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The novel coronavirus commonly referred to as COVID-19 became a global pandemic in the March of 2020 and createdunprecedented challenges for health care systems worldwide. Early case reports demonstrated a high risk of aerosolizationand infection of operating room staff during endoscopic endonasal approaches, highlighting the need for safe managementstrategies in patients with COVID-19 with acute pathology. During periods of epidemiologic infectious surges, elective caseshave often been suspended. However, patients presenting with urgent pathology, such as pituitary apoplexy or acute visualcompromise from sellar or parasellar lesions still require treatment regardless of infectious status. Here, we present a caseof an asymptomatic COVID-19 patient with progressive vision loss that underwent successful microscopic resection ofpituitary adenoma, without evidence of spread to the operating room staff. We hypothesize that during microscopicapproaches to the sella, there is relatively less forceful irrigation, and as a result, potentially less aerosolization. This maydecrease the risk of viral spread to the surgeons and the operating room staff. Additionally, we report that fluorescent insitu hybridization studies of tumor tissue for SARS-CoV-2 may not reliably be able to detect viral infections. In conclusion,for asymptomatic patients at high risk for COVID, microscopic transsphenoidal approaches may provide a safer alternative.These patients should undergo preoperative testing, and repeat testing should be considered if possible for negative results.Proper PPE should however still be utilized to maximize safety of the operating room staff.

Introduction: For elderly adults in the United States, stroke is the fifth leading cause of death of which ischemic strokes comprise a vast majority. Optimal pharmacological management of elderly ischemic stroke patients involves both reperfusion and supportive care. Recent research into pharmacological management has focused on vascular, immunomodulatory, cytoprotective, and alternative agents, some of which have shown limited success in clinical trials. However, no treatments have been established as a reliable mode for management of cerebral ischemia for elderly adults beyond acute thrombolysis.Areas covered: The authors conducted a literature search for ischemic stroke management in the elderly and a search for human drug studies for managing ischemic stroke on clinicaltrials.gov. Here, they describe recent progress in the pharmacological management of cerebral ischemia in the elderly.Expert opinion: Many drug classes (antihypertensive, cytoprotective and immunomodulatory, and alternative agents) have been explored with limited success in managing ischemic stroke, though some have shown preventative benefits. We generally observed a broad gap in evidence on elderly patients from studies across all drug classes, necessitating further studies to gain an understanding of effective management of ischemic stroke in this large demographic of patients.

Dorsal arachnoid webs (DAWs) are rare pathological abnormalities of the arachnoid layer of the spinal cord that can result in pain and myelopathy.To present clinical, imaging, and pathological characteristics of patients diagnosed with DAW, case illustrations, and a review of the literature.Seventeen cases of DAW between 2015 and 2019 at a tertiary medical center were retrospectively identified through a case log search. Patient characteristics, preoperative imaging, operative notes, and pathology reports were collected. Our main outcome assessed was postoperative resolution of symptoms. Odds ratios were used to determine associations between preoperative signs and symptoms with postoperative symptom resolution.The mean age of the cohort was 50.5 years (IQR = 16) and presented primarily with back pain (64.7%). On imaging, all patients were found to have the "scalpel sign," and nearly half had a syrinx present (41.2%). All DAWs were located in the thoracic spine, with the most common location being the midthoracic (70.6%). The mean follow-up length for all patients was 4.3 months. There were no preoperative symptoms significantly associated with postoperative symptom resolution; however, a trend was noted with the presence of a preoperative syrinx. Pathology samples consistently demonstrated fibroconnective or collagenous tissue with no evidence of inflammation or neoplasm.DAW is a rare pathology that can result in myelopathy or inappropriate interventions if misdiagnosed. Surgical intervention using laminectomy with intradural exploration should be considered in symptomatic patients with DAW because it is curative with a strong chance of preoperative symptom resolution with relatively low complication rates.

