Pathophysiology and Optimal Treatment of Intracranial Branch Atheromatous Disease

Abstract

Intracranial branch atheromatous disease (BAD) is a pathological condition characterized by the occlusion of a relatively large perforating branch (700-800 µm) near the orifice of a parent artery due to atherosclerotic plaque-based thrombus (microatheroma). BAD is refractory to treatment and follows a course of progressive exacerbation, especially motor paralysis. Uniform treatment for common atherothrombotic cerebral infarction or lacunar infarction does not prevent the progressive exacerbation of BAD, and consequently affects functional prognosis. To date, various combinations of treatments have been investigated and proposed to attenuate the worsening symptoms of BAD. However, no therapy with established efficacy is yet available for BAD. Since it is the most difficult condition to treat in the area of cerebral infarction, the establishment of optimal treatment methods for BAD is keenly awaited. This review presents an overview of the acute treatments available for BAD and discusses the prospects for optimal treatment.

Keywords: Alteplase; Branch atheromatous disease; Dual-antiplatelet treatment; Lenticulostriate artery.

Fig.1. Schematic diagram of a perforating branch lesions of the middle cerebral artery causing the branch atheromatous disease (BAD) or lacunar infarction

The branches of the lenticulostriate arteries (LSA) are thicker and steeply angled toward the outer side of M1 and run in the opposite direction of blood flow in M1, i.e., inward. These anatomical characteristics of LSA are based on the generation of microatheroma, leading to platelet activation by shear stress. Some LSAs may have lipohyalinosis, which causes lacunar infarction instead of BAD. Solid circles, enlarged views of inside of the blood vessel ACA, anterior cerebral artery; ICA, internal carotid artery; MCA M1, proximal segment of the middle cerebral artery