Injury patterns and mortality associated with near-hanging in children.

BACKGROUND: The pathophysiology of near-hanging in children is different from that of adults due to anatomic, physiologic, and injury-related mechanisms, with evidence suggesting that blunt cerebrovascular injuries (BCVI) and cervical spine injuries (CSI) are uncommon. We sought to estimate the incidence of secondary injuries and their association with mortality in pediatric near-hanging victims. METHODS: We performed a retrospective observational study of children (≤17 years) with a diagnosis code for hanging between October 1, 2015 and February 28, 2023 who presented to one of 47 geographically diverse US children's hospitals. We evaluated the incidence of the following secondary injuries: cerebral edema, pneumothorax, pulmonary edema, BCVI, and CSI. We performed Fisher's exact test with Bonferroni correction to identify associations between intentionality, sex, age, and secondary injuries with mortality. RESULTS: We included 1929 children, of whom 33.8% underwent neuroimaging, 45.9% underwent neck imaging, and 38.7% underwent neck angiography. The most common injury was cerebral edema (24.0%), followed by pulmonary edema (3.2%) and pneumothorax (2.8%). CSI (2.1%) and BCVI (0.9%) occurred infrequently. Cerebral edema, pneumothorax, pulmonary edema, and younger age (≤12 years) were associated with mortality. CONCLUSIONS: In this multi-center study of pediatric near-hanging victims, BCVI and CSI occurred rarely and were not associated with mortality. While children in our study underwent neck imaging more frequently than head imaging, cerebral edema occurred more often than other injury types and imparted the highest mortality risk. Given the rarity of BCVI and CSI, a selective approach to neck imaging may be warranted in pediatric near-hanging events.

CSF-Based Volumetric Imaging Biomarkers Highlight Incidence and Risk Factors for Cerebral Edema After Ischemic Stroke.

BACKGROUND: Cerebral edema has primarily been studied using midline shift or clinical deterioration as end points, which only captures the severe and delayed manifestations of a process affecting many patients with stroke. Quantitative imaging biomarkers that measure edema severity across the entire spectrum could improve its early detection, as well as identify relevant mediators of this important stroke complication. METHODS: We applied an automated image analysis pipeline to measure the displacement of cerebrospinal fluid (ΔCSF) and the ratio of lesional versus contralateral hemispheric cerebrospinal fluid (CSF) volume (CSF ratio) in a cohort of 935 patients with hemispheric stroke with follow-up computed tomography scans taken a median of 26 h (interquartile range 24-31) after stroke onset. We determined diagnostic thresholds based on comparison to those without any visible edema. We modeled baseline clinical and radiographic variables against each edema biomarker and assessed how each biomarker was associated with stroke outcome (modified Rankin Scale at 90 days). RESULTS: The displacement of CSF and CSF ratio were correlated with midline shift (r = 0.52 and - 0.74, p < 0.0001) but exhibited broader ranges. A ΔCSF of greater than 14% or a CSF ratio below 0.90 identified those with visible edema: more than half of the patients with stroke met these criteria, compared with only 14% who had midline shift at 24 h. Predictors of edema across all biomarkers included a higher National Institutes of Health Stroke Scale score, a lower Alberta Stroke Program Early CT score, and lower baseline CSF volume. A history of hypertension and diabetes (but not acute hyperglycemia) predicted greater ΔCSF but not midline shift. Both ΔCSF and a lower CSF ratio were associated with worse outcome, adjusting for age, National Institutes of Health Stroke Scale score, and Alberta Stroke Program Early CT score (odds ratio 1.7, 95% confidence interval 1.3-2.2 per 21% ΔCSF). CONCLUSIONS: Cerebral edema can be measured in a majority of patients with stroke on follow-up computed tomography using volumetric biomarkers evaluating CSF shifts, including in many without visible midline shift. Edema formation is influenced by clinical and radiographic stroke severity but also by chronic vascular risk factors and contributes to worse stroke outcomes.

Increased volume of cerebral oedema is associated with risk of acute seizure activity and adverse neurological outcomes in encephalitis - regional and volumetric analysis in a multi-centre cohort.

