Mecanismos fisiopatológicos asociados al daño neurológico por Covid-19

Pathophysiological mechanisms involved in neurological damage by Covid-19

Contenido principal del artículo

Jose Gaya
Odalys Puentes Corrales
Iliana Alonso Rodríguez
Liliam Leyva Medrano
Adonisbel Mario Valero Sanchez
Yoelvis Cesar Del Pozo Burgos

Resumen

Introducción: en diciembre 2019, se reportó en China la presencia de un nuevo coronavirus que, se clasificó y denominó como Síndrome Respiratorio Agudo Severo-Coronavirus 2 (SARS-CoV-2), causante de la enfermedad pandémica Covid-19. Este virus es capaz de producir daño adicional en el sistema nervioso y provocar síntomas y complicaciones neurológicas. Objetivo: describir los principales mecanismos fisiopatológicos que explican el daño neurológico reportado en la enfermedad Covid-19. Métodos: se realizó una selección de artículos científicos publicados entre 2019 y 2021, utilizando el repositorio electrónico de PubMed/ScienceDirect (y artículos de libre acceso en las Bases/Datos de Scopus, MedLine, Scielo y LILACs) según las recomendaciones del tesauro DeCS (Descriptores en Ciencias de la Salud) para operadores lógicos y descriptores sobre esta temática. Resultados: aunque, se considera una enfermedad típicamente respiratoria, se han descrito una serie de manifestaciones extra-pulmonares como posibles síntomas de presentación y/o complicaciones, en pacientes con Covid-19. El coronavirus SARS-CoV-2, tiene propiedades neuroinvasivas, neurotrópicas y pro-inflamatorias capaces de exacerbar el proceso neurodegenerativo que provoca la enfermedad. Se ha reportado que entre 30-80% de los pacientes con Covid-19 suelen presentar síntomas neurológicos. Conclusión: esta revisión describe los principales fundamentos fisiopatológicos invocados para intentan explicar los mecanismos que determinan la generación de enfermedad y complicaciones neurológicas en la infección por Covid-19. Las manifestaciones neurológicas reportadas en los pacientes infectados pueden deberse a invasión viral directa (propiedades neurotrópicas) o mecanismos indirectos (derivados del estado infeccioso post-inflamatorio, alteraciones metabólicas y desregulaciones de la respuesta inmune).

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