Gadolinium ethoxybenzyl-diethylenetriaminepentaacetic acid is a hepatobiliary-specific contrast agent used for enhanced magnetic resonance imaging (EOB-MRI). It can provide specific information on hepatobiliary phase images. In addition to dynamic contrast studies, it is excellent for the detection and characterization of liver lesions.

　Various benign neoplastic and non-non-neoplastic liver lesions have been reported. Among them, benign hepatocellular nodules, including focal nodular hyperplasia (FNH), FNH-like lesions, and hepatocellular adenoma with β-catenin mutation, can be characterized as hyperintensity in hepatobiliary phase images. Arterio-portal shunts can be accurately diagnosed by being detected in hepatobiliary phase images. In addition to focal nodular lesions, EOB-MRI has affected the diagnosis and detection of impaired sinusoidal perfusion disorders, such as sinusoidal obstruction syndrome and porto-sinusoidal vascular disorder. The distinctive features of EOB-MRI have made it indispensable for the diagnosis of benign neoplastic and non-neoplastic liver lesions in clinical settings over the past 15 years.

　Moyamoya disease is a rare cerebrovascular disease of unknown origin that causes stenooclusive changes in major intracranial arteries and chronic cerebral ischemia. Although no fundamental cure exists, revascularization surgery can improve cerebral ischemia. Recent studies have shown that patients with moyamoya disease suffer from central nervous system (CNS) interstitial fluidopathy. Imaging findings of CNS interstitial fluidopathy reported in this disease include enlarged perivascular spaces, white matter hyperintensity, medullary streaks, interstitial free water measured with multi-shell diffusion magnetic resonance imaging, an index of diffusivity along the perivascular spaces, choroid plexus perfusion, and volume. These changes are, at least in some parts, reversible if revascularization surgery improves the cerebral ischemia. Decreased arterial input may result in disrupted function of intramural peri-arterial drainage pathways and the glymphatic system, and thus, disrupted CSF homeostasis. Because arterial input is a driving force of waste clearance in the brain, it is reasonable to infer that disrupted CSF homeostasis under chronic cerebral ischemia induces pathological changes in Alzheimer’s disease. However, regarding this aspect serum biomarkers and positron emission tomography studies have not revealed amyloid beta accumulation in patients with moyamoya disease. Further studies are required to investigate whether CSF interstitial fluidopathy in moyamoya disease should be the treatment target for neuronal damage induced by chronic cerebral ischemia.