External validation and comparison of MBE, EDEMA, and modified EDEMA scores for predicting malignant cerebral EDEMA in Chinese patients with large hemispheric infarction patients without revascularization.

BACKGROUND: Malignant cerebral edema (MCE) is a severe condition characterized by rapid neurological deterioration and a potentially poor prognosis. Scoring systems including the malignant brain edema (MBE) score, Enhanced Detection of Edema in Malignant Anterior Circulation Stroke score (EDEMA), and modified EDEMA score, have been developed to predict MCE in patients with large hemispheric infarction (LHI). We aimed to externally validate and comparethe predictive efficacy of these scores in LHI patients within 48 h of onset and not undergoing reperfusion therapy. METHODS: Demographic, clinical and radiological data were retrospectively collected from LHI patients within 48 h of onset and not receiving reperfusion therapy. Patients were divided into MCE and non-MCE group. The calibration, discrimination, and clinical practicability of the three scores were verified using Hosmer-Lemeshow goodness-of-fit test, receiver operating characteristic (ROC) curve analysis and decision curve analysis (DCA), respectively. Finally, continuous net reclassification improvement (NRI) and integrated discrimination improvement (IDI) were applied to determine the discrimination performance of the three scores. RESULTS: A total of 314 patients were included in the study, with 122 cases being MCE patients. The Hosmer-Lemeshow goodness-of-fit test showed excellent fitting ability across the MBE (p = 0.36), EDEMA (p = 0.61), and modified EDEMA scores (p = 0.62) in our patients. The MBE, EDEMA, and modified EDEMA scores had the AUCs of 0.855 (95 % CI 0.818-0.898), 0.782 (95 % CI 0.727-0.837) and 0.878 (95 % CI 0.844-0.919) respectively. The MBE (NRI, 0.33; 95 % CI, 0.11-0.56, p = 0.003 and IDI, 0.11; 95 % CI, 0.03-0.18; p = 0.004) and modified EDEMA scores (NRI, 1.10; 95 % CI, 0.94-1.26; p < 0.001 and IDI, 0.17; 95 % CI, 0.13-0.20, p < 0.001) showed better performance than the EDEMA score. DCA demonstrated that the modified EDEMA score outperformed the other two scores, possessing heightened clinical usefulness. CONCLUSIONS: The MBE, EDEMA, and modified EDEMA scores for predicting MCE are also applicable in non-revascularization LHI patients within 48 h of onset. Both the MBE and modified EDEMA scores demonstrated higher predictive validity as predictive tools for MCE in LHI patients than the EDEMA score. Furthermore, the modified EDEMA score could be a suitable prediction tool in Chinese patients for its excellent clinical utility.

Subclonal Cancer Driver Mutations Are Prevalent in the Unresected Peritumoral Edema of Adult Diffuse Gliomas.

Adult diffuse gliomas commonly recur regardless of therapy. As recurrence typically arises from the peritumoral edema adjacent to the resected bulk tumor, the profiling of somatic mutations from infiltrative malignant cells within this critical, unresected region could provide important insights into residual disease. A key obstacle has been the inability to distinguish between next-generation sequencing (NGS) noise and the true but weak signal from tumor cells hidden among the noncancerous brain tissue of the peritumoral edema. Here, we developed and validated True2 sequencing to reduce NGS-associated errors to <1 false positive/100 kb panel positions while detecting 97.6% of somatic mutations with an allele frequency ≥0.1%. True2 was then used to study the tumor and peritumoral edema of 22 adult diffuse gliomas including glioblastoma, astrocytoma, oligodendroglioma, and NF1-related low-grade neuroglioma. The tumor and peritumoral edema displayed a similar mutation burden, indicating that surgery debulks these cancers physically but not molecularly. Moreover, variants in the peritumoral edema included unique cancer driver mutations absent in the bulk tumor. Finally, analysis of multiple samples from each patient revealed multiple subclones with unique mutations in the same gene in 17 of 22 patients, supporting the occurrence of convergent evolution in response to patient-specific selective pressures in the tumor microenvironment that may form the molecular foundation of recurrent disease. Collectively, True2 enables the detection of ultralow frequency mutations during molecular analyses of adult diffuse gliomas, which is necessary to understand cancer evolution, recurrence, and individual response to therapy. SIGNIFICANCE: True2 is a next-generation sequencing workflow that facilitates unbiased discovery of somatic mutations across the full range of variant allele frequencies, which could help identify residual disease vulnerabilities for targeted adjuvant therapies.

