RESUMO
Hepatic myelopathy is a complication seen in patients with chronic liver failure with physiologic or iatrogenic portosystemic shunting. The main symptom is progressive lower limb dyskinesia. The role of the brain motor control center in hepatic myelopathy is unknown. This study aimed to investigate the gray matter changes in patients with hepatic myelopathy secondary to transjugular intrahepatic portosystemic shunt and to examine their clinical relevance. This was a cross-sectional study. Twenty-three liver failure patients with hepatic myelopathy (hepatic myelopathy group), 23 liver failure patients without hepatic myelopathy (non-hepatic myelopathy group) after transjugular intrahepatic portosystemic shunt, and 23 demographically matched healthy volunteers were enrolled from March 2014 to November 2016 at Xijing Hospital, Air Force Military Medical University (Fourth Military Medical University), China. High-resolution magnetization-prepared rapid gradient-echo brain imaging was acquired. Group differences in regional gray matter were assessed using voxel-based morphometry analysis. The relationship between aberrant gray matter and motor characteristics was investigated. Results demonstrated that compared with the non-hepatic myelopathy group, gray matter volume abnormalities were asymmetric, with decreased volume in the left insula (P = 0.003), left thalamus (P = 0.029), left superior frontal gyrus (P = 0.006), and right middle cingulate cortex (P = 0.021), and increased volume in the right caudate nucleus (P = 0.017), corrected with open-source software. The volume of the right caudate nucleus in the hepatic myelopathy group negatively correlated with the lower limb clinical rating of the Fugl-Meyer Assessment (r = -0.53, P = 0.01). Compared with healthy controls, patients with and without hepatic myelopathy exhibited overall increased gray matter volume in both thalami, and decreased gray matter volume in both putamen, as well as in the globus pallidus, cerebellum, and vermis. The gray matter abnormalities we found predominantly involved motor-related regions, and may be associated with motor dysfunction. An enlarged right caudate nucleus might help to predict weak lower limb motor performance in patients with preclinical hepatic myelopathy after transjugular intrahepatic portosystemic shunt. This study was approved by the Ethics Committee of Xijing Hospital, Air Force Military Medical University (Fourth Military Medical University), China (approval No. 20140227-6) on February 27, 2014.
RESUMO
We aimed to detect alterations in diffusion characteristics of brain white matter in hepatic myelopathy (HM) patients. Liver cirrhosis patients with (n=25) and without (n=18) HM after transjugular intrahepatic portosystemic shunt and 26 healthy controls were enrolled in this study. All participants were scanned with diffusion tensor imaging on a 3T Siemens scanner. Tract-based spatial statistics analysis was used to detect abnormalities of intracranial white matter tracts. Correlations between clinical characteristics and diffusion metrics were also calculated. HM patients showed widespread decreased fractional anisotropy values in association fibers, callosal fibers, thalamic fibers, and limbic system fibers (P<0.01, family-wise error-corrected) compared with healthy controls. In addition, HM patients showed lower fractional anisotropy values in the corpus callosum, corona radiata, external capsule, and superior longitudinal fasciculus compared with cirrhosis patients without myelopathy (P<0.01, family-wise error-corrected). Furthermore, limb muscle strength grading was correlated with the diffusion characteristics of the corpus callosum and superior longitudinal fasciculus in HM patients (P<0.05). HM patients suffer from more distinct changes of white matter fiber tracts than cirrhosis patients without myelopathy. In addition, alterations of the corpus callosum and superior longitudinal fasciculus may be associated with the major motor disturbance in HM. Our finding may shed light on the underlying neuropathological mechanism of HM.