[Concept, pathophysiology and treatment for branch atheromatous disease].

Small deep brain infarcts are often caused by two different vascular pathologies: 1. atheromatous occlusion at the orifice of large caliber penetrating arteries termed branch atheromatous disease (BAD) and 2. lipohyallinotic degenerative changes within the course of penetrating arteries termed lipohyalinitic degeneration. Representative vascular territories of BAD type infarcts are lenticulostriate artery (LSA), pontine paremedian artery (PPA) and less frequently anterior choroidal artery. BAD type infarcts are strongly associated with progressive motor deficits (PMD) leading to a worse functional outcome, because they affect pyramidal tract at corona radiata, pontine base or internal capsule. In our study, female sex and initial severity of motor deficits were common predictors for PMD in both groups with LSA and PPA. Single infarcts without concomitant silent lacunar infarcts and preceding lacunar transient ischemic attack (TIA) in the LSA group, and diabetes mellitus in the PPA group were independent predictors for PMD in penetrating artery infarctions. There were different characteristics between the groups of LSA and PPA. Prevalence of male gender, diabetes mellitus and intracranial atherosclerosis were significantly higher in the PPA group than in the LSA group. The combined treatment of cilostazol and edarabone significantly improved functional outcome especially in the PPA infarct group. Adjoining clopidgrel on aforementioned combined treatment further improved functional outcome in the LSA group. The actions of vasodilatation and endothelial protection in cilostazol and inhibition of shear-induced platelet activation in clopidogrel, as well as scavenging free radicals in edaravone might work effectively.