Neurological Manifestations In COVID-19 Patients: An Imaging Review

Background: The COVID-19 pandemic that started in late 2019, has posed a great health challenge to India rapidly elevating our country to the second most affected nation after the United States. While the respiratory manifestations of COVID-19 are widely-known, there is paucity of information on its neurological manifestations in Indian literature. The imaging features of the diverse neurological presentations such as stroke, encephalitis, demyelination, hemorrhages and vascular involvement are reviewed in this article. Objective of the review is to discuss the spectrum of neuroimaging features in COVID-19. Method(s): Multiple publications from systematic and cohort studies on neuroimaging are reviewed in this article. Due permission was obtained from the publishers to reproduce the illustrations because of lack of adequate neuroimaging data in our country. Result(s): Ischemic infarcts, micro-hemorrhages, parenchymal hematomas and white matter changes, both diffuse and focal were the most common manifestations. Acute necrotizing hemorrhagic encephalitis, features resembling posterior reversible encephalopathy syndrome (PRES) and acute demyelinating encephalomyelitis (ADEM), arterial dissections, dural sinus and deep venous thrombosis were reported. Olfactory bulb and white matter signal ratios were elevated in anosmic patients. Micro-structural changes such as remyelination and neurogenesis indicated processes of repair. Conclusion(s): Ischemic and hemorrhagic lesions are the most common neuroimaging abnormalities in COVID-19 patients, though 40% of the studies are normal. Awareness of the imaging features is essential for management of these patients in the current pandemic. Severity of illness and risk of spread of infection are major constraints for neuroimaging. Copyright © 2022 International Medical Sciences Academy. All rights reserved.

Virus-cell interactions of the ChAdOx1 viral vector give insights into vaccine-induced immune thrombotic thrombocytopenia

The ChAdOx1 nCoV-19 vaccine (AZD1222/Vaxzervia) adapted from the chimpanzee adenovirus Y25 (ChAd-Y25) has been critical in combatting the severe acute respiratory coronavirus 2 (SARS-CoV-2) pandemic. However, as part of the largest vaccination campaign in history, a potentially lifethreatening clotting disorder, thrombosis with thrombocytopenia, resembling heparin-induced thrombocytopenia (HIT), has been observed in a minority of AZD1222 patients following the first but not the second dose. Vaccine-induced immune thrombotic thrombocytopenia (VITT) is characterised by development of thromboses at uncommon sites such as the cerebral venous sinuses and the splanchnic veins, with concomitant thrombocytopaenia. Therefore, to determine how ChAdOx1 may contribute to this novel disorder, it is critical to investigate the vector-host interactions of ChAdOx1. Structural and in vitro analysis of the fiber knob responsible for the primary virus-cell interaction suggests that coxsackie and adenovirus receptor (CAR) is the primary ChAdOx1 receptor. However, ChAdOx1 infection of CAR(-) human vascular endothelial cells has been demonstrated in vitro, suggesting ChAdOx1 may be using additional receptors. Dual tropism has been demonstrated in other human adenoviruses, with HAdV-D26 and HAdV-D37 both using sialic acid and CAR for transduction. Furthermore, coagulation factor X (FX), a factor demonstrated to bind to the hexon and facilitate human adenovirus type 5 (HAdV-C5) transduction via a CARindependent pathway does not increase ChAdOx1 infection, with amino acid alignment between the hexon proteins suggesting ChAdOx1 is unable to bind FX. Taken together, these findings suggest ChAdOx1 uses additional as yet unknown mechanisms for transduction, which may further contribute to the pathogenesis of VITT.