High altitude retinopathy: An overview and new insights.

High altitude retinopathy (HAR) is a common ocular disorder that occurs on ascent to high altitude. There are many clinical symptoms, retinal vascular dilatation, retinal edema and hemorrhage are common. These usually do not or slightly affect vision; rarely, severe cases develop serious or permanent vision loss. At present, the research progress of HAR mainly focuses on hemodynamic changes, blood-retinal barrier damage, oxidative stress and inflammatory response. Although the related studies on HAR are limited, it shows that HAR still belongs to hypoxia, and hypobaric hypoxia plays an aggravating role in promoting the development of the disease. Various studies have demonstrated the correlation of HAR with acute mountain sickness (AMS) and high-altitude cerebral edema (HACE), so a deeper understanding of HAR is important. The slow ascent rates and ascent altitude are the key to preventing any altitude sickness. Research on traditional chinese medicine (TCM) and western medicine has been gradually carried out. Further exploration of the pathogenesis and prevention strategies of HAR will provide better guidance for doctors and high-altitude travelers.

Systematically Treating the Extra Sweet Pediatric Patient, Without Inadvertently Giving Them a Big Head.

Treating pediatric patients with diabetic ketoacidosis (DKA) during transport can be complex and multifactorial. Cerebral edema is a frequent occurrence in pediatric patients with DKA; however, the signs often occur in a subtle manner. Overzealous correction of their blood glucose may result in cerebral edema as well as a cascade of electrolyte abnormalities. Pediatric patients with diabetes mellitus are prone to developing DKA. Serious complications from DKA in pediatrics often present acutely and rapidly.

Radiological Differentiation Between Intracranial Meningioma and Solitary Fibrous Tumor/Hemangiopericytoma: A Systematic Literature Review.

BACKGROUND: Intracranial solitary fibrous tumor (SFT) is characterized by aggressive local behavior and high post-resection recurrence rates. It is difficult to distinguish between SFT and meningiomas, which are typically benign. The goal of this study was to systematically review radiological features that differentiate meningioma and SFT. METHODS: We performed a systematic review in accordance with PRISMA guidelines to identify studies that used imaging techniques to identify radiological differentiators of SFT and meningioma. RESULTS: Eighteen studies with 1565 patients (SFT: 662; meningiomas: 903) were included. The most commonly used imaging modality was diffusion weighted imaging, which was reported in 11 studies. Eight studies used a combination of diffusion weighted imaging and T1- and T2-weighted sequences to distinguish between SFT and meningioma. Compared to all grades/subtypes of meningioma, SFT is associated with higher apparent diffusion coefficient, presence of narrow-based dural attachments, lack of dural tail, less peritumoral brain edema, extensive serpentine flow voids, and younger age at initial diagnosis. Tumor volume was a poor differentiator of SFT and meningioma, and overall, there were less consensus findings in studies exclusively comparing angiomatous meningiomas and SFT. CONCLUSIONS: Clinicians can differentiate SFT from meningiomas on preoperative imaging by looking for higher apparent diffusion coefficient, lack of dural tail/narrow-based dural attachment, less peritumoral brain edema, and vascular flow voids on neuroimaging, in addition to younger age at diagnosis. Distinguishing between angiomatous meningioma and SFT is much more challenging, as both are highly vascular pathologies. Tumor volume has limited utility in differentiating between SFT and various grades/subtypes of meningioma.

[Postmortem assessment of cerebral edema]. / Posmertnaya otsenka oteka golovnogo mozga.

