Explore the vast range of titles available.

The aim of this study was to compare the diagnostic value of post-mortem computed tomography angiography (PMCTA) to conventional, ante-mortem computed tomography (CT)-scan, CT-angiography (CTA) and digital subtraction angiography (DSA) in the detection and localization of the source of bleeding in cases of acute hemorrhage with fatal outcomes. The medical records and imaging scans of nine individuals who underwent a conventional, ante-mortem CT-scan, CTA or DSA and later died in the hospital as a result of an acute hemorrhage were reviewed. Post-mortem computed tomography angiography, using multi-phase post-mortem CTA, as well as medico-legal autopsies were performed. Localization accuracy of the bleeding was assessed by comparing the diagnostic findings of the different techniques. The results revealed that data from ante-mortem and post-mortem radiological examinations were similar, though the PMCTA showed a higher sensitivity for detecting the hemorrhage source than did ante-mortem radiological investigations. By comparing the results of PMCTA and conventional autopsy, much higher sensitivity was noted in PMCTA in identifying the source of the bleeding. In fact, the vessels involved were identified in eight out of nine cases using PMCTA and only in three cases through conventional autopsy. Our study showed that PMCTA, similar to clinical radiological investigations, is able to precisely identify lesions of arterial and/or venous vessels and thus determine the source of bleeding in cases of acute hemorrhages with fatal outcomes.

We present a case of a young male patient with a fatal pulmonary air embolism following a penetrating gunshot head injury. He suffered from severe head trauma including a laceration of the superior sagittal sinus. Operative neurosurgical intervention did not establish a watertight closure of the wounds. Eight days after the trauma, the patient suddenly collapsed and died after an attempt to mobilise him to the vertical. Forensic autopsy indicated pulmonary air embolism as the cause of death. Retrospectively, we postulate an entry of air to the venous system via the incompletely occluded wounds and the lacerated superior sagittal sinus while mobilisation to the vertical created a negative pressure in the dural sinus.

A 27-year-old man suffered a relatively minor trauma. He developed signs of raised intracranial pressure three days after injury. Investigations revealed superior sagittal sinus and torcular thrombosis.

A 26-year-old male sustained simultaneous massive bilateral frontal extradural haematomas following a head injury as a result of a large tear of the superior sagittal sinus, without fracturing of the skull vault.

Background Cerebral venous sinus thrombosis (CVST) is a rare neurovascular disorder with highly variable manifestations and clinical courses. Animal models properly matched to the clinical form of CVST are necessary for elucidating the pathophysiology of the disease. In this study, we aimed to establish a rat model that accurately recapitulates the clinical features of CVST in human patients. Methods This study consisted of a clinical analysis and animal experiments. Clinical data for two centres obtained between January 2016 and May 2021 were collected and analysed retrospectively. In addition, a Sprague–Dawley rat model of CVST was established by inserting a water-swellable rubber device into the superior sagittal sinus, following which imaging, histological, haematological, and behavioural tests were used to investigate pathophysiological changes. Principal component analysis and hierarchical clustering heatmaps were used to evaluate the similarity between the animal models and human patients. Results The imaging results revealed the possibility of vasogenic oedema in animal models. Haematological analysis indicated an inflammatory and hypercoagulable state. These findings were mostly matched with the retrospective clinical data. Pathological and serological tests further revealed brain parenchymal damage related to CVST in animal models. Conclusions We successfully established a stable and reproducible rat model of CVST. The high similarity between clinical patients and animal models was verified via cluster analysis. This model may be useful for the study of CVST pathophysiology and potential therapies.

Cerebral venous thrombosis (CVT) is a neurovascular disease with recently increasing incidence. Aseptic inflammatory responses play an important role in the pathology of CVT. Recent studies report that neutrophil extracellular traps (NETs) are major triggers of thrombosis and inflammation in stroke, but their effect on brain injury in CVT requires further validation. In this study, two CVT animal models were used to simulate superior sagittal sinus thrombosis and cortical vein thrombosis. The effects of brain tissue infiltration of NETs and the molecular mechanisms associated with NET formation were deeply explored in combination with proteomics, histology, and serology. The results showed that the cortical vein thrombosis model could be combined with more severe blood–brain barrier (BBB) disruption and showed more severe cerebral hemorrhage. Decreased Sirtuin 1 (SIRT1) expression promotes high mobility group box 1 (HMGB1) acetylation, causing increased cytosolic translocation and extracellular release, and HMGB1 can promote NET formation and recruitment. In addition, corticocerebral accumulation of NETs contributes to BBB damage. This establishes a vicious cycle between BBB damage and NET accumulation. SIRT1 mediated-HMGB1 deacetylation may play a critical role in attenuating BBB damage following CVT. This study employed a combined validation using models of venous sinus thrombosis and cortical vein thrombosis to investigate the deacetylation role of SIRT1, aiming to offer new insights into the pathological mechanisms of brain injury following CVT.

