Characterization of Cortical Microvascularization in Adult Moyamoya Disease

Abstract

Background and Purpose— Increased cortical microvascularization has been proposed to be a Moyamoya disease (MMD)–specific characteristic. It was the aim of our study to characterize the anatomic pattern and microhemodynamics of cortical microvascularization in MMD. Methods— Intraoperative indocyanine green videoangiography was performed in 16 adult MMD patients, 15 patients with atherosclerotic cerebrovascular disease (ACVD), and 10 control patients. Cortical microvascularization and microvascular hemodynamics were categorized and analyzed according to anatomic and functional indocyanine green angiographic aspects. Anatomic analysis included microvascular density, microvascular diameter, and microvascular surface per analyzed area. Microhemodynamic analysis included microvascular transit time, arterial microvascular transit time, and venous microvascular transit time. Results— Microvascular density and diameter were significantly increased in MMD patients (1.8±0.2 mm/mm 2 and 0.24±0.03 mm, respectively) compared with those in ACVD patients (1.5±0.2 mm/mm 2 and 0.20±0.02 mm, respectively) and controls (1.5±0.1 mm/mm 2 and 0.19±0.03 mm, respectively). This resulted in significantly increased microvascular surface per analyzed area in MMD (67±13%) vs ACVD patients (47±7%) and controls (45±6%). Anatomic changes were paralleled by significantly increased microvascular and arterial microvascular transit times in MMD patients (11.55±3.50 and 6.79±2.96 seconds, respectively) compared with those in ACVD patients (8.13±1.78 and 4.34±1.30 seconds, respectively) and controls (8.04±2.16 and 4.50±1.87 seconds, respectively). Conclusion— Cortical microvascularization in MMD is characterized by significantly increased microvascular density and microvascular diameter, leading to increased microvascular surface. These anatomic alterations are accompanied by prolonged microvascular hemodynamics. These observations might represent an MMD-specific compensation mechanism for impaired cerebral blood flow.