Dysfunction of the hemostasis systemin patients with multiple sclerosis and coronavirus infection

Abstract

Multiple sclerosis is a chronic demyelinating disease of the central nervous system, accompanied by a disruption of the blood-brain barrier, the development of neuroinflammation, demyelination, and neurodegeneration. The coronavirus infection pandemic can manifest symptoms affecting the nervous system and exacerbate existing neurological pathology. The SARS-CoV-2 virus disrupts the integrity of the blood-brain barrier through the massive release of cytokines and proteases, activating microglia and oligodendrocytes, which initiate neuroinflammatory and neurodegenerative processes. Experimental studies have demonstrated that coronaviruses can lead to demyelination and provoke exacerbations of multiple sclerosis in affected women. Dysfunction of cerebral endothelium and platelet activation plays a crucial role both in the pathophysiology of multiple sclerosis and coronavirus infection, linking disorders of the primary hemostasis system with neuroinflammation. A close connection has been established between coagulation, inflammation, and immune reactions that occur within the vascular system. There is a hypothesis that coagulation activation at the neurovascular level may contribute to the emergence and maintenance of inflammatory reactions characteristic of multiple sclerosis pathogenesis. This occurs as a result of fibrinogen penetration through the compromised blood-brain barrier, which correlates with areas of axonal damage and results in the unwanted activation of microglia and macrophages, intensifying neuroinflammation. Dysfunction of the hemostasis system in patients with multiple sclerosis and COVID-19 can lead to a worsening of the disease course, deterioration of neurological status, and unsatisfactory treatment outcomes.