Fiona Smith1, Hanan Mardini, Christopher Record, Andrew M. Blamire1
1Newcastle MR Centre & Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, United Kingdom
Liver cirrhosis kills more than 750,000 people worldwide each year. Almost 30% of patients with cirrhosis experience hepatic encephalopathy (HE), a neuropsychiatric complication potentially linked to formation of cerebral edema driven by elevated blood ammonia. We used DTI and proton MRS to monitor edema and metabolite changes during induced hyperammonaemia by amino acid challenge in HE patients. Elevated blood ammonia was accompanied by increased ADC and decreased myo-Inositol. Absolute increase in blood ammonia significantly correlated with ADC and inversely correlated with myo-Inositol in the individual patients strongly supporting ammonia driven brain edema as a neurochemical mechanism for HE in cirrhosis.