Covid-19-Induced Dysautonomia: A Menace of Sympathetic Storm.
ASN Neuro
; 13: 17590914211057635, 2021.
Article
in English
| MEDLINE | ID: covidwho-1511685
ABSTRACT
Among the plethora of debilitating neurological disorders of COVID-19 syndrome in survivors, the scope of SARS-CoV-2-induced dysautonomia (DNS) is yet to be understood, though the implications are enormous. Herein, we present an inclusive mini-review of SARS-CoV-2-induced DNS and its associated complications. Although, the direct link between Covid-19 and DSN is still speculative, the hypothetical links are thought to be either a direct neuronal injury of the autonomic pathway or a para/post-infectious immune-induced mechanism. SARS-CoV-2 infection-induced stress may activate the sympathetic nervous system (SNS) leading to neuro-hormonal stimulation and activation of pro-inflammatory cytokines with further development of sympathetic storm. Sympathetic over-activation in Covid-19 is correlated with increase in capillary pulmonary leakage, alveolar damage, and development of acute respiratory distress syndrome. Furthermore, SARS-CoV-2 can spread through pulmonary mechanoreceptors and chemoreceptors to medullary respiratory center in a retrograde manner resulting in sudden respiratory failure. Taken together, DSN in Covid-19 is developed due to sympathetic storm and inhibition of Parasympathetic nervous system-mediated anti-inflammatory effect with development of cytokine storm. Therefore, sympathetic and cytokine storms together with activation of Renin-Angiotensin-System are the chief final pathway involved in the development of DSN in Covid-19.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Renin-Angiotensin System
/
Angiotensin-Converting Enzyme Inhibitors
/
Angiotensin II Type 1 Receptor Blockers
/
COVID-19
Type of study:
Cohort study
/
Observational study
/
Prognostic study
Limits:
Aged
/
Female
/
Humans
/
Male
/
Middle aged
Country/Region as subject:
Europa
Language:
English
Journal:
ASN Neuro
Journal subject:
Neurology
/
Chemistry
Year:
2021
Document Type:
Article
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