Cognitive disorders of patients with cerebrovascular disorders who suffered from COVID-19

doi:10.26565/2312-5675-2023-22-03

Mischenko Vladyslav State Institution ‘‘Institute of Neurology, Psychiatry and Narcology of the National Academy of Medical Sciences of Ukraine’’, Akademika Pavlova, 46, Kharkiv, Ukraine, 61068 https://orcid.org/0000-0003-0429-8572
Dmytriieva Olena State Institution ‘‘Institute of Neurology, Psychiatry and Narcology of the National Academy of Medical Sciences of Ukraine’’, Akademika Pavlova, 46, Kharkiv, Ukraine, 61068 https://orcid.org/0009-0006-5595-1390
Zdesenko Iryna State Institution ‘‘Institute of Neurology, Psychiatry and Narcology of the National Academy of Medical Sciences of Ukraine’’, Akademika Pavlova, 46, Kharkiv, Ukraine, 61068 https://orcid.org/0000-0001-8811-2004
Lehka Mariia State Institution ‘‘Institute of Neurology, Psychiatry and Narcology of the National Academy of Medical Sciences of Ukraine’’, Akademika Pavlova, 46, Kharkiv, Ukraine, 61068

DOI: https://doi.org/10.26565/2312-5675-2023-22-03

Keywords: COVID-19, cognitive disorders, cerebrovascular pathology

Abstract

The purpose of the research was to study the features of cognitive functions in COVID-19 patients with chronic cerebrovascular
disorders. It has been discovered, that by all patients, who have recovered from COVID-19, moderate and severe cognitive impairments
were identified. In this group of patients a significant progression of cognitive deficit was noted in compared to the group of patients
without COVID-19. The main forms of disorders in COVID-19 patients with cerebrovascular pathology, were violations of attention and
decreasing of information processing speed, and disorders of short-term working memory, instead long-term memory and recognition
memory suffered much less. Our research demonstrated better sensitivity of the MoCA scale for detecting cognitive impairment in
COVID-19 patients with cerebrovascular pathology. The majority of patients had cognitive impairment within 6 months after recovery from
COVID-19, what indicated the necessity for long-term monitoring and timely treatment of these patients.

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References

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doi.org/10.1371/journal.pone.0246590

Girard T.D., Thompson J.L., Pandharipande P.P. et al. Clini¬cal phenotypes of delirium during critical illness and severity of sub¬sequent long-term cognitive impairment: a prospective cohort study. Lancet Respir. Med. 2018. 6(3). Р. 213-22. doi: 10.1016/S2213- 2600(18)30062-6. PMID: 29508705; PMCID: PMC6709878.

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Desforges M., Le Coupanec A., Brison E., Meessen-Pi¬nard M., Talbot P.J. Neuroinvasive and neurotropic human respiratory coronaviruses: potential neurovirulent agents in humans. Adv. Exp. Med. Biol. 2014. 807. P. 75-96. doi:10.1007/978-81-322-1777-06.

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Sankowski R., Mader S., Valdés-Ferrer S.I. Systemic inflam¬mation and the brain: novel roles of genetic, molecular, and environ¬mental cues as drivers of neurodegeneration. Front. Cell. Neurosci. 2015. 9(28). P. 28. doi:10.3389/fncel.2015.00028.

Panariello F., Cellini L., Speciani M., De Ronchi D., Atti A.R. How Does SARS-CoV-2 Affect the Central Nervous System? A Wor-king Hypothesis. Front. Psychiatry. 2020. 11. P. 582345. doi: 10.3389/ fpsyt.2020.582345.

Hoffmann M., Kleine-Weber H., Schroeder S. et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell. 2020. 181(2). P. 271-280.

doi:10.1016/j.cell.2020.02.052.

Chen R., Wang K., Yu J. et al. The Spatial and Cell-Type Distribution of SARS-CoV-2 Receptor ACE2 in the Human and Mouse Brains. Front Neurol. 2021. 11. P. 573095. doi: 10.3389/ fneur.2020.573095.

