Traumatic Brain Injury Lesions Research Articles

Clinical and Imaging Characteristics, Care Pathways, and Outcomes of Traumatic Epidural Hematomas: A Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury Study.

Guideline recommendations for surgical management of traumatic epidural hematomas (EDHs) do not directly address EDHs that co-occur with other intracranial hematomas; the relative rates of isolated vs nonisolated EDHs and guideline adherence are unknown. We describe characteristics of a contemporary cohort of patients with EDHs and identify factors influencing acute surgery. This research was conducted within the longitudinal, observational Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury cohort study which prospectively enrolled patients with traumatic brain injury from 65 hospitals in 18 European countries from 2014 to 2017. All patients with EDH on the first scan were included. We describe clinical, imaging, management, and outcome characteristics and assess associations between site and baseline characteristics and acute EDH surgery, using regression modeling. In 461 patients with EDH, median age was 41 years (IQR 24-56), 76% were male, and median EDH volume was 5 cm3 (IQR 2-20). Concomitant acute subdural hematomas (ASDHs) and/or intraparenchymal hemorrhages were present in 328/461 patients (71%). Acute surgery was performed in 99/461 patients (21%), including 70/86 with EDH volume ≥30 cm3 (81%). Larger EDH volumes (odds ratio [OR] 1.19 [95% CI 1.14-1.24] per cm3 below 30 cm3), smaller ASDH volumes (OR 0.93 [95% CI 0.88-0.97] per cm3), and midline shift (OR 6.63 [95% CI 1.99-22.15]) were associated with acute surgery; between-site variation was observed (median OR 2.08 [95% CI 1.01-3.48]). Six-month Glasgow Outcome Scale-Extended scores ≥5 occurred in 289/389 patients (74%); 41/389 (11%) died. Isolated EDHs are relatively infrequent, and two-thirds of patients harbor concomitant ASDHs and/or intraparenchymal hemorrhages. EDHs ≥30 cm3 are generally evacuated early, adhering to Brain Trauma Foundation guidelines. For heterogeneous intracranial pathology, surgical decision-making is related to clinical status and overall lesion burden. Further research should examine the optimal surgical management of EDH with concomitant lesions in traumatic brain injury, to inform updated guidelines.

Ex vivo method for rapid quantification of post traumatic brain injury lesion volumes using ultrasound

BackgroundStudies of traumatic brain injury often involve the quantification of the lesion volume as a major outcome measure. The determination of lesion volume typically employs the cutting and mounting of brain tissue, and the calculation of the cross-sectional area of the lesion within each section of brain after histological staining. This is a time consuming and laborious task often requiring many weeks to determine the lesion volume for an individual brain. MethodsIn this report we present a method for determining the lesion volume within the brain following traumatic brain injury that involves the use of ultrasound imaging. With this process the lesion volume can be determined within a time period of 90 min per brain rather than weeks and months. Moreover, we have developed a pipeline that will combine the cross-sectional ultrasound images of the brain with the Allen Mouse Brain Atlas to provide the precise anatomical structures that are affected by traumatic injury to the brain. The anatomical detail was lastly paired with behavioral data showing neurological deficits correlated with specific areas of brain injury. ResultsThe accuracy and precision of this method was shown to be highly consistent with the traditional histological approach. Additionally, the mapping process and behavioral data show that neurological recovery from 1 to 3 weeks post injury is not correlated with gross anatomical recovery of the TBI lesion in our TBI model. ConclusionTogether these approaches will enhance the pipeline for processing brain tissue in experimental conditions where the lesion volume is an important outcome parameter and provide more high resolution information about the identity of the damaged regions of the brain.

Evaluation of overuse of Head Computerized Tomography scan on traumatic brain injury pediatric patients

Traumatic brain injury (TBI) is a leading cause of morbidity and mortality among pediatric patients. Head Computerized Tomography (CT) scan has the undoubtedly benefit of diagnosing TBI lesions but is also associated with increased risk of cancer due to radiation. This study was composed of 190 patients evaluated in the emergency setting of a pediatric Brazilian hospital from January 2019 to December 2021. The results of the study demonstrated an increased amount of CT scans in patients with mild TBI during this period. Besides, we noticed that many of these CT scans showed normal results or clinically insignificant findings such as subgaleal hematomas. Knowing the risks related to radiation exposure at such a young age makes us question the validity of the hospital protocol we are following. Also, we believe that a future solution to this issue would be to implement radiation-free complimentary exams such as Magnetic Resonance Imaging (MRI) to our hospital protocol. Emphasizing the importance of justification of procedures and optimization of radiation doses are also crucial to prevent cancer development in pediatric patients.