An analysis of literature data on the methods of post-mortem assessment of cerebral edema is presented. Based on the mechanisms of development, two main types of cerebral edema are distinguished: cytotoxic (intracellular) and vasogenic (extracellular). To determine cerebral edema, a number of methods are used, both direct and indirect, invasive and non-invasive assessment. Direct methods for assessing cerebral edema are based on determining the amount of water in its tissue. Indirect methods include morphological and radiation studies. Traditionally, the most evidence-based criteria for the diagnosis of cerebral edema are macroscopic and microscopic changes determined at autopsy. Methods are also indicated for determining the content of water in brain tissue by comparing the mass of wet and dry brain, as well as estimating the specific density of brain tissue.

Bihemispheric Cerebral Oximetry Monitoring's Functionality in Suspected Cerebral Edema Diabetic Ketoacidosis With Therapeutic 3% Hyperosmolar Therapy in a Pediatric Emergency Department.

BACKGROUND: Suspected cerebral edema diabetic ketoacidosis (SCEDKA) is more common than perceived with symptoms including altered mentation, headache with vomiting, depressed Glasgow coma scale (GCS), abnormal motor or verbal responses, combativeness, and neurological depression. Suspected cerebral edema diabetic ketoacidosis has been associated with initial diabetic ketoacidosis (DKA) presentation and at start of DKA therapy.Cerebral oximetry (bihemispheric regional cerebral oxygen saturation [rcSO2] and cerebral blood volume index [CBVI]) can detect increased intracranial pressure (ICP)-induced altered bihemispheric cerebral physiology (rcSO2) (Crit Care Med 2006;34:2217-2223, J Pediatr 2013;163: 1111-1116, Curr Med Chem 2009;16:94-112, Diabetologia 1985;28:739-742, Pediatr Crit Care Med 2013;14:694-700). In pediatrics, rcSO2 of less than 60% or rcSO2 of greater than 85% reflects increased ICP and cerebral edema (Crit Care Med 2006;34:2217-2223, J Pediatr 2013;163: 1111-1116, Curr Med Chem 2009;16:94-112, Diabetologia 1985;28:739-742, Pediatr Crit Care Med 2013;14:694-700). Cerebral oximetry can detect increased ICP-induced altered bihemispheric cerebral physiology (rcSO2, CBVI) and cerebral physiological changes (rcSO2, CBVI changes) during therapeutic mechanical cerebral spinal fluid removal to decrease increased ICP (Crit Care Med 2006;34:2217-2223, J Pediatr 2013;163: 1111-1116, Curr Med Chem 2009;16:94-112, Diabetologia 1985;28:739-742, Pediatr Crit Care Med 2013;14:694-700).In the pediatric intensive care units, SCEDKA patients with nonbihemispheric cerebral oximetry showed an initial rcSO2 of greater than 90%. Bihemispheric rcSO2 with CBVI in SCEDKA patients has the potential to detect the abnormal cerebral physiology and disruptive autoregulation while detecting 3% hypertonic saline solution (HTS) effects on the SCEDKA altered cerebral physiology (rcSO2). PURPOSE: The purposes of this study were to analyze and compare 3% HTS effect on bihemispheric rcSO2 readings, neurological and biochemical parameters in SCEDKA with 3% HTS infusion to non-SCEDKA patients in pediatric emergency department (PED). METHODS: An observational retrospective comparative analysis study of bihemispheric rcSO2 readings, neurological and biochemical parameters in 2 groups of PED DKA patients were performed: PED DKA patients with SCEDKA +3% HTS infusions versus non-SCEDKA without 3% HTS infusions. RESULTS: From 2008 to 2013, of the 1899 PED DKA patients, 60 SCEDKA patients received 3% HTS (5 mL/kg via peripheral intravenous) infusion (median age of 5 years [range, 3.7-7 years]), with 42 new DKA insulin dependent diabetes mellitus onset. Suspected cerebral edema diabetic ketoacidosis patients had GCS of 11 (range, 11-12), with consistent SCEDKA signs and symptoms (severe headaches with vomiting, confusion, blurred vision, altered speech, lethargy, and combativeness). Suspected cerebral edema diabetic ketoacidosis patients' initial (0-5 minutes) left rcSO2 readings were 91.4% (range, 88.4%-94.1%) and right was 90.3% (range, 88.6%-94.1%) compared with non-SCEDKA patients' left rcSO2 readings of 73.2% (range, 69.7%-77.8%) and right of 73.2% (range, 67.6%-77%) (P < 0.0001). The rcSO2 monitoring time before 3% HTS infusion was 54.9 minutes (range, 48.3-66.8 minutes) with 3% HTS time effect change: pre-3% HTS (54.9 minutes [range, 48.3-66.8 minutes]). Before 3% HTS infusion, the left rcSO2 readings were 90.0% (range, 89%-95%) and right was 91% (range, 86%-95%). The 30 to 45 minutes post-3% HTS showed that left was 64% (range, 62%-69%) and right was 65.4% (range, 63%-70%) (P < 0.0001). rcSO2 Δ change for post-3% HTS (0-20 minutes) to pre-3% HTS was as follows: left, -26.58 (-29.5 to -23.7) (P < 0.0001); right, -25.2 (-27.7 to -22.6) (P < 0.0001). Post-3% HTS GCS (14,15) and biochemistry compared with pre-3% HTS infusions all improved (P < 0.001). CONCLUSIONS: In PED SCEDKA patients, the pre-3% HTS bihemispheric rcSO2 readings were greater than 90% and had lower GCS than non-SCEDKA patients. The post-3% HTS infusion rcSO2 readings showed within minutes a substantial reduction compared with non-SCEDKA patients, with no complications. Changes in rcSO2 readings after 3% HTS correlated with improved SCEDKA indicators (improved mental status, headache, and GCS) without any complications. We showed that cerebral oximetry in PED SCEDKA patients has shown an initial bihemispheric of greater than 90% readings signifying abnormal bihemispheric cerebral physiology. We also showed the cerebral oximetry's functionality in detecting 3% HTS therapeutic effects on SCEDKA's abnormal cerebral physiology and the beneficial therapeutic effects of 3% HTS infusion in SCEDKA patients. Using cerebral oximetry in pediatric DKA patients' initial cerebral assessment could have a significant impact in detecting SCEDKA patients. Further SCEDKA research using cerebral oximetry should be considered.