BACKGROUND: Seizures can occur unpredictably in patients with acute encephalitis syndrome (AES), and many suffer from poor long-term neurological sequelae. Establishing factors associated with acute seizures risk and poor outcomes could support clinical care. We aimed to conduct regional and volumetric analysis of cerebral oedema on magnetic resonance imaging (MRI) in patients with AES. We assessed the relationship of brain oedema with acute seizure activity and long-term neurological outcome. METHODS: In a multi-centre cohort study, adults and children presenting with an AES were recruited in the UK. The clinical and brain MRI data were retrospectively reviewed. The outcomes variables were inpatient acute seizure activity and neurological disability at six-months post-discharge. A poor outcome was defined as a Glasgow outcome score (GOS) of 1-3. We quantified regional brain oedema on MRI through stereological examination of T2-weighted images using established methodology by independent and blinded assessors. Clinical and neuroimaging variables were analysed by multivariate logistic regression to assess for correlation with acute seizure activity and outcome. RESULTS: The study cohort comprised 69 patients (mean age 31.8 years; 53.6% female), of whom 41 (59.4%) had acute seizures as inpatients. A higher Glasgow coma scale (GCS) score on admission was a negative predictor of seizures (OR 0.61 [0.46-0.83], p = 0.001). Even correcting for GCS on admission, the presence of cortical oedema was a significant risk factor for acute seizure activity (OR 5.48 [1.62-18.51], p = 0.006) and greater volume of cerebral oedema in these cortical structures increased the risk of acute seizures (OR 1.90 [1.12-3.21], p = 0.017). At six-month post-discharge, 21 (30.4%) had a poor neurological outcome. Herpes simplex virus encephalitis was associated with higher risk of poor outcomes in univariate analysis (OR 3.92 [1.08-14.20], p = 0.038). When controlling for aetiology, increased volume of cerebral oedema was an independent risk factor for adverse neurological outcome at 6 months (OR 1.73 [1.06-2.83], p = 0.027). CONCLUSIONS: Both the presence and degree of cerebral oedema on MRIs of patients with AES may help identify patients at risk of acute seizure activity and subsequent long-term morbidity.

Acute Ischemic Stroke and COVID-19: An Analysis of 27 676 Patients.

BACKGROUND AND PURPOSE: Acute ischemic stroke may occur in patients with coronavirus disease 2019 (COVID-19), but risk factors, in-hospital events, and outcomes are not well studied in large cohorts. We identified risk factors, comorbidities, and outcomes in patients with COVID-19 with or without acute ischemic stroke and compared with patients without COVID-19 and acute ischemic stroke. METHODS: We analyzed the data from 54 health care facilities using the Cerner deidentified COVID-19 dataset. The dataset included patients with an emergency department or inpatient encounter with discharge diagnoses codes that could be associated to suspicion of or exposure to COVID-19 or confirmed COVID-19. RESULTS: A total of 103 (1.3%) patients developed acute ischemic stroke among 8163 patients with COVID-19. Among all patients with COVID-19, the proportion of patients with hypertension, diabetes, hyperlipidemia, atrial fibrillation, and congestive heart failure was significantly higher among those with acute ischemic stroke. Acute ischemic stroke was associated with discharge to destination other than home or death (relative risk, 2.1 [95% CI, 1.6-2.4]; P<0.0001) after adjusting for potential confounders. A total of 199 (1.0%) patients developed acute ischemic stroke among 19 513 patients without COVID-19. Among all ischemic stroke patients, COVID-19 was associated with discharge to destination other than home or death (relative risk, 1.2 [95% CI, 1.0-1.3]; P=0.03) after adjusting for potential confounders. CONCLUSIONS: Acute ischemic stroke was infrequent in patients with COVID-19 and usually occurs in the presence of other cardiovascular risk factors. The risk of discharge to destination other than home or death increased 2-fold with occurrence of acute ischemic stroke in patients with COVID-19.

Effect of Recanalization on Cerebral Edema in Ischemic Stroke Treated With Thrombolysis and/or Endovascular Therapy.

Background and Purpose- A large infarct and expanding cerebral edema (CED) due to a middle cerebral artery occlusion confers a 70% mortality unless treated surgically. Reperfusion may cause blood-brain barrier disruption and a risk for cerebral edema and secondary parenchymal hemorrhage (PH). We aimed to investigate the effect of recanalization on development of early CED and PH after recanalization therapy. Methods- From the SITS-International Stroke Treatment Registry, we selected patients with signs of artery occlusion at baseline (either Hyperdense Artery Sign or computed tomography/magnetic resonance imaging angiographic occlusion). We defined recanalization as the disappearance of radiological signs of occlusion at 22 to 36 hours. Primary outcome was moderate to severe CED and secondary outcome was PH on 22- to 36-hour imaging scans. We used logistic regression with adjustment for baseline variables and PH. Results- Twenty two thousand one hundred eighty-four patients fulfilled the inclusion criteria (n=18 318 received intravenous thrombolysis, n=3071 received intravenous thrombolysis+thrombectomy, n=795 received thrombectomy). Recanalization occurred in 64.1%. Median age was 71 versus 71 years and National Institutes of Health Stroke Scale score 15 versus 16 in the recanalized versus nonrecanalized patients respectively. Recanalized patients had a lower risk for CED (13.0% versus 23.6%), adjusted odds ratio (aOR), 0.52 (95% CI, 0.46-0.59), and a higher risk for PH (8.9% versus 6.5%), adjusted odds ratio, 1.37 (95% CI, 1.22-1.55), than nonrecanalized patients. Conclusions- In patients with acute ischemic stroke, recanalization was associated with a lower risk for early CED even after adjustment for higher rate for PH in recanalized patients.

