Adolescent subdural empyema in setting of COVID-19 infection: illustrative case.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is an ongoing viral pandemic that has affected modern medical practice and can complicate known pathology. The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes symptoms that may mimic a viral pneumonia, with potential for serious sequelae, including acute respiratory distress syndrome, coagulopathy, multiorgan dysfunction, systemic vascular abnormalities, and secondary infection. OBSERVATIONS: The authors describe a case of a 15-year-old boy who presented with a right subdural empyema and sinusitis while having active COVID-19 infection. The patient initially presented with left-sided weakness, frontal sinusitis, and subdural empyema. Emergent surgery was performed for evacuation of empyema and sinus debridement. Samples of purulent material within the subdural space were tested for SARS-CoV-2 by reverse transcriptase polymerase chain reaction. The patient had a successful recovery and regained the use of his right side after combined treatment. To our knowledge, this is the first reported case of a bacterial subdural empyema associated with frontal sinusitis in a coinfected patient with COVID-19 without evidence of COVID-19 intracranial infection. LESSONS: A subdural empyema, which is a surgical emergency, was likely a superinfection caused by COVID-19. This, along with the coagulopathy caused by the virus, introduced unique challenges to the treatment of a known pathology.

Encephaloduroarteriosynangiosis Operative Technique and Intraoperative Anesthesia Management: Treatment From Both Sides of the Curtain.

BACKGROUND: Encephaloduroarteriosynangiosis (EDAS) is a form of indirect revascularization for cerebral arterial steno-occlusive disorders. EDAS has gained growing interest as a technique applicable to pediatric and adult populations for several types of ischemic cerebral steno-occlusive conditions. OBJECTIVE: To present a team-oriented, multidisciplinary update of the EDAS technique for application in challenging adult cases of cerebrovascular stenosis/occlusion, successfully implemented in more than 200 cases. METHODS: We describe and demonstrate step-by-step a multidisciplinary-modified EDAS technique, adapted to maintain uninterrupted intensive medical management of patients' stroke risk factors and anesthesia protocols to maintain strict hemodynamic control. RESULTS: A total of 216 EDAS surgeries were performed in 164 adult patients, including 65 surgeries for patients with intracranial atherosclerotic disease and 151 operations in 99 patients with moyamoya disease. Five patients with intracranial atherosclerotic disease had recurrent strokes (3%), and there was one perioperative death. The mean clinical follow-up was 32.9 mo with a standard deviation of 31.1. There was one deviation from the surgical protocol. There were deviations from the anesthesia protocol in 3 patients (0.01%), which were promptly corrected and did not have any clinical impact on the patients' condition. CONCLUSION: The EDAS protocol described here implements a team-oriented, multidisciplinary adaptation of the EDAS technique. This adaptation resides mainly in 3 points: (1) uninterrupted administration of intensive medical management, (2) strict hemodynamic control during anesthesia, and (3) meticulous standardized surgical technique.

Air Pollution Particulate Matter Exposure and Chronic Cerebral Hypoperfusion and Measures of White Matter Injury in a Murine Model.

