Encephalopathy in COVID-19 patients; viral, parainfectious, or both?

We describe the clinical, laboratory and radiological features of 3 critically ill patients with COVID-19 who developed severe encephalopathy. The first patient did not regain consciousness when sedation was removed at the end of 2 weeks of intensive care. He had received treatment with convalescent...

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Autores:
Tipo de recurso:
Article of investigation
Fecha de publicación:
2020
Institución:
Universidad de Bogotá Jorge Tadeo Lozano
Repositorio:
Expeditio: repositorio UTadeo
Idioma:
eng
OAI Identifier:
oai:expeditiorepositorio.utadeo.edu.co:20.500.12010/14269
Acceso en línea:
https://doi.org/10.1016/j.ensci.2020.100275
http://hdl.handle.net/20.500.12010/14269
Palabra clave:
Encephalopathy
COVID-19
Patients
Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
Rights
License
Abierto (Texto Completo)
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dc.title.spa.fl_str_mv Encephalopathy in COVID-19 patients; viral, parainfectious, or both?
title Encephalopathy in COVID-19 patients; viral, parainfectious, or both?
spellingShingle Encephalopathy in COVID-19 patients; viral, parainfectious, or both?
Encephalopathy
COVID-19
Patients
Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
title_short Encephalopathy in COVID-19 patients; viral, parainfectious, or both?
title_full Encephalopathy in COVID-19 patients; viral, parainfectious, or both?
title_fullStr Encephalopathy in COVID-19 patients; viral, parainfectious, or both?
title_full_unstemmed Encephalopathy in COVID-19 patients; viral, parainfectious, or both?
title_sort Encephalopathy in COVID-19 patients; viral, parainfectious, or both?
dc.subject.spa.fl_str_mv Encephalopathy
COVID-19
Patients
topic Encephalopathy
COVID-19
Patients
Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
dc.subject.lemb.spa.fl_str_mv Síndrome respiratorio agudo grave
COVID-19
SARS-CoV-2
Coronavirus
description We describe the clinical, laboratory and radiological features of 3 critically ill patients with COVID-19 who developed severe encephalopathy. The first patient did not regain consciousness when sedation was removed at the end of 2 weeks of intensive care. He had received treatment with convalescent plasma. His clinical examination was remarkable for intact brainstem reflexes, roving eye movements, later transient ocular flutter; and then what appeared to be slow ocular dipping. He had no coherent volitional response to the environment. The second patient recovered with measurable cognitive deficits after a prolonged period of encephalopathy. He had received combination treatment with interferon beta 1b and lopinavir/ritonavir. The third patient remained in persistent, severe agitated delirium and died 3 months into his illness. The MRI of the 3 patients showed multifocal abnormalities predominantly in the cerebral white matter, with varying involvement of the grey matter, brainstem and spinal cord. Case 1’s MRI changes were consistent with acute disseminated encephalomyelitis. The patients also displayed blood markers, to varying degree, of autoimmunity and hypercoagulability. We were not able to convincingly show, from microbiological as well as immunological evaluation, if the effects of COVID-19 on these patients’ nervous system were a direct consequence of the virus, proinflammatory-thrombotic state or a combination. Patient 1 responded partially to empirical, albeit delayed, therapy with intravenous immunoglobulins. Patient 2 recovered with no specific treatment. These cases illustrate the need to understand the full spectrum of encephalopathy associated with COVID-19 so as to better guide its management. (word count 247)
publishDate 2020
dc.date.accessioned.none.fl_str_mv 2020-10-06T19:30:48Z
dc.date.available.none.fl_str_mv 2020-10-06T19:30:48Z
dc.date.created.none.fl_str_mv 2020
dc.type.local.spa.fl_str_mv Artículo
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format http://purl.org/coar/resource_type/c_2df8fbb1
dc.identifier.issn.spa.fl_str_mv 2405-6502
dc.identifier.other.spa.fl_str_mv https://doi.org/10.1016/j.ensci.2020.100275
dc.identifier.uri.none.fl_str_mv http://hdl.handle.net/20.500.12010/14269
dc.identifier.doi.spa.fl_str_mv https://doi.org/10.1016/j.ensci.2020.100275
identifier_str_mv 2405-6502
url https://doi.org/10.1016/j.ensci.2020.100275
http://hdl.handle.net/20.500.12010/14269
dc.language.iso.spa.fl_str_mv eng
language eng
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dc.rights.local.spa.fl_str_mv Abierto (Texto Completo)
rights_invalid_str_mv Abierto (Texto Completo)
http://purl.org/coar/access_right/c_abf2
dc.format.extent.spa.fl_str_mv 23 páginas
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dc.publisher.spa.fl_str_mv eNeurologicalSci
dc.source.spa.fl_str_mv reponame:Expeditio Repositorio Institucional UJTL
instname:Universidad de Bogotá Jorge Tadeo Lozano
instname_str Universidad de Bogotá Jorge Tadeo Lozano
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reponame_str Expeditio Repositorio Institucional UJTL
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spelling 2020-10-06T19:30:48Z2020-10-06T19:30:48Z20202405-6502https://doi.org/10.1016/j.ensci.2020.100275http://hdl.handle.net/20.500.12010/14269https://doi.org/10.1016/j.ensci.2020.100275We describe the clinical, laboratory and radiological features of 3 critically ill patients with COVID-19 who developed severe encephalopathy. The first patient did not regain consciousness when sedation was removed at the end of 2 weeks of intensive care. He had received treatment with convalescent plasma. His clinical examination was remarkable for intact brainstem reflexes, roving eye movements, later transient ocular flutter; and then what appeared to be slow ocular dipping. He had no coherent volitional response to the environment. The second patient recovered with measurable cognitive deficits after a prolonged period of encephalopathy. He had received combination treatment with interferon beta 1b and lopinavir/ritonavir. The third patient remained in persistent, severe agitated delirium and died 3 months into his illness. The MRI of the 3 patients showed multifocal abnormalities predominantly in the cerebral white matter, with varying involvement of the grey matter, brainstem and spinal cord. Case 1’s MRI changes were consistent with acute disseminated encephalomyelitis. The patients also displayed blood markers, to varying degree, of autoimmunity and hypercoagulability. We were not able to convincingly show, from microbiological as well as immunological evaluation, if the effects of COVID-19 on these patients’ nervous system were a direct consequence of the virus, proinflammatory-thrombotic state or a combination. Patient 1 responded partially to empirical, albeit delayed, therapy with intravenous immunoglobulins. Patient 2 recovered with no specific treatment. These cases illustrate the need to understand the full spectrum of encephalopathy associated with COVID-19 so as to better guide its management. 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