GABA abnormalities are thought to contribute to hepatic encephalopathy, perhaps mediated by branched chain and aromatic amino acids acting as false neurotransmitters [31] . Excess GABA activity, such as that which occurs after withdrawal from chronic ethanol or benzodiazepine use, is a well known and quite dangerous cause of delirium [32] . Acutely, sedatives that stimulate GABA receptors, such as benzodiazepines and (probably) propofol, impair cognitive function and are deliriogenic [8, [33] [34] [35] . This raises the possibility that strategies to minimize sedative drug accumulation, such as daily interruption of sedative infusions [36] , which have been shown to reduce duration of mechanical ventilation, and ICU and hospital length of stay, might also reduce the incidence or duration of delirium. Whether these sedative drugs lead to neurocognitive deficits long after their use is unknown, but this has been suggested in certain high-risk groups, such as the very old (>75 years) and those with pre-existing cognitive impairment [37, 38] .