T2 hyperintensity along the cortico-spinal tract in cirrhosis relates to functional abnormalities

被引:54
作者
Córdoba, J
Raguer, N
Flavià, M
Vargas, V
Jacas, C
Alonso, J
Rovira, A
机构
[1] Univ Autonoma Barcelona, Hosp Univ Vall Hebron, Serv Med Interna Hepatol, Barcelona, Spain
[2] Univ Autonoma Barcelona, Hosp Univ Vall Hebron, Serv Neurofisiol Clin, Barcelona, Spain
[3] Univ Autonoma Barcelona, Hosp Univ Vall Hebron, Unitat Neuropsicol Geriatr, Barcelona, Spain
[4] Univ Autonoma Barcelona, Hosp Univ Vall Hebron, Unitat Ressonancia Magnet, Barcelona, Spain
关键词
D O I
10.1053/jhep.2003.50406
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Magnetic resonance has shown T2 hyperintensity along the cortico-spinal tract in the brain of cirrhotic patients. This abnormality, which is reversible after liver transplantation, appears to correspond to mild edema. Because astrocytic edema present in hepatic encephalopathy may be responsible for neuronal dysfunction, we studied whether T2 hyperintensity along the cortico-spinal tract may relate to functional abnormalities. Twenty patients with cirrhosis underwent neuropsychologic tests, neurophysiologic study of the cortico-spinal tract with transcranial magnetic stimulation, and H-1-magnetic resonance. The study was repeated 6 months after liver transplantation (n = 15) and was compared with a control group of healthy subjects (n = 11). Cirrhotic patients exhibited increased T2 signal and several functional abnormalities along the cortico-spinal tract (increased central motor conduction time, increased motor cortical threshold, and decreased motor-evoked potential amplitude). Functional abnormalities reversed after liver transplantation and were associated with normalization of T2 cortico-spinal hyperintensity and with improvement of minimal hepatic encephalopathy. In conclusion, T2 hyperintensity along the cortico-spinal tract in cirrhosis relates to functional abnormalities that are reversible after liver transplantation. These findings suggest that mild cerebral edema along the cortico-spinal pathway may cause neuronal dysfunction. These results support the participation of astrocytic edema in the pathogenesis of hepatic encephalopathy.
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页码:1026 / 1033
页数:8
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