| Autor: |
Voznyuk, I. A., Pivovarova, L. P., Gogoleva, E. A., Osipova, I. V., Ariskina, O. B., Morozova, E. M., Chernyavsky, I. V., Markelova, E. V. |
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| Zdroj: |
Neuroscience & Behavioral Physiology; May2023, Vol. 53 Issue 4, p503-508, 6p |
| Abstrakt: |
Objectives. To study the pathogenetic and clinical significance of hypoxic brain damage and inflammatory mediators as factors in the development of cerebral stroke and to improve diagnosis using laboratory markers of brain damage and inflammation in patients with acute cerebrovascular accident (aCVA). Materials and methods. A total of 55 patients with ischemic-type stroke at age 74 (67; 80) years were investigated, along with a reference group consisting of 25 people without stroke at age 65 (62; 66.5) years. Depending on stroke outcome, groups of patients were formed – discharged and deceased. Patients' neurological status was assessed using standard scales and a comorbidity index. Serum and cerebrospinal fluid (CSF) concentrations of S100b protein, glial fibrillary acidic protein (GFAP), and interleukin-6 (IL-6) were determined; serum neuron-specific enolase (NSE) and cortisol were estimated by immunoenzyme assay (IFA), clinical blood tests were run, and fibrinogen content was assessed on days 1, 3, and 10 of stroke. Results. Increases in blood and CSF levels of markers of brain tissue damage and systemic inflammation in response to cerebral ischemia reflected synergy of these pathological processes in patients with stroke and their association with the severity of cerebral stroke and its outcome. Conclusions. The data obtained here indicate that the postischemic release of neuron-specific proteins, along with increases in IL-6, C-reactive protein (CRP), and cortisol levels, provide additional characterization of the severity of cerebral stroke and the body's response to damage, and also predict disease outcome. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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