COVID-19 virus may have neuroinvasive potential and cause neurological complications: a perspective review.

Coronavirus disease 2019 (COVID-19) was reported at the end of 2019 in China for the first time and has rapidly spread throughout the world as a pandemic. Since COVID-19 causes mild to severe acute respiratory syndrome, most studies in this field have only focused on different aspects of pathogenesis in the respiratory system. However, evidence suggests that COVID-19 may affect the central nervous system (CNS). Given the outbreak of COVID-19, it seems necessary to perform investigations on the possible neurological complications in patients who suffered from COVID-19. Here, we reviewed the evidence of the neuroinvasive potential of coronaviruses and discussed the possible pathogenic processes in CNS infection by COVID-19 to provide a precise insight for future studies.

Evaluation of Epidemiologic Factors, Radiographic Features, and Pathologic Findings for Predicting Peritumoral Brain Edema in Meningiomas.

BACKGROUND: Despite several treatment options that are available for meningiomas, surgery is the only method currently practiced. Peritumoral brain edema (PTBE) in meningiomas causes difficulty marginalizing the dissection in an intraoperative setting. PURPOSE: To evaluate whether the epidemiological variables, imaging characteristics, and pathologic parameters are correlated with the presence of PTBE in meningiomas. STUDY TYPE: Retrospective study from 2015 to 2018. SUBJECTS: In all, 550 patients with histopathologically confirmed meningioma were included. After exclusion of patients with extradural, spinal, and intraventricular meningiomas and those with image artifacts, a total of 441 patients were included in the final analysis. FIELD STRENGTH/SEQUENCE: Images were performed with 3T MR scanners and axial/sagittal T1 WI, axial/coronal T2 WI and axial/sagittal/coronal contrast-enhanced T1 WI after administration of 0.1 mmol/kg of body weight of Gd-DTPA. ASSESSMENT: Fourteen variables were patients' age, sex, skull changes, calcification, density, location, margin, volume, cerebrospinal fluid (CSF) cleft, signal intensity (SI) on T2 WI, degree and pattern of contrast enhancement, WHO histological classification, and Ki-67 labeling index. STATISTICAL TESTS: The relationship between each factor and the formation of PTBE was examined by multivariate logistic regression analysis. RESULTS: After multivariate logistic regression, the absence of CSF cleft (odds ratio [OR]: 63.43, 95% confidence interval [CI]: 27.24-121.42, P = 1.2 × 10-8 ), non-skull base location (OR: 15.32, 95% CI: 5.81-28.23, P = 0.0008), high SI on T2 WI (OR: 5.05, 95% CI: 2.27-14.88, P = 0.01), and G I uncommon subtypes (OR: 4.75, 95% CI: 1.42-15.94, P = 0.01) were found to be significant independent factors associated with the occurrence of PTBE in meningiomas. In patients with PTBE-positive meningiomas, there was no significant correlation between the volume of PTBE and the volume of the tumor (r = 0.17, P = 0.60). DATA CONCLUSION: These factors may be suggestive of anticipating the formation of PTBE. LEVEL OF EVIDENCE: 3 Technical Efficacy Stage: 3 J. Magn. Reson. Imaging 2020;52:174-182.

ß-Caryophyllene Liposomes Attenuate Neurovascular Unit Damage After Subarachnoid Hemorrhage in Rats.

This study was conducted to prepare ß-caryophyllene loaded liposomes (BCP-LP) and investigated their effects on neurovascular unit (NVU) damage after subarachnoid hemorrhage (SAH) in rats. A blood injection into the pre-chiasmatic cistern was used to achieve SAH. BCP-LP were prepared, characterized and administrated to rats with SAH. The prepared BCP-LP were spherical with a size distribution of approximately 189.3 nm and Zeta potential of - 13.9 mV. Neurological scoring, the balance beam test, cerebral blood flow monitoring, brain edema and biochemical analyses were applied to evaluate the effects of BCP-LP on rat NVU damage after SAH. The results demonstrated that BCP-LP treatment improved neurological function disorder, balance ability and cerebral blood perfusion in rats. Brain edema detection and blood-brain barrier permeability detection revealed that BCP-LP could reduce brain edema and promote repairment of blood-brain barrier after SAH. Using the western blot experiments, we demonstrated that BCP-LP attenuated the loss of tight junction proteins Occludin and Zonula occludens-1, inhibit the high expression of VEGFR-2 and GFAP, and promote the repair of laminin. These results demonstrate the protective effect BCP-LP exert in the NVU after SAH in rats, and supports the use of BCP-LP for future study and therapy of SAH.

