Prevention and management of cerebral small vessel disease

Abstract

Lacunar infarcts/lacunes, white matter hyperintensities (WMH), and cerebral microbleeds (CMBs) are considered various manifestations of cerebral small vessel disease (SVD). Since the exact mechanisms of these manifestations differ, their associated risk factors differ. High blood pressure is the most consistent risk factor for all of these manifestations. How­ever, a “J curve” phenomenon in terms of blood pressure probably exists for WMH. The as­sociation between cholesterol levels and lacunar infarcts/lacunes or WMH was less consis­tent and sometimes conflicting; a low cholesterol level probably increases the risk of CMBs. Homocysteinemia appears to be associated with WMH. It is noteworthy that the risk factors profile may also differ between different lacunar patterns and CMBs located at different parts of the brain. Thrombolysis, antihypertensives, and statins are used to treat patients with symptomatic lacunar infarction, just as in those with other stroke subtypes. However, it should be remembered that bleeding risks increase in patients with extensive WMH and CMBs after thrombolysis therapy. According to the Secondary Prevention of Small Subcorti­cal Strokes trial results, a blood pressure reduction to <130 mmHg is recommended in pa­tients with symptomatic lacunar infarction. However, an excessive blood pressure decrease may induce cognitive decline in older patients with extensive WMH. Dual antiplatelet ther­apy (aspirin plus clopidogrel) should be avoided because of the excessive risk of intracere­bral hemorrhage. Although no particular antiplatelet is recommended, drugs such as cilo­stazol or triflusal may have advantages for patients with SVD since they are associated with less frequent bleeding complications than aspirin.