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BackgroundTraumatic brain injury (TBI) causes early seizures and is the leading cause of post-traumatic epilepsy. We prospectively assessed structural imaging biomarkers differentiating patients who develop seizures secondary to TBI from patients who do not.DesignMulticentre prospective cohort study starting in 2018. Imaging data are acquired around day 14 post-injury, detection of seizure events occurred early (within 1 week) and late (up to 90 days post-TBI).ResultsFrom a sample of 96 patients surviving moderate-to-severe TBI, we performed shape analysis of local volume deficits in subcortical areas (analysable sample: 57 patients; 35 no seizure, 14 early, 8 late) and cortical ribbon thinning (analysable sample: 46 patients; 29 no seizure, 10 early, 7 late). Right hippocampal volume deficit and inferior temporal cortex thinning demonstrated a significant effect across groups. Additionally, the degree of left frontal and temporal pole thinning, and clinical score at the time of the MRI, could differentiate patients experiencing early seizures from patients not experiencing them with 89% accuracy.Conclusions and relevanceAlthough this is an initial report, these data show that specific areas of localised volume deficit, as visible on routine imaging data, are associated with the emergence of seizures after TBI.

Purpose Contusion expansion is a key determinant of outcome after traumatic brain injury (TBI). Because many patients develop acute coagulopathy, it has been proposed that hemostatic changes may drive this expansion, but the link remains uncertain. Methods In this retrospective single-center cohort, we included adults with isolated moderate-to-severe TBI and no pre-injury antithrombotic therapy. The hemostatic markers activated partial thromboplastin time (APTT), prothrombin time (PT, reported as INR), platelet count (PLT), and fibrinogen were measured on admission and during the first 72 h. Contusion volumes were derived from serial CT scans. Associations between hemostatic markers and contusion volumes over time were analyzed using generalized additive mixed models (GAMMs), adjusting for confounders. Results Among 109 patients, median admission values were fibrinogen 2.4 g/L, PT-INR 1.0, APTT 29 s, and PLT 233 × 10 9 /L. After admission, fibrinogen and PLT declined, whereas PT-INR and APTT increased modestly. Contusion volume increased from a median of 0.7 ml at baseline to 4.6 ml on the third CT. In univariable models, higher APTT and PT-INR values and lower platelet counts were associated with larger contusion volumes, but these associations lost significance after adjustment for age and time from injury. Conclusion Hemostatic disturbances, as measured by standard coagulation assays, were common after TBI but not independently associated with contusion volume over time.

Background Cortical contusions are common in moderate-severe traumatic brain injury (TBI). Cortical contusions often expand, potentially causing neuro-worsening several hours to days post-trauma. While contusion expansion (CE) may affect outcome, potential clinical and radiological markers that can predict CE have been insufficiently explored. In the present single-center retrospective observational cohort study, we evaluated clinical outcome by the Glasgow Outcome Scale extended (GOSE) scale and evaluated risk factor for CE. Method Adult TBI patients > 18 years of age, and of all injury severities, were included. Main variables of interest were low platelet count, defined as < 150 × 10 9 /L, presence of bifrontal contusions and CE, defined as absolute contusion volume increase in cm 3 . Factors associated with CE and clinical outcome according to GOSE were analyzed. Results Between 2012–2022, 272 patients were included. Contusion size on admission correlated positively with CE, as did the Marshall and Rotterdam radiological classification scores. Bifrontal contusions were significantly larger at admission, experienced larger CE, and had a worse outcome than contusions in other locations. Patients with a platelet count < 150 × 10 9 /L experienced a greater volume CE and had a worse outcome when compared to patients with a normal platelet count. In a multivariate analysis, CE remained significantly associated with a poor outcome six months post- injury. Conclusion Contusion volume at admission, Marshall CT classification and Rotterdam CT score, positively correlated to CE. Bifrontal contusions and a platelet count < 150 × 10 9 /L were associated with CE, and a poor clinical outcome. Large CE volumes were associated with a worse clinical outcome, and CE was per se associated with outcome in a multivariate analysis. Management of these risk factors for CE in the acute post-injury setting may be needed to attenuate contusion expansion and to improve clinical outcome in TBI patients suffering from cortical contusion injuries.