Luteolin Protects Against CIRI, Potentially via Regulation of the SIRT3/AMPK/mTOR Signaling Pathway.

Mitochondrial abnormalities accelerate the progression of ischemic brain damage. Sirtuin 3 (SIRT3) is mainly found in mitochondria and affects almost all major aspects of mitochondrial function. Luteolin, a flavonoid with diverse biological properties, including antioxidant activity, inhibition of cell apoptosis and regulation of autophagy. It also modulates the activity of AMP activated kinase and/or sirtuin 1 (SIRT 1) by regulating the expression of sirtuins. We investigated the protective effects of luteolin on cerebral ischemia-reperfusion. It was found through experiments that luteolin reduced the infarcted area of MCAO rat model, and based on the experimental results, it was inferred that luteolin affected the AMPK, mTOR and SIRT3 pathways, thereby protecting brain cells. As expected, we found that luteolin can reduce the neurological function score, the degree of cerebral edema, the cerebral infarction volume, alleviate morphological changes in the cortex and hippocampus, increase neuron survival and decrease the number of apoptotic neurons. At the same time, luteolin significantly reduced the number of GFAP and Iba-1 positive glial cells in the hippocampus while enhanced the scavenging of oxygen free radicals and the activity of SOD in mitochondria. Addtionally, it can also enhance antioxidant capacity via the reversal of mitochondrial swelling and the mitochondrial transmembrane potential. Moreover, luteolin can increase SIRT3-targeted expression in mitochondria, decrease the phosphorylation of AMPK, and increase phosphor-mTOR (p-mTOR) levels, which may have occurred specifically through activation of the SIRT3/AMPK/mTOR pathway. We speculate that luteolin reduces the pathological progression of CIRI by increasing SIRT3 expression and enhancing mitochondrial function. Therefore, the results indicate that luteolin can increase the transduction of SIRT3, providing a potential mechanism for neuroprotective effects in patients with cerebral ischemia.

Docosahexaenoic Acid Protects Traumatic Brain Injury by Regulating NOX2 Generation via Nrf2 Signaling Pathway.

Docosahexaenoic acid (DHA) is verified to have neuroprotective effects on traumatic brain injury (TBI) rats by activating Nrf2 signaling pathway, but the role of NOX2 in this effect has not been illuminated. So this study explored the role of NOX2 in TBI models treated with DHA, aiming to complete the mechanism of DHA. TBI rat models were constructed with or without DHA treatment, and H2O2-induced hippocampal neurons were pretreated with DHA alone or in combination with Nrf2 inhibitor brusatol. The neurological function, cognitive ability, and cerebral edema degree of rats were assessed. The apoptosis rate and viability of cells was measured. The generation of NOX2, Nrf2, HO-1 and NQO-1 expression levels, and ROS content in hippocampal CA1 region and hippocampal neurons were detected. DHA could not only improve the neurological function, brain edema and cognitive ability in TBI rats, but also decrease effectively the contents of NOX2 and ROS in hippocampal CA1 region and hippocampal neurons. DHA promoted the nuclear transposition of Nrf2 and the expression levels of HO-1 and NQO-1 in hippocampal CA1 region and hippocampal neurons. On the contrary, Nrf2 inhibitor brusatol inhibited the nuclear transposition of Nrf2 and the expression levels of HO-1 and NQO-1 in hippocampal neurons, promoted the generation of ROS and NOX2, and accelerated cell apoptosis. Both in vivo and in vitro experiments demonstrated that DHA treated TBI by reducing NOX2 generation that might function on Nrf2 signaling pathway, providing a potential evidence for its clinical application.

MCC950 Inhibits NLRP3 Inflammasome and Alleviates Axonal Injures in Early Stages of Diffuse Axonal Injury in Rats.