A review of the skeletal effects of exposure to high altitude and potential mechanisms for hypobaric hypoxia-induced bone loss.

Mountaineering and exposure to high altitude result in physiological adaptations to the reduced inspiratory oxygen availability. Acute mountain sickness (AMS), high altitude pulmonary edema (HAPE), and high altitude cerebral edema (HACE) are well-described harmful effects of exposure to high altitude. Common to AMS, HAPE, and HACE are distinct clinical signs and symptoms of impaired function. However, several studies have suggested that high altitude might result in a substantial bone loss, which usually does not produce any apparent symptoms. This review aims to provide a comprehensive overview of, and map current knowledge of the skeletal effects of hypobaric hypoxia and high altitude. PubMed and Embase were searched from inception to September 6, 2021, to identify studies investigating the skeletal effects of exposure to hypobaric hypoxia and high altitude. Three hundred sixty titles and abstracts were screened, and 20 full-text articles were included (16 in vivo studies and four real-world human studies). In rodents, simulated high altitude up to 2900 m did not result in any adverse skeletal effects. In contrast, studies exposing animals to very high altitude (3500-5500 m) reported substantial reductions in BMD, cortical morphology, and bone strength, as well as deteriorated trabecular microstructure. Detrimental microstructural effects were also reported in rats exposed to simulated extreme altitude (6000 m). Finally, real-world human studies in mountaineers suggested high altitude exposure reduced bone mineral density (BMD) and that the harmful skeletal effects of hypobaric hypoxia were not entirely recovered after 12 months. In conclusion, in vivo and real-world studies demonstrated high altitude exposure results in adverse skeletal effects. The underlying mechanism for hypobaric hypoxia-induced bone loss is not elucidated.