Clinical characteristics and functional outcome of surgically treated adult head trauma patients with acute subdural hematoma: Ethiopian tertiary hospitals experience

BackgroundAcute subdural hematoma (ASDH) is one of the most common and devastating lesions in traumatic brain injury with a mortality rate upto 60 % especially in low-income countries. The present study aimed to determine the clinical characteristics and functional outcomes and the associated factors of surgically treated head trauma patients with ASDH. MethodsBetween January 2018 and January 2021 we identified 140 head trauma patients with ASDH who underwent surgical evacuation in three tertiary hospitals. Epidemiological data were collected; the six-month functional outcome was studied using an extended Glasgow outcome score (EGOS) and associated factors were also studied. Univariate analysis was performed at first, and variables with a P-value of <0.05 were entered into the multivariable logistic regression model. ResultsMale predominance was seen accounting for 87 % and assault was the most common mechanism of injury (35.7 %). Sixty-five (56.5 %) of patients achieved favorable functional recovery (EGOS of 5–8) and 50 (43.5 %) of patients had unfavorable recovery (EGOS of 1–4) after 6 months of follow-up. In multivariate logistic regression models, GCS <5, Pupillary abnormality, hypotension, oxygen saturation <90 at presentation, and hospital-acquired pneumonia were the independent factors associated with unfavorable functional outcomes. ConclusionIn our setup, most of the patients are male from assault injuries. There is still a high rate of unfavorable outcomes in patients with acute subdural hematoma. GCS <5, pupillary abnormality, hypotension and desaturation at presentation, and postoperative hospital-acquired infection are predictors for unfavorable functional outcomes.

Prediction of therapeutic intensity level from automatic multiclass segmentation of traumatic brain injury lesions on CT-scans

The prediction of the therapeutic intensity level (TIL) for severe traumatic brain injury (TBI) patients at the early phase of intensive care unit (ICU) remains challenging. Computed tomography images are still manually quantified and then underexploited. In this study, we develop an artificial intelligence-based tool to segment brain lesions on admission CT-scan and predict TIL within the first week in the ICU. A cohort of 29 head injured patients (87 CT-scans; Dataset1) was used to localize (using a structural atlas), segment (manually or automatically with or without transfer learning) 4 or 7 types of lesions and use these metrics to train classifiers, evaluated with AUC on a nested cross-validation, to predict requirements for TIL sum of 11 points or more during the 8 first days in ICU. The validation of the performances of both segmentation and classification tasks was done with Dice and accuracy scores on a sub-dataset of Dataset1 (internal validation) and an external dataset of 12 TBI patients (12 CT-scans; Dataset2). Automatic 4-class segmentation (without transfer learning) was not able to correctly predict the apparition of a day of extreme TIL (AUC = 60 ± 23%). In contrast, manual quantification of volumes of 7 lesions and their spatial location provided a significantly better prediction power (AUC = 89 ± 17%). Transfer learning significantly improved the automatic 4-class segmentation (DICE scores 0.63 vs 0.34) and trained more efficiently a 7-class convolutional neural network (DICE = 0.64). Both validations showed that segmentations based on transfer learning were able to predict extreme TIL with better or equivalent accuracy (83%) as those made with manual segmentations. Our automatic characterization (volume, type and spatial location) of initial brain lesions observed on CT-scan, publicly available on a dedicated computing platform, could predict requirements for high TIL during the first 8 days after severe TBI. Transfer learning strategies may improve the accuracy of CNN-based segmentation models.Trial registrations Radiomic-TBI cohort; NCT04058379, first posted: 15 august 2019; Radioxy-TC cohort; Health Data Hub index F20220207212747, first posted: 7 February 2022.

A narrative review of the effects of dexamethasone on traumatic brain injury in clinical and animal studies: focusing on inflammation.