Increasing evidence has revealed that neuroinflammation plays a pivotal role in axonal injures. Nucleotide oligomerization domain (NOD)-like receptor protein (NLRP3) inflammasome is reported to be widely involved with the pathology of central nervous system disorders. But the role of NLRP3 in diffuse axonal injury (DAI) are rarely reported. The purpose of this study was to investigate the expression of NLRP3 after diffuse axonal injury and the role of NLRP3 in axonal injures. The lateral head rotation device was used to establish DAI model of rats. Immunohistochemical staining for ß-amyloid precursor protein and Bielschowsky silver staining were used to assess axonal injures and axonal loss. Terminal Deoxynucleotidyl Transferase-Mediated Digoxigenin-dUTP-Biotin Nick-End Labelling Assay was used to detect cell apoptosis. Brain water content was used to assess cerebral edema and the modified Neurologic Severity Score was used to assess the neurological deficits. Components of NLRP3 inflammasome, such as NLRP3, apoptosis-associated speck-like (ASC) adapter protein and caspase-1, and pro-inflammatory cytokines, for example IL-18 and IL-1ß, were over-expressed in early stages of DAI. MCC950, a selective small-molecule inhibitor of NLRP3 inflammasome, inhibited the over-expression of NLRP3 inflammasome and pro-inflammatory cytokines after DAI. MCC950 alleviated axonal injures and cell apoptosis. MCC950 also decreased brain water content and alleviated neurologic deficits 1 day and 3 days after DAI but not 7 days after DAI. These results suggest that MCC950 treatment in the early stages of DAI has a time limiting effect in preventing from axonal injuries and neurological deficits, and that NLRP3 inflammasome plays an important role in axonal injures and may be a potential candidate for axonal injures following DAI.

Symptomatic peritumoral edema is associated with surgical outcome: a consecutive series of 72 supratentorial meningioma patients ≥ 80 years of age.

PURPOSE: To assess the association of peritumoral brain edema (PTBE) with postoperative outcome in old (≥ 80 years) meningioma patients. METHODS: All supratentorial meningioma patients (≥ 80 years old) who underwent surgery between 2010 and 2018 were retrospectively identified. Patients were classified into poor (≤ 40), intermediate (50-70), or good (≥ 80) preoperative Karnofsky Performance Status (KPS) subgroups. Outcome was evaluated at 3 months and at last follow-up within the first year after surgery, and categorized as improved, stable, or deteriorated. Three-dimensional volumetric assessment of tumor and PTBE volume was conducted. Volumes were categorized as small (< 10 cm3), medium (10-50 cm3), large (> 50 cm3). RESULTS: Seventy-two patients (mean age 83 ± 3 years, median 83; median follow-up 3 years) were included. The mean tumor volume was 39 ± 31 cm3 (median 27), and mean PTBE volume was 57 ± 79 cm3 (median 27). The mean preoperative KPS and at last follow-up was 58 ± 16 (median 60) and 59 ± 30 (median 70). Thirty-three patients were classified as improved, 16 as stable, and 23 deteriorated; eleven patients died within the first year. Large PTBE volume was more common for patients with poor preoperative status (p = 0.001). However, patients with large PTBE and poor preoperative status improved most frequently following surgery (p = 0.037 at 3 months, p = 0.074 at last follow-up). Large PTBE volume was not associated with treatment-associated complications (p = 0.538) or mortality (p = 0.721). A decision support tool to predict outcome was developed (p = 0.038). CONCLUSION: Elderly patients with large PTBE volumes usually had a poor preoperative performance status, but appeared to benefit most often from surgery.

Interrelated Pathogenesis? Neuronal Intranuclear Inclusion Disease Combining With Hemiplegic Migraine.

BACKGROUND: Neuronal intranuclear inclusion disease (NIID) is considered a heterogeneous disease because of its highly variable clinical manifestations. To date, there are no reports of NIID patients presenting with hemiplegic migraine (HM)-like headache, or of HM and NIID co-occurring as comorbidity, and the connection between these 2 seemingly unrelated clinical conditions has yet to be established. METHOD: We present a patient with NIID who was previously diagnosed with HM. To determine the pathogenesis of HM in this NIID patient, we systematically reviewed published NIID and HM cases and cataloged them based on their clinical manifestations. RESULT: The clinical manifestations of NIID is highly various; however, there is no case reported to date that shows HM-like symptoms or cerebral edema. All documented symptomatic HM cases show vascular dysfunction to various degrees, but none of them has been shown to be correlated with NIID. CONCLUSION: Our patient is the first documented case in which HM and NIID occur simultaneously. Vascular dysfunctions that cause cerebral hypoperfusion and glucose hypometabolism, two of the dominant causes of symptomatic HM, may be associated with the accumulation of eosinophilic hyaline inclusions that cause NIID. However, the existence of inclusions may also alter neuronal behavior and indirectly cause cerebral hypoperfusion and glucose hypometabolism. Further research and observations are needed to examine the relationship between HM and NIID.