An autopsy case of unexpected death due to Addison's disease caused by adrenal tuberculosis.

BACKGROUND: Adrenal tuberculosis is difficult to diagnose due to non-specific symptom. Unexpected death due to adrenal insufficiency after trauma surgery is rare. CASE PRESENTATION: A 45-year-old man, who was admitted to hospital because of trauma to the right hand, died unexpectedly on the 13th day after replantation of amputated fingers. He was diagnosed with brain edema and diluted hyponatremia. Autopsy and histopathologic examination revealed severe brain edema combined with cerebellar tonsillar hernia, extensive destruction of adrenal gland caused by bilateral adrenal tuberculosis and right lung invasive pulmonary tuberculosis. CONCLUSIONS: Trauma and pulmonary tuberculosis complicated with adrenal tuberculosis induced the adrenal crisis, which eventually lead to severe cerebral edema and hernia, and finally death from respiratory and circulatory failure. This autopsy and histopathologic examination suggested a possible pathophysiologic mechanism of sudden death due to diluted hyponatremia after trauma surgery.

Correlation analysis between TSP2, MMP-9 and perihematoma edema, as well as the short-term prognosis of patients with hypertensive intracerebral hemorrhage.

BACKGROUND: To analyze the correlation between thrombospondin-2 (TSP2), matrix metalloproteinase (MMP)-9, and perihematomal edema, as well as the short-term prognosis of patients with hypertensive intracerebral hemorrhage. METHODS: The clinical data of 114 patients with hypertensive intracerebral hemorrhage admitted to our hospital from January 2018 to February 2020 were collected and divided into groups according to the levels of TSP2 and MMP-9. We compared edema indexes in patients with different levels of TSP2 and MMP-9, and analyzed the correlation between TSP2, MMP-9 and relative edema volume index (REI), edema change index (AEI). We also assessed the TSP2 and MMP-9 levels in patients with different prognoses, and analyzed the predictive value of TSP2 and MMP-9 for poor prognosis of patients. RESULTS: (I) There was no difference in the REI and AEI values between the low and high TSP2 groups at admission and 24 h after admission (P>0.05), while the REI and AEI values of the high TSP2 group at 5 and 15 d after admission were significantly lower than those of the low TSP2 group (P<0.05); (II) the REI and AEI values of patients with different MMP-9 levels were not different between admission and 24 h after admission (P>0.05), while the REI and AEI values of the high MMP-9 group were significantly higher than those of the low MMP-9 group at 5 and 15 d after admission (P<0.05); (III) Pearson correlation analysis showed that MMP-9 was positively correlated with REI and AEI, while TSP2 was negatively correlated (P<0.05); (IV) among 114 patients, 39 had poor prognosis, 75 had good prognosis The MMP-9 levels of patients with a poor prognosis were significantly higher than those of patients with a good prognosis, and the TSP2 level was the opposite (P<0.05); (V) receiver operating characteristic (ROC) curve showed that the sensitivity, specificity and the area under the curve (AUC) of the TSP2 + MMP-9 combination in the diagnosis of hypertensive cerebral hemorrhage were significantly higher than when TSP2 and MMP-9 were tested separately (P<0.05). CONCLUSIONS: In patients with hypertensive intracerebral hemorrhage, TSP2 is negatively correlated with edema around the hematoma, while MMP-9 is positively correlated.

Reversible bilateral optic tract edema following pipeline-assisted coiling of a large ophthalmic aneurysm: A case report.