Background Traumatic brain injury is a common and devastating injury that is the leading cause of neurological disability and death worldwide. Patients with cerebral lobe contusion received conservative treatment because of their mild manifestations, but delayed intracranial hematoma may increase and even become life-threatening. We explored the noninvasive method to predict the prognosis of progression and Glasgow Outcome Scale (GOS) by using a quantitative radiomics approach and statistical analysis. Methods Eighty-eight patients who were pathologically diagnosed were retrospectively studied. The radiomics method developed in this work included image segmentation, feature extraction, and feature selection. The nomograms were established based on statistical analysis and a radiomics method. We conducted a comparative study of hematoma progression and GOS between the clinical factor alone and fusion radiomics features. Results Nineteen clinical factors, 513 radiomics features, and 116 locational features were considered. Among clinical factors, international normalized ratio, prothrombin time, and fibrinogen were enrolled for hematoma progression. As for GOS, treatment strategy, age, Glasgow Coma Scale score, and blood platelet were associated factors. Eight features for GOS and five features for hematoma progression were filtered by using sparse representation and locality preserving projection-combined method. Four nomograms were constructed. After fusion radiomics features, area under the curve of hematoma progression prediction increased from 0.832 to 0.899, whereas GOS prediction went from 0.794 to 0.844. Conclusions A radiomic-based model that merges radiomics and clinical features is a noninvasive approach to predict hematoma progression and clinical outcomes of cerebral contusions in traumatic brain injury.

Traumatic cerebral contusion and intracerebral hemorrhages (ICH) commonly result from traumatic brain injury and are associated with high morbidity and mortality rates. Current animal models require craniotomy and provide less control over injury severity. This study proposes a highly reproducible and controllable traumatic contusion and ICH model using non-invasive extracorporeal shockwaves (ESWs). Rat heads were exposed to ESWs generated by an off-the-shelf clinical device plus intravenous injection of microbubbles to enhance the cavitation effect for non-invasive induction of injury. Results indicate that injury severity can be effectively adjusted by using different ESW parameters. Moreover, the location or depth of injury can be purposefully determined by changing the focus of the concave ESW probe. Traumatic contusion and ICH were confirmed by H&E staining. Interestingly, the numbers of TUNEL-positive cells (apoptotic cell death) peaked one day after ESW exposure, while Iba1-positive cells (reactive microglia) and GFAP-positive cells (astrogliosis) respectively peaked seven and fourteen days after exposure. Cytokine assay showed significantly increased expressions of IL-1β, IL-6, and TNF-α. The extent of brain edema was characterized with magnetic resonance imaging. Conclusively, the proposed non-invasive and highly reproducible preclinical model effectively simulates the mechanism of closed head injury and provides focused traumatic contusion and ICH.

Background Failure of cerebral autoregulation and progression of intracranial lesion have both been shown to contribute to poor outcome in patients with acute traumatic brain injury (TBI), but the interplay between the two phenomena has not been investigated. Preliminary evidence leads us to hypothesize that brain tissue adjacent to primary injury foci may be more vulnerable to large fluctuations in blood flow in the absence of intact autoregulatory mechanisms. The goal of this study was therefore to assess the influence of cerebrovascular reactivity measures on radiological lesion expansion in a cohort of patients with acute TBI. Methods We conducted a retrospective cohort analysis on 50 TBI patients who had undergone high-frequency multimodal intracranial monitoring and for which at least two brain computed tomography (CT) scans had been performed in the acute phase of injury. We first performed univariate analyses on the full cohort to identify non-neurophysiological factors (i.e., initial lesion volume, timing of scan, coagulopathy) associated with traumatic lesion growth in this population. In a subset analysis of 23 patients who had intracranial recording data covering the period between the initial and repeat CT scan, we then correlated changes in serial volumetric lesion measurements with cerebrovascular reactivity metrics derived from the pressure reactivity index (PRx), pulse amplitude index (PAx), and RAC (correlation coefficient between the pulse amplitude of intracranial pressure and cerebral perfusion pressure). Using multivariate methods, these results were subsequently adjusted for the non-neurophysiological confounders identified in the univariate analyses. Results We observed significant positive linear associations between the degree of cerebrovascular reactivity impairment and progression of pericontusional edema. The strongest correlations were observed between edema progression and the following indices of cerebrovascular reactivity between sequential scans: % time PRx > 0.25 ( r  = 0.69, p  = 0.002) and % time PAx > 0.25 ( r  = 0.64, p  = 0.006). These associations remained significant after adjusting for initial lesion volume and mean cerebral perfusion pressure. In contrast, progression of the hemorrhagic core and extra-axial hemorrhage volume did not appear to be strongly influenced by autoregulatory status. Conclusions Our preliminary findings suggest a possible link between autoregulatory failure and traumatic edema progression, which warrants re-evaluation in larger-scale prospective studies.

