No abstract

KEY WORDSHepatic encephalopathy; Brain imaging; Magnetic resonance imaging; Magnetic resonance spectroscopy, Computed tomography, Single photon emission computed tomography; Positron emission tomography. 2 SYNOPSISNovel imaging techniques are allowing hepatologists to investigate the structural and functional neuropathology of hepatic encephalopathy (HE) in greater detail but only limited techniques are applicable to the clinic. Computed tomography and magnetic resonance imaging (MRI) can rule out other diagnoses and in the case of MRI, give certain key diagnostic features in widely available sequences. While increased brain water content is a hallmark of HE, the localisation of low-grade cerebral edema, the extent of regional swelling or atrophy and the different functional characteristics of affected brain regions continue to be debated. More specialised volumetric, diffusion-tensor, magnetization transfer, functional magnetic resonance imaging and magnetic resonance spectroscopy, in conjunction with positron emission tomography continue to enrich the investigative findings in HE. Nevertheless an internationally accepted diagnostic framework that includes an objective imaging test to replace or augment psychometry remains elusive. Quantitative MRI is likely to be the best candidate to become such a test and the utility of MR and nuclear medical techniques to the clinic and results from recent research are described in this article.3

SummaryBackgroundBrain change can occur in primary biliary cholangitis (PBC), potentially as a result of cholestatic and/or inflammatory processes. This change is linked to systemic symptoms of fatigue and cognitive impairment.AimTo identify whether brain change occurs early in PBC. If the change develops early and is progressive, it may explain the difficulty in treating these symptoms.MethodsEarly disease brain change was explored in 13 patients with newly diagnosed biopsy‐proven precirrhotic PBC using magnetisation transfer, diffusion‐weighted imaging and 1H magnetic resonance spectroscopy. Results were compared to 17 healthy volunteers.ResultsCerebral magnetisation transfer ratios were reduced in early PBC, compared to healthy volunteers, in the thalamus, putamen and head of caudate with no greater reduction in patients with greater symptom severity. Mean apparent diffusion coefficients were increased in the thalamus only. No 1H magnetic resonance spectroscopy abnormalities were seen. Serum manganese levels were elevated in all PBC patients, but no relationship was seen with imaging or symptom parameters. There were no correlations between neuroimaging data, laboratory data, symptom severity scores or age.ConclusionsThis is the first study to be performed in this precirrhotic patient population, and we have highlighted that neuroimaging changes are present at a much earlier stage than previously demonstrated. The neuroimaging abnormalities suggest that the brain changes seen in PBC occur early in the pathological process, even before significant liver damage has occurred. If such changes are linked to symptom pathogenesis, this could have important implications for the timing of second‐line‐therapy use.