Traumatic brain injury (TBI) is a type of brain injury resulting from a sudden physical force to the head. TBI can range from mild, such as a concussion, to severe, which might result in long-term complications or even death. The initial impact or primary injury to the brain is followed by neuroinflammation, excitotoxicity, and oxidative stress, which are the hallmarks of the secondary injury phase, that can further damage the brain tissue. Dexamethasone (DXM) has neuroprotective effects. It reduces neuroinflammation, a critical factor in secondary injury-associated neuronal damage. DXM can also suppress the microglia activation and infiltrated macrophages, which are responsible for producing pro-inflammatory cytokines that contribute to neuroinflammation. Considering the outcomes of this research, some of the effects of DXM on TBI include: (1) DXM-loaded hydrogels reduce apoptosis, neuroinflammation, and lesion volume and improves neuronal cell survival and motor performance, (2) DXM treatment elevates the levels of Ndufs2, Gria3, MAOB, and Ndufv2 in the hippocampus following TBI, (3) DXM decreases the quantity of circulating endothelial progenitor cells, (4) DXM reduces the expression of IL1, (5) DXM suppresses the infiltration of RhoA + cells into primary lesions of TBI and (6) DXM treatment led to an increase in fractional anisotropy values and a decrease in apparent diffusion coefficient values, indicating improved white matter integrity. According to the study, the findings show that DXM treatment has neuroprotective effects in TBI. This indicates that DXM is a promising therapeutic approach to treating TBI.

Epidemiology and Assessment of Traumatic Spinal Cord Injury With Concomitant Brain Injury: An Observational Study in a Regional Trauma Center.

: To analyze the epidemiological information of patients with traumatic spinal cord injury (SCI) and concomitant traumatic brain injury (TBI) and to suggest points to be aware of during the initial physical examination of patients with SCI. : This study was a retrospective, observational study conducted in a regional trauma center. All the records of patients diagnosed with traumatic SCI between 2016 and 2020 were reviewed. A total of 627 patients with confirmed traumatic SCI were hospitalized. A retrospective study was conducted on 363 individuals. : The epidemiological data of 363 individuals were investigated. Changes in American Spinal Injury Association Impairment Scale (AIS) scores in patients with SCI were evaluated. The initial evaluation was performed on average 11 days after the injury, and a follow-up examination was performed 43 days after. Fourteen of the 24 patients identified as having AIS A and SCI with concomitant TBI in the initial evaluation showed neurologic level of injury (NLI) recovery with AIS B or more. The conversion rate in patients with SCI and concomitant TBI exceeded that reported in previous studies in individuals with SCI. : Physical, cognitive, and emotional impairments caused by TBI present significant challenges in rehabilitating patients with SCI. In this study, the influence of concomitant TBI lesions could have caused the initial AIS assessment to be incorrect.

The kinase inhibitory region of SOCS3 attenuates reactive astrogliosis and astroglial scar in mice after traumatic brain injury

Traumatic brain injury (TBI) leads to reactive astrogliosis that impedes neural repair/regeneration. It has been proven that SOCS3 attenuates astrocyte activation by inhibiting the JAK2-STAT3 pathway. However, whether the kinase inhibitory region (KIR) of SOCS3 can be directly applied to mediate astrocyte activation after TBI is not clear. The present study aimed at investigating the inhibitory effect of KIR on reactive astrogliosis and its potential neuroprotection after TBI insult. For this purpose, A TBI model was developed by the free impact of heavy objects in adult mice. KIR was linked to the TAT peptide (TAT-KIR) to facilitate cell membrane penetration and intracranially injected into the cerebral cortex adjacent to the TBI lesion. Then reactive astrogliosis, activity of JAK2-STAT3 pathway, neuron loss, and function deficit were observed. Our results showed a decrease in neuron loss and an improvement in neural function. Meanwhile, Intracranial injection of TAT-KIR in TBI mice demonstrated a reduction of GFAP-positive astrocytes as well as C3/GFAP double-labeled A1 reactive astrocytes. Western blot analysis illustrated that the activity of the JAK2-STAT3 pathway was significantly inhibited by TAT-KIR. We conclude that exogenous treatment TAT-KIR, through suppression of JAK2-STAT3 activity, inhibits TBI -induced reactive astrogliosis induced, thereby alleviating the loss of neurons and relieving the neural function deficit. This investigation suggests that TAT-KIR could be a potential therapeutic strategy for enhancing neural regeneration following

Novel, thalidomide-like, non-cereblon binding drug tetrafluorobornylphthalimide mitigates inflammation and brain injury

