scholarly journals Neurologic Complications in Adult and Pediatric Patients with SARS-CoV-2 Infection

2021 ◽  
Vol 6 (1) ◽  
pp. 1
Author(s):  
Kendall Howard ◽  
Taylor Williams ◽  
Elizabeth Fitch ◽  
Heather Ots ◽  
Esther Pototskiy ◽  
...  
Keyword(s):  
Hemorrhagic Stroke ◽  
Neuronal Damage ◽  
Neural Tissue ◽  
Neurological Complications ◽  
Neurologic Manifestations ◽  
Molecular Events ◽  
Neuroprotective Therapy ◽  
Level Of Consciousness ◽  
Patients At Risk ◽  
Enzyme I

SARS-CoV-2 has an impact on the nervous system as a result of pathological cellular and molecular events at the level of vascular and neural tissue. Severe neurologic manifestations including stroke, ataxia, seizure, and depressed level of consciousness are prevalent in patients with SARS-CoV-2 infection. Although the mechanism is still unclear, SARS-CoV-2 has been associated with the pathogenesis of intravascular coagulation and angiotensin-converting enzyme-I, both exacerbating systemic inflammation and contributing to hypercoagulation or blood–brain barrier leakage, resulting in ischemic or hemorrhagic stroke. On the other hand, the SARS-CoV-2 spike protein in neural tissue and within the cerebrospinal fluid may induce neural dysfunction, resulting in neuroinflammation, which is exacerbated by peripheral and neural hypercytokinemia that can lead to neuronal damage and subsequent neuroinflammation. A deeper understanding of the fundamental biological mechanisms of neurologic manifestations in SARS-CoV-2 infection can pave the way to identifying a single biomarker or network of biomarkers to help target neuroprotective therapy in patients at risk for developing neurological complications.

scholarly journals SARS-CoV-2 and the Nervous System: From Clinical Features to Molecular Mechanisms

2020 ◽  
Vol 21 (15) ◽  
pp. 5475 ◽  
Author(s):  
Manuela Pennisi ◽  
Giuseppe Lanza ◽  
Luca Falzone ◽  
Francesco Fisicaro ◽  
Raffaele Ferri ◽  
...  
Keyword(s):  
Nervous System ◽  
Molecular Mechanisms ◽  
Neuronal Damage ◽  
Neurological Complications ◽  
Neurological Manifestations ◽  
Wide Range ◽  
Inflammatory State ◽  
Acute Polyneuropathy ◽  
The Central Nervous System ◽  
The Impact

Increasing evidence suggests that Severe Acute Respiratory Syndrome-coronavirus-2 (SARS-CoV-2) can also invade the central nervous system (CNS). However, findings available on its neurological manifestations and their pathogenic mechanisms have not yet been systematically addressed. A literature search on neurological complications reported in patients with COVID-19 until June 2020 produced a total of 23 studies. Overall, these papers report that patients may exhibit a wide range of neurological manifestations, including encephalopathy, encephalitis, seizures, cerebrovascular events, acute polyneuropathy, headache, hypogeusia, and hyposmia, as well as some non-specific symptoms. Whether these features can be an indirect and unspecific consequence of the pulmonary disease or a generalized inflammatory state on the CNS remains to be determined; also, they may rather reflect direct SARS-CoV-2-related neuronal damage. Hematogenous versus transsynaptic propagation, the role of the angiotensin II converting enzyme receptor-2, the spread across the blood-brain barrier, the impact of the hyperimmune response (the so-called “cytokine storm”), and the possibility of virus persistence within some CNS resident cells are still debated. The different levels and severity of neurotropism and neurovirulence in patients with COVID-19 might be explained by a combination of viral and host factors and by their interaction.

