Brain metabolism in minimal hepatic encephalopathy assessed by 3.0-Tesla magnetic resonance spectroscopy

2015 ◽  
Vol 46 (4) ◽  
pp. 269-276 ◽  
Author(s):  
Yohei Kooka ◽  
Kei Sawara ◽  
Ryujin Endo ◽  
Akinobu Kato ◽  
Kazuyuki Suzuki ◽  
...  
2012 ◽  
Vol 46 (5) ◽  
pp. 436-442 ◽  
Author(s):  
Irena Ciećko-Michalska ◽  
Tomasz Dziedzic ◽  
Robert Banyś ◽  
Magdalena Senderecka ◽  
Marek Binder ◽  
...  

2018 ◽  
Vol 17 ◽  
pp. 153601211774905 ◽  
Author(s):  
Su Xu ◽  
Wenjun Zhu ◽  
Yamin Wan ◽  
JiaBei Wang ◽  
Xi Chen ◽  
...  

Minimal hepatic encephalopathy (MHE) is highly prevalent, observed in up to 80% of patients with liver dysfunction. Minimal hepatic encephalopathy is defined as hepatic encephalopathy with cognitive deficits and no grossly evident neurologic abnormalities. Clinical management may be delayed due to the lack of in vivo quantitative methods needed to reveal changes in brain neurobiochemical biomarkers. To gain insight into the development of alcoholic liver disease–induced neurological dysfunction (NDF), a mouse model of late-stage alcoholic liver fibrosis (LALF) was used to investigate changes in neurochemical levels in the thalamus and hippocampus that relate to behavioral changes. Proton magnetic resonance spectroscopy of the brain and behavioral testing were performed to determine neurochemical alterations and their relationships to behavioral changes in LALF. Glutamine levels were higher in both the thalamus and hippocampus of alcohol-treated mice than in controls. Thalamic levels of taurine and creatine were significantly diminished and strongly correlated with alcohol-induced behavioral changes. Chronic long-term alcohol consumption gives rise to advanced liver fibrosis, neurochemical changes in the nuclei, and behavioral changes which may be linked to NDF. Magnetic resonance spectroscopy represents a sensitive and noninvasive measurement of pathological alterations in the brain, which may provide insight into the pathogenesis underlying the development of MHE.


2019 ◽  
Vol 70 (8) ◽  
pp. 2959-2962
Author(s):  
Cristian Scheau ◽  
Ioana Anca Badarau ◽  
Ioana Gabriela Lupescu ◽  
Ioana Raluca Papacocea ◽  
Gratiela Livia Mihai ◽  
...  

The glutamate-glutamine cycle is essential for sustaining the neuronal secretion of the excitatory neurotransmitter glutamate. Hepatic encephalopathy, even in its most discreet form, minimal hepatic encephalopathy (MHE), interferes with the glutamate and glutamine balance due to the increase in ammonia levels in the central nervous system (CNS), induced by a combination of liver dysfunction, increased blood-brain barrier permeability and many other factors. An experimental study on 21 patients with chronic liver disease and 11 healthy volunteers was performed. Magnetic resonance spectroscopy demonstrated an increase of the glutamate-glutamine complex peak, with high predictive value for MHE, especially when the metabolites are referenced to creatine, a stabile metabolite in the CNS. This paper also explores the pathophysiology of MHE with emphasis on the involvement of the glutamate-glutamine cycle in the development of this complication.


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