BACKGROUND: Exposure to ambient air pollution particulate matter (PM) is associated with increased risk of dementia and accelerated cognitive loss. Vascular contributions to cognitive impairment are well recognized. Chronic cerebral hypoperfusion (CCH) promotes neuroinflammation and blood-brain barrier weakening, which may augment neurotoxic effects of PM. OBJECTIVES: This study examined interactions of nanoscale particulate matter (nPM; fine particulate matter with aerodynamic diameter ≤200 nm) and CCH secondary to bilateral carotid artery stenosis (BCAS) in a murine model to produce white matter injury. Based on other air pollution interactions, we predicted synergies of nPM with BCAS. METHODS: nPM was collected using a particle sampler near a Los Angeles, California, freeway. Mice were exposed to 10 wk of reaerosolized nPM or filtered air (FA) for 150 h. CCH was induced by BCAS surgery. Mice (C57BL/6J males) were randomized to four exposure paradigms: a) FA, b) nPM, c) FA + BCAS, and d) nPM + BCAS. Behavioral outcomes, white matter injury, glial cell activation, inflammation, and oxidative stress were assessed. RESULTS: The joint nPM + BCAS group exhibited synergistic effects on white matter injury (2.3× the additive nPM and FA + BCAS scores) with greater loss of corpus callosum volume on T2 magnetic resonance imaging (MRI) (30% smaller than FA group). Histochemical analyses suggested potential microglial-specific inflammatory responses with synergistic effects on corpus callosum C5 immunofluorescent density and whole brain nitrate concentrations (2.1× and 3.9× the additive nPM and FA + BCAS effects, respectively) in the joint exposure group. Transcriptomic responses (RNA-Seq) showed greater impact of nPM + BCAS than individual additive effects, consistent with changes in proinflammatory pathways. Although nPM exposure alone did not alter working memory, the nPM + BCAS cohort demonstrated impaired working memory when compared to the FA + BCAS group. DISCUSSION: Our data suggest that nPM and CCH contribute to white matter injury in a synergistic manner in a mouse model. Adverse neurological effects may be aggravated in a susceptible population exposed to air pollution. https://doi.org/10.1289/EHP8792.

Transvenous Pressure Monitoring Guides Endovascular Treatment of Vein of Galen Malformation: A Technical Note.

INTRODUCTION: Vein of Galen malformations (VGMs) are complex congenital arteriovenous malformations that generally require serial endovascular treatment sessions to slowly correct the high-flow fistulous connections that cause increased venous pressures and ultimately lead to the classic presentations of heart failure, hydrocephalus, and intracranial hemorrhages. Despite the advances in endovascular technology and embolic materials, the resolution of embolization is often limited to the subjective view of diminished flow on angiograms. CASE REPORT: An 8-month-old patient with a VGM developed clinical signs of heart failure and growing head circumference with ventriculomegaly. The patient was treated endovascularly with a transvenous approach for coil embolization while undergoing continuous monitoring of the post-malformation venous pressures. The arterial and venous systolic blood pressures (SBP) were collected at serial time points and used to measure estimated 95% confidence interval bounds for arteriovenous SBP gradients and determine when sufficient coil embolization and flow reduction was thought to be achieved. CONCLUSION: The transvenous pressure monitoring demonstrated progressively increasing pressure gradients between the arterial and venous systems that correlated with the degree of flow reduction on angiographic runs. The patient underwent successful coil embolization of the VGM and had improvement of heart failure and ventricular size in follow-up at 8-month post-op. This provides a novel technique to introduce an objective measurement that can guide the embolization of a VGM.

Encephaloduroarteriosynangiosis Averts Stroke in Atherosclerotic Patients With Border-Zone Infarct: Post Hoc Analysis From a Performance Criterion Phase II Trial.

BACKGROUND: Intracranial atherosclerotic disease (ICAD) is one of the leading causes of stroke worldwide. Patients with ICAD who initially present with ischemia in border-zone areas and undergo intensive medical management (IMM) have the highest recurrence rates (37% at 1 yr) because of association with hemodynamic failure and poor collaterals. OBJECTIVE: To evaluate the effect of encephaloduroarteriosynagiosis (EDAS) on stroke recurrence in patients with ICAD and border-zone stroke (BDZS) at presentation. METHODS: A phase II clinical trial of EDAS revascularization for symptomatic ICAD failing medical management (EDAS Revascularization for Symptomatic Intracranial Atherosclerosis Steno-occlusive [ERSIAS]) was recently concluded. We analyze the outcomes of the subgroup of patients with BDZS at presentation treated with EDAS vs the previously reported Stenting versus Aggressive Medical Management for Preventing Recurrent stroke in Intracranial Stenosis (SAMMPRIS) IMM subgroup with BDZS at presentation. RESULTS: Of 52 patients included in the ERSIAS trial, 35 presented with strokes at baseline, and 28 had a BDZ pattern, including 15 (54%) with exclusive BDZS and 13 (46%) with mixed patterns (BDZ plus other distribution). Three of the 28 (10.7%) had recurrent strokes up to a median follow-up of 24 months. The rate of recurrent stroke in ICAD patients with BDZS at presentation after EDAS was significantly lower than the rate reported in the SAMMPRIS IMM subgroup with BDZS at presentation (10.7% vs 37% P = .004, 95% CI = 0.037-0.27). CONCLUSION: ICAD patients with BDZS at presentation have lower rates of recurrent stroke after EDAS surgery than those reported with medical management in the SAMMPRIS trial. These results support further investigation of EDAS in a randomized clinical trial.