Risk factors and control of seizures in 778 Chinese patients undergoing initial resection of supratentorial meningiomas.

This retrospective study explored the risk factors for the occurrence of seizures in the pre- and postoperative period in patients undergoing supratentorial meningiomas surgery to investigate those who are likely to benefit from prophylactic antiepileptic drugs (AEDs). We reviewed the medical records of 778 supratentorial meningiomas patients who were operated at our institution between 2011 and 2012. A total of 100 (12.9%) patients experienced preoperative seizures; 41 patients (5.3%) experienced postoperative in-hospital seizures, and 91 (13.5%, n = 673) patients experienced postoperative seizures after discharge. Multivariate analysis revealed that motor cortex involvement (odds ratio [OR] 3.243, P < 0.001) and peritumoral edema ≥ 1 cm (OR 3.936, P < 0.001) were significant risk factors of preoperative seizures. Whereas presenting with headache (OR 0.259, P < 0.001) and age ≥ 55 years at surgery (OR 0.514, P = 0.009) showed decreased incidence of preoperative seizures. The involvement of motor cortex (OR 3.290, P = 0.003), postoperative Karnofsky Performance Scale (KPS) ≤ 70 (OR 5.389, P < 0.001), preoperative seizure (OR 4.003, P < 0.001), and occurrence of any medical/surgical complication (OR 3.925, P = 0.001) were significant risk factors for postoperative in-hospital seizures. Postoperative seizures after discharge were associated with tumor maximal diameter ≥ 3.5 cm (OR 1.903, P = 0.022), preoperative seizures (OR 4.350, P < 0.001), postoperative in-hospital seizures (OR 6.385, P < 0.001), and tumor recurrence/progression (OR 7.642, P < 0.001). The probability of seizure freedom in the 5-year follow-up was roughly 59% among patients with preoperative seizures, and 87% among patients without preoperative seizures. Cox regression analysis showed that tumor recurrence/progression (relative risk 2.987, 95% CI 1.517, 5.879, P = 0.002) was the only predictor of postoperative seizures in patients without a history of preoperative epilepsy. The use of postoperative prophylactic antiepileptic drug (AED) did not reduce the incidence of seizures in our analysis. Understanding the risk factors for seizures might help clinicians to predict their occurrence and develop effective anti-epileptic treatment strategies. Further prospective randomized controlled trials are needed to determine the risk factors for seizures and the efficacy of AED prophylaxis.

External Validation and Modification of the EDEMA Score for Predicting Malignant Brain Edema After Acute Ischemic Stroke.

BACKGROUND: Accurate prediction of malignant brain edema (MBE) after stroke is paramount to facilitate close monitoring and timely surgical intervention. The Enhanced Detection of Edema in Malignant Anterior Circulation Stroke (EDEMA) score was useful to predict potentially lethal malignant edema in Western populations. We aimed to validate and modify it to achieve a better predictive value for MBE in Chinese patients. METHODS: Of ischemic stroke patients consecutively admitted in the Department of Neurology, West China Hospital between January 2010 and December 2017, we included patients with anterior circulation stroke, early signs of brain edema on computed tomography within 24 h of onset, and admission National Institutes of Health Stroke Scale (NIHSS) score ≥ 8. MBE was defined as the development of signs of herniation (including decrease in consciousness and/or anisocoria), accompanied by midline shift ≥ 5 mm on follow-up imaging. The EDEMA score consisted of five parameters: glucose, stroke history, reperfusion therapy, midline shift, and cistern effacement. We created a modified score by adding admission NIHSS score to the original EDEMA score. The discrimination of the score was assessed by the area under the receiver operating characteristics curve (AUC). Calibration was assessed by Hosmer-Lemeshow test and calibration plot. We compared the discrimination of the original and modified score by AUC, net reclassification improvement (NRI), and integrated discrimination improvement (IDI). Clinical usefulness of the two scores was compared by plotting net benefits at different threshold probabilities in the decision curve analysis. RESULTS: Of the 478 eligible patients (mean age 67.3 years; median NIHSS score 16), 93 (19%) developed MBE. The EDEMA score showed moderate discrimination (AUC 0.72, 95% confidence interval [CI] 0.67-0.76) and good calibration (Hosmer-Lemeshow test, P = 0.77). The modified score showed an improved discriminative ability (AUC 0.80, 95% CI 0.76-0.84, P < 0.001; NRI 0.67, 95% CI 0.55-0.78, P < 0.001; IDI 0.07, 95% CI 0.06-0.09, P < 0.001). Decision curves showed that the modified score had a higher net benefit than the original score in a range of threshold probabilities lower than 60%. CONCLUSIONS: The original EDEMA score showed an acceptable predictive value for MBE in Chinese patients. By adding the admission NIHSS score, the modified score allowed for a more accurate prediction and clinical usefulness. Further validation in large cohorts of different ethnicities is needed to confirm our findings.

