Vascular cognitive impairment (VCI) defines a continuum of disorders ranging from mild cognitive impairment to full-blown dementia, attributable to cerebrovascular causes. Major morphological types - multi-infarct encephalopathy, strategic infarct type, subcortical arteriosclerotic leukoencephalopathy, multilacunar state, postischemic encephalopathy - result from systemic, cardiac and local large or small vessel disease. Cognitive decline is commonly caused by widespread small cerebrovascular lesions (CVLs) affecting regions/networks essential for cognition, memory and behavior. CVLs often coexist with Alzheimer-type and other pathologies, which interact in promoting dementia, but in many nondemented elderly individuals, mixed brain pathologies are also present. Due to the high variability of CVLs, no validated clinical and neuropathological criteria for VCI are available. Cholinesterase inhibitors and memantine produce small cognitive improvement but without essential effect. Antihypertensive treatment, cardiovascular control and lifestyle modifications reducing vascular risk factors are essential. Given its growing health, social and economic burden, prevention and treatment of VCI are a major challenge of neuroscience.
Keywords: cerebrovascular lesions; large and small vessel disease; neuropathology; pathogenic factors; prevention and therapeutics; subcortical vascular lesions; vascular cognitive impairment.