Edema coursing the optic apparatus has traditionally been associated with sellar and para-sellar tumors. However, postoperative aneurysmal volume expansion following endovascular treatment has been reported to induce cranial neuropathies, such as vision loss in rare instances. Here, we present a case report of worsening optic tract edema associated with bilateral visual acuity deficit following treatment of a large left paraophthalmic aneurysm with pipeline-assisted coiling. Rapid resolution of visual deficit was observed following administration of corticosteroids. A 42-year-old female with a 6-month history of worsening left eye vision and sentinel headache presented with left visual field cut and decreased left visual acuity. She was found to have a large paraophthalmic aneurysm which was treated with pipeline-assisted coiling. Within one week post-treatment, the patient presented to the emergency department with worsening right visual complaints. On magnetic resonance imaging, T2 hyperintensities coursing the right posterior optic nerve, optic chiasm, and bilateral optic tracts were noted. Angiography demonstrated an expanding neck remnant. The patient was treated with oral corticosteroids and repeat pipeline stenting. At four week follow up, she demonstrated significant improvement of symptoms and reduced T2 hyperintensities. With the advancement in endovascular technique for the treatment of large aneurysms, more patients are electing endovascular treatment over microsurgical clipping. Given the possibility of continued growth following endovascular treatment, patient counseling regarding risks and side effects is paramount.

Whole brain in vivo neuropathology: Imaging site-specific changes in brain structure over time following trimethyltin exposure in rats.

Presented is a diffusion weighted imaging protocol with measures of apparent diffusion coefficient which when registered to a 3D MRI rat brain atlas provides site-specific information on 173 different brain areas. This protocol coined "in vivo neuropathology" was used to follow the progressive neurotoxic effects of trimethyltin on global gray matter microarchitecture. Four rats were given an IP injection of 7 mg/kg of the neurotoxin trimethyltin and imaged for changes in water diffusivity at 3- and 7-days post injections. At 3 days, there was a significant decrease in apparent diffusion coefficient, a proxy for cytotoxic edema, in several cortical areas and cerebellum. At 7 days the level of injury expanded to include most of the cerebral cortex, hippocampus, olfactory system, and cerebellum/brainstem corroborating much of the work done with traditional histopathology. Analysis is achieved with a minimum number of rats adhering to the laws and regulations around the humane care and use of laboratory animals, providing an alternative to the traditional tests for assessing drug neurotoxicity. "In vivo neuropathology" can minimize the cost, expedite the process, and identify subtle changes in site-specific brain microarchitecture across the entire brain.

Attenuation of cerebral edema facilitates recovery of glymphatic system function after status epilepticus.

Status epilepticus (SE) is a neurological emergency usually accompanied by acute cerebral edema and long-term cognitive impairment, and is characterized by neurodegeneration and aberrant hyperphosphorylated tau protein (p-tau) aggregation. The glia-lymphatic (glymphatic) system plays a central role in facilitating the clearance of metabolic waste from the brain, but its relationship with cerebral edema and cognitive dysfunction after SE is unclear. We hypothesized that cerebral edema after SE might impair glymphatic system function through compression, thus leading to impaired removal of metabolic waste, and ultimately affecting long-term cognitive function. Our results showed that glymphatic system function was temporarily impaired, as evidenced by 2-photon imaging, MRI enhancement, imaging of brain sections, and astrocytic water channel aquaporin 4 (AQP4) protein polarization. The severity of cerebral edema on MRI correlated well with glymphatic system dysfunction within 8 days following SE. Moreover, when cerebral edema was alleviated by glibenclamide treatment or genetic deletion of Trpm4, post-SE glymphatic system function recovered earlier, along with fewer p-tau-deposited neurons and neuronal degeneration and better cognitive function. These findings suggest that SE-induced cerebral edema may cause glymphatic system dysfunction and render the post-SE brain vulnerable to p-tau aggregation and neurocognitive impairment.

Transependymal Edema as a Predictor of Endoscopic Third Ventriculostomy Success in Pediatric Hydrocephalus.

