7 This finding is consistent with the results of studies using magnetization transfer, an MR sequence that enables selleck compound indirect estimate of the accumulation of water in the brain.8 However, contrary to what would be expected from the pathogenetic hypothesis of edema secondary to astrocyte swelling, diffusion-weighted imaging in cirrhosis suggests that the increased water content is located in the extracellular compartment.9 Diffusion imaging analysis using a biexponential approach (in contrast to standard monoexponential analysis) supports the presence of two components that can be ascribed to water bound to membranes (mostly intracellular) or unbound to membranes (mostly extracellular). Although the interpretation is controversial, the results of applying this method in cirrhosis patients are in accordance with an increase in water content in the extracellular compartment.

10 Most studies of MR related to HE have been performed in patients with cirrhosis (chronic liver damage) with only minimal HE (no obvious changes in mental status). There are few data in episodic HE with follow-up. Only one study11 has controlled for individual variables by reassessing the same patient during HE and after recovery. This study showed at baseline the characteristic pattern associated with HE: an increase in the Glx peak (a combination of glutamate and glutamine) and a decrease in myo-inositol and choline derivatives. The study by Poveda also showed a decrease in apparent diffusion coefficient (ADC) after improvement of HE, which was interpreted as water flux from extracellular to intracellular compartments and the existence of vasogenic brain edema during HE.

However, they could not relate changes in MR spectrum to HE, which may be explained by the use of a 1.5 Tesla (1.5-T) scanner and by the fact that the interval between grading HE and MR imaging (MRI) assessment was up to 24hours. The aim of this study was to investigate brain water and metabolite changes in patients with cirrhosis and HE and relate them to the time course and severity of the condition. The MR was performed with a 3-T scanner, which allows specific assessment of brain glutamine,12 a key factor in ammonia-related neurotoxicity.13 The ultimate purpose was to obtain further data related to the pathogenesis of HE and to seek potential diagnostic biomarkers of this condition.

In addition, astroglial protein S100 beta concentration, an indicator of glial injury and BBB dysfunction,14, 15 was assessed in serum. Materials and methods Design In this prospective study, clinical and brain MRI characteristics were assessed in a group of cirrhosis patients admitted to the hospital for an episode of overt HE. The patients were clinically stable and had no manifestations Entinostat of neurologic impairment before the HE episode (within 5 days before admission).