OBJECTIVE
To assess phenotype and identify biomarkers of cognitive impairment (CI) of varying severity in patients in the acute period of ischemic stroke (IS) based on the analysis of clinical and paraclinical indicators.
MATERIAL AND METHODS
Two hundred and forty patients with diagnosed IS and presence of CI were examined. Depending on the scores on the Montreal Cognitive Assessment Scale, patients were divided into two groups: group 1 (n=182) with mild CI, group 2 (n=58) with dementia. On admission, stroke severity according to the National Institutes of Health Stroke Scale (NIHSS), activities of daily living assessed by the Barthel Scale and patient independence assessed by the modified Rankin Scale (mRS) were determined. Neuropsychological examination was performed on day 14 and included investigation of episodic memory, executive functions, speech, gnosis, praxis, and the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) parameters. Immunological diagnostics included a study of the concentration of cytokines of various groups (interleukin (IL)-1b, IL-6, IL-16, granulocyte-macrophage colony-stimulating factor (GM-CSF), chemokines CXCL10, CXCL11, CXCL9, tumor necrosis factor α (TNFα)). Neuroimaging parameters were assessed using brain MRI data with verification of the STRIVE criteria and the medial temporal lobe atrophy scale (MTA). The standard application software package SPSS Statistics, Pandas and SciPy libraries were used for statistical analysis.
RESULTS
Patients of group 2 had lower scores in all cognitive domains with the greatest reduction in perception, constructive praxis, semantic information processing and mnestic function. These analyses revealed a higher degree of IQCODE, prevalence of features corresponding to STRIVE/MTA criteria in patients of group 2, while patients of group 1 had higher NIHSS and mRS scores. When serum concentrations of cytokines were assessed, patients of group 1 showed higher concentrations of IL-1b, IL-6, GM-CSF and TNFα, while group 2 patients had higher concentrations of cytokine CXCL10.
CONCLUSION
The presence of pre-stroke CI, baseline indicators of the patient’s functional status, neuroimaging parameters of MTA/STRIVE and age are reflected in the structure and severity of cognitive deficit in the acute period of IS. Investigation of the role of interleukins, GM-CSF, TNFα and CXCL10 in the pathogenesis of IS and their association with the progression of post-stroke CI requires further studies with a larger sample size and longer follow-up period.
