consciousness may indicate an acute life-threatening increase in intracranial pressure (ICP), necessitating immediate neurosurgical intervention. TBI assessment often utilizes the Glasgow Coma Scale (GCS), classifying injuries as mild (GCS 13-15), moderate (GCS 9-12), or severe (GCS <9). Even mild TBI can lead to long-term complications. TBI should be viewed as a disease process rather than a singular event. Primary brain damage results from shearing forces on the parenchyma, manifesting as contusions, hematomas, or diffuse axonal injury. Secondary brain damage is driven by mechanisms such as inflammation and spreading depolarizations. Treatment aims not only to secure immediate survival but also to reduce secondary injuries, with ICP management being crucial. Neurosurgical interventions are guided by cranial pathologies, with options including ICP monitoring, burr hole trepanation, craniotomy. In severe TBI cases with refractory ICP elevation, decompressive craniectomy may be performed as a last resort, significantly reducing mortality but often resulting in high morbidity and vegetative states, necessitating careful consideration of indications.

The Effect of Repetitive Transcranial Magnetic Stimulation on Cognition in Diffuse Axonal Injury in a Rat Model.

Diffuse axonal injury (DAI) following sudden acceleration and deceleration can lead to cognitive function decline. Various treatments have been proposed. Repetitive transcranial magnetic stimulation (rTMS), a non-invasive stimulation technique, is a potential treatment for enhancing neuroplasticity in cases of brain injury. The therapeutic efficacy of rTMS on cognitive function remains unconfirmed. This study investigated the effects of rTMS and the underlying molecular biomechanisms using a rat model of DAI. Sprague-Dawley rats (n = 18) were randomly divided into two groups: one receiving rTMS after DAI and the other without brain stimulation. All rats were subjected to sudden acceleration and deceleration using a DAI modeling machine to induce damage. MRI was performed to confirm the DAI lesion. The experimental group received rTMS at a frequency of 1 Hz over the frontal cortex for 10 min daily for five days. To assess spatial memory, we conducted the Morris water maze (MWM) test one day post-brain damage and one day after the five-day intervention. A video tracking system recorded the escape latency. After post-MWM tests, all rats were euthanized, and their brain tissues, particularly from the hippocampus, were collected for immunohistochemistry and western blot analyses. The escape latency showed no difference on the MWM test after DAI, but a significant difference was observed after rTMS between the two groups. Immunohistochemistry and western blot analyses indicated increased expression of BDNF, VEGF, and MAP2 in the hippocampal brain tissue of the DAI-T group. In conclusion, rTMS improved cognitive function in the DAI rat model. The increased expression of BDNF, VEGF, and MAP2 in the DAI-T group supports the potential use of rTMS in treating cognitive impairments associated with DAI.