BACKGROUND: The Endoscopic Third Ventriculostomy Success Score (ETVSS) is based on the clinical features of hydrocephalus except for radiological findings. A previous study suggested that transependymal edema (TEE) as a radiological finding may be a reliable predictor of endoscopic third ventriculostomy (ETV) success in patients of all ages. We aimed to investigate whether TEE on preoperative magnetic resonance imaging can predict ETV success in pediatric patients. METHODS: Medical and radiological records of all pediatric patients with an initial ETV in our hospital between 2013 and 2019 were retrospectively reviewed. RESULTS: This study included 32 patients with hydrocephalus. The median age at surgery was 10.0 years (interquartile range: 5.6-12.9 years). There were 20 patients in the high ETVSS (90-80) group and 12 patients in the moderate ETVSS (70-50) group. The median follow-up period was 29.0 months (interquartile range: 12.9-46.2 months). The ETV success rate at the final follow-up was 81%. Preoperative brain magnetic resonance imaging revealed TEE in 20 patients and third ventricle floor ballooning in 25 patients, of whom 19 (95%) and 22 (88%), respectively, achieved successful ETV. Patients with TEE had a significantly better outcome than patients without TEE (95% vs. 58%, P = 0.018). Multivariate analysis demonstrated that the presence of TEE (odds ratio 13.6, 95% confidence interval 1.3-137.5, P = 0.027) is a significant predictor of ETV success. CONCLUSIONS: In our cohort with a high or moderate ETVSS, the ETV success rate in patients with TEE was significantly higher than in patients without TEE, suggesting that TEE may be a useful predictor of ETV success in pediatric hydrocephalus.

Predicting hemorrhagic transformation after large vessel occlusion stroke in the era of mechanical thrombectomy.

Serum biomarkers are associated with hemorrhagic transformation and brain edema after cerebral infarction. However, whether serum biomarkers predict hemorrhagic transformation in large vessel occlusion stroke even after mechanical thrombectomy, which has become widely used, remains uncertain. In this prospective study, we enrolled patients with large vessel occlusion stroke in the anterior circulation. We analyzed 91 patients with serum samples obtained on admission. The levels of matrix metalloproteinase-9 (MMP-9), amyloid precursor protein (APP) 770, endothelin-1, S100B, and claudin-5 were measured. We examined the association between serum biomarkers and hemorrhagic transformation within one week. Fifty-four patients underwent mechanical thrombectomy, and 17 patients developed relevant hemorrhagic transformation (rHT, defined as hemorrhagic changes ≥ hemorrhagic infarction type 2). Neither MMP-9 (no rHT: 46 ± 48 vs. rHT: 15 ± 4 ng/mL, P = 0.30), APP770 (80 ± 31 vs. 85 ± 8 ng/mL, P = 0.53), endothelin-1 (7.0 ± 25.7 vs. 2.0 ± 2.1 pg/mL, P = 0.42), S100B (13 ± 42 vs. 12 ± 15 pg/mL, P = 0.97), nor claudin-5 (1.7 ± 2.3 vs. 1.9 ± 1.5 ng/mL, P = 0.68) levels on admission were associated with subsequent rHT. When limited to patients who underwent mechanical thrombectomy, the level of claudin-5 was higher in patients with rHT than in those without (1.2 ± 1.0 vs. 2.1 ± 1.7 ng/mL, P = 0.0181). APP770 levels were marginally higher in patients with a midline shift ≥ 5 mm than in those without (79 ± 29 vs. 97 ± 41 ng/mL, P = 0.084). The predictive role of serum biomarkers has to be reexamined in the mechanical thrombectomy era because some previously reported serum biomarkers may not predict hemorrhagic transformation, whereas the level of APP770 may be useful for predicting brain edema.

An amplitude-based characteristic parameter extraction algorithm for cerebral edema detection based on electromagnetic induction.

