Cargando…
COVID-19 Encephalopathy in Adults
Many patients with COVID-19 are asymptomatic. However, among the patients that are symptomatic, influenza-like illnesses including fever, myalgia and respiratory symptoms seem to be the most common presentation across age groups. Though respiratory illness seems to be the primary presentation, about...
Autores principales: | , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cureus
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7885743/ https://www.ncbi.nlm.nih.gov/pubmed/33643747 http://dx.doi.org/10.7759/cureus.13052 |
Sumario: | Many patients with COVID-19 are asymptomatic. However, among the patients that are symptomatic, influenza-like illnesses including fever, myalgia and respiratory symptoms seem to be the most common presentation across age groups. Though respiratory illness seems to be the primary presentation, about 36.4% to 69% of hospitalized COVID-19 patients have exhibited neurological manifestations. We present two patients who were hospitalized for the presenting symptom of acute encephalopathy. Both the patients regained consciousness within 24 to 48 hours of initiating treatment. The first patient was known to have mild cognitive impairment and a thorough work-up was done in the emergency department which did not reveal any other causes apart from positive SARS-CoV-2 rapid PCR test. The second patient was from a long-term care facility with underlying dementia, usually alert, awake and oriented to self and presented with severe encephalopathy with a Glasgow Coma Scale of 3 on admission. Her work up was notable only for a positive SARS-CoV-2 rapid polymerase chain reaction test. Both patients responded well to standard remdesivir and steroid therapy and returned to baseline cognition. SARS-COV 2 virus appears to be a causative agent of acute onset encephalopathy. Very little is known about the pathophysiology of neurological manifestations in COVID-19 illness. There are several theoretical possibilities of pathogenesis such as of blood-brain barrier disruption secondary to SARS-CoV-2 binding to angiotensin-converting enzyme 2, autoimmune sequelae, ischemic injury via systemic hypoxia or local vascular endothelial information or thrombosis, toxic metabolic encephalopathies and long-term impact of systemic proinflammatory state that have been considered. |
---|