The mechanical properties of the cerebral bridging veins (CBVs) were studied using advanced microtensile equipment. Detailed high-quality curves were obtained at different strain rates, showing a clearly nonlinear stress–strain response. In addition, the tissue of the CBVs exhibits stress relaxation and a preconditioning effect under cyclic loading, unequivocal indications of viscoelastic behavior. Interestingly, most previous literature that conducts uniaxial tensile tests had not found significant viscoelastic effects in CBVs, but the use of more sensitive tests allowed to observe the viscoelastic effects. For that reason, a careful mathematical analysis is presented, clarifying why in uniaxial tests with moderate strain rates, it is difficult to observe any viscoelastic effect. The analysis provides a theoretical explanation as to why many recent studies that investigated mechanical properties did not find a significant viscoelastic effect, even though in other circumstances, the CBV tissue would clearly exhibit viscoelastic behavior. Finally, this study provides reference values for the usual mechanical properties, as well as calculations of constitutive parameters for nonlinear elastic and viscoelastic models that would allow more accurate numerical simulation of CBVs in Finite Element-based computational models in future works.

Background. Gastric pentadecapeptide BPC 157 therapy in rats compensated irremovable occlusion of various vessels and counteracted the consequent multiorgan dysfunction syndromes by activation of the corresponding collateral bypassing loops. Thus, we used BPC 157 therapy against the irremovable occlusion of the end of the superior mesenteric vein. Methods. Assessments, for 30 min (gross recording, venography, ECG, pressure, microscopy, biochemistry, and oxidative stress) include the portal and caval hypertension, aortal hypotension, and centrally, the superior sagittal sinus hypertension, systemic arterial and venous thrombosis, ECG disturbances, MDA-tissue increase, and heart, lung, liver, kidney and gastrointestinal tract, in particular, and brain (cortex (cerebral, cerebellar), hypothalamus/thalamus, hippocampus) lesions. Rats received BPC 157 medication (10 µg/kg, 10 ng/kg) intraperitoneally at 1 or 15 min ligation time. Results. BPC 157 rapidly activated the superior mesenteric vein–inferior anterior pancreati-coduodenal vein–superior anterior pancreaticoduodenal vein–pyloric vein–portal vein pathway, reestablished superior mesenteric vein and portal vein connection and reestablished blood flow. Simultaneously, toward inferior caval vein, an additional pathway appears via the inferior mesenteric vein united with the middle colic vein, throughout its left colic branch to ascertain alternative bypassing blood flow. Consequently, BPC 157 acts peripherally and centrally, and counteracted the intracranial (superior sagittal sinus), portal and caval hypertension, aortal hypotension, ECG disturbances attenuated, abolished progressing venous and arterial thrombosis. Additionally, BPC 157 counteracted multiorgan dysfunction syndrome, heart, lung, liver, kidney and gastrointestinal tract, and brain lesions, and oxidative stress in tissues. Conclusion. BPC 157 therapy may be specific management also for the superior mesenteric vein injuries.

Acute subdural hematoma (ASDH) is one of the most frequent traumatic brain injuries (TBIs) with high mortality rate. Bridging vein (BV) ruptures is a major cause of ASDH. The KTH finite element head model includes bridging veins to predict acute subdural hematoma due to BV rupture. In this model, BVs were positioned according to Oka et al. (1985). The aim of the current study is to investigate whether the location and entry angles of these BVs could be modelled using data from a greater statistical sample, and what the impact of this improvement would be on the model’s predictive capability of BV rupture. From the CT angiogram data of 78 patients, the relative position of the bridging veins and their entry angles along the superior sagittal sinus was determined. The bridging veins were repositioned in the model accordingly. The performance of the model, w.r.t. BV rupture prediction potential was tested on simulations of full body cadaver head impact experiments. The experiments were simulated on the original version of the model and on three other versions which had updated BV positions according to mean, maximum and minimum entry angles. Even though the successful prediction rate between the models stayed the same, the location of the rupture site significantly improved for the model with the mean entry angles. Moreover, the models with maximum and minimum entry angles give an insight of how BV biovariability can influence ASDH. In order to further improve the successful prediction rate, more biofidelic data are needed both with respect to bridging vein material properties and geometry. Furthermore, more experimental data are needed in order to investigate the behaviour of FE head models in depth.