Alonso Juli, Córdoba Juan, Rovira Alex
Departament de Radiologia, Unitat de Ressonància Magnètica (IDI), Hospital Vall d'Hebron, Vall d'Hebron Institut of Research (VHIR), Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, Spain.
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, Spain; Departament de Medicina, Universitat Autònoma de Barcelona, Barcelona, Spain; Servei de Medicina Interna-Hepatologia, Hospital Vall d'Hebron, Vall d'Hebron Institut of Research (VHIR), Barcelona, Spain.
Semin Ultrasound CT MR. 2014 Apr;35(2):136-52. doi: 10.1053/j.sult.2013.09.008.
The term hepatic encephalopathy (HE) covers a wide spectrum of neuropsychiatric abnormalities caused by portal-systemic shunting. The diagnosis requires demonstration of liver dysfunction or portal-systemic shunts and exclusion of other neurologic disorders. Most patients with this condition have liver dysfunction caused by cirrhosis, but it also occurs in patients with acute liver failure and less commonly, in patients with portal-systemic shunts that are not associated with hepatocellular disease. Various magnetic resonance (MR) techniques have improved our knowledge about the pathophysiology of HE. Proton MR spectroscopy and T1-weighted imaging can detect and quantify accumulations of brain products that are normally metabolized or eliminated such as glutamine and manganese. Other MR techniques such as T2-weighted and diffusion-weighted imaging can identify white matter abnormalities resulting from disturbances in cell volume homeostasis secondary to brain hyperammonemia. Partial or complete recovery of these abnormalities has been observed with normalization of liver function or after successful liver transplantation. MR studies have undoubtedly improved our understanding of the mechanisms involved in the pathogenesis of HE, and some findings can be considered biomarkers for monitoring the effects of therapeutic measures focused on correcting this condition.
肝性脑病(HE)这一术语涵盖了由门体分流引起的广泛的神经精神异常。诊断需要证实肝功能障碍或门体分流,并排除其他神经系统疾病。大多数患有这种疾病的患者肝功能障碍是由肝硬化引起的,但它也发生在急性肝衰竭患者中,较少见于与肝细胞疾病无关的门体分流患者。各种磁共振(MR)技术增进了我们对肝性脑病病理生理学的了解。质子磁共振波谱和T1加权成像可以检测和量化通常会被代谢或清除的脑内产物,如谷氨酰胺和锰的蓄积。其他MR技术,如T2加权和扩散加权成像,可以识别因脑内高氨血症继发的细胞体积稳态紊乱导致的白质异常。随着肝功能正常化或成功进行肝移植后,已观察到这些异常部分或完全恢复。MR研究无疑增进了我们对肝性脑病发病机制的理解,一些研究结果可被视为生物标志物,用于监测旨在纠正这种疾病的治疗措施的效果。