Interrelation of cognitive functions and neural networks with blood flow velocity through the internal jugular vein in patients with chronic cerebral ischemia
- Authors: Fokin V.F.1, Medvedev R.B.1, Ponomareva N.V.1, Konovalov R.N.1, Lagoda O.V.1, Krotenkova M.V.1, Tanashyan M.M.1
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Affiliations:
- Research Center of Neurology
- Issue: Vol 40, No 4 (2021)
- Pages: 107-112
- Section: Original articles
- URL: https://journals.rcsi.science/RMMArep/article/view/83637
- DOI: https://doi.org/10.17816/rmmar83637
- ID: 83637
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Abstract
Understanding age-related and functional changes in cerebral venous circulation is critical for the development of new preventive, diagnostic and therapeutic approaches to maintaining brain health in the elderly. Chronic cerebral ischemia is one of the widespread socially significant vascular diseases caused by a decrease in the level of blood circulation. To assess the role of venous outflow through the internal jugular veins in cognitive decline and neural networks in patients with chronic cerebral ischemia, 30 men and 40 women (average age 66.5 years), cognitive functions and organization of neural networks were studied at high and low levels of cerebral venous blood flow through the internal jugular veins. To assess the venous outflow, the systolic blood flow rate was measured by the internal jugular veins. A higher rate of venous outflow through internal jugular veins is associated with a more successful performance of the Luria test for verbal memory. A higher or lower blood flow rate affects the formation of neural networks of the brain. At a higher blood flow rate, the predominant areas of the resting neural networks (the passive mode network of the brain and the salient network) are localized in the frontal regions, at a low blood flow rate, the predominant neural network (frontal-parietal) is located in the left hemisphere. The state of faster and slower venous outflow forms neural networks using different neural formations that affect verbal memory. Reorganization of neural networks in this case, apparently, is the central mechanism responsible for cognitive decline in chronic cerebral ischemia (2 figs, 1 table, bibliography: 10 refs)
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##article.viewOnOriginalSite##About the authors
Vitaly F. Fokin
Research Center of Neurology
Email: fvf@mail.ru
ORCID iD: 0000-0003-2915-9384
SPIN-code: 1208-3796
D.Sc. (Biology), Professor
Russian Federation, MoscowRoman B. Medvedev
Research Center of Neurology
Email: medvedev-roman@yandex.ru
ORCID iD: 0000-0003-3887-0418
Scopus Author ID: 54994882700
ResearcherId: B-5185-2012
Ph.D. (Medicine)
MoscowNatalia V. Ponomareva
Research Center of Neurology
Email: ponomare@yandex.ru
ORCID iD: 0000-0002-9771-0775
SPIN-code: 1307-3591
D.Sc. (Medicine)
Russian Federation, MoscowRodion N. Konovalov
Research Center of Neurology
Email: krn_74@mail.ru
ORCID iD: 0000-0001-5539-245X
Scopus Author ID: 23497502900
ResearcherId: B-6834-2012
Ph.D. (Medicine)
Russian Federation, MoscowOlga V. Lagoda
Research Center of Neurology
Email: olga.lagoda@gmail.com
ORCID iD: 0000-0001-7562-4991
Scopus Author ID: 6507370001
ResearcherId: C-5395-2012
Ph.D. (Medicine)
Russian Federation, MoscowMarina V. Krotenkova
Research Center of Neurology
Email: krotenkova_mrt@mail.ru
ORCID iD: 0000-0003-3820-4554
Scopus Author ID: 23497494200
ResearcherId: B-5783-2012
D.Sc. (Medicine)
Russian Federation, MoscowMarine M. Tanashyan
Research Center of Neurology
Author for correspondence.
Email: m_tanashyan2004@mail.ru
ORCID iD: 0000-0002-5883-8119
Scopus Author ID: 6506228066
ResearcherId: F-8483-2014
Corresponding Member of the Russian Academy of Sciences, M.D., D.Sc. (Medicine), Professor
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