Intracranial branch atheromatous disease (BAD) was proposed by Caplan in order to clarify problematic cases that do not fit into the dichotomatous separations of cases into lipohyalinotic penetrating artery disease or large artery occlusive disease. Narrowing or occlusion of the mouth of the branching artery by an atheromatous plaque results in deep infarcts of more than 10mm diameter with classical lacunar syndromes including pure motor hemiparesis. Both lenticulostriate and paramedian pontine arteries are likely to be involved in BAD. Neurological worsening after admission and poor functional outcome at discharge are usually observed in BAD patients. Once the patients show any neurological or radiological sign of BAD, they are treated intensively with anti-thrombotic drug and edaravone. Plaque stabilization and improvement of endothelial function would be the therapeutic targets for treatment of BAD in the future.