A deceased man in his 50 s was found with his neck over a broken glass door frame, with blood around the body. A non-contrast postmortem computed tomography (PMCT) scan revealed subcutaneous hemorrhage, temporal bone fracture, and cerebral contusion. Also, wounds extending from the anterior to posterior neck and the presence of air in the cervical vessels suggested cervical vascular injury. A virtual angioscopy image reconstructed from PMCT angiography data revealed a ruptured left common carotid artery and allowed accurate measurement of the injury. This case demonstrates the effectiveness of postmortem virtual angioscopy for visualization and evaluation of vascular injuries, providing valuable insights for forensic investigation.

Cerebral Contusion (CC) is one of the most serious injury types in patients with traumatic brain injury (TBI). Traumatic intraparenchymal hematoma (TICH) expansion severely affects the patient’s prognosis. In this study, the baseline data, imaging features, and laboratory examinations of patients with CC were summarized and analyzed to develop and validate a nomogram predictive model assessing the risk factors for TICH expansion. Totally 258 patients were included and retrospectively analyzed herein, who met the CC inclusion criteria, from July 2018 to July 2021. TICH expansion was defined as increased hematoma volume ≥ 30% relative to primary volume or an absolute hematoma increase ≥ 5 ml at CT review. Univariate and binary logistic regression analyses were performed to screen out the independent predictors significantly correlated with TICH expansion: Age, subdural hematoma (SDH), contusion site, multihematoma fuzzy sign (MFS), contusion volume, and traumatic coagulation abnormalities (TCA). Based on these, the nomogram model was established. The differences between the contusion volume and glasgow outcome scale (GOS) were analyzed by the nonparametric tests. Larger contusion volume was associated with poor prognosis. This study established a Nomogram model to predict TICH expansion in patients with CC. Meanwhile, the study found that the risk of bleeding tended to decrease when the hematoma volume was > 15 ml, but the larger initial hematoma volume would indicate worse prognosis. We advocate the use of predictive models for TICH expansion risk assessment in hospitalized CC patients, which is low-cost and easy-to-apply, especially in acute settings. •This study provides an easy-to-use tool to predict Traumatic intraparenchymal hematoma (TICH) risk in patients with Cerebral Contusion (CC) and to help optimize the classification and management of patients with CC. In this study, the baseline and clinical data of patients were integrated, and age, SDH, contusion volume, contusion site, Multihematoma fuzzy sign (MFS) and Traumatic coagulation abnormalities (TCA) were identified as significant influencing factors for TICH expansion.In addition, we found that the bleeding tendency decreased when the contusion volume was > 15ml, contrary to previous reports.•This study is a multi-center retrospective study with high persuasiveness based on the CC patients admitted to 3 authoritative hospitals in China in recent 3 years.•We provide the scores corresponding to various risk factors of TICH in CC patients, which can help doctors quickly judge the condition in clinical practice, especially in acute environment.

Background Spreading depolarizations (SDs) occur in 50–60% of patients after surgical treatment of severe traumatic brain injury (TBI) and are independently associated with unfavorable outcomes. Here we performed a pilot study to examine the relationship between SDs and various types of intracranial lesions, progression of parenchymal damage, and outcomes. Methods In a multicenter study, fifty patients (76% male; median age 40) were monitored for SD by continuous electrocorticography (ECoG; median duration 79 h) following surgical treatment of severe TBI. Volumes of hemorrhage and parenchymal damage were estimated using unbiased stereologic assessment of preoperative, postoperative, and post-ECoG serial computed tomography (CT) studies. Neurologic outcomes were assessed at 6 months by the Glasgow Outcome Scale-Extended. Results Preoperative volumes of subdural and subarachnoid hemorrhage, but not parenchymal damage, were significantly associated with the occurrence of SDs ( P ’s < 0.05). Parenchymal damage increased significantly (median 34 ml [Interquartile range (IQR) − 2, 74]) over 7 (5, 8) days from preoperative to post-ECoG CT studies. Patients with and without SDs did not differ in extent of parenchymal damage increase [47 ml (3, 101) vs. 30 ml (− 2, 50), P  = 0.27], but those exhibiting the isoelectric subtype of SDs had greater initial parenchymal damage and greater increases than other patients ( P ’s < 0.05). Patients with temporal clusters of SDs (≥ 3 in 2 h; n  = 10 patients), which included those with isoelectric SDs, had worse outcomes than those without clusters ( P  = 0.03), and parenchymal damage expansion also correlated with worse outcomes ( P  = 0.01). In multivariate regression with imputation, both clusters and lesion expansion were significant outcome predictors. Conclusions These results suggest that subarachnoid and subdural blood are important primary injury factors in provoking SDs and that clustered SDs and parenchymal lesion expansion contribute independently to worse patient outcomes. These results warrant future prospective studies using detailed quantification of TBI lesion types to better understand the relationship between anatomic and physiologic measures of secondary injury.