Neuropathogenesis and Neurological Manifestations of SARS-CoV-2

Lavienraj Premraj; Rakesh C. Arora; Sung Min Cho

doi:10.1007/978-3-030-94992-1_8

Neuropathogenesis and Neurological Manifestations of SARS-CoV-2

Lavienraj Premraj, Rakesh C. Arora, Sung Min Cho

School of Medicine

Research output: Chapter in Book/Report/Conference proceeding › Chapter

Abstract

Neurological complications of COVID-19 contribute significantly to mortality in the intensive care unit (ICU). Preventive therapy, though discussed in literature, is limited for COVID-19 neurological manifestations and treatment algorithms continue to rely on evidence from previous pandemics. Thus, in this chapter we evaluate current in vitro, in vitro, histopathological studies to ascertain the most likely mechanisms of SARS-CoV-2 central nervous system entry. From this understanding, we determine probable mechanisms for neurological compilations observed in COVID-19 as relevant to the clinician. SARS-CoV-2 infection of nasal epithelium and the respiratory tract may allow for a systemic inflammatory response that results in neuroinflammation. While most neurological complications are inflammatory in etiology, rarely, SARS-CoV-2 may enter into the central nervous system and mediate neuronal damage.

Original language	English (US)
Title of host publication	COVID-19 Critical and Intensive Care Medicine Essentials
Publisher	Springer International Publishing
Pages	85-100
Number of pages	16
ISBN (Electronic)	9783030949921
ISBN (Print)	9783030949914
DOIs	https://doi.org/10.1007/978-3-030-94992-1_8
State	Published - Jan 1 2022

Keywords

Angiotensin converting enzyme-2 cellular receptor
Blood-brain-barrier
Blood-cerebrospinal fluid-barrier
COVID-19
Intracranial hemorrhage
Magnetic resonance imaging
Olfactory epithelium
Olfactory sense neurons
Transmembrane protease, ser ine 2

ASJC Scopus subject areas

General Medicine
General Immunology and Microbiology

Access to Document

10.1007/978-3-030-94992-1_8

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abstract = "Neurological complications of COVID-19 contribute significantly to mortality in the intensive care unit (ICU). Preventive therapy, though discussed in literature, is limited for COVID-19 neurological manifestations and treatment algorithms continue to rely on evidence from previous pandemics. Thus, in this chapter we evaluate current in vitro, in vitro, histopathological studies to ascertain the most likely mechanisms of SARS-CoV-2 central nervous system entry. From this understanding, we determine probable mechanisms for neurological compilations observed in COVID-19 as relevant to the clinician. SARS-CoV-2 infection of nasal epithelium and the respiratory tract may allow for a systemic inflammatory response that results in neuroinflammation. While most neurological complications are inflammatory in etiology, rarely, SARS-CoV-2 may enter into the central nervous system and mediate neuronal damage.",

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author = "Lavienraj Premraj and Arora, {Rakesh C.} and Cho, {Sung Min}",

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AU - Cho, Sung Min

N1 - Publisher Copyright: © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2022.

PY - 2022/1/1

Y1 - 2022/1/1

N2 - Neurological complications of COVID-19 contribute significantly to mortality in the intensive care unit (ICU). Preventive therapy, though discussed in literature, is limited for COVID-19 neurological manifestations and treatment algorithms continue to rely on evidence from previous pandemics. Thus, in this chapter we evaluate current in vitro, in vitro, histopathological studies to ascertain the most likely mechanisms of SARS-CoV-2 central nervous system entry. From this understanding, we determine probable mechanisms for neurological compilations observed in COVID-19 as relevant to the clinician. SARS-CoV-2 infection of nasal epithelium and the respiratory tract may allow for a systemic inflammatory response that results in neuroinflammation. While most neurological complications are inflammatory in etiology, rarely, SARS-CoV-2 may enter into the central nervous system and mediate neuronal damage.

AB - Neurological complications of COVID-19 contribute significantly to mortality in the intensive care unit (ICU). Preventive therapy, though discussed in literature, is limited for COVID-19 neurological manifestations and treatment algorithms continue to rely on evidence from previous pandemics. Thus, in this chapter we evaluate current in vitro, in vitro, histopathological studies to ascertain the most likely mechanisms of SARS-CoV-2 central nervous system entry. From this understanding, we determine probable mechanisms for neurological compilations observed in COVID-19 as relevant to the clinician. SARS-CoV-2 infection of nasal epithelium and the respiratory tract may allow for a systemic inflammatory response that results in neuroinflammation. While most neurological complications are inflammatory in etiology, rarely, SARS-CoV-2 may enter into the central nervous system and mediate neuronal damage.

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KW - Blood-cerebrospinal fluid-barrier

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KW - Magnetic resonance imaging

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KW - Olfactory sense neurons

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PB - Springer International Publishing

ER -

Neuropathogenesis and Neurological Manifestations of SARS-CoV-2

Abstract

Keywords

ASJC Scopus subject areas

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