Preclinical models of alcohol-related neurological syndromes include studies on on WE/KS and HE. A thiamine-deficient diet over 3–4 weeks can reduce thiamine, but administration of a thiamine pyrophosphokinase inhibitor such as pyrithiamine is often required to recapitulate human symptoms in animals (Hazell & Butterworth, 2009). Structural MRI findings in thiamine-deficient rats show hyperintense signals on T2-weighted images in thalamus, collicular bodies, mammillary bodies, corpus callosum, and cerebellar peduncles (Figure 2A;B) (Dror et al., 2010; Pfefferbaum, Adalsteinsson, Bell, & Sullivan, 2007; Zahr, Alt, et al., 2014). Current rodent models of HE are deemed unsatisfactory by the International Society for Hepatic Encephalopathy (Butterworth et al., 2009). Nevetheless, a study using carbon tetrachloride (CCl4) as an agent to induce acute liver failure in rodents revealed brain morphological changes in lateral ventricles (top arrow) and cisterns (Figure 2C) (Zahr, Sullivan, et al., 2016).