Abstract W P313: Effects of Organized Stroke Care on In-Hospital Mortality and Morbidity of Patients With Ischemic and Hemorrhagic Stroke: J-ASPECT Study

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Kunihiro Nishimura ◽  
Satoru Kamitani ◽  
Michikazu Nakai ◽  
Akiko Kada ◽  
Fumiaki Nakamura ◽  
...  
Keyword(s):  
Hospital Mortality ◽  
Hemorrhagic Stroke ◽  
Strong Association ◽  
Stroke Care ◽  
Stroke Subtype ◽  
Mortality And Morbidity ◽  
Hierarchical Logistic Regression ◽  
Team Assessment ◽  
Stroke Team ◽  
Level Of Consciousness

Background and Purpose: The effectiveness of organized stroke care on stroke mortality and morbidity remains uncertain. We examined whether organized stroke care index (OCI), which graded 0-3 based on the presence of rehabilitation, stroke team assessment, and admission to a stroke unit developed by Saposnik (Neurology 2010) influence in-hospital mortality and morbidity of patients with ischemic and hemorrhagic stroke in a nationwide study. Methods: Of the 1369 certified training institutions in Japan, 749 hospitals responded to a questionnaire survey regarding comprehensive stroke care capacities. Among the institutions that responded, data on patients hospitalized between April 1, 2010 and March 31, 2011, because of stroke were obtained from the Japanese Diagnosis Procedure Combination database. In-hospital mortality morbidity was analyzed using hierarchical logistic regression analysis adjusted for age, sex, level of consciousness on admission, and the number of OCI fulfilled in each component and in total.It was supported by Grants-in-Aid from the Ministry of Health, Labour and Welfare of Japan Results: Data from 265 institutions and 53,170 emergency-hospitalized patients were analyzed. Patients fulfilled the criteria for admission to a SCU, stroke team assessment and the presence of rehabilitation were 28.9%, 42.1% and 95.1%, respectively. Mortality adjusted for age, sex, and level of consciousness was significantly correlated with admission to a SCU (OR=0.87, p=0.039), SCU team assessment (OR=0.88,p=0.029), and OCI ( OR=0.93, p=0.031). Modified ranking scale 0 to 2 rate were also associated with significantly SCU admission (p=0.003) .These association holds for ischemic stroke and subarachnoid hemorrhage. Conclusion: A strong association between organized stroke care and lower mortality was apparent. These data suggest that organized stroke care should be provided to stroke patients regardless of stroke subtype.

scholarly journals 2587. Etiology and Outcome of Acute Neonatal Infectious Encephalitis

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S899-S899
Author(s):  
Craig Frankel ◽  
Hilary Whyte ◽  
Vann Chau ◽  
Daune MacGregor ◽  
Sanjay Mahant ◽  
...  
Keyword(s):  
Influenza A ◽  
Hemorrhagic Stroke ◽  
Peripheral Leukocyte ◽  
Eeg Abnormalities ◽  
Level Of Consciousness ◽  
Neurologic Sequelae ◽  
Csf Pleocytosis ◽  
Ischemic Encephalopathy ◽  
Infectious Encephalitis ◽  
Infectious Etiology

Abstract Background There are very few studies on acute encephalitis with onset during the neonatal period. The objectives of this study were to investigate the etiology and salient clinical features of neonatal encephalitis. Methods Neonates with possible infectious encephalitis (IE) were prospectively enrolled. Inclusion criteria included encephalopathy (altered/fluctuating level of consciousness ≥24 hours) plus ≥2 of: fever/temperature instability; seizure(s); focal neurologic findings; CSF pleocytosis; EEG abnormalities consistent with encephalitis; neuroimaging abnormalities consistent with encephalitis. Neonates with a clear diagnosis of post-perinatal asphyxial encephalopathy or culture proven bacterial meningitis were excluded. Results shown as absolute numbers, proportions or medians [interquartile range] as appropriate. Results Fifty-nine neonates fulfilled the inclusion/exclusion criteria (June 2013–November 2018). Empiric acyclovir was initiated in 49 (83.1%) cases. An infectious etiology was identified in 25 (42.4%): enteroviruses (n = 15), HSV (n = 5), HHV6 (n = 2), parainfluenza 3 (n = 1), influenza A (n = 1), CMV (n = 1). A noninfectious cause was confirmed in 20 (33.9%): missed hypoxic-ischemic encephalopathy (n = 10), genetic/metabolic disorders (n = 7), ischemic/hemorrhagic stroke (n = 3). No specific etiology was identified in 14 (23.7%). Thirteen (52%) neonates with IE either died (n = 7) or suffered neurologic sequelae (n = 6). Deaths were attributable to HSV (n = 4), enteroviruses (n = 2) and HHV6 (n = 1). Neurocognitive sequelae were documented in one case each of enterovirus, HSV2, HHV6, CMV, parainfluenza 3 and influenza A. Differences between neonates with and without IE, respectively, included age in days of symptom onset (7 [6, 10] vs. 1 [0, 3]; P < 0.001), gestational age (37.0 [36.0, 39.0] vs. 38.6 [37.6, 40.0]; P = 0.045), peripheral leukocyte count (10.5 [IQR 5.9, 14.6] vs. 14.3 [IQR 10.7, 21.7]; P = 0.008) and CSF glucose (2.80 [IQR 2.3, 3.2] vs. 3.10 [2.8, 3.8]; P = 0.003). Conclusion Enteroviruses and HSV are the predominant causes of neonatal IE. Outcome of neonatal IE is poor with approximately half dying or suffering neurologic sequelae. Disclosures All authors: No reported disclosures.