DURAL VENOUS SINUS THROMBOSIS: A RARE PRESENTING CONSEQUENCE OF COVID-19

SESSION TITLE: Post-COVID-19 Infection Complications SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: The severe acute respiratory syndrome coronavirus (SARS-COV2) and its resulting coronary virus 2019 syndrome (COVID-19) has resulted in an unprecedented global pandemic affecting more than 250 million people and resulting in at least 5 million deaths worldwide. Clinical manifestations of the Covid-19 disease process include but are not limited to respiratory dysfunction and failure, coagulopathy, malaise and cytokine storm. We report a case of dural sinus thrombosis (DST) as a sequelae to COVID-19. CASE PRESENTATION: A 26-year-old woman with a history of migraines presented with sudden diffuse headache and photosensitivity. She reported no palpitations, oral ulcers, dizziness, diaphoresis, slurred speech, weakness, paresthesias or recent head trauma. Her presenting vital signs were within normal range. Physical exam was negative for focal neurologic deficits, weakness, or sensory loss. A rapid pregnancy test was negative. D-dimer was 7,200 ng/mL (reference <500 ng/mL). A COVID test was positive. A computed tomography (CT) of the head revealed diffuse hypodensity in the torcula and the transverse sinuses bilaterally extending into the cerebellar folia, suspicious for DST, which was confirmed on magnetic resonance venography. A full hypercoagulable panel resulted negative. It was determined that the patient's coronavirus disease infection resulted in a prothrombotic state and her dural sinus vein thromboses. The patient was started on a high intensity heparin drip for seven days, then transitioned to Dabigatran and Topiramate for management of headache upon discharge. DISCUSSION: COVID-19 typically manifests as fever, hypoxia, and dyspnea. If coagulopathy were to occur, the most common of them are deep vein thromboses. Cerebral thrombotic events, specifically, a DST has been underreported in literature. It is suspected that the burden of cerebral thrombosis in COVID-19 patients is 0.08%. In the same study, it was also identified that 31% of those who developed a cerebral thrombosis also had other hypercoagulable risk factors not present in this patient. Advancement in neuroimaging has allowed these thrombotic issues to be identified, however, early recognition, especially with a lack of risk factors, creates a less straightforward management plan. Our patient manifested a DST in the setting of an active COVID-19 infection. Higher levels of evaluation are required in patients who test positive for Covid-19 when clinically indicated. Such indications include headaches that are new in onset, severe in nature, and diffuse. Delayed diagnosis and management can be permanently damaging. CONCLUSIONS: Dural venous sinus thrombosis is a rare, yet deadly complication of COVID-19. All risk factors and other etiologies of hypercoagulable states should be ruled out followed by early detection based on clinical and physical exam, and accompanied by appropriate imaging followed by prompt intervention. Reference #1: Baldini, T., Asioli, G. M., Romoli, M., Carvalho Dias, M., Schulte, E. C., Hauer, L., Aguiar De Sousa, D., Sellner, J., & Zini, A. (2021). Cerebral venous thrombosis and severe acute respiratory syndrome coronavirus-2 infection: A systematic review and meta-analysis. European journal of neurology, 28(10), 3478–3490. https://doi.org/10.1111/ene.14727 Reference #2: Hemasian, H., & Ansari, B. (2020). First case of Covid-19 presented with cerebral venous thrombosis: A rare and dreaded case. Revue neurologique, 176(6), 521–523. https://doi.org/10.1016/j.neurol.2020.04.013 Reference #3: Thompson, A., Morgan, C., Smith, P., Jones, C., Ball, H., Coulthard, E. J., Moran, E., Szewczyk-Krolikowski, K., & Rice, C. M. (2020). Cerebral venous sinus thrombosis associated with COVID-19. Practical neurology, practneurol-2020-002678. Advance online publication. https://doi.org/10.1136/practneurol-2020-002678 DISCLOSURES: No relevant relationships by Steven Douedi No relevant relationships by slam Elkherpitawy No relevant relationships by Justin Ilagan No relevant relationships by David Kountz No relevant relationships by Anton Mararenko No relevant relationships by Mihir Odak

Idiopathic Intracranial Hypertension and its management in an increasingly obese population

Background and aims: Idiopathic Intracranial Hypertension (IIH) is caused by elevated cerebrospinal fluid pressure of unknown aetiology predominantly affecting obese women of childbearing age. This study looked into the management of this patient population in a country with a rising obesity rate. Methods: Patients diagnosed with IIH were identified through the national Maltese database and further data was retrospectively collected from patients' files. Results: 59 patients were identified with an average age of 34 (14-68yr), and BMI 36.3 (26.7-49.1). Most underwent repeated lumbar punctures (Graph 1). The average opening pressure was 31.71cm of water (17-72cm of water). Visual field testing (75%), fundal photos (44%) and optical coherence tomography (21%) were often employed to assess papilledema. MRI showed typical IIH changes in 75% (Table 1). All patients were started on acetazolamide. Magnitude and specific strategies for weight loss were not routinely documented. 17% were offered surgical management;including shunt insertion (15%), and dural venous sinus stenting (5%). (Figure Presented) Conclusion: With rising obesity rates, this has become an increasingly prevalent disorder. Moreover, several patients either presented or relapsed following weight gain at the beginning of the COVID-19 pandemic. This study confirmed that more focus should be employed towards weight loss, which was often poorly documented and not aggressively targeted. Patients were undergoing frequent lumbar punctures rather than repeat, non-invasive ophthalmological investigations - this was tackled locally by involving an ophthalmologist with a special interest in the disorder. A multidisciplinary task force and new local guidelines have been instrumental in standardising and optimising management for these patients.

Cerebral Venous Sinus Thrombosisin the Setting of an AVMWhile on Anticoagulation: A Case Report