BACKGROUND: Cerebral edema is a common condition secondary to any type of neurological injury. The early diagnosis and monitoring of cerebral edema is of great importance to improve the prognosis. In this article, a flexible conformal electromagnetic two-coil sensor was employed as the electromagnetic induction sensor, associated with a vector network analyzer (VNA) for signal generation and receiving. Measurement of amplitude data over the frequency range of 1-100 MHz is conducted to evaluate the changes in cerebral edema. We proposed an Amplitude-based Characteristic Parameter Extraction (Ab-CPE) algorithm for multi-frequency characteristic analysis over the frequency range of 1-100 MHz and investigated its performance in electromagnetic induction-based cerebral edema detection and distinction of its acute/chronic phase. Fourteen rabbits were enrolled to establish cerebral edema model and the 24 h real-time monitoring experiments were carried out for algorithm verification. RESULTS: The proposed Ab-CPE algorithm was able to detect cerebral edema with a sensitivity of 94.1% and specificity of 95.4%. Also, in the early stage, it can detect cerebral edema with a sensitivity of 85.0% and specificity of 87.5%. Moreover, the Ab-CPE algorithm was able to distinguish between acute and chronic phase of cerebral edema with a sensitivity of 85.0% and specificity of 91.0%. CONCLUSION: The proposed Ab-CPE algorithm is suitable for multi-frequency characteristic analysis. Combined with this algorithm, the electromagnetic induction method has an excellent performance on the detection and monitoring of cerebral edema.

Estimation of the Morphofunctional Status of the Brain in Hypertensive Wistar Rats Using Diffusion-Weighted MRI.

Morphofunctional changes of the brain tissues of Wistar rats were studied based on the development of a multifactor cardiovasorenal model of arterial hypertension using MRI. An increase of the signal on the diffusion brain maps was recorded in 3 months, which indicated fluid accumulation in the intra- and extracellular space of the brain tissue. The data characterize the development of the pathogenetic mechanism of the hypervolemic variant of experimental arterial hypertension. The development of endothelial dysfunction in the brain vessels was manifested by predominance of abnormal constrictor reactions. In 6 months after arterial hypertension simulation, structural changes in the brain developed, such as leukoareosis, cystic encephalomalacia with dilated cerebrospinal fluid spaces and limited blood supply to brain tissue in the basins of the large cerebral arteries.

Safety and efficacy of normobaric oxygenation on rescuing acute intracerebral hemorrhage-mediated brain damage-a protocol of randomized controlled trial.

BACKGROUND: All of the existing medication and surgical therapies currently cannot completely inhibit intracerebral hemorrhage (ICH)-mediated brain damage, resulting in disability in different degrees in the involved patients. Normobaric oxygenation (NBO) was reported attenuating ischemic brain injury. Herein, we aimed to explore the safety and efficacy of NBO on rescuing the damaged brain tissues secondary to acute ICH, especially those in the perihematoma area being threatened by ischemia and hypoxia. METHODS: A total of 150 patients confirmed as acute spontaneous ICH by computed tomography (CT) within 6 h after symptoms onset, will enroll in this study after signing the informed consent, and enter into the NBO group or control group randomly according to a random number. In the NBO group, patients will inhale high-flow oxygen (8 L/min, 1 h each time for 6 cycles daily) and intake low-flow oxygen (2 L/min) in intermittent periods by mask for a total of 7 days. While in the control group, patients will breathe in only low-flow oxygen (2 L/min) by mask for 7 consecutive days. Computed tomography and perfusion (CT/CTP) will be used to evaluate cerebral perfusion status and brain edema. CT and CTP maps in the two groups at baseline and day 7 and 14 after NBO or low-flow oxygen control will be compared. The primary endpoint is mRS at both Day14 post-ICH and the end of the 3rd month follow-up. The secondary endpoints include NIHSS and plasma biomarkers at baseline and Day-1, 7, and 14 after treatment, as well as the NIHSS at the end of the 3rd month post-ICH and the incidence of bleeding recurrence and the mortalities within 3 months post-ICH. DISCUSSION: This study will provide preliminary clinical evidence about the safety and efficacy of NBO on correcting acute ICH and explore some mechanisms accordingly, to offer reference for larger clinical trials in the future. TRIAL REGISTRATION: ClinicalTrials.gov NCT04144868 . Retrospectively registered on October 29, 2019.