scholarly journals Sav1 Loss Induces Senescence and Stat3 Activation Coinciding with Tubulointerstitial Fibrosis

2017 ◽  
Vol 37 (12) ◽  
Author(s):  
Janet Y. Leung ◽  
Harper L. Wilson ◽  
Kristin J. Voltzke ◽  
Lindsay A. Williams ◽  
Hyo Jin Lee ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
End Stage Renal Disease ◽  
Tubulointerstitial Fibrosis ◽  
Renal Epithelium ◽  
Molecular Events ◽  
Phenotypic Manifestation ◽  
Patients At Risk ◽  
Secretory Phenotype ◽  
Stage Renal Disease ◽  
End Stage

ABSTRACT Tubulointerstitial fibrosis (TIF) is recognized as a final phenotypic manifestation in the transition from chronic kidney disease (CKD) to end-stage renal disease (ESRD). Here we show that conditional inactivation of Sav1 in the mouse renal epithelium resulted in upregulated expression of profibrotic genes and TIF. Loss of Sav1 induced Stat3 activation and a senescence-associated secretory phenotype (SASP) that coincided with the development of tubulointerstitial fibrosis. Treatment of mice with the YAP inhibitor verteporfin (VP) inhibited activation of genes associated with senescence, SASPs, and activation of Stat3 as well as impeded the development of fibrosis. Collectively, our studies offer novel insights into molecular events that are linked to fibrosis development from Sav1 loss and implicate VP as a potential pharmacological inhibitor to treat patients at risk for developing CKD and TIF.

scholarly journals N-Methyl-d-Aspartate (NMDA) Receptor Blockade Prevents Neuronal Death Induced by Zika Virus Infection

mBio ◽  
2017 ◽  
Vol 8 (2) ◽  
Author(s):  
Vivian V. Costa ◽  
Juliana L. Del Sarto ◽  
Rebeca F. Rocha ◽  
Flavia R. Silva ◽  
Juliana G. Doria ◽  
...  
Keyword(s):  
Global Health ◽  
Drug Treatment ◽  
Zika Virus ◽  
Neuronal Death ◽  
Neuronal Damage ◽  
Neurological Complications ◽  
Zikv Infection ◽  
Experimental Animals

ABSTRACT Zika virus (ZIKV) infection is a global health emergency that causes significant neurodegeneration. Neurodegenerative processes may be exacerbated by N-methyl-d-aspartate receptor (NMDAR)-dependent neuronal excitoxicity. Here, we have exploited the hypothesis that ZIKV-induced neurodegeneration can be rescued by blocking NMDA overstimulation with memantine. Our results show that ZIKV actively replicates in primary neurons and that virus replication is directly associated with massive neuronal cell death. Interestingly, treatment with memantine or other NMDAR blockers, including dizocilpine (MK-801), agmatine sulfate, or ifenprodil, prevents neuronal death without interfering with the ability of ZIKV to replicate in these cells. Moreover, in vivo experiments demonstrate that therapeutic memantine treatment prevents the increase of intraocular pressure (IOP) induced by infection and massively reduces neurodegeneration and microgliosis in the brain of infected mice. Our results indicate that the blockade of NMDARs by memantine provides potent neuroprotective effects against ZIKV-induced neuronal damage, suggesting it could be a viable treatment for patients at risk for ZIKV infection-induced neurodegeneration. IMPORTANCE Zika virus (ZIKV) infection is a global health emergency associated with serious neurological complications, including microcephaly and Guillain-Barré syndrome. Infection of experimental animals with ZIKV causes significant neuronal damage and microgliosis. Treatment with drugs that block NMDARs prevented neuronal damage both in vitro and in vivo. These results suggest that overactivation of NMDARs contributes significantly to the neuronal damage induced by ZIKV infection, and this is amenable to inhibition by drug treatment. IMPORTANCE Zika virus (ZIKV) infection is a global health emergency associated with serious neurological complications, including microcephaly and Guillain-Barré syndrome. Infection of experimental animals with ZIKV causes significant neuronal damage and microgliosis. Treatment with drugs that block NMDARs prevented neuronal damage both in vitro and in vivo. These results suggest that overactivation of NMDARs contributes significantly to the neuronal damage induced by ZIKV infection, and this is amenable to inhibition by drug treatment.

