Investigating the possible mechanisms of autonomic dysfunction post-COVID-19.
Auton Neurosci
; 245: 103071, 2023 03.
Article
in English
| MEDLINE | ID: covidwho-2231377
ABSTRACT
Patients with long COVID suffer from many neurological manifestations that persist for 3 months following infection by SARS-CoV-2. Autonomic dysfunction (AD) or dysautonomia is one complication of long COVID that causes patients to experience fatigue, dizziness, syncope, dyspnea, orthostatic intolerance, nausea, vomiting, and heart palpitations. The pathophysiology behind AD onset post-COVID is largely unknown. As such, this review aims to highlight the potential mechanisms by which AD occurs in patients with long COVID. The first proposed mechanism includes the direct invasion of the hypothalamus or the medulla by SARS-CoV-2. Entry to these autonomic centers may occur through the neuronal or hematogenous routes. However, evidence so far indicates that neurological manifestations such as AD are caused indirectly. Another mechanism is autoimmunity whereby autoantibodies against different receptors and glycoproteins expressed on cellular membranes are produced. Additionally, persistent inflammation and hypoxia can work separately or together to promote sympathetic overactivation in a bidirectional interaction. Renin-angiotensin system imbalance can also drive AD in long COVID through the downregulation of relevant receptors and formation of autoantibodies. Understanding the pathophysiology of AD post-COVID-19 may help provide early diagnosis and better therapy for patients.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Autonomic Nervous System Diseases
/
Orthostatic Intolerance
/
COVID-19
Type of study:
Screening_studies
Topics:
Long Covid
Limits:
Humans
Language:
English
Journal:
Auton Neurosci
Journal subject:
Neurology
Year:
2023
Document Type:
Article
Affiliation country:
J.autneu.2022.103071
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