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COVID-19-Associated Encephalopathy: Systematic Review of Case Reports
BACKGROUND AND PURPOSE: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily attacks the respiratory system, but there are also several reports of the involvement of the central nervous system, with one of the manifestations being encephalopathy. The relatively new emergence of COV...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Korean Neurological Association
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8926776/ https://www.ncbi.nlm.nih.gov/pubmed/35196749 http://dx.doi.org/10.3988/jcn.2022.18.2.194 |
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author | Siahaan, Yusak Mangara Tua Puspitasari, Vivien Pangestu, Aristo |
author_facet | Siahaan, Yusak Mangara Tua Puspitasari, Vivien Pangestu, Aristo |
author_sort | Siahaan, Yusak Mangara Tua |
collection | PubMed |
description | BACKGROUND AND PURPOSE: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily attacks the respiratory system, but there are also several reports of the involvement of the central nervous system, with one of the manifestations being encephalopathy. The relatively new emergence of COVID-19 means that few studies have investigated the clinical profile of encephalopathy associated with this disease. This study aimed to determine the clinical profile, laboratory, and imaging results of encephalopathy associated with COVID-19. METHODS: Three databases, namely PubMed/MEDLINE, Embase, and Scopus, were systematically searched for case reports and case series related to COVID-19-associated encephalopathy published from January 1, 2019 to July 20, 2020. RESULTS: This review included 24 studies involving 33 cases. The most-reported neurological symptoms were disorientation/confusion (72.72%), decreased consciousness (54.54%), and seizures (27.27%). Laboratory examinations revealed increases in the C-reactive protein level (48.48%), the lactate dehydrogenase level (30.30%), and lymphopenia (27.27%). Brain imaging did not produce any pathological findings in 51.51% of the cases. Electroencephalography showed generalized slowing in 45.45% of the cases. Elevated protein (42.42%) and lymphocytosis (24.24%) were found in the cerebrospinal fluid. Fifteen patients were reportedly discharged from the hospital in a stable condition, while four cases of mortality were recorded. CONCLUSIONS: The clinical, laboratory, and imaging findings in this review support the hypothesis that cerebral damage in COVID-19-associated encephalopathy is caused by cytokine-immune-mediated inflammation rather than by direct invasion. |
format | Online Article Text |
id | pubmed-8926776 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Korean Neurological Association |
record_format | MEDLINE/PubMed |
spelling | pubmed-89267762022-03-24 COVID-19-Associated Encephalopathy: Systematic Review of Case Reports Siahaan, Yusak Mangara Tua Puspitasari, Vivien Pangestu, Aristo J Clin Neurol Original Article BACKGROUND AND PURPOSE: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily attacks the respiratory system, but there are also several reports of the involvement of the central nervous system, with one of the manifestations being encephalopathy. The relatively new emergence of COVID-19 means that few studies have investigated the clinical profile of encephalopathy associated with this disease. This study aimed to determine the clinical profile, laboratory, and imaging results of encephalopathy associated with COVID-19. METHODS: Three databases, namely PubMed/MEDLINE, Embase, and Scopus, were systematically searched for case reports and case series related to COVID-19-associated encephalopathy published from January 1, 2019 to July 20, 2020. RESULTS: This review included 24 studies involving 33 cases. The most-reported neurological symptoms were disorientation/confusion (72.72%), decreased consciousness (54.54%), and seizures (27.27%). Laboratory examinations revealed increases in the C-reactive protein level (48.48%), the lactate dehydrogenase level (30.30%), and lymphopenia (27.27%). Brain imaging did not produce any pathological findings in 51.51% of the cases. Electroencephalography showed generalized slowing in 45.45% of the cases. Elevated protein (42.42%) and lymphocytosis (24.24%) were found in the cerebrospinal fluid. Fifteen patients were reportedly discharged from the hospital in a stable condition, while four cases of mortality were recorded. CONCLUSIONS: The clinical, laboratory, and imaging findings in this review support the hypothesis that cerebral damage in COVID-19-associated encephalopathy is caused by cytokine-immune-mediated inflammation rather than by direct invasion. Korean Neurological Association 2022-03 2022-02-14 /pmc/articles/PMC8926776/ /pubmed/35196749 http://dx.doi.org/10.3988/jcn.2022.18.2.194 Text en Copyright © 2022 Korean Neurological Association https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Siahaan, Yusak Mangara Tua Puspitasari, Vivien Pangestu, Aristo COVID-19-Associated Encephalopathy: Systematic Review of Case Reports |
title | COVID-19-Associated Encephalopathy: Systematic Review of Case Reports |
title_full | COVID-19-Associated Encephalopathy: Systematic Review of Case Reports |
title_fullStr | COVID-19-Associated Encephalopathy: Systematic Review of Case Reports |
title_full_unstemmed | COVID-19-Associated Encephalopathy: Systematic Review of Case Reports |
title_short | COVID-19-Associated Encephalopathy: Systematic Review of Case Reports |
title_sort | covid-19-associated encephalopathy: systematic review of case reports |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8926776/ https://www.ncbi.nlm.nih.gov/pubmed/35196749 http://dx.doi.org/10.3988/jcn.2022.18.2.194 |
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