Table 1.
List of Pathomechanisms Suspected in the Development of Long-COVID/PASC and Their Potential Effect on the Outcome After Various Severities of TBI
Pathomechanism(s) (selected) | Level of evidence in the pathomechanism of long-COVID/PASC |
Potential influence/effect on outcome after
|
||
---|---|---|---|---|
miTBI | MoTBI | sTBI | ||
Direct | ||||
Direct viral invasion and/or viral reservoirs in the CNS | Low/uncertain67,68,244,245 | ? | ? | ? |
Definition: presence of the virus and/or viral particles in cells of the CNS | ||||
Indirect | ||||
Endothelial damage/dysfunction/(micro)vascular injury | Moderate to high64,70,75–77,93 | +++ | +++ | +++ |
Definition: abnormal vascular functions, more reactive endothelial phenotype, injury, blockage of small vessels including capillaries | ||||
Abnormal coagulation | High (after severe COVID-19)79,246,247 | +++ | +++ | +++ |
Definition: disruptions in the body's ability to control blood clotting | ||||
Inflammation | High (after severe COVID-19)81,89,107,248–250 | +/– | ++ | +++ |
Definition: maladaptive immune response | ||||
Abnormal immunometabolism | Moderate84–87,251 | +/– | ++ | +++ |
Definition: changes in intracellular metabolic pathways of immune cells that alter their functionality |
PASC, post-acute sequelae of SARS-CoV-2 infection; TBI, traumatic brain injury; CNS, central nervous system; COVID-19, coronavirus disease 19.