Objective: To increase the awareness of neurological complications of arteriovenous malformation (AVM) due to obstruction of the venous drainage despite being on anticoagulants. Background: Cerebral AVMs are high-flow intracranial vascular malformation comprised of feeding arteries, a nidus of vessels with intervening brain parenchyma through which arteriovenous shunting occurs and dilated draining veins allowing significant hemodynamic gradient without an interposed resistance. Venous drainage stenosis or occlusion will increase the hemodynamic pressure gradient within the AVM compartments and potentially lead to redistribution of flow resulting in cerebral venous sinus thrombosis or hemorrhagic stroke from nidus rupture. This effect might be worsened in the presence of a generalized hypercoagulable state causing microvascular injury and thrombosis;despite adequate anticoagulation therapy. Design/Methods: N/A Results: 66-year-old obese woman with history of atrial fibrillation, coronary artery disease, diabetes, hypertension, hyperlipidemia, prior stroke, small left frontal AVM diagnosed on conventional angiogram and recent COVID-19 infection presented to our comprehensive stroke center with seizures and right hemiparesis. MRI brain showed T2/FLAIR hyperintense lesion in the left frontal/parasagittal region with an extensive vasogenic edema, heterogeneous diffusion restriction, and gyriform contrast enhancement. Conventional angiogram showed AVM without nidus opacification but with an associated mass effect correlating with parenchyma edema and early venous shunting. Patient was initially misdiagnosed as low-grade neoplasm although accurate diagnosis of left parasagittal frontal venous infarct in the setting of spontaneous venous thrombosis of left frontal AVM was made with conventional angiogram. Conclusions: Venous infarct due to CVST is a devastating complication of AVM. The hemodynamic pressure gradient within the AVM might play a larger role in contributing to hypercoagulable state within the venous system leading to cerebral venous sinus thrombosis despite patient being on therapeutic anticoagulation.

Modern a COVID-19 Vaccine-Induced Immune Thrombosis of Central Retinal Artery-Report of a Case

Objective: To report a rarely isolated central retinal artery occlusion (CRAO) following Coronavirus disease 2019 (COVID-19) Vaccine Moderna (mRNA-1273). Background: COVID-19 caused by severe acute respiratory syndrome coronavirus was firstly reported in Dec 2019 and became pandemic as of Mar 2020. Fortunately, novel rapidly developed COVID-19 vaccines are capable of lessening the pandemic effectively. As billions of people vaccinated, however, COVID-19 vaccine-induced thrombosis (VIT) are gradually emerging. Design/Methods: A previously healthy 70-year-old man presented with acute painless visual loss of the right eye five days after the first dose of Moderna vaccine. On examination of the right eye, visual acuity (VA) was counting finger at 15 cm. Fundoscopy revealed a diffuse whitened retina with cherry-red spot. Optical coherence tomography (OCT) showed hyperreflectivity. Screening tests for platelet and D-Dimer levels were unremarkable. CRAO was treated with clopidogrel and hyperbaric oxygen therapy. The serum level of anti-platelet factor-4 (PF4) antibody was 73.34 ng/ml (ref, 0-49.99 ng/ml).Two months later, VA was counting finger at 10 cm3 and OCT revealed hyperreflectivity and mild inner retina atrophy Results: COVID-19 vaccine-induced thrombosis and thrombocytopenia (VITT) based on the victims receiving AstraZeneca and Johnson & Johnson vaccines is through autoimmune antibody against PF4. VITT is typically manifested within 6-24 days post-vaccination;thrombotic sites are in the cerebral sinus, portal vein, splanchnic vein, and pulmonary emboli;as well as thrombocytopenia and increased level of D-Dimer. Our patient had isolated CRAO five days post-Moderna vaccination but normal platelet count and D-Dimer level. Moreover, VIT with isolated CRAO was not published on PubMed. Conclusions: VIT could occur in the unusual site such as CRAO in our case. Normal platelet and D-Dimer levels might not be sensitive tools to exclude VIT. Suspected patient with thrombotic event after COVID-19 vaccines should have anti-PF4 antibody test to assure an effective treatment.

Retrograde cerebral air embolism in a patient on venovenous ECMO

INTRODUCTION: Retrograde cerebral air embolism (CAE) is rarely described in literature that may be associated with manipulation of central or peripheral venous catheters. During a literature review, there were no described occurrences of CAE in patients on veno-venous (V-V) ECMO. DESCRIPTION: A 42-year-old male with ARDS secondary to COVID-19 pneumonitis was cannulated for V-V ECMO outside our facility and transferred to our cardiovascular intensive care unit. Upon arrival, he was noted to have a right femoral drainage cannula and right internal jugular (RIJ) venous antegrade cannula. On day 10 of his hospital stay he was converted to a RIJ Protek duo cannula and the right femoral drainage cannula was removed. This cannula was repositioned multiple times after placement due to flow issues. Due to poor oxygenator membrane function, it became necessary to exchange the oxygenator on day 25. During the exchange, the patient experienced sudden-onset bradycardia that progressed to several seconds of asystole. He regained spontaneous cardiac activity after a bolus dose of IV glycopyrrolate. Following this, he had several episodes of bradycardia and eventually asystole that resolved after one round of ACLS and IV atropine. The bradycardic episodes continued after this event and were associated with hypertension. On day 25, the patient suffered a decline in neurologic status from a GCS of 11T to 3T. The patient was sent emergently for non-contrast CT head. This scan revealed pneumocephalus with diffuse foci of air emboli in the subarachnoid and intraventricular spaces, the choroid plexus, and dural venous sinuses. After a family discussion, care was withdrawn from the patient on day 27. DISCUSSION: This patient suffered a massive retrograde CAE peri-ECMO circuit oxygenator exchange. It is our understanding that this a novel clinical situation for this phenomenon and not previously described in literature. This emphasizes that manipulation of any vascular cannula may result in the entrainment of air in a retrograde venous fashion into the cerebral vasculature.