HE, occurring in acute or chronic liver disease, including acute liver failure and cirrhosis, is believed to arise, at least partially, from high levels of ammonia circulating in the blood. HE patients may appear confused and disoriented and have poor coordination (Prakash and Mullen 2010; Vaquero et al. 2003). T1-weighted images of HE show bilateral, symmetrical, and high-intensity signals in basal ganglia structures, particularly the globus pallidus and substantia nigra (Binesh et al. 2006; Cordoba et al. 2002; Naegele et al. 2000; Pujol et al. 1996; Taylor-Robinson et al. 1995) (see figure 3). T2-weighted FLAIR images show hyperintense signals along the corticospinal tract and diffuse increases in white-matter signal intensities in the cerebral hemispheres (Rovira et al. 2002, 2008). These in vivo MR features correspond with evidence of increased numbers of nonneuronal (i.e., glial) cells called astrocytes in basal ganglia and cerebral cortex of HE brains (Caine et al. 1997). Although discriminating features of WE and HE have been outlined, these diseases can be difficult to differentially diagnose and distinguish, because patients can appear to have similar symptoms and comparable MRI results, especially among alcoholics (Thorarinsson et al. 2011).