BackgroundQuelling microglial-induced excessive neuroinflammation is a potential treatment strategy across neurological disorders, including traumatic brain injury (TBI), and can be achieved by thalidomide-like drugs albeit this approved drug class is compromised by potential teratogenicity. Tetrafluorobornylphthalimide (TFBP) and tetrafluoronorbornylphthalimide (TFNBP) were generated to retain the core phthalimide structure of thalidomide immunomodulatory imide drug (IMiD) class. However, the classical glutarimide ring was replaced by a bridged ring structure. TFBP/TFNBP were hence designed to retain beneficial anti-inflammatory properties of IMiDs but, importantly, hinder cereblon binding that underlies the adverse action of thalidomide-like drugs.MethodsTFBP/TFNBP were synthesized and evaluated for cereblon binding and anti-inflammatory actions in human and rodent cell cultures. Teratogenic potential was assessed in chicken embryos, and in vivo anti-inflammatory actions in rodents challenged with either lipopolysaccharide (LPS) or controlled cortical impact (CCI) moderate traumatic brain injury (TBI). Molecular modeling was performed to provide insight into drug/cereblon binding interactions.ResultsTFBP/TFNBP reduced markers of inflammation in mouse macrophage-like RAW264.7 cell cultures and in rodents challenged with LPS, lowering proinflammatory cytokines. Binding studies demonstrated minimal interaction with cereblon, with no resulting degradation of teratogenicity-associated transcription factor SALL4 or of teratogenicity in chicken embryo assays. To evaluate the biological relevance of its anti-inflammatory actions, two doses of TFBP were administered to mice at 1 and 24 h post-injury following CCI TBI. Compared to vehicle treatment, TFBP reduced TBI lesion size together with TBI-induction of an activated microglial phenotype, as evaluated by immunohistochemistry 2-weeks post-injury. Behavioral evaluations at 1- and 2-weeks post-injury demonstrated TFBP provided more rapid recovery of TBI-induced motor coordination and balance impairments, versus vehicle treated mice.ConclusionTFBP and TFNBP represent a new class of thalidomide-like IMiDs that lower proinflammatory cytokine generation but lack binding to cereblon, the main teratogenicity-associated mechanism. This aspect makes TFBP and TFNBP potentially safer than classic IMiDs for clinical use. TFBP provides a strategy to mitigate excessive neuroinflammation associated with moderate severity TBI to, thereby, improve behavioral outcome measures and warrants further investigation in neurological disorders involving a neuroinflammatory component.Graphical

An end-end deep learning framework for lesion segmentation on multi-contrast MR images—an exploratory study in a rat model of traumatic brain injury

Traumatic brain injury (TBI) engenders traumatic necrosis and penumbra-areas of secondary neural injury which are crucial targets for therapeutic interventions. Segmenting manually areas of ongoing changes like necrosis, edema, hematoma, and inflammation is tedious, error-prone, and biased. Using the multi-parametric MR data from a rodent model study, we demonstrate the effectiveness of an end-end deep learning global-attention-based UNet (GA-UNet) framework for automatic segmentation and quantification of TBI lesions. Longitudinal MR scans (2h, 1, 3, 7, 14, 30, and 60days) were performed on eight Sprague-Dawley rats after controlled cortical injury was performed. TBI lesion and sub-regions segmentation was performed using 3D-UNet and GA-UNet. Dice statistics (DSI) and Hausdorff distance were calculated to assess the performance. MR scan variations-based (bias, noise, blur, ghosting) data augmentation was performed to develop a robust model.Training/validation median DSI for U-Net was 0.9368 with T2w and MPRAGE inputs, whereas GA-UNet had 0.9537 for the same. Testing accuracies were higher for GA-UNet than U-Net with a DSI of 0.8232 for the T2w-MPRAGE inputs.Longitudinally, necrosis remained constant while oligemia and penumbra decreased, and edema appearing around day 3 which increased with time. GA-UNet shows promise for multi-contrast MR image-based segmentation/quantification of TBI in large cohort studies.

Association between Blood and Computed Tomographic Imaging Biomarkers in a Cohort of Mild Traumatic Brain Injury Patients.

The objective of this work was to analyze the relationships between traumatic brain injury (TBI) on computed tomographic (CT) imaging and blood concentration of glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase-L1 (UCH-L1), and S100B. This prospective cohort study involved 644 TBI patients referred to Stanford Hospital's Emergency Department between November 2015 and April 2017. Plasma and serum samples of 462 patients were analyzed for levels of GFAP, UCH-L1, and S100B. Glial neuronal ratio (GNR) was calculated as the ratio between GFAP and UCH-L1 concentrations. Admission head CT scans were reviewed for TBI imaging common data elements, and performance of biomarkers for identifying TBI was assessed via area under the receiver operating characteristic curve (ROC). We also dichotomized biomarkers at established thresholds and estimated standard measures of classification accuracy. We assessed the ability of GFAP, UCH-L1, and GNR to discriminate small and large/diffuse lesions based on CT imaging using an ROC analysis. In our cohort of mostly mild TBI patients, GFAP was significantly more accurate in detecting all types of acute brain injuries than UCH-L1 in terms of area under the curve (AUC) values (p < 0.001), and also compared with S100B (p < 0.001). UCH-L1 and S100B had similar performance (comparable AUC values, p = 0.342). Sensitivity exceeded 0.8 for each biomarker across all different types of TBI injuries, and no significant differences were observed by type of injury. There was a significant difference between GFAP and GNR in distinguishing between small lesions and large/diffuse lesions in all injuries (p = 0.004, p = 0.007). In conclusion, GFAP, UCH-L1, and S100B show high sensitivity and negative predictive values for all types of TBI lesions on head CT. A combination of negative blood biomarkers (GFAP and UCH-L1) in a patient suspected of TBI may be used to safely obviate the need for a head CT scan. GFAP is a promising indicator to discriminate between small and large/diffuse TBI lesions.