Endoscopic Surgery Without Decompressive Craniectomy in Large Putaminal Intracerebral Hemorrhage: Assessment of Efficacy and Safety.

BACKGROUND: Decompressive craniectomy (DC) is performed conventionally for large putaminal intracerebral hemorrhage (ICH). However, DC causes local skull defect and leads to post-surgical cranioplasty. The aim of this study is to investigate the effectiveness and safety of an endoscopic procedure to treat large putaminal ICH without DC. METHODS: This retrospective study included 112 large putaminal ICH patients who underwent hematoma evacuations with either an endoscopic procedure (group A) or with DC (group B) between January 2009 and June 2017. The efficacy was evaluated by mean modified Rankin Scale (mRS) three months after surgery. Safety was evaluated by mortality rate and postoperative complications. Univariate and multivariate logistic regression analyses were performed to determine the risk factors for clinical outcomes. RESULTS: The study included 49 patients in group A and 63 in group B. The mRS scores in both groups were similar after 3 months' follow-up (p = 0.709). There was no difference in the mortality rate between the two groups (p = 0.538). The rate of complications was lower in group A than that in group B (p = 0.024). Smaller preoperative midline shift (p = 0.008) and absent intraventricular extension (p = 0.044) have contributed significantly to better outcomes. CONCLUSION: Endoscopic hematoma evacuation without DC is safe and effective for patients with large putaminal ICH and deserves further investigation, preferably in a randomized controlled setting.

Asymmetric cerebral edema presenting with severe neurologic impairment and seizures after cardiac and thoracic interventions.

INTRODUCTION: A syndrome of focal neurologic deficits with characteristic imaging features, acute encephalopathy, and seizures after cardiac and thoracic interventions has been previously briefly reported in the literature. In a retrospective observational study, we aim to identify the prevalence and characteristics of this syndrome, in addition to discussing the possible underlying pathophysiology. METHODS: In a retrospective study, we reviewed records of consecutive adult patients (≥18 years old) who underwent cardiac and thoracic procedures at a single institution between September 2014 to September 2019 and found to have evidence of focal cerebral edema following their procedure. We included and reported clinical course of patients who developed post-operative neurologic dysfunction and underwent magnetic resonance imaging (MRI) showing (1) asymmetric cerebral edema with (2) cortical diffusion restriction and (3) T2 cortical or subcortical hyperintensity and (4) no proximal vascular occlusion. RESULTS: Three out of 107 patients (2.8%) met our inclusion criteria. These represented one male and two females with age at presentation of 63, 81 and 69, respectively. All patients developed severe neurologic impairment on the same day following their procedure (sternotomy with valve or bypass surgery in 2 patients; esophageal dilatation procedure in 1 patient). All patients underwent MRI of the brain and vessel imaging qualifying our inclusion criteria. Two patients improved neurologically prior to discharge, and one patient expired after family elected to withdraw care. CONCLUSION: We present a series of cases with a rare syndrome after cardiac and thoracic interventions. Although the exact mechanism of this syndrome remains unclear, we believe it to be related to relative cerebral hyperperfusion and cerebral dysautoregulation following anesthesia and thoracic manipulation. Future studies should focus on understanding the true prevalence and pathophysiology of this syndrome.

Copeptin Kinetics in Acute Ischemic Stroke May Differ According to Revascularization Strategies: Pilot Data.

Background and Purpose- Prognostic value of copeptin in acute ischemic stroke has been widely reported. This study aimed to evaluate copeptin temporal profile according to revascularization strategies and the development of brain edema and hemorrhagic transformation. Methods- Plasma copeptin and brain edema and hemorrhagic transformation assessed by computed tomography/magnetic resonance imaging were evaluated upon admission (T0), at 24 hours (T1), and between the third and fifth day of hospitalization (T2) in 34 acute ischemic stroke patients. Results- Median copeptin concentration was 50.71 pmol/L at T0, 18.31 pmol/L at T1, and 10.92 pmol/L at T2. Copeptin at T1 was higher in patients with medium/severe brain edema at T2 (32.25 versus 13.67 pmol/L; P=0.038) and hemorrhagic transformation at T1 (93.10 versus 13.67 pmol/L; P<0.003) and T2 (85.70 versus 14.45 pmol/L; P=0.024). Copeptin level drop (CopΔT1-T0) was significantly steeper in patients receiving revascularization, particularly in those undergoing combined therapy (-129.34 versus -5.43 pmol/L; P=0.038). ΔT1-T0 also correlated with Thrombolysis in Cerebral Infarction score (P<0.001). Conclusions- Copeptin resulted associated with brain edema and hemorrhagic transformation in acute ischemic stroke, and its drop at 24 hours may mirror effective brain vessel recanalization.

