Title:Coagulopathy and Brain Injury Pathogenesis in Post-Covid-19 Syndrome
Volume: 20
Issue: 3
Author(s): Basheer Abdullah Marzoog*
Affiliation:
- National Research Mordovia State University, Bolshevitskaya Street, 68, Saransk 430005, Rep. Mordovia
Keywords:
Homeostasis & hemostasis, COVID-19 & SARS-CoV2, coagulopathy, endothelial dysfunction, pathogenesis & pathophysiology, post-COVID syndrome, neurology.
Abstract: The post-COVID neurological syndrome has been coined, which describes the functional
and structural sequelae of coronavirus infection disease-19 (COVID-19) in the brain.
Mild/severe manifestations of the post-COVID neurological syndrome have been identified in
approximately 33.00% of COVID-19 survivors. The presence of neurological complications after
COVID allowed neuropathologists to investigate in-depth the role of viral infection in neurons.
The pathophysiology of the post-COVID neurological syndrome involved the development of a
systematic response, including coagulopathy characterized by the formation of microthrombi. Coagulopathy,
an old term for a new disease, describes the discrepancy between pro-coagulant and
anticoagulant systems due to overexpression of pro-coagulant substances and or their receptors in
addition to suppression of the anticoagulant molecules and or their receptors. Vascular endothelial
cells and hepatocytes play a central role in the regulation of hemostasis that is disrupted during the
acute phase response (APR) of coronavirus-19 (COVID-19). Currently, coagulopathy and inflammation
are termed together since both form a complementary system, indicated by the elevation of
inflammatory biomarkers (APR) and fibrinolysis biomarkers (D-dimer/fibrin). The later events of
the post-COVID neurological syndrome are primarily induced by coagulopathy and direct viral
tropism. Therefore, the paper introduces the hypothesis of coagulopathy induced post-COVID
neurological syndrome.