A hybrid method for traumatic brain injury lesion segmentation

&lt;span&gt;Traumatic brain injuries are significant effects of disability and loss of life. Physicians employ computed tomography (CT) images to observe the trauma and measure its severity for diagnosis and treatment. Due to the overlap of hemorrhage and normal brain tissues, segmentation methods sometimes lead to false results. The study is more challenging to unitize the AI field to collect brain hemorrhage by involving patient datasets employing CT scans images. We propose a novel technique free-form object model for brain injury CT image segmentation based on superpixel image processing that uses CT to analyzing brain injuries, quite challenging to create a high outstanding simple linear iterative clustering (SLIC) method. The maintains a strategic distance of the segmentation image to reduced intensity boundaries. The segmentation image contains marked red hemorrhage to modify the free-form object model. The contour labelled by the red mark is the output from our free-form object model. We proposed a hybrid image segmentation approach based on the combined edge detection and dilation technique features. The approach diminishes computational costs, and the show accomplished 96.68% accuracy. The segmenting brain hemorrhage images are achieved in the clustered region to construct a free-form object model. The study also presents further directions on future research in this domain.&lt;/span&gt;

Neural stem cell therapy in conjunction with curcumin loaded in niosomal nanoparticles enhanced recovery from traumatic brain injury

Despite a great amount of effort, there is still a need for reliable treatments of traumatic brain injury (TBI). Recently, stem cell therapy has emerged as a new avenue to address neuronal regeneration after TBI. However, the environment of TBI lesions exerts negative effects on the stem cells efficacy. Therefore, to maximize the beneficial effects of stem cells in the course of TBI, we evaluated the effect of human neural stem/progenitor cells (hNS/PCs) and curcumin-loaded niosome nanoparticles (CM-NPs) on behavioral changes, brain edema, gliosis, and inflammatory responses in a rat model of TBI. After TBI, hNS/PCs were transplanted within the injury site and CM-NPs were orally administered for 10 days. Finally, the effect of combination therapy was compared to several control groups. Our results indicated a significant improvement of general locomotor activity in the hNS/PCs + CM-NPs treatment group compared to the control groups. We also observed a significant improvement in brain edema in the hNS/PCs + CM-NPs treatment group compared to the other groups. Furthermore, a significant decrease in astrogliosis was seen in the combined treatment group. Moreover, TLR4-, NF-κB-, and TNF-α- positive cells were significantly decreased in hNS/PCs + CM-NPs group compared to the control groups. Taken together, this study indicated that combination therapy of stem cells with CM-NPs can be an effective therapy for TBI.

PD-L1 signaling in reactive astrocytes counteracts neuroinflammation and ameliorates neuronal damage after traumatic brain injury

