Zafiris Oliver, Kircheis Gerald, Rood Hermann A, Boers Frank, Häussinger Dieter, Zilles Karl
Institute of Medicine, Research Center Jülich, Germany.
Neuroimage. 2004 Jun;22(2):541-52. doi: 10.1016/j.neuroimage.2004.01.038.
An altered brain metabolism in the parietal and prefrontal regions of the cerebral cortex as well as cognitive alterations have been found in patients suffering from hepatic encephalopathy. The neural mechanisms underlying these metabolically induced cognitive alterations, however, are not known. Since patients with liver cirrhosis without clinically overt encephalopathy already show an impaired performance in a flicker light test, the aim of this study was to analyze the normal and pathologically impaired neural mechanisms of these patients using functional magnetic resonance imaging (fMRI). Nine subjects at the early stage of encephalopathy [nonmanifest hepatic encephalopathy (nmHE)] and ten controls underwent scanning, while they indicated the apparent transition from a steady light to the onset of a flicker light, that is, the critical flicker frequency (CFF). Judgement-related blood oxygenation level-dependent (BOLD) activation was decreased in nmHE compared to controls in the right inferior parietal cortex (IPL). Furthermore, the analysis of psychophysiologic interaction suggests impaired neural interaction in patients with nmHE, especially between the IPL and the parietooccipital cortex (Poc), the intraparietal sulcus, the anterior cingulate cortex (ACC), the right prefrontal cortex (PFC), the medial temporal lobe, and the extrastriate cortex V5. In contrast, nonmanifest patients revealed an enhanced coupling between IPL and the postcentral cortex. Our findings provide evidence of an early-impaired and compensatory neural mechanism during visual judgement already in the earliest stages of hepatic encephalopathy and suggest an aberrant coupling between cerebral regions in the dysmetabolic brain.
在肝性脑病患者中,已发现大脑皮层顶叶和前额叶区域的脑代谢改变以及认知改变。然而,这些代谢诱导的认知改变背后的神经机制尚不清楚。由于无临床明显脑病的肝硬化患者在闪烁光测试中已表现出功能受损,本研究的目的是使用功能磁共振成像(fMRI)分析这些患者正常和病理受损的神经机制。9名处于脑病早期[非显性肝性脑病(nmHE)]的受试者和10名对照组接受了扫描,同时他们指出从稳定光到闪烁光开始的明显转变,即临界闪烁频率(CFF)。与对照组相比,nmHE患者右侧顶下小叶(IPL)中与判断相关的血氧水平依赖(BOLD)激活降低。此外,心理生理相互作用分析表明,nmHE患者存在神经相互作用受损,尤其是在IPL与顶枕叶皮层(Poc)、顶内沟、前扣带回皮层(ACC)、右侧前额叶皮层(PFC)、内侧颞叶和纹外皮层V5之间。相比之下,非显性患者显示IPL与中央后皮层之间的耦合增强。我们的研究结果提供了证据,表明在肝性脑病的最早阶段,视觉判断过程中已经存在早期受损和代偿性神经机制,并提示代谢异常大脑中脑区之间存在异常耦合。