Propensity for different vascular distributions and cerebral edema of intraparenchymal brain metastases from different primary cancers.

PURPOSE: This study seeks to ascertain whether different primary tumor types have a propensity for brain metastases (BMs) in different cerebral vascular territories and cerebral edema. METHODS: Consecutive adult patients who underwent surgical resection of a BM at a tertiary care institution between 2001 and 2011 were retrospectively reviewed. Only patients with the most common primary cancers (lung, breast, skin-melanoma, colon, and kidney) were included. Preoperative MRIs were reviewed to classify all tumors by cerebral vascular territory (anterior cerebral artery-ACA, lenticulostriate, middle cerebral artery-MCA, posterior cerebral artery-PCA, posterior fossa, and watershed), and T2-weighted FLAIR widths were measured. Chi square analyses were performed to determine differences in cerebral vascular distribution by primary tumor type, and one-way ANOVA analyses were performed to determine FLAIR signal differences. RESULTS: 669 tumors from 388 patients were classified from lung (n = 316 BMs), breast (n = 144), melanoma (n = 119), renal (n = 47), and colon (n = 43). BMs from breast cancer were less likely to be located in PCA territory (n = 18 [13%]; χ2 = 6.10, p = 0.01). BMs from melanoma were less likely to be located in cerebellar territory (n = 11 [9%]; χ2 = 14.1, p < 0.001), and more likely to be located in lateral (n = 5 [4%]; χ2 = 4.56, p = 0.03) and medial lenticulostriate territories (n = 2 [2%]; χ2 = 6.93, p = 0.009). BMs from breast and melanoma had shorter T2-FLAIR widths, with an average [IQR] of 47.2 [19.6-69.2] mm (p = 0.01) and 41.2 [14.4-62.7] mm (p = 0.002) respectively. Conversely, BMs from renal cancer had longer T2-FLAIR widths (64.2 [43.6-80.8] mm, p = 0.002). CONCLUSIONS: These findings suggest that different primary tumor types could have propensities for different cerebral vascular territories and cerebral edema.

WHO grade of intracranial meningiomas differs with respect to patient's age, location, tumor size and peritumoral edema.

PURPOSE: To analyse whether the WHO grade of intracranial meningiomas differs itself depending on patients and meningioma characteristics at diagnosis. METHODS: Single center retrospective study of a series of consecutive patients with primary intracranial meningiomas who underwent surgery between January 2007 and March 2014. Patients (age, sex, outcome) and meningioma characteristics (histological diagnosis, tumor location, WHO grading, size, extend of peritumoral edema and tumor recurrence rate) were analysed. RESULTS: Of 240 included patients, 184 (76.7%) were female and 56 (23.3%) were male. 17 patients (7.1%) were in age group 20-40 years, 112 (46.7%) in group 41-60 years and 111 (46.3%) were in age group > 60 years. 189 patients (78.8%) were diagnosed with WHO grade I, 49 (20.4%) WHO grade II and 2 (0.8%) had a WHO grade III meningioma. WHO grade II meningiomas were significantly more frequent in the age group 20-40 years compared to age group 41-60 years (chi-square p < 0.05). Convexity meningiomas were significantly more frequent classified as WHO grade II meningiomas compared to all other locations (chi-square, p < 0.01). Mean calculated tumor volume and the tumor volume determined by volumetric measurement was significantly larger in grade II meningioma patients compared to grade I (46.3 ± 40.5 cc grade II versus 21.8 ± 27.8 cc grade I and 45.3 ± 38.2 cc versus 23.1 ± 30.0 cc respectively; t test < 0.01). Extend of the peritumoral edema was significantly larger in patients with grade II meningiomas (Wilcoxon test, p < 0.05). Short term outcome did not differ between different age groups nor was it associated with tumor size. During a mean follow up of 49 months (min 3, max 144 months) recurrence rate was significantly higher in WHO grade II (4 out of 49 [8.2]%) compared to WHO grade I patients (3 out if 186, [1.6%]; Chi-square, p < 0.05). CONCLUSION: In this series atypical meningioma was associated with younger age, location on the convexity, larger tumor size and more peritumoral edema.