BackgroundTissue damage and cellular destruction are the major events in traumatic brain injury (TBI), which trigger sterile neuroimmune and neuroinflammatory responses in the brain. While appropriate acute and transient neuroimmune and neuroinflammatory responses facilitate the repair and adaptation of injured brain tissues, prolonged and excessive neuroimmune and neuroinflammatory responses exacerbate brain damage. The mechanisms that control the intensity and duration of neuroimmune and neuroinflammatory responses in TBI largely remain elusive.MethodsWe used the controlled cortical impact (CCI) model of TBI to study the role of immune checkpoints (ICPs), key regulators of immune homeostasis, in the regulation of neuroimmune and neuroinflammatory responses in the brain in vivo.ResultsWe found that de novo expression of PD-L1, a potent inhibitory ICP, was robustly and transiently induced in reactive astrocytes, but not in microglia, neurons, or oligodendrocyte progenitor cells (OPCs). These PD-L1+ reactive astrocytes were highly enriched to form a dense zone around the TBI lesion. Blockade of PD-L1 signaling enlarged brain tissue cavity size, increased infiltration of inflammatory Ly-6CHigh monocytes/macrophages (M/Mɸ) but not tissue-repairing Ly-6CLowF4/80+ M/Mɸ, and worsened TBI outcomes in mice. PD-L1 gene knockout enhanced production of CCL2 that is best known for its ability to interact with its cognate receptor CCR2 on Ly-6CHigh M/Mϕ to chemotactically recruit these cells into inflammatory sites. Mechanically, PD-L1 signaling in astrocytes likely exhibits dual inhibitory activities for the prevention of excessive neuroimmune and neuroinflammatory responses to TBI through (1) the PD-1/PD-L1 axis to suppress the activity of brain-infiltrating PD-1+ immune cells, such as PD-1+ T cells, and (2) PD-L1 intrinsic signaling to regulate the timing and intensity of astrocyte reactions to TBI.ConclusionsPD-L1+ astrocytes act as a gatekeeper to the brain to control TBI-related neuroimmune and neuroinflammatory responses, thereby opening a novel avenue to study the role of ICP–neuroimmune axes in the pathophysiology of TBI and other neurological disorders.

Порушення натрієвого балансу у хворих з ураженням гіпоталамо-гіпофізарної ділянки при черепно-мозковій травмі

Актуальність. Черепно-мозкова травма (ЧМТ) до цього часу залишається провідною причиною смерті людей працездатного віку. В Україні частота ЧМТ щорічно становить у різних регіонах від 2,3 до 6 випадків (у середньому 4–4,2) на 1000 населення. Пацієнти з первинним ураженням головного мозку і гіпоталамо-гіпофізарної системи становлять групу ризику з розвитку набряку головного мозку через виникнення у них порушення водно-електролітної рівноваги та відповідно порушення рівноваги осмолярності між клітинним та позаклітинним простором. Порушення водно-електролітного балансу як наслідок ураження гіпоталамо-гіпофізарної системи при ЧМТ в літературі висвітлено недостатньо. Мало вивчені особливості функціонування центральних та периферичних ланцюжків ендокринної системи залежно від локалізації, характеру і тяжкості травми. Недостатньо вивчене питання про діагностичні та прогностичні цінності різних показників волемічного статусу у хворих із ЧМТ. Мета: вивчити види дизнатріємії у хворих з ізольованою ЧМТ і ураженням гіпоталамо-гіпофізарної ділянки головного мозку; вияснити вплив виду порушення натрієвого балансу на летальність у хворих із ЧМТ та ураженням гіпоталамо-гіпофізарної ділянки головного мозку. Матеріали та методи. Нами було обстежено 74 пацієнтів (чоловіків/жінок = 60/14) із вогнищевим забоєм головного мозку й ураженням гіпоталамічної ділянки. Серед 74 хворих з ізольованою ЧМТ і ураженням гіпоталамо-гіпофізарної ділянки головного мозку в 47 хворих було діагностовано гіповолемію, що поєднувалась з гіпонатріємією. У 15 хворих було виявлено гіпернатріємію з гіперволемією. Моніторинг внутрішньочерепного тиску здійснювали за допомогою поліфункціонального монітора (Monitor Model BSM-3562 (Nihon Konden Corporation, Японія, 2018)) із лінією для інвазивного вимірювання тиску. Постійне неінвазивне вимірювання оксигенації тканин органів (rSO2) проводили на моніторі Somanetics Invos Oximeter Cerebral/Somatik (Covidien, Mansfield, MA, США, 2020). В усіх хворих визначали рівень електролітів плазми крові. Висновки. У хворих із ЧМТ і ураженням гіпоталамо-гіпофізарної системи виникають різнонаправлені зміни водно-натрієвого балансу, що вимагають диференційованого підходу до їх лікування. Зважаючи на невелику кількість спостережень, ми не наважуємося пов’язувати вид дизнатріємії у хворих із ЧМТ і ураженням гіпоталамо-гіпофізарної ділянки головного мозку з летальністю. Вважаємо за доцільне продовжувати дослідження в цьому напрямку.