Shang J., Wan Y., Luo C.et al. Cell entry mechanisms of SARS-CoV-2. Proc Natl Acad Sci USA. 2020. 117. P. 11727-34.

doi: 10.1073/pnas.2003138117.

Lazaroni T.L.N., Raslan A.C.S., Fontes W.R.P. et al. Angio¬tensin-(1–7)/Mas axis integrity is required for the expression of object recognition memory. Neurobiol. Learn. Mem. 2012. 97. P. 113-23.

doi: 10.1016/j.nlm.2011.10.003.

Wang X.-L., Iwanami J., Min L.-J. et al. Deficiency of angiotensin-converting enzyme 2 causes deterioration of cognitive function. NPJ Aging Mech. Dis. 2016. 2. P. 16024. doi: 10.1038/ npjamd.2016.24.

Kehoe P.G., Hibbs E., Palmer L.E., Miners J.S. Angiotensin- III is Increased in Alzheimer’s Disease in Association with Amyloid-β and Tau Pathology. J. Alzheimers Dis. 2017. 58(1). P. 203-214. doi: 10.3233/JAD-161265. PMID: 28387670.

Miners J.S., Ashby E., Van Helmond Z. et al. Angiotensin-converting enzyme (ACE) levels and activity in Alzheimer’s disease, and relationship of perivascular ACE-1 to cerebral amyloid angio-pathy. Neuropathol. Appl. Neurobiol. 2008. 34(2). P. 181-93. doi: 10.1111/j.1365-2990.2007.00885.x.

Miners S., Ashby E., Baig S. et al. Angiotensin-converting enzyme levels and activity in Alzheimer’s disease: differences in brain and CSF ACE and association with ACE1 genotypes. Am. J. Transl. Res. 2009. 1(2). P. 163-77. PMID: 19956428.

Miners S., Kehoe P.G., Love S. Cognitive impact of COVID-19: looking beyond the short term. Alzheimers Res. Ther. 2020. 12(1). P. 170. doi: 10.1186/s13195-020-00744-w.

Huang C., Wang Y., Li X. et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China [published cor¬rection appears in Lancet. 2020 Jan 3]. Lancet. 2020. 395(10223). P. 497-506. doi:10.1016/S0140-6736(20)30183-5.

Chakrabarty T., Torres I.J., Bond D.J., Yatham L.N. In¬flammatory cytokines and cognitive functioning in early-stage bipolar I disorder. J. Affect. Disord. 2019. 245. P. 679-685. doi: 10.1016/j. jad.2018.11.018.

Duarte P.O., Duarte M.G.F., Pelichek A., Pfrimer K., Fer¬riolli E., Moriguti J.C., Lima N.K.C. Cardiovascular risk factors and inflammatory activity among centenarians with and without dementia. Aging Clin. Exp. Res. 2017. 29(3). P. 411-417. doi: 10.1007/s40520- 016-0603-9.

Zheng F., Xie W. High-sensitivity C-reactive protein and cog¬nitive decline: the English Longitudinal Study of Ageing. Psychol. Med. 2018. 48(8). P. 1381-1389. doi: 10.1017/S0033291717003130.

Zhou H., Lu S., Chen J. et al. The landscape of cognitive function in recovered COVID-19 patients. J. Psychiatr. Res. 2020. 129. P. 98-102. doi:10.1016/j.jpsychires.2020.06.022.

Vintimilla R., Hall J., Johnson L., O’Bryant S. The re¬lationship of CRP and cognition in cognitively normal older Mexican Americans: A cross-sectional study of the HABLE co¬hort. Medicine (Baltimore). 2019. 98(19). e15605. doi:10.1097/ MD.0000000000015605.

Han H.B., Lee K.E., Choi J.H. Functional Dissociation of θ Oscillations in the Frontal and Visual Cortices and Their Long-Range Network during Sustained Attention. eNeuro. 2019. 6(6). ENEU¬RO.0248-19.2019. doi:10.1523/ENEURO.0248-19.2019.

