Abstract
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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