OBJECTIVE High-grade spinal glioma (HGSG) is a rare but aggressive tumor that occurs in both adults and children. Histone H3 K27M mutation correlates with poor prognosis in children with diffuse midline glioma. However, the role of H3 K27M mutation in the prognosis of adults with HGSG remains unclear owing to the rarity of this mutation, conflicting reports, and the absence of multicenter studies on this topic. METHODS The authors studied a cohort of 30 adult patients with diffuse HGSG who underwent histological confirmation of diagnosis, surgical intervention, and treatment between January 2000 and July 2020 at six tertiary academic centers. The primary outcome was the effect of H3 K27M mutation status on progression-free survival (PFS) and overall survival (OS). RESULTS Thirty patients (18 males and 12 females) with a median (range) age of 50.5 (19–76) years were included in the analysis. Eighteen patients had H3 K27M mutation–positive tumors, and 12 had H3 K27M mutation–negative tumors. The median (interquartile range) PFS was 3 (10) months, and the median (interquartile range) OS was 9 (23) months. The factors associated with increased survival were treatment with concurrent chemotherapy/radiation (p = 0.006 for PFS, and p ≤ 0.001 for OS) and American Spinal Injury Association grade C or better at presentation (p = 0.043 for PFS, and p < 0.001 for OS). There were no significant differences in outcomes based on tumor location, extent of resection, sex, or H3 K27M mutation status. Analysis restricted to HGSG containing necrosis and/or microvascular proliferation (WHO grade IV histological features) revealed increased OS for patients with H3 K27M mutation–positive tumors (p = 0.017). CONCLUSIONS Although H3 K27M mutant–positive HGSG was associated with poor outcomes in adult patients, the outcomes of patients with H3 K27M mutant–positive HGSG were somewhat more favorable compared with those of their H3 K27M mutant–negative HGSG counterparts. Further preclinical animal studies and larger clinical studies are needed to further understand the age-dependent effects of H3 K27M mutation.

Background: Growing evidence suggests that chronic subdural hematoma (CSDH) may have long-term adverse effects even after surgical evacuation. Hematoma recurrence is commonly reported as a short-term, postoperative outcome measure for CSDH, but other measures such as hematoma resolution may provide better insight regarding mechanisms behind longer-term sequelae. This study aims to characterize postoperative resolution times and identify predictors for this relatively unexplored metric. Methods: Consecutive cases (N = 122) of burr hole evacuation for CSDH by a single neurosurgeon at Columbia University Irving Medical Center from 2000 to 2019 were retrospectively identified. Patient characteristics, presenting factors, and date of hematoma resolution were abstracted from the electronic health record. Outcome measures included CSDH resolution at 6 months, surgery-to-resolution time, and inpatient mortality. Univariate and multivariate analyses were performed to determine predictors of outcome measures. Results: Hematoma resolution at 6 months was observed in 58 patients (47.5%), and median surgery-to-resolution time was 161 days (IQR: 85–367). Heavy drinking was predictive of non-resolution at 6 months and longer surgery-to-resolution time, while increased age was predictive of non-resolution at 6 months. Antiplatelet agent resumption was associated with non-resolution at 6 months and longer surgery-to-resolution time on univariate analysis but was not significant on multivariate analysis. Conclusion: Postoperative resolution times for most CSDHs are on the order of several months to a year, and delayed resolution is linked to heavy drinking and advanced age. Subsequent prospective studies are needed to directly assess the utility of hematoma resolution as a potential metric for long-term functional and cognitive outcomes of CSDH.

The mitochondrial Bit1 protein exerts tumor-suppressive function in NSCLC through induction of anoikis and inhibition of EMT. Having this dual tumor suppressive effect, its downregulation in the established human lung adenocarcinoma A549 cell line resulted in potentiation of tumorigenicity and metastasis in vivo. However, the exact role of Bit1 in regulating malignant growth and transformation of human lung epithelial cells, which are origin of most forms of human lung cancers, has not been examined. To this end, we have downregulated the endogenous Bit1 expression in the immortalized non-tumorigenic human bronchial epithelial BEAS-2B cells. Knockdown of Bit1 enhanced the growth and anoikis insensitivity of BEAS-2B cells. In line with their acquired anoikis resistance, the Bit1 knockdown BEAS-2B cells exhibited enhanced anchorage-independent growth in vitro but failed to form tumors in vivo. The loss of Bit1-induced transformed phenotypes was in part attributable to the repression of E-cadherin expression since forced exogenous E-cadherin expression attenuated the malignant phenotypes of the Bit1 knockdown cells. Importantly, we show that the loss of Bit1 expression in BEAS-2B cells resulted in increased Erk activation, which functions upstream to promote TLE1-mediated transcriptional repression of E-cadherin. These collective findings indicate that loss of Bit1 expression contributes to the acquisition of malignant phenotype of human lung epithelial cells via Erk activation-induced suppression of E-cadherin expression.