Remarks on patients with traumatic brain injury due to traffic accident related to alcohol comsumption treated in Vietduc hospital after implementing the decree 100

Purpose: Traumatic Brain Injury (TBI) is still considered as a leading cause of morbidity and mortality of victims by traffic accident. Despite a fact that many measurements and preventions have been applied, the rate of TBI is remained high. Aim of this study was to investigate treatment process of TBI caused by road traffic accident at Viet Duc Hospital after the Decree 100 which has been issued in Vietnam in early 2020. Materials and method: A retrospective and prospective study has been conducted in Viet Duc Hospital from Dec, 2020 to March, 2021. All the patients with TBI by road traffic accident were enrolled. Severity of TBI was identified by Glasgow Scale (GCS) and BAC (Blood Alcohol Concentration) test taken on arrival. The data was collected from medical record as well as autopsy report and analysed by SPSS.20.0 Results: A total of 150 patients with TBI by road traffic accidents were enrolled, age group from 21 to 60 years old accounted for 64%, male accounted for 86.7%. Associated injuries were maxillofacial lesions 48%, extremities 24.7%, chest accounted for 20%. Severity of TBI with GCS 6 - 8 was the highest rate 52%, from 3 - 5 GCS accounted for 30%. 40% were operated on emergency; BAC was positive 46.7%, of which over from 50 mg/L accounted for 32.6%. The patients with GCS from 6 to 8 were BAC positive accounted for a higher rate than groups with GCS above 9 or below 5. The most common TBI lesions were subarachnoid hemorrhage, subdural hematoma and cerebral edema accounted for 67.3%, 60% and 58% respectively. Overall mortality was 26% including in-hospital death and discharged to die. Conclusions and recommendations: Data from the study has shown that many young men with severe TBI by road traffic accident were BAC positive which can results in the high risk of death and disability. Thus, we highly recommend counterparts should constantly strengthen the propaganda and enforcement measures in order to reduce traffic accidents and TBI patients. Keywords: traffic accidents; injury; brain trauma severity.

Quantification of Alcohol Dehydrogenase Concentration for Traumatic Brain Injury in Alcohol-intoxicated Patients as a Predictor of Severity and Prognosis

BACKGROUND: Traumatic brain injury (TBI) stills the leading cause of public health problem and disabilities in many countries, especially in lower-middle-income countries. Motor vehicle crashes, especially motorized two-wheeler riders, are the major cause of TBI, followed by fall and assault. During 2013–2014, a total of 2108 TBI cases (65.4% of them being caused by motor vehicle crashes) were documented in the Emergency Unit of Dr. Hasan Sadikin Hospital (RSHS) Bandung. Among these, 30.7% of cases were categorized as moderate and severe TBI, with a mortality rate of 29.2%. Half of the cases arrived at RSHS within 6 h and 14.0% of these cases were alcohol-intoxicated. Individuals with low activity of alcohol-metabolizing enzymes have low tolerance to alcohol and are therefore rapidly intoxicated, making them more susceptible to more serious injuries from motor vehicle crashes. METHODS: A prospective study was designed by consecutive sampling from January to August 2017 to review 30 intoxicated patients with TBI on hospital admission by measuring their serum alcohol dehydrogenase (ADH) concentration using an ELISA and then correlated it with the severity, type of TBI lesions, and the outcome. RESULTS: Demonstrated an ADH level of l d0.24 ng/ml in patients with TBI with a history of alcohol intoxication, which statistically correlated with lower initial Glasgow coma scale (GCS) scores on admission by approximately 6.53 times (p &lt; 0.001), thus increasing the risk of developing multiple lesions by 3.98 times (p = 0.029) and worse outcomes by 5.27 times (p = 0.003), but it did not correlate with length of stay (p = 0.392). CONCLUSIONS: ADH concentrations in intoxicated TBI patients can be taken into consideration to decide about the therapeutic action and further informed consent to the family.

CX3CR1 deficiency aggravates brain white matter injury and affects expression of the CD36/15LO/NR4A1 signal

