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.