Role of MRI in detection of minimal hepatic encephalopathy

Hepatic encephalopathy (HE) is a metabolic induced disorder of the brain which is induced by acute or chronic liver disease. HE usually presents with a whole spectrum of neurological symptoms. Minimal HE (mHE) represents the starting point of this spectrum with no neurological symptoms but usually with cognitive deficits, which can be assessed by cognitive testing only. Recent studies have shown, that cognition in mHE can be improved if treatment starts early. However, a prerequisite for treatment are sensitive diagnostic tools. In this context, magnetic resonance imaging (MRI) of the brain is one of the most promising methods because it has the potential to depict mHE related tissue changes. In this international research project, research teams from the Medical University Graz and the Medical Faculty of the University of Ljubljana will evaluate newest MRI sequences to improve the detection of mHE related brain changes und to improve the understanding of the patholphysiological mechanisms behind mHE.

Our international project, that was performed in collaboration with the Medical University of Ljubljana, aimed to investigate brain changes in patients with liver cirrhosis using magnetic resonance imaging (MRI) techniques. This study included 34 patients with liver cirrhosis and 18 healthy controls, with no significant differences in age observed between the two groups. MR spectroscopy was used to measure levels of the metabolite GABA in the striatum region of the brain. GABA is a neurotransmitter that is relevant for communication between neurons. Patients with liver cirrhosis showed significantly Iower levels of GABA compared to healthy controls. Furthermore, a correlation was observed between Iower GABA levels and Iower cognitive scores as measured by the STROOP and PHES tests. Quantitative susceptibility mapping (QSM) was utilized to investigate susceptibility changes in multiple brain regions. The analysis revealed that significant changes in susceptibility were only found in the hippocampi and caudate accumbens regions of patients with liver cirrhosis when compared to healthy controls. This finding was confirmed using R2* mapping. We hypothesize that the observed decrease in susceptibility may be due to a higher concentration of calcium in these regions, which could be a result of altered calcium metabolism or neuro-degenerative processes associated with liver cirrhosis. Enlarged perivascular spaces may also have contributed to our findings. Overall, our study suggests that liver cirrhosis is associated with changes in brain metabolites and susceptibility in specific regions. The observed decrease in susceptibility in the hippocampi and caudate-accumbens regions may indicate altered neuronal function or structure, which could contribute to the cognitive deficits observed in patients with liver cirrhosis. Further studies are needed to explore the underlying mechanisms and potential therapeutic targets for this condition.