Abstract
Aim. To study the role of neuroinflammation and cerebral structural factors in the development of cognitive impairment in the recovery period of ischemic stroke. 
 Methods. In 55 patients with ischemic stroke the assessment of global cognitive status in acute and recovery period of ischemic stroke, evaluation of cytokine concentrations (interleukin-1β, interleukin-4, interleukin-6, interleukin-10 and tumor necrosis factor α) in cerebrospinal fluid and blood serum, as well as a number of MRI morphometric and diffusion tensor parameters were performed. 
 Results. Predictors of stable cognitive status were low concentration of interleukin-6 and -10 and interleukin-1β and -10 dominance in cerebrospinal fluid, high fractional anisotropy of ipsilateral superior longitudinal fasciculus in the acute phase of stroke. Predictors of positive trend of cognitive status include low level of C-reactive protein, intermediate values of fractional anisotropy of the designated tract, high level of high-density lipoproteins in serum and interleukin-10 in cerebrospinal fluid, codominance of interleukin-1β and -6 in serum and interleukin-10 in cerebrospinal fluid, predominance of interleukin-10 over interleukin-1β in serum, as well as lesser degree of stenosis of the ipsilateral internal carotid artery. Predominance of interleukin-1β over interleukin-10 in serum, large volume of the brain ventricles, lower values of fractional anisotropy of ipsilateral superior longitudinal fasciculus, low level of high-density lipoproteins and greater degree of stenosis of the ipsilateral internal carotid artery can be considered as predictors of negative trend of cognitive status. 
 Conclusion. The trajectory of cognitive status in the recovery period of ischemic stroke is determined by the profile of neuroinflammation in conjunction with microstructural integrity of the ipsilateral superior longitudinal fasciculus, as well as severity of atherosclerosis of the carotid artery on the side of stroke, level of high-density lipoproteins and ventricular dilation in the acute period of the disease.
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