Stroke patients are at higher risk of developing cognitive impairment. Cognitive dysfunctions, especially progressive ones, worsen stroke prognosis and outcome. A longitudinal follow-up of cognitive disorders, however, is rendered difficult by their heterogeneity and the lack of definitions generally agreed upon. Stroke is a major cause of cognitive deficit. The identification of risk factors, clinical determinants and laboratory markers of post-stroke cognitive deficit may help detect patients at increased risk of cognitive deterioration, and prevent or delay the occurrence of poststroke cognitive impairments. Though inflammatory processes have been implicated in the pathogenesis of stroke, their role in the complex pathophysiological mechanisms of post-stroke cognitive impairment is not completely understood. Evidence suggests that elevated serum Creactive protein is associated with both the increased risk of stroke and post-stroke cognitive deficit. The hypothesis of a possible relationship between markers of systemic inflammation and cognitive dysfunctions raises the question of how rational the option of applying non-steroidal antiinflammatory drugs in a proper therapeutic window will be, especially during the acute phase of stroke, to prevent cognitive decline and dementia.

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Background/aim: Evidence suggests that the risk for dementia increases after stroke. This study investigated the dynamics of the neurological and cognitive status of patients with no baseline dementia over a 1-year period after ischemic stroke. Materials and methods:We examined 47 ischemic stroke patients admitted within 48 h of ictus. Their neurological and cognitive statuses, blood biochemical parameters, and microalbuminuria levels were prospectively evaluated over a 1-year period post-stroke.Results: A more severe neurological deficit was found in the cognitively impaired patients (P = 0.003). The NIHSS score over a 1-year follow-up period improved only in patients with normal cognition (P = 0.000). Time-varying dynamics of the MMSE score were observed in both patient groups (P = 0.000). Age (Р = 0.000), education (Р = 0.004), sex (Р = 0.041), history of diabetes (Р = 0.045), and serum high sensitive C-reactive protein (hs-CRP) on admission (Р = 0.003) were significant determinants of cognitive decline 1 year after a stroke. The albumin-to-creatinine ratio was high during the whole follow-up period in the cognitively impaired group after adjusting for sex and age (P = 0.010). Binary logistic regression showed that hs-CRP (Р = 0.013) and age (Р = 0.010) were independent predictors of patients' cognitive status 1 year after stroke. Conclusion:The level of inflammatory markers could be considered as an additional criterion of long-term cognitive impairment.

The spontaneous and the stimulated extracellular generation of reactive oxygen species (ROS) by peripheral phagocytes, the blood antioxidant capacity and the degree of oxidative damage were evaluated in patients with severe ischemic and hemorrhagic stroke in the chronic phase of disease. It was found in patients compared to the control group that: (i) the spontaneous phagocyte oxidative activity was enhanced independently of the type of stroke and the time elapsed after stroke onset; (ii) there was no difference in the extracellular ROS generation stimulated by opsonin-dependent and independent receptor mechanisms; (iii) there was no change in the indices of blood antioxidant capacity; (iv) the concentration of plasma lipid peroxides was enhanced regardless of the type of stroke, but it significantly increased over time; and (v) the concentration of blood thiobarbituric acid-reactive material was also enhanced. It was independent of the type of stroke and remained elevated during the whole period studied. We have demonstrated an enhanced spontaneous phagocyte oxidative activity and oxidative damage to lipids in patients in the chronic phase after stroke. The elimination of generated ROS and products of lipid peroxidation from the circulation could prevent the aggravation of chronic vascular injury in patients and could reduce the possibility of a subsequent stroke. This suggests the need for complex therapy, including antioxidant treatment directed to exclude the effects of free radicals, after the oxidative stress of stroke.

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The activity of peripheral phagocytes to generate reactive oxygen species (ROS) was studied in healthy individuals and patients with ischaemic stroke. The aim was to clarify the relationship between phagocyte activity, the time elapsed after the onset of disease and stroke severity. The total and extracellular production of ROS were evaluated by luminol chemiluminescence. Simultaneously the plasma oxidant activity was determined. When stimulated by opsonized zymosan, phagocytes in patients with stroke (regardless of its severity) showed fast activation. The total ROS generation increased over time in all stroke cases studied. However, the extracellular ROS generation was found to be greater in patients with severe stroke than in those with mild neurological deficiency. When stimulated by formyl-methionyl-leucyl-phenylalanine, the total oxidative phagocyte capacity (regardless of stroke severity) increased over time, but there was no change in the amount of extracellularly generated ROS. In patients with stroke the oxidant activity of plasma was enhanced. We conclude that circulating phagocytes in patients with ischaemic stroke are primed for enhanced ROS production by opsonin receptor-mediated stimulation and for increased secretion of myeloperoxidase by opsonin receptor-independent stimulation. The enhanced extracellular generation of ROS through opsonin receptor-dependent stimulation may be considered an oxidative stress biomarker in cerebral ischaemia.

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