Evaluation of tortuous vertebral arteries before cervical spine surgery: illustrative case.

BACKGROUND: Cervical spine surgery sometimes necessitates complex ventral/dorsal approaches or osteotomies that place the vertebral artery (VA) at risk of inadvertent injury. Tortuosity of the VA poses increased risk of vessel injury during anterior decompression or placement of posterior instrumentation. OBSERVATIONS: In this report, the authors describe a patient with degenerative cervical spondylotic myelopathy and focal kyphotic deformity requiring corrective surgery via a combined ventral/dorsal approach. Computed tomography (CT) and CT angiography (CTA) of the spine identified a left medially enlarged C4 transverse foramen and tortuous VA V2 segment forming a potentially dangerous medial loop into the vertebral body, respectively. The patient's presentation and management are described. LESSONS: The course of the VA is variable, and a tortuous VA with significant medial or lateral displacement may be dangerous during ventral and dorsal approaches to the cervical spine. CTA of the cervical spine is warranted in cases in which atlantoaxial fixation is needed or suspicious transverse foramen morphology is identified to understand the course of the VA and identify anatomical variations that would put the VA at risk during cervical spine surgery.

Symptomatic Cervical Tumoral Calcinosis due to Cosmetic Body Contouring Mineral Oil Injections.

Tumoral calcinosis (TC) is an uncommon disease that has been linked to familial genetic mutations but can often be due to secondary causes such as chronic renal failure and hyperparathyroidism. There are rare instances of tumoral calcinosis induced by foreign body injections, often for cosmetic purposes. Here we describe operative management of spinal cord compression due to mineral oil injection induced tumoral calcinosis. A 54-year-old transgender female presented with signs of myelopathy so severe that she had become wheelchair bound. Labs demonstrated hypercalcemia and imaging of the neuroaxis revealed significant calcification resulting in cervicothoracic and lumbar central canal stenosis. Given symptomatic cervical spinal cord compression, she was taken to the OR for urgent laminectomy and decompression. Postoperatively, she recovered well and was ambulating independently by postoperative day (POD) 9. This is the first reported case of localized mineral oil injections causing distant calcification with subsequent symptomatic cord compression requiring operative intervention.

Experimental chronic cerebral hypoperfusion results in decreased pericyte coverage and increased blood-brain barrier permeability in the corpus callosum.

Murine chronic cerebral hypoperfusion (CCH) results in white matter (WM) injury and behavioral deficits. Pericytes influence blood-brain barrier (BBB) integrity and cerebral blood flow. Under hypoxic conditions, pericytes detach from perivascular locations increasing vessel permeability and neuronal injury. This study characterizes the time course of BBB dysfunction and pericyte coverage following murine experimental CCH secondary to bilateral carotid artery stenosis (BCAS). Mice underwent BCAS or sham operation. On post-procedure days 1, 3, 7 and 30, corpus callosum BBB permeability was characterized using Evans blue (EB) extravasation and IgG staining and pericyte coverage/count was calculated. The BCAS cohort demonstrated increased EB extravasation on postoperative days 1 ( p = 0.003) 3 ( p = 0.002), and 7 ( p = 0.001) when compared to sham mice. Further, EB extravasation was significantly greater ( p = 0.05) at day 3 than at day 30 in BCAS mice. BCAS mice demonstrated a nadir in pericyte coverage and count on post-operative day 3 ( p < 0.05, compared to day 7, day 30 and sham). Decreased pericyte coverage/count and increased BBB permeability are most pronounced on postoperative day 3 following murine CCH. This precedes any notable WM injury or behavioral deficits.