Cerebral infarction and femoral venous thrombosis detected in a patient with diabetic ketoacidosis and heterozygous factor V Leiden G1691A and PAI-1 4G/5G mutations

2015 ◽  
Vol 28 (9-10) ◽  
Author(s):  
Selcen Yaroglu Kazanci ◽  
Osman Yesilbas ◽  
Melike Ersoy ◽  
Hasan Serdar Kihtir ◽  
Hamdi Murat Yildirim ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Venous Thrombosis ◽  
Diabetic Ketoacidosis ◽  
Factor V Leiden ◽  
Neurological Complications ◽  
Factor V ◽  
Altered Level ◽  
Femoral Catheter ◽  
Level Of Consciousness ◽  
Pai 1

AbstractCerebral infarction is one of the serious neurological complications of diabetic ketoacidosis (DKA). Especially in patients who are genetically prone to thrombosis, cerebral infarction may develop due to inflammation, dehydration, and hyperviscocity secondary to DKA. A 6-year-old child with DKA is diagnosed with cerebral infarction after respiratory insufficiency, convulsion, and altered level of consciousness. Femoral and external iliac venous thrombosis also developed in a few hours after central femoral catheter had been inserted. Heterozygous type of factor V Leiden and

scholarly journals Microscopic Examination Of Postcapillary Cerebral Venues In Hemorrhagic Stroke

2021 ◽  
Vol 03 (08) ◽  
pp. 69-73
Author(s):  
Khaidarov Nodir Kadyrovich ◽  
◽  
Shomurodov Kahramon Erkinovich ◽  
Kamalova Malika Ilhomovna ◽  
◽  
...  
Keyword(s):  
Hemorrhagic Stroke ◽  
Surgical Intervention ◽  
Neurological Complications ◽  
World Health ◽  
Timely Manner ◽  
Global Response ◽  
Adequate Treatment ◽  
The World ◽  
Circulatory Disorders ◽  
Health Organization

Hemorrhagic stroke among acute cerebral circulatory disorders is characterized by severe neurological complications and the need to choose between surgical intervention or therapeutic therapy. According to the World Health Organization (WHO)". Globally, stroke deaths will reach 7.8 million by 2030 unless an aggressive global response to the epidemic is put in place" 1. Subarachnoid haemorrhage, which accounts for half of the non-traumatic intracerebral haemorrhage, affects the most active and able-bodied population. The most important medical and social objectives are to monitor the course of the disease from the first hours after the onset of stroke, to prescribe adequate treatment in a timely manner, and to reduce mortality and disability rates [5,9].

scholarly journals Modeling Poliovirus Infection Using Human Engineered Neural Tissue Enriched With Motor Neuron Derived From Embryonic Stem Cells

2021 ◽  
Vol 8 ◽  
Author(s):  
Érika Cosset ◽  
Youssef Hibaoui ◽  
Sten Ilmjärv ◽  
Pierre-Yves Dietrich ◽  
Caroline Tapparel ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Motor Neuron ◽  
Motor Neurons ◽  
Embryonic Stem ◽  
Neural Tissue ◽  
Enveloped Virus ◽  
Standardized Protocol ◽  
Molecular Events