ObjectiveTo study the effects of CX3CR1 on white matter injury, neurofunction, recognition, and expression of the CD36/15LO/NR4A1 signal in mice with traumatic brain injury (TBI). MethodsCX3CR1GFP/GFP, CX3CR1GFP/+ and C57BL/6 male mice were randomly divided into 3 groups. We used a controlled cortical impact (CCI) to establish a TBI model and T2wt MRI to detect the TBI lesion. FA and DTI allowed for quantitative evaluation of the structural integrity of white matter tracts. Several behavior tests were used to investigate nerve function; a computer-based tracing system was used to trace and analyze dendrites and cell bodies of microglia and astrocytes in the peri-lesional brain areas. We also used RT-PCR and western blot to detect the effect of CX3CL1/CX3CR1 axis on CD36/15LO/NR4A1 signal. ResultsThe fractional anisotropy (FA) at the corpus callosum area of brain was decreased at 3 days post TBI, the average lesion volume CX3CR1GFP/GFP group was increased, and the neurologic deficit scores of mice of Cx3Cr1GFP/+ and wild-type groups were significantly increased compared to Cx3Cr1GFP/GFP group mice. In the Corner turn test, TBI induced impairments in forelimb function that were more severe than Cx3Cr11GFP/+ and wild-type TBI mice. We operated the Y-maze at 3 days post-TBI and the NOR test at 28 days after TBI. There was a significant TBI effect induced in decreased percentage entries into the novel arm in Cx3Cr1GFP/+ and wild-type TBI mice, compared with Cx3Cr1GFP/GFP; Cx3Cr1GFP/+. Wild-type mice showed decreased exploration time in new objects compared with Cx3Cr1GFP/GFP. Those two behavior tests demonstrated that Cx3Cr1 knock-out increased the damage caused by TBI to memory. In the tail suspension and force swimming tests, there was no significant difference between those three groups. CD36 increased in Cx3Cr1GFP/GFP compared with the other three groups at 3 days after TBI. TBI inhibited the expression of NR4A1 at 3 d after damage. Cx3Cr1 deficiency can induce high expression of 15LO, this was unaffected by TBI. ConclusionCX3CR1 deletion can enhance white matter injury. It increased the expression of CD36 and 15LO and increased expression of NR4A1. The lack of CX3CR1 can affect the recovery of nerve function.

Pediatric traumatic brain injury: a new relation between outcome and neutrophil-to-lymphocite ratio.

Leading causes of death in industrialized countries are traumatic injuries and acquired disability, and entry to the emergency department in childhood. TBI (traumatic brain injury) may involve the onset of both primary lesions and a complex immune response (sterile immune reaction to brain injury), which, in addition to neuro-protective effects, can mediate secondary neurological injury. The neutrophil-to-lymphocyte ratio (NLR), as a circulating inflammatory marker, has been related to outcomes in adult patients with non-neurologic diseases (such as gut tumours) or neurologic diseases (such as stroke or brain tumours), and to the prognosis of traumatic brain injury in adolescents and adults. However, the potential role of NLR in predicting outcomes in paediatric head trauma is not clearly defined. The aim of this retrospective observational study is to evaluate the association between clinical features predictive of intracranial and extracranial lesions in TBI and NLR and to establish whether an elevation of NLR is indirectly associated with adverse outcomes in pediatric patients with TBI. We analysed a sample of 219 pediatric patients, between 2-18 years old, after a TBI, and evaluated if differences in NLR were associated with neurological signs or positive CT in pediatric patients. We then compared the NLR values between healthy subjects and patients with TBI. (www.actabiomedica.it)

Multiclass semantic segmentation and quantification of traumatic brain injury lesions on head CT using deep learning: an algorithm development and multicentre validation study

CT is the most common imaging modality in traumatic brain injury (TBI). However, its conventional use requires expert clinical interpretation and does not provide detailed quantitative outputs, which may have prognostic importance. We aimed to use deep learning to reliably and efficiently quantify and detect different lesion types. Patients were recruited between Dec 9, 2014, and Dec 17, 2017, in 60 centres across Europe. We trained and validated an initial convolutional neural network (CNN) on expert manual segmentations (dataset 1). This CNN was used to automatically segment a new dataset of scans, which we then corrected manually (dataset 2). From this dataset, we used a subset of scans to train a final CNN for multiclass, voxel-wise segmentation of lesion types. The performance of this CNN was evaluated on a test subset. Performance was measured for lesion volume quantification, lesion progression, and lesion detection and lesion volume classification. For lesion detection, external validation was done on an independent set of 500 patients from India. 98 scans from one centre were included in dataset 1. Dataset 2 comprised 839 scans from 38 centres: 184 scans were used in the training subset and 655 in the test subset. Compared with manual reference, CNN-derived lesion volumes showed a mean difference of 0·86 mL (95% CI -5·23 to 6·94) for intraparenchymal haemorrhage, 1·83 mL (-12·01 to 15·66) for extra-axial haemorrhage, 2·09 mL (-9·38 to 13·56) for perilesional oedema, and 0·07 mL (-1·00 to 1·13) for intraventricular haemorrhage. We show the ability of a CNN to separately segment, quantify, and detect multiclass haemorrhagic lesions and perilesional oedema. These volumetric lesion estimates allow clinically relevant quantification of lesion burden and progression, with potential applications for personalised treatment strategies and clinical research in TBI. European Union 7th Framework Programme, Hannelore Kohl Stiftung, OneMind, NeuroTrauma Sciences, Integra Neurosciences, European Research Council Horizon 2020.