International Medical Journal, Vol. 27., Iss. 1, 2021, P. 67−72.
CEREBROVASCULAR DISORDERS IN PATIENTS WITH COVID-19
Kharkiv Medical Academy of Postgraduate Education, Ukraine
COVID−19 is an acute respiratory viral disease caused by the RNA virus of the SARS−CoV−2 (2019 nCoV) coronavirus family and can have both mild course in the form of acute respiratory viral infection and severe one with frequent complications such as pneumonia, thrombosis, cerebrovascular disorders and high mortality. Hypoxia of the brain and spinal cord is associated with impaired gas exchange in the pulmonary alveoli, progressive respiratory failure with subsequent decompensation of function and structural damage to all organs and systems. Neurological disorders in COVID−19, observed in almost a half of patients, can be divided into three groups: manifestations of the central nervous system, lesions of the peripheral nervous system, myopathy. In order to study the lesion of the nervous system in patients with COVID−19, a history of acute cerebrovascular disorders and clinical picture of stroke without the emergence of new foci in neuroimaging, three clinical cases were analyzed. All patients complained of speech impairment, disorientation in time and space, numbness and weakness in the extremities on the background of acute cerebrovascular accident in the anamnesis, accompanied by general weakness and fever to subfebrile figures. COVID−19 pneumonia was observed during computed tomography of the lungs. However, during neuroimaging new foci of infarction were not identified. Thus, given the lack of new foci of infarction during neuroimaging, lack of hypercoagulation and cardiac causes, it can be concluded that focal symptoms in patients with COVID−19 with a history of stroke cause hypoxia of brain cells in the area around the necrotic foci resulted from previous heart attacks.
Key words: nervous system, lesions, COVID−19, coronaviruses, encephalopathy, hypoxia.
1. Temporary guidelines for the prevention, diagnosis, and treatment of new coronavirus infection (COVID−19) / E. G. Kamkin et al. Version 6 (28.04.2020). (In Russ.). URL: https://static−1. rosminzdrav.ru/system/attachments/attaches/000/050/116/ original/28042020_ %D0 %9CR_COVID−19_v6.pdf (accessed: 12.05.2020)
2. David L. Heymann, Nahoko Shindo. COVID−19: what is next for public health? // The Lancet. 2020. doi: 10.1016/S0140−6736(20)30374−3
3. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China / C. Huang et al. // The Lancet. 2020. Vol. 395 (10223). P. 497−506.
4. Pezzini A., Padovani A. Lifting the mask on neurological manifestations of COVID−19 // Nat. Rev. Neurol. 2020. Vol. 16 (11). P. 636. https://doi.org/10.1038/s41582−020−0398−3
5. Neurochemical evidence of astrocytic and neuronal injury commonly found in COVID−19 / N. Kanberg et al. // Neurology. 2020. Vol. 95 (12). e1754. https://doi.org/10.1212/wnl.0000000000010111
6. Cerebral microbleeds and leukoencephalopathy in critically ill patients with COVID−19 / S. Agarwal et al. // Stroke. 2020. Vol. 51 (9). P. 2649. https://doi.org/10.1161/strokeaha.120.030940
7. Coronavirus infections in the central nervous system and respiratory tract show distinct features in hospitalized children / Y. Li et al. // Intervirology. 2016. Vol. 59 (3). P. 163−169. https://doi.org/10.1159/000453066
8. Non−invasive bioluminescence imaging of HCoV−OC43 infection and therapy in the central nervous system of live mice / J. Niu et al. // Antiviral Res. 2020. Vol. 173. P. 104646. https://doi.org/10.1016/j.antiviral.2019.104646
9. Activation of human monocytes after infection by human coronavirus 229E / M. Desforges et al. // Virus Res. 2007. Vol. 130 (1−2). P. 228−240. https://doi.org/10.1016/j.virusres.2007.06.016
10. Expression of severe acute respiratory syndrome coronavirus receptors, ACE2 and CD209L in different organ derived microvascular endothelial cells // Zhonghua Yi Xue Za Zhi. 2007. Vol. 87 (12). P. 833−837.
11. Neurotropic virus tracing suggests a membranous−coating−mediated mechanism for transsynaptic communication / Y. C. Li et al. // J. Comp. Neurol. 2013. Vol. 521 (1). P. 203−212. https://doi.org/10.1002/cne.23171
12. Neurologic manifestations of hospitalized patients with coronavirus disease 2019 in Wuhan, China / L. Mao et al. // JAMA Neurol. 2020. Vol. 77 (6). P. 683.
13. Neurologic Features in Severe SARS−CoV−2 Infection / J. Helms et al. // Engl. J. Med. 2020. Vol. 382 (23). P. 2268.
14. Neurological manifestations of COVID−19 and other coronavirus infections: A systematic review / V. Montalvan et al. // Clin. Neurol. Neurosurg. 2020. Vol. 194. P. 105921. https://doi.org/10.1016/j.clineuro.2020.105921
15. Neurologic manifestations in hospitalized patients with COVID−19: The ALBACOVID registry / C. M. Romero−Sánchez et al. // Neurology. 2020. Vol. 95 (8). e1060.
16. Koralnik I. J., Tyler K. L. COVID−19: A global threat to the nervous system // Ann. Neurol. 2020. Vol. 88 (1). P. 1.
17. New onset neurologic events in people with COVID−19 in 3 regions in China / W. Xiong et al. // Neurology. 2020. Vol. 95 (11):e1479.
18. Machado C., Gutierrez J. Brainstem dysfunction SAR−COV−2 infection can be a potentional cause of respiratory distress (Review article). Preprint. April 2020. doi: 10.20944/preprints202004.0330.v1
19. Liu W., Li H. COVID−19 attacks the 1−beta chain of hemoglobin and captures the porphyrin to inhibit human heme metabolism // ChemRxiv. 2020. Preprint.
20. Hypercoagulability of COVID−19 patients in Intensive Care Unit. A report of thromboelastography findings and other parameters of hemostasis / M. Panigada et al. // J. Thromb. Haemost. 2020. https://doi.org/10.1111/jth.14850
21. Tang N., Li D., Wang X., Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia // J. Thromb. Haemost. 2020. Vol. 18. P. 844−847. https://doi.org/10.1111/jth.14768