Poliomyelitis is caused by poliovirus (PV), a positive strand non-enveloped virus. Since its discovery in the 1950s, several cell culture and molecular methods have been developed to detect and characterize the various strains of PV. Here, we provide an accurate and standardized protocol to differentiate human embryonic stem cells (hESCs) toward engineered neural tissue enriched with motor neurons (MN ENTs). These MN ENTs expressed markers of motor neuron CHAT and Hb-9 as revealed by immunofluorescence staining and quantitative RT-PCR. Interestingly, our results suggest that motor neurons are responsible for the permissiveness of poliovirus within the MN ENTs. Moreover, our study revealed the molecular events occurring upon PV-3 infection in the MN ENTs and highlighted the modulation of a set of genes involved in EGR-EP300 complex. Collectively, we report the development of a reliable in vitro model to investigate the pathophysiology of PV infection, allowing to both design and assess novel therapeutic approaches against PV infection.

scholarly journals Markers of ischemic neuronal damage, neurological complications of carotid endarterectomy and their management depending on anesthesia type

2013 ◽  
Vol 94 (1) ◽  
pp. 13-17
Author(s):  
V V Shmelev ◽  
M I Neymark
Keyword(s):  
Carotid Endarterectomy ◽  
Neurological Disorders ◽  
Neuronal Damage ◽  
Brain Perfusion ◽  
Neurological Status ◽  
Neurological Complications ◽  
Inhalational Anesthesia ◽  
Intravenous Anesthesia ◽  
Cervical Plexus Block ◽  
Plexus Block

Aim. to identify the anesthesia method for carotid endarterectomy providing minimal ischemic neuronal damage and decreasing the number of post-surgical complications; to adjust the optimal treatment for associated neurological disorders. Methods. An assessment of anesthesia methods was performed in 190 patients who underwent the carotid endarterectomy. The intravenous anesthesia with propofol (first group, 60 patients), regional anesthesia using deep cervical plexus block (second group, 60 patients), and inhalational anesthesia with sevoflurane (third group, 70 patients) were compared. Brain perfusion parameters, neurological status, ischemic neuronal damage markers were examined. Results. In patients undergoing carotid endarterectomy an ischemic neuronal damage is provoked due to brain perfusion decrease as a result of common carotid artery clipping regardless of anesthesia method. Inhalational anesthesia was associated with relatively lower ischemic neuronal damage markers levels. Some patients form every group have developed serious post-surgical neurological complications (stroke, transient cerebral ischemic attack, neurological status deterioration). Post-surgical complications were registered in 10 (16.7%) patients from the first group, in 9 (15%) patients form the second group, in 3 (4.3%) patients from the third group. Citicoline was the most effective drug for associated neurological disorders treatment. Conclusion. Inhalational anesthesia with sevoflurane compared to intravenous anesthesia with propofol and regional anesthesia using deep cervical plexus block limits the neuronal damage and is associated with lower number of post-surgical neurological complications, which can be treated with citicoline.

scholarly journals Neurologic Manifestations of SARS-CoV-2, the Virus that Causes COVID-19

2020 ◽  
Vol 2 (6) ◽  
Author(s):  
Hassan Naji
Keyword(s):  
Neuronal Damage ◽  
Transmission Rate ◽  
Case Reports ◽  
Cerebrovascular Disorders ◽  
Case Series ◽  
Cardiac Complications ◽  
Neurologic Manifestations ◽  
Neurological Manifestations ◽  
The Past ◽  
Acute Encephalitis

Coronaviruses have been associated with many outbreaks in the past and the recent pandemic caused by SARS-CoV-2 has spread around the globe due to its high transmission rate. SARS-CoV-2 has reported to be associated with respiratory and cardiac complications, but recent case series and case reports of COVID-19 patients suggest that it is also associated with neurological manifestations. The most commonly observed neurological manifestation are headache, anomia, ageusia, dizziness, delirium and the complications include Guillain-Barre syndrome (GBS), acute encephalitis, acute myelitis, and cerebrovascular disorders. The pathways leading to neuronal damage are the retrograde neuronal and hematogenous pathway. This paper is aimed to explain the neurological manifestations associated with COVID-19 patients and the possible pathophysiological mechanisms of neuronal invasion.

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