Mitko A., Rothlein D., Poole V. et al. Individual differences in sustained attention are associated with cortical thickness. Hum. Brain Mapp. 2019. 40(11). P. 3243-3253. doi:10.1002/hbm.24594.

Sasannejad C., Ely E.W., Lahiri S. Long-term cognitive im¬pairment after acute respiratory distress syndrome: a review of clinical impact and pathophysiological mechanisms.Crit.Care Lond. Engl. 2019. 23. 352. doi:10.1186/s13054-019-2626-z.

Wilcox M.E., Brummel N.E., Archer K. et al. Cognitive dysfunction in ICU patients: risk factors, predictors, and rehabilita¬tion interventions. Crit. Care Med. 2013. 41. S81-98. doi:10.1097/ CCM.0b013e3182a16946.

Mikkelsen M.E., Christie J.D., Lanken P.N. et al. The adult respiratory distress syndrome cognitive outcomes study: long-term neuropsychological function in survivors of acute lung injury. Am. J. Respir. Crit. Care Med. 2012. 185. P. 1307-1315. doi:10.1164/rccm. 201111-2025OC.

Beaud V., Crottaz-Herbette S., Dunet V. et al. Pat¬tern of cognitive deficits in severe COVID-19. J. Neurol Neuro¬surg. Psychiatry. 2021. 92. P. 67-568. doi: 10.1136/jnnp-2020- 325173.

Hopkins R.O., Weaver L.K., Collingridge D. et al. Two-year cognitive, emotional, and quality-of-life outcomes in acute respira¬tory distress syndrome. Am. J. Respir. Crit. Care Med. 2005. 171(4). P. 340-7. doi: 10.1164/rccm.200406-763OC.

Helms J., Kremer S., Merdji H. et al. Delirium and en¬cephalopathy in severe COVID-19: a cohort analysis of ICU pa¬tients. Crit. Care. 2020. 24(1). P. 491. doi: 10.1186/s13054-020- 03200-1.

Hopkins R.O., Gale S.D., Weaver L.K. Brain atro¬phy and cognitive impairment in survivors of Acute Respira¬tory Distress Syndrome. Brain Inj. 2006. 20(3). P. 263-71. doi: 10.1080/02699050500488199.

Maydych V. The Interplay Between Stress, Inflammation, and Emotional Attention: Relevance for Depression. Front Neurosci. 2019. 13. P. 384. doi: 10.3389/fnins.2019.00384.

Carfì A., Bernabei R., Landi F. Gemelli Against COVID-19 Post-Acute Care Study Group. Persistent Symptoms in Patients After Acute COVID-19. JAMA. 2020. 324(6). P. 603-605. doi: 10.1001/ jama.2020.12603.

Garrigues E., Janvier P., Kherabi Y. et al. Post-discharge persistent symptoms and health-related quality of life after hospi¬talization for COVID-19. J. Infect. 2020. 81. e4-e6. doi:10.1016/j. jinf.2020.08.029.

Mahase E. Long covid could be four different syndromes, review suggests. BMJ. 2020. 371. m3981. doi: 10.1136/bmj.m3981.

Miskowiak K.W., Johnsen S., Sattler S.M. et al. Cogni¬tive impairments four months after COVID-19 hospital discharge: Pattern, severity and association with illness variables. Eur. Neu¬ropsychopharmacol. 2021. 46. P. 39-48. doi: 10.1016/j.euroneu¬ro.2021.03.019.

Vinkers C.H., van Amelsvoort T., Bisson J.I. et al. Stress resi-lience during the coronavirus pandemic. Eur. Neuropsychopharmacol. 2020. 35. P. 12-16. doi: 10.1016/j.euroneuro.2020.05.003.

Folstein M., Folstein S., McHugh PR. Mini-mental state: a practical method for grading the cognitive state ofpatients for the clinical //J. Psychiatr. Res. - 1975. - Vol. 12. - P. 189-198.