Current rodent models to study HE include models of acute and chronic liver failure (Butterworth et al. 2009; Diaz-Gomez et al. 2011). According to the International Society for Hepatic Encephalopathy, however, “At this time, there are no satisfactory animal models of Type C HE resulting from end-stage alcoholic liver disease or viral hepatitis, the most common etiologies encountered in patients” (Butterworth et al. 2009, p. 783). In addition, no MR-imaging studies to date have used rodent models of HE. Imaging studies in cats, dogs, and monkeys (Moon et al. 2012; Torisu et al. 2005; Zhou et al. 2012) typically recapitulate the human condition, showing nonspecific sulcal widening and hyperintensities in lentiform nuclei (i.e., putamen and globus pallidus of the basal ganglia) (Torisu et al. 2005; Zhou et al. 2012). Animal models of HE have been used to evaluate potential mechanisms of pathology, such as the contribution of excess ammonia in the blood (i.e., hyperammonemia) (Cauli et al. 2014) or lactate (Bosoi et al. 2014). Animal models of HE have also been used to explore treatment strategies for HE (e.g., hypothermia) (Barba et al. 2008).
