Depression as the cause and consequence of cerebrovascular diseases

Recent epidemiological, clinical, neuroimaging and neuropathological studies have reported substantial evidence on the complex interactive relationships between depression and cerebrovascular diseases, especially in older populations, and plausible explanations of the etiopathogenetic mechanisms in both directions have been proposed Although there is no general consensus regarding its prevalence, it is widely accepted that major depression after stroke is common and that it should be recognized as a key factor in rehabilitation and outcome following stroke. The "vascular depression" hypothesis presupposes that late-onset depression may often result from vascular damage to frontal-subcortical circuits implicated in mood regulation. This concept has stimulated many researches and the obtained results support the proposed hypothesis. Recent large studies have emphasised the role of depression per se in the development ofsubsequent stroke. Mechanisms proposed to explain the increased risk of cerebrovascular diseases in depressed patients There are a number ofplausible mechanisms that could explain why depression may increase the risk of subsequent cerebrovascular disease, the most important being sympathoadrenal hyperactivity, platelet activation, an increase in inflammatory cytokines and an increased risk of arrhythmias. Thorough clinical examinations determining the conventional stroke risk factors in the population with depression, as well as management of depression as part of the overall measures for the reduction of cerebrovascular risk factors are of utmost importance.