“…The present study hypothesizes that the long-term effects of isoleucine leads to a higher increase in cerebral perfusion than that obtained by leucine, thus promoting different degrees of recovery from HE according to the amino acid received by the subjects. Hence, the study was focused on brain areas that are known for being more affected by hypoperfusion, such as the basal ganglia ( Bizzi et al, 1996 ; Kumar et al, 1991 ; Sims and Pulsinelli, 1987 ), as well as regions where altered perfusion was already reported in HE and/or acquired hepatocerebral degeneration, such as the hippocampus, prefrontal cortex, medial temporal cortex, anterior cingulate cortex and parietooccipital regions ( Lockwood et al, 1993 ; O'Carroll et al, 1991 ; Sunil et al, 2012 ; Ueki et al, 2002 ; Zafiris et al, 2004 ). Perfusion alterations in some of these regions were already associated with HE symptoms in prior studies, while some areas were reported as having dissimilar blood flow responses after BCAA administration ( Catafau et al, 2000 ; Iwasa et al, 2003 ; Lockwood et al, 1993 ; O'Carroll et al, 1991 ; Ueki et al, 2002 ).…”