Increased Hospital Surgical Volume Reduces Rate of 30- and 90-Day Readmission After Acoustic Neuroma Surgery.

BACKGROUND: Hospital readmissions are commonly linked to elevated health care costs, with significant financial incentive introduced by the Affordable Care Act to reduce readmissions. OBJECTIVE: To study the association between patient, hospital, and payer factors with national rate of readmission in acoustic neuroma surgery. METHODS: All adult inpatients undergoing surgery for acoustic neuroma in the newly introduced Nationwide Readmissions Database from 2013 to 2014 were included. We identified readmissions for any cause with a primary diagnosis of neurological, surgical, or systemic complication within 30- and 90-d after undergoing acoustic neuroma surgery. Multivariable models were employed to identify patient, hospital, and administrative factors associated with readmission. Hospital volume was measured as the number of cases per year. RESULTS: We included patients representing a weighted estimate of 4890 admissions for acoustic neuroma surgery in 2013 and 2014, with 355 30-d (7.7%) and 341 90-d (9.1%) readmissions. After controlling for patient, hospital, and payer factors, procedural volume was significantly associated with 30-d readmission rate (OR [odds ratio] 0.992, p = 0.03), and 90-d readmission rate (OR 0.994, p = 0.047). The most common diagnoses during readmission in both 30- and 90-d cohorts included general central nervous system complications/deficits, hydrocephalus, infection, and leakage of cerebrospinal fluid (rhinorrhea/otorrhea). CONCLUSION: After controlling for patient, hospital, and payer factors, increased procedural volume is associated with decreased 30- and 90-d readmission rate for acoustic neuroma surgery. Future studies seeking to improve outcomes and reduce cost in acoustic neuroma surgery may seek to further evaluate the role of hospital procedural volume and experience.

Nanoparticulate matter exposure results in neuroinflammatory changes in the corpus callosum.

Epidemiological studies have established an association between air pollution particulate matter exposure (PM2.5) and neurocognitive decline. Experimental data suggest that microglia play an essential role in air pollution PM-induced neuroinflammation and oxidative stress. This study examined the effect of nano-sized particulate matter (nPM) on complement C5 deposition and microglial activation in the corpus callosum of mice (C57BL/6J males). nPM was collected in an urban Los Angeles region impacted by traffic emissions. Mice were exposed to 10 weeks of re-aerosolized nPM or filtered air for a cumulative 150 hours. nPM-exposed mice exhibited reactive microglia and 2-fold increased local deposition of complement C5/ C5α proteins and complement component C5a receptor 1 (CD88) in the corpus callosum. However, serum C5 levels did not differ between nPM and filtered air cohorts. These findings demonstrate white matter C5 deposition and microglial activation secondary to nPM exposure. The C5 upregulation appears to be localized to the brain.

Estradiol Protects White Matter of Male C57BL6J Mice against Experimental Chronic Cerebral Hypoperfusion.

BACKGROUND AND PURPOSE: Estradiol is a sex steroid hormone known to protect the brain against damage related to transient and global cerebral ischemia. In the present study, we leverage an experimental murine model of bilateral carotid artery stenosis (BCAS) to examine the putative effects of estradiol therapy on chronic cerebral hypoperfusion. We hypothesize that long-term estradiol therapy protects against white matter injury and declarative memory deficits associated with chronic cerebral hypoperfusion. METHODS: Adult male C57BL/6J mice underwent either surgical BCAS or sham procedures. Two days after surgery, the mice were given oral estradiol (Sham+E, BCAS+E) or placebo (Sham+P, BCAS+P) treatments daily for 31-34 days. All mice underwent Novel Object Recognition (NOR) testing 31-34 days after the start of oral treatments. Following sacrifice, blood was collected and brains fixed, sliced, and prepared for histological examination of white matter injury and extracellular signal-regulated kinase (ERK) expression. RESULTS: Animals receiving long-term oral estradiol therapy (BCAS-E2 and Sham-E2) had higher plasma estradiol levels than those receiving placebo treatment (BCAS-P and Sham-P). BCAS-E2 mice demonstrated less white matter injury (Klüver-Barrera staining) and performed better on the NOR task compared to BCAS-P mice. ERK expression in the brain was increased in the BCAS compared to sham cohorts. Among the BCAS mice, the BCAS-E2 cohort had a greater number of ERK + cells. CONCLUSION: This study demonstrates a potentially protective role for oral estradiol therapy in the setting of white matter injury and declarative memory deficits secondary to murine chronic cerebral hypoperfusion.

Predictors of 30- and 90-day readmission following craniotomy for malignant brain tumors: analysis of nationwide data.

Hospital readmissions are a major contributor to increased health care costs and are associated with worse patient outcomes after neurosurgery. We used the newly released Nationwide Readmissions Database (NRD) to describe the association between patient, hospital and payer factors with 30- and 90-day readmission following craniotomy for malignant brain tumor. All adult inpatients undergoing craniotomy for primary and secondary malignant brain tumors in the NRD from 2013 to 2014 were included. We identified all cause readmissions within 30- and 90-days following craniotomy for tumor, excluding scheduled chemotherapeutic procedures. We used univariate and multivariate models to identify patient, hospital and administrative factors associated with readmission. We identified 27,717 admissions for brain tumor craniotomy in 2013-2014, with 3343 (13.2%) 30-day and 5271 (25.7%) 90-day readmissions. In multivariate analysis, patients with Medicaid and Medicare were more likely to be readmitted at 30- and 90-days compared to privately insured patients. Patients with two or more comorbidities were more likely to be readmitted at 30- and 90-days, and patients discharged to skilled nursing facilities or home health care were associated with increased 90-day readmission rates. Finally, hospital procedural volume above the 75th percentile was associated with decreased 90-day readmission rates. Patients treated at high volume hospitals are less likely to be readmitted at 90-days. Insurance type, non-routine discharge and patient comorbidities are predictors of postoperative non-scheduled readmission. Further studies may elucidate potentially modifiable risk factors when attempting to improve outcomes and reduce cost associated with brain tumor surgery.

Chronic cerebral hypoperfusion induced by bilateral carotid artery stenosis causes selective recognition impairment in adult mice.

OBJECTIVES: Chronic cerebral hypoperfusion (CCH) can result in vascular dementia and small vessel white matter ischemic injury. These findings have previously been demonstrated in a murine experimental model of CCH secondary to bilateral common carotid artery stenosis (BCAS). This study sought to elucidate the effects of CCH on recognition memory as assessed by the novel object recognition (NOR) test and histological analysis of the hippocampus and perirhinal cortex. METHODS: Studies were performed on ten-week-old male mice using bilateral 0.18 mm microcoils to narrow the carotid arteries in accordance with prior publications. Following surgery, BCAS (n = 6) and sham (n = 6) mice were evaluated using NOR and 8-arm radial maze testing paradigms. Tissue damage was assessed using H&E staining on a parallel cohort of mice (n = 6 BCAS, n = 7 sham). RESULTS: In the NOR paradigm, BCAS mice demonstrated significant deficits in short-term memory. Consistent with prior studies, BCAS mice also performed significantly worse on 8-arm radial maze testing. BCAS mice exhibited significantly more neuronal injury in the perirhinal cortex when compared to sham-operated mice. However, no significant differences in neuronal damage were observed in the CA1 region of the hippocampus. DISCUSSION: Experimental CCH secondary to BCAS results in recognition memory deficits on NOR testing. Damage to the perirhinal cortex, rather than to the hippocampus, may underlie this impairment.

Neuroprotective strategies following intraparenchymal hemorrhage.

Intracerebral hemorrhage and, more specifically, intraparenchymal hemorrhage, are devastating disease processes with poor clinical outcomes. Primary injury to the brain results from initial hematoma expansion while secondary hemorrhagic injury occurs from blood-derived products such as hemoglobin, heme, iron, and coagulation factors that overwhelm the brains natural defenses. Novel neuroprotective treatments have emerged that target primary and secondary mechanisms of injury. Nonetheless, translational application of neuroprotectants from preclinical to clinical studies has yet to show beneficial clinical outcomes. This review summarizes therapeutic agents and neuroprotectants in ongoing clinical trials aimed at targeting primary and secondary mechanisms of injury after intraparenchymal hemorrhage.

Selective embolization of ruptured feeding artery aneurysm followed by resection of arteriovenous malformation.

This is the case of a man in his 40s who suffered sudden collapse into a deep coma as a result of a ruptured arteriovenous malformation (AVM) feeding artery aneurysm within the lateral ventricle. The ruptured aneurysm was successfully treated with Onyx embolization of the feeding pedicle. The AVM and the feeding artery aneurysm were then removed via a transcallosal approach. This case highlights the utility of interrogating the AVM with microcatheterization of the feeding pedicles in order to define the exact anatomical features necessary for treatment planning. It also reviews the anatomy of the choroidal fissure. The video can be found here: https://youtu.be/UeqFzhTRU1Q .

Clinical effects of air pollution on the central nervous system; a review.

The purpose of this review is to describe recent clinical and epidemiological studies examining the adverse effects of urban air pollution on the central nervous system (CNS). Air pollution and particulate matter (PM) are associated with neuroinflammation and reactive oxygen species (ROS). These processes affect multiple CNS pathways. The conceptual framework of this review focuses on adverse effects of air pollution with respect to neurocognition, white matter disease, stroke, and carotid artery disease. Both children and older individuals exposed to air pollution exhibit signs of cognitive dysfunction. However, evidence on middle-aged cohorts is lacking. White matter injury secondary to air pollution exposure is a putative mechanism for neurocognitive decline. Air pollution is associated with exacerbations of neurodegenerative conditions such as Alzheimer's and Parkinson's diseases. Increases in stroke incidences and mortalities are seen in the setting of air pollution exposure and CNS pathology is robust. Large populations living in highly polluted environments are at risk. This review aims to outline current knowledge of air pollution exposure effects on neurological health.

Neuroprotective delivery platforms as an adjunct to mechanical thrombectomy.

Despite the success of numerous neuroprotective strategies in animal and preclinical stroke models, none have effectively translated to clinical medicine. A multitude of influences are likely responsible. Two such factors are inefficient recanalization strategies for large vessel occlusions and suboptimal delivery methods/platforms for neuroprotective agents. The recent endovascular stroke trials have established a new paradigm for large vessel stroke treatment. The associated advent of advanced mechanical revascularization devices and new stroke technologies help address each of these existing gaps. A strategy combining effective endovascular revascularization with administration of neuroprotective therapies is now practical and could have additive, if not synergistic, effects. This review outlines past and current neuroprotective strategies assessed in acute stroke trials. The discussion focuses on delivery platforms and their potential applicability to endovascular stoke treatment.

Stroke Damage Is Exacerbated by Nano-Size Particulate Matter in a Mouse Model.

This study examines the effects of nano-size particulate matter (nPM) exposure in the setting of murine reperfused stroke. Particulate matter is a potent source of inflammation and oxidative stress. These processes are known to influence stroke progression through recruitment of marginally viable penumbral tissue into the ischemic core. nPM was collected in an urban area in central Los Angeles, impacted primarily by traffic emissions. Re-aerosolized nPM or filtered air was then administered to mice through whole body exposure chambers for forty-five cumulative hours. Exposed mice then underwent middle cerebral artery occlusion/ reperfusion. Following cerebral ischemia/ reperfusion, mice exposed to nPM exhibited significantly larger infarct volumes and less favorable neurological deficit scores when compared to mice exposed to filtered air. Mice exposed to nPM also demonstrated increases in markers of inflammation and oxidative stress in the region of the ischemic core. The findings suggest a detrimental effect of urban airborne particulate matter exposure in the setting of acute ischemic stroke.