Sun Qing, Fan Wenliang, Liu Yuan, Kou Zhifeng, Han Ping
Department of Radiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hubei Provincial Clinical Research Center for Precision Radiology and Interventional Medicine, Wuhan, China.
Front Hum Neurosci. 2025 Jul 18;19:1600100. doi: 10.3389/fnhum.2025.1600100. eCollection 2025.
Although neural activity abnormalities have been reported in cirrhosis patients with minimal hepatic encephalopathy (MHE), the neurophysiological mechanisms underlying microstructural brain alterations remain poorly understood. This prospective study aimed to assess microstructural abnormalities in both gray matter and white matter of MHE patients by using diffusion kurtosis imaging (DKI), and to examine associations between these alterations and neurocognitive and clinical measurements.
Thirty-one Hepatitis B Virus-related cirrhotic patients without MHE (NMHE), thirty Hepatitis B Virus-related cirrhotic patients with MHE, and 59 gender-, age-, education-matched healthy controls underwent diffusional kurtosis imaging and neurocognitive assessments. We used tract-based spatial statistics (TBSS) analysis to estimate group differences of white matter (WM) microstructure and voxel-based morphometry analysis to determine gray matter (GM) abnormalities. Correlation analyses were further performed to assess relationships between altered diffusional parameters and clinical variables, such as neurocognitive performances and disease duration.
The TBSS analysis results showed that MHE patients had significantly decreased fractional anisotropy (FA) in the temporal part of the left superior longitudinal fasciculus and decreased kurtosis fractional anisotropy (KFA) in the left corticospinal tract and anterior thalamic radiation ( < 0.05, threshold-free cluster enhancement corrected). Notably, lower KFA in WM regions correlated with worse neurocognitive test scores in MHE patients. For GM, MHE patients exhibited increased volume of thalamus. No significant WM or GM differences were observed between NMHE patients and the other two groups.
Minimal hepatic encephalopathy patients demonstrated microstructural abnormalities in both WM and GM, predominantly affecting regions involved in cognitive, attention, and motor functions. These findings suggest that disruption of microstructural integrity may underlie the pathophysiological underpinnings of neurocognitive dysfunction in MHE, offering neuroimaging evidence for disease mechanisms.
尽管已有报道称肝硬化合并轻微肝性脑病（MHE）患者存在神经活动异常，但大脑微观结构改变背后的神经生理机制仍知之甚少。这项前瞻性研究旨在通过扩散峰度成像（DKI）评估MHE患者灰质和白质的微观结构异常，并研究这些改变与神经认知及临床指标之间的关联。
31例无MHE的乙型肝炎病毒相关肝硬化患者（非MHE组）、30例乙型肝炎病毒相关肝硬化合并MHE患者以及59名性别、年龄、教育程度匹配的健康对照者接受了扩散峰度成像和神经认知评估。我们采用基于纤维束的空间统计（TBSS）分析来估计白质（WM）微观结构的组间差异，并采用基于体素的形态计量学分析来确定灰质（GM）异常。进一步进行相关性分析以评估扩散参数改变与临床变量（如神经认知表现和病程）之间的关系。
TBSS分析结果显示，MHE患者左侧上纵束颞部的分数各向异性（FA）显著降低，左侧皮质脊髓束和丘脑前辐射的峰度分数各向异性（KFA）降低（<0.05，经无阈值簇增强校正）。值得注意的是，MHE患者白质区域较低的KFA与较差的神经认知测试分数相关。对于灰质，MHE患者丘脑体积增加。非MHE患者与其他两组之间未观察到显著的白质或灰质差异。
轻微肝性脑病患者在白质和灰质中均表现出微观结构异常，主要影响涉及认知、注意力和运动功能的区域。这些发现表明，微观结构完整性的破坏可能是MHE神经认知功能障碍病理生理基础，